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Columbia  SJntomitp 
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College  of  SßfasLitiansL  anb  burgeon« 
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PRE  SBNTED  IN  ME  MORY  OP 

WILLIAMHENRYDRAPER 

1830-1901- P  and  S-1855 
AND  HIS  SON 

WIMJÄM  KINNICUTT  DRAPER  | 
1863-1926-P.AND  S-1888 


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http://www.archive.org/details/textbookofmedici1893str 


A 

TEXT-BOOK  OF  MEDICINE 


FOR  STUDENTS  AND  PRACTITIONERS 


BY 

Dk.   ADOLF    STRÜMPELL 

PROFESSOR  AND   DIRECTOR   OF   THE   MEDICAL   CLINIQUE   AT   ERLANGEN 


Scconb  American  (Edition 

TRANSLATED  BY  PERMISSION  FROM  THE  SECOND  AND  THIRD,  AND 
THOROUGHLY  REVISED  FROM  THE  SIXTH  GERMAN  EDITION,  BY 

HERMAN  F.  VICKERY,    A.B.,    M.D. 

INSTRUCTOR  IN  CLINICAL  MEDICINE,  HARVARD  UNIVERSITY;   PHYSICIAN  TO  OUT-PATIENTS,  MASSACHUSETTS 
GENERAL    HOSPITAL  ;   FELLOW    OF   THE    MASSACHUSETTS   MEDICAL    SOCIETY,   ETC. 

AND 

PHILIP  COOMBS  KNAPP,    A.M.,    M.D. 

CLINICAL   INSTRUCTOR   IN   DISEASES   OF   THE   NERVOUS    SYSTEM,  HARVARD    UNIVERSITY  ;    PHYSICIAN 

TO    OUT-PATIENTS    WITH    DISEASES   OF   THE   NERVOUS    SYSTEM,   BOSTON   CITY    HOSPITAL^ 

MEMBER   OF   THE   AMERICAN    NEUROLOGICAL   ASSOCIATION  ;   FELLOW    OF 

THE   MASSACHUSETTS   MEDICAL    SOCIETY,   ETC. 


WITH  EDITORIAL  NOTES  BY 

FREDERICK   C.   SHATTUCK,    A.M.,    M.D. 

jackson  professor  of  clinical  medicine,  harvard  university;  visiting  physician  to  the 

massachusetts  general  hospital  ;  member  of  the  association  of  american 

physicians;  fellow  of  the  Massachusetts  medical  society,  etc. 


WITH  ONE  HUNDEED   AND   NINETEEN  ILLUSTRATIONS 


NEW    YOEK 
D .    APPLETON    AND. COMPANY 

1893 


Copyright,  1886,  1893, 
By  D.   APPLETON  AND  COMPANY. 


All  rights  reserved. 


Electrotyped  and  Printed 
at  the  Appleton  Press,  U.  S.  A. 


f 


PREFACE   TO    TH^    SIXTH   EDITION. 


Although  the  fifth  edition  of  this  text-book  was  very  large,  a  year's  time 
has  brought  so  pressing  a  demand  for  a  new  one,  that  the  author,  in  preparing 
it,  has  been  obliged  to  confine  himself  to  the  most  essential  improvements  and 
additions.  There  is  an  entirely  new  chapter  on  influenza,  a  disease  which  had 
almost  been  forgotten,  when  the  last  great  epidemic  brought  it  prominently  to 
medical  attention.  Quite  important  changes  and  additions  have  been  made  in 
the  chapters  on  cholera,  malaria,  diseases  of  the  nose  and  larynx,  syringo- 
myelia, and  diabetes.  The  appendix  on  poisons  has  also  been  considerably 
enlarged. 

The  author  sends  out  this  new  edition  with  the  wish  that  it  may  not  only 
be  of  practical  benefit  to  those  for  whom  it  is  written,  but  may  also  add  to 
their  pleasure  and  interest  in  their  vocation. 

Adolf  Strümpell. 

Erlangen,  May,  1890. 


PREFACE  TO  THE  FIRST  EDITIOK 


In  the  work  which  is  now  offered  to  the  public  I  have  made  an  attempt 
to  give  an  account  of  our  present  knowledge  in  the  field  of  the  special 
pathology  and  treatment  of  internal  diseases.  This  account,  although  brief, 
I  have  endeavored  to  make  as  complete  as  possible  in  regard  to  all  impor- 
tant and  certainly  established  facts.  While  everything  hypothetical  has 
been  wholly  omitted  or  only  briefly  referred  to,  I  have  tried,  on  the  other 
hand,  not  only  to  enumerate  the  facts  of  clinical  experience  with  sufficient 
accuracy,  but  also  and  especially  to  make  the  reader  comprehend  the  develop- 
ment and  the  internal  connection  of  the  different  morbid  phenomena  by 
constantly  referring  to  the  data  of  general  pathological  and  anatomical 
research.  In  regard  to  treatment,  the  limits  of  our  knowledge  will  often  be 
apparent,  but  I  believe  that  I  have  paid  a  sufficient  regard  to  the  needs  of 
practice.  In  order  to  avoid  repetitions,  only  a  small  number  of  complete 
prescriptions  have  been  inserted  in  the  text,  but  an  abundant  and  well- 
arranged  formulary  has  been  added  as  an  appendix  at  the  end  of  the  work.* 

Although  in  the  composition  of  this  text-book  I  have  of  course  made  very 
great  use  of  the  later  literature  of  medicine,  still  the  experienced  reader 
will  recognize  in  not  a  few  places  the  results  of  the  author's  own  experience 
and  observation.  These  results  are  drawn  from  more  than  six  years*1  active 
work  in  the  medical  clinicpie  here,  to  the  abundant  material  of  which  I  have 
been  fortunate  enough  to  have  access  as  assistant  first  to  C.  Wunderlich 
and  then  to  E.  Wagner. 

Adolf  Strümpell. 

Leipsic,  1  Jlarch,  1883. 

[*  Owing  to  the  differences  between  our  Pharmacopoeia  and  practice  and  those  of  Germany,  it  has 
been  thought  best  to  omit  this  appendix.— Teahs.] 


TEANSLATOES'  PEEFAOE 
TO   THE   REVISED   EDITION. 


This  translation  is  already  used  as  a  text-book  or  as  a  work  of  reference 
in  some  twenty-eight  medical  schools  in  America,  and  we  trust  that  it  will 
continue  to  meet  with  approval.  After  preparing  this  revised  edition,  the 
translators  feel  moved  to  express  their  admiration  of  the  industry  and  care- 
fulness as  well  as  the  sound  judgment  and  great  learning  of  their  author. 
Scarcely  a  page  has  escaped  some  correction  or  addition ;  so  that  the  work 
is  thoroughly  brought  up  to  date. 

The  Tkaxslatoks. 

Boston,  June,  1892. 


TEANSLATOES1  PEEFAOE 

TO   THE   FIRST   AMERICAN  EDITION. 


This  translation  was  made  from  the  second  German  edition.  After  the 
work  had  been  sent  to  the  press  in  Ma}T,  we  learned  that  a  third  edition  of 
the  volume  on  nervous  diseases  had  appeared  in  Germany.  "We  therefore 
recalled  our  manuscript,  and  incorporated  into  it  all  the  changes  and  addi- 
tions that  had  been  made  in  that  edition. 

We  have  tried  to  make  the  translation  as  exact  as  possible,  but,  in  a  few 
instances,  we  have  taken  the  liberty  of  adding  a  word  or  a  phrase  to  make 
the  meaning  clearer.  With  Dr.  Shattuck's  approval  we  have  added  a  few 
foot-notes  to  the  section  on  nervous  diseases,  embodying  the  results  of  investi- 
gations made  subsequently  to  the  appearance  of  the  original. 

In  regard  to  the  nomenclature  of  physical  signs  in  diseases  of  the  lungs, 
we  have  departed  somewhat  from  the  original  in  order  to  have  our  nomen- 
clature conform  to  that  proposed  at  the  meeting  of  the  American  Medical 
Association  in  May,  1885/  by  the  late  Dr.  Austin  Flint,  chairman  of  a  com- 
mittee appointed  to  prepare  such  a  nomenclature  at  the  International  Medi- 
cal Congress  in  1881.  This  may  explain  certain  unusual  terms,  such  as 
"small  rales." 

We  have  not  attempted  to  adapt  the  treatment  to  the  United  States 
Pharmacopoeia.  As  a  rule,  when  the  preparation  mentioned  was  described 
in  Stille  and  Maisch's  National  Dispensatory  (second  edition,  1879),  we  have 
made  no  comment.  In  other  cases  we  have  added  the  formula  of  the  prepa- 
ration either  in  a  foot-note  or  in  parenthesis.  In  a  very  few  cases  we  have 
substituted  an  officinal  (U.  S.  P.)  preparation  which  was  almost  identical.  As 
the  metric  system  is  not  yet  in  active  use,  we  have  substituted  for  it  approxi- 
mate equivalents  in  the  old  system.  We  have  considered  it  needlessly  pre- 
cise, however,  to  give  the  exact  equivalents  in  tenths  of  a  degree  or  hun- 
dredths of  a  grain.  In  every  instance  we  have  retained  the  author's  figures 
in  parenthesis,  and  we  have  added  tables  of  weights  and  measures  in  an 
appendix.     Measures  of  length  have  been  left  in  the  metric  system. 


TRANSLATORS'  PREFACE.  vii 

In  place  of  the  original  Fig.  106,  page  763— specimens  of  handwriting  in 
general  paralysis,  in  German  script,  and  in  the  German  language— we  have 
substituted  other  specimens  selected  from  a  large  number  kindly  sent  us  by 
Dr.  E.  P.  Elliot,  first  assistant  at  the  Danvers  Lunatic  Hospital. 

Our  thanks  are  due  to  Dr.  G.  L.  Walton,  of  this  city,  for  his  assistance  at 
a  critical  moment  in  the  work,  and  to  other  friends  who  have  given  us  aid 
and  encouragement  during  the  progress  of  our  labors. 

The  Translators. 

Boston,  November,  1886. 


EDITOR'S  PREFACE. 


The  appearance  of  a  sixth  German  edition,  and  the  demand  for  a  revised 
edition  of  the  American  translation,  seem  to  show  that  the  high  estimate 
formed  of  this  work  was  reasonable. 

In  the  present  edition  some  notes  have  been  omitted,  others  changed,  and 
some  new  ones  added.  For  most  of  the  new  notes  in  the  section  on  Nervous 
Diseases  I  have  to  thank  Dr.  Knapp,  one  of  the  translators.  His  additions 
have  been  signed  "  K."  For  the  others,  with  all  sins  of  omission  and  com- 
mission, I  alone  am  responsible. 

Frederick  C.  Shattuck. 

Boston,  September,  1892. 


COIN  TENTS. 


CHAPTER 
I. 


II. 
III. 

IV. 

V. 

VI. 

VII. 


VIII. 

IX. 

X. 

XI. 

XII. 

XIII. 

XIV. 


XV. 

XVI. 

XVII. 

XVIII. 

XIX. 

XX. 

XXI. 

XXII. 

XXIII. 


Acute  General  Infectious  Diseases. 

»  PAGE 

Typhoid  Fever 1 

Phenomena  and  Complications  relating  to  the  Separate  Organs ....  9 

Peculiarities  in  the  Course  of  the  Disease 18 

Relapses  of  Typhoid  Fever    .        .        .        .  ' 19 

Typhus  Fever 28 

Relapsing  Fever 31 

Scarlet  Fever 36 

Measles 46 

Röthein .51 

Small-pox 52 

Variola  Vera 53 

Varioloid 54 

Varicella 60 

Erysipelas 61 

Diphtheria 65 

Influenza        .        . 74 

Dysentery                                .     ■ 77 

Cholera 81 

Malarial  Diseases 90 

Intermittent  Fever 92 

Pernicious  Intermittent  Fever 94 

Remittent  and  Continuous  Forms  of  Malarial  Fever  ......  95 

Chronic  Malarial  Cachexia ♦  .95 

Masked  Intermittent  Fever 95 

Typho-malarial  Fever 98 

Dengue 99 

Yellow  Fever ' 100 

Epidemic  Cerebro-spinal  Meningitis 103 

Septic  and  Pya?mic  Diseases 108 

Hydrophobia  (Rabies  canina) 113 

Glanders  (Farcy) ' 116 

Malignant  Pustule  (Anthrax.     Mycosis  intestinalis) 117 

Trichinosis 121 


Diseases  of  the  Respiratory  Organs. 
SECTION  I. 

DISEASES   OF   THE  NOSE. 


I.    Coryza    . 
II.    Chronic  Rhinitis 
III.    Nose-bleed 


125 
126 

129 


(ix") 


CONTENTS. 


SECTION  II. 

DISEASES   OF   THE   LARYNX. 
CHAPTER  pAQE 

I.    Acute  Laryngeal  Catarrh  (Acute  Laryngitis) 130 

II.     Chronic  Laryngitis  (Chronic  Laryngeal  Catarrh) 132 

III.  Laryngeal  Perichondritis 134 

IV.  CEderaa  of  the  Glottis 135 

V.     Tuberculosis  of  the  Larynx  (Consumption  of  the  Larynx) 136 

VI.     Paralyses  of  the  Laryngeal  Muscles 139 

Paralyses  in  the  Distribution  of  the  Superior  Laryngeal  Nerve  ....  139 
Paralyses  in  the  Distribution  of  the  Inferior  Laryngeal  or  Recurrent  Nerve     .  139 

VII.    Spasm  of  the  Glottis 142 

VIII.    Disturbances  of  Sensibility  in  the  Larynx 143 

IX.    New  Growths  in  the  Lai-ynx 144 

Benignant  New  Growths  in  the  Larynx 144 

Malignant  New  Growths.     Carcinoma  of  the  Larynx 145 

SECTION  III. 

DISEASES   OF   THE  TRACHEA   AND   THE   BRONCHI. 

I.    Acute  Catarrh  of  the  Trachea  and  the  Bronchi 146 

The  Milder  Forms  of  Acute  Bronchitis        . 148 

Severe  Febrile  Acute  Bronchitis 148 

Catarrh  of  the  Finer  Bronchi.     Capillary  Bronchitis 148 

II.     Chronic  Bronchitis 151 

III.  Foetid  Bronchitis  (Putrid  Bronchitis) 155 

IV.  Croupous  Bronchitis  (Fibrinous  Bronchitis) 158 

V.  Whooping  Cough  (Pertussis) 160 

VI.    Bronchiectasis 164 

VII.     Stenosis  of  the  Trachea  and  Bronchi 166 

Tracheal  Stenosis 166 

Bronchial  Stenosis 167 

VIII.     Bronchial  Asthma 168 

SECTION  IV. 

DISEASES   OF  THE   LUNGS. 

I.    Pulmonary  Emphysema 173 

Clinical  History  and  Symptoms 176 

Other  Pulmonary  Symptoms  and  Phenomena  in  other  Organs    ....  178 
II.    Pulmonary  Atelectasis  (Compression  of  the  Lungs.     Aplasia  of  the  Lungs)        .  181 

III.  Pulmonary  CEdema 183 

IV.  Catarrhal  Pneumonia  (Broncho-pneumonia.     Lobular  Pneumonia)   .        .        .  184 
V.     Croupous  Pneumonia 189 

Description  of  Single  Symptoms  and  Complications 193 

Special  Peculiarities  and  Anomalies  in  the  Course  of  Pneumonia        .        .        .  200 
VI.     Tuberculosis  of  the  Lungs  (Pulmonary  Phthisis.     Pulmonary  Consumption)     .  207 

General  Pathology  and  iEtiology  of  Tuberculosis 207 

-«Etiology  of  Tuberculosis  in  Man 208 

Pathological  Anatomy  of  Tuberculosis,  especially  of  Pulmonary  Tuberculosis  .  212 
Clinical  History  of  Tuberculosis  in  General,  and  of  Pulmonary  Tuberculosis  in 

Particular 215 

Special  Symptoms  and  Complications 218 

Contraction  of  the  Lungs  (Fibroid  Phthisis) 223 

Disseminated  Pulmonary  Tuberculosis 224 


CONTENTS.  xi 

CHAPTER  PAGE 

VII.    Acute  General  Miliary  Tuberculosis 236 

VIII.    Gangrene  of  the  Lungs 241 

IX.     Diseases  from  the  Inhalation  of  Dust  (Pneumonoconiosis) 245 

X.  Embolic  Processes  in  the  Lungs  (Ilaimorrhagic  Infarction  of  the  Lungs)  .        .  247 

XI.    Brown  Induration  of  the  Lungs  (Lungs  of  Heart  Disease) 249 

XII.  Tumors  of  the  Lungs.     Cancer  of  the  Lungs.      Echinococcus  in  the  Lungs. 

Pulmonary  Syphilis 250 

SECTION  V. 

DISEASES   OF   THE   PLEURA. 

I.     Pleurisy 253 

Physical  Signs 257 

Different  Forms  of  Pleurisy  ....  - 261 

II.    Peripleuritis .        .  267 

III.  Pneumothorax 267 

IV.  Hydrothorax.    Hsematothorax 271 

V.    New  Growths  of  the  Pleura 272 

VI.     Mediastinal  Tumors 273 

VII.    Actinomycosis  of  the  Thoracic  Cavity 274 

Diseases  of  the  Circulatory  Organs. 

SECTION  I. 

DISEASES   OF   THE   HEART. 

I.    Acute  Endocarditis  (Endocarditis  verrucosa  and  ulcerosa)  .        .        .        .        .  276 

II.    Valvulvar  Disease  of  the  Heart 280 

General  Pathology  of  Valvular  Disease  of  the  Heart 281 

Insufficiency  of  the  Mitral  Valve 283 

Stenosis  of  the  Mitral  Orifice  (Mitral  Stenosis)     .......  285 

Insufficiency  of  the  Semilunar  Valves  of  the  Aorta     .        .•       .        .        .        .  287 

Stenosis  of  the  Aortic  Orifice 290 

Insufficiency  of  the  Tricuspid  Valve 291 

Stenosis  of  the  Tricuspid  Orifice 292 

Insufficiency  of  the  Pulmonary  Valve 293 

Stenosis  of  the  Pulmonary  Orifice  (Pulmonary  Stenosis)  and  the  other  Con- 
genital Lesions  of  the  Heart 293 

Combined  Valvular  Diseases  of  the  Heart 294 

General  Comparison  of  the  most  Important  Physical  Signs  in  Valvular  Disease 

of  the  Heart 295 

General  Sequelae  and  Complications  of  Valvular  Disease  of  the  Heart  .  .  295 
General  Course  and  Prognosis  of  Valvular  Disease  of  the  Heart  .  .  .  301 
Treatment  of  Valvular  Heart  Disease 303 

III.  Myocarditis  (Indurated  Degeneration.     Myodegeneration)         ....  307 

IV.  Idiopathic  Hypertrophy  and  Dilatation  of  the  Heart  (Overexertion   of   the 

Heart.     Weakened  Heart) 312 

V.    Fatty  Heart 315 

Appendix.     Remarks  on  the  So-called  Mechanical  Treatment  of  Circulatory 

Disturbances 316 

VI.    Neuroses  of  the  Heart 318 

Angina  Pectoris  (Stenocardia) 318 

Nervous  Palpitation 319 

Tachycardia 320 


xii  CONTENTS. 

SECTION  II. 

DISEASES   OF  THE   PERICARDIUM. 
CHAPTER  PAGB 

I.     Pericarditis 321 

Pericarditis  externa  and  Mediastino-pericarditis  (Pleuro-pericarditis)         .        .  325 
Obliteration  of  the  Pericardial  Cavity  (Adhesive  Pericarditis)    ....  326 

Tubercular  Pericarditis 327 

II.    Hydro-pericardium,  Haamo-pericardium,  and  Pneumopericardium     .        .        .  329 

Hydro-pericardium  (Dropsy  of  the  Pericardium) 329 

Hsemo-pericardium  (Blood  in  the  Pericardial  Sac) 330 

Pneumopericardium  (Air  in  the  Pericardial  Sac) 330 

SECTION  III. 

DISEASES   OF   THE   VESSELS. 

I.  Arterio-sclerosis  (Endarteritis  chronica  deformans.    Atheroma  of  the  Vessels)  331 

II.    Aneurism  of  the  Thoracic  Aorta 334 

III.  Aneurisms  of  the  Other  Vessels 339 

IV.  Rupture  of  the  Aorta 339 

V.     Narrowing  of  the  Aorta 340 

Diseases  of  the  Digestive  Organs. 

SECTION  I. 

DISEASES   OF   THE   MOUTH,   TONGUE,   AND   SALIVARY   GLANDS. 

I.    Stomatitis  (Inflammation  of  the  Mouth) 341 

II.     Ulcerative  Stomatitis  (Stomacace) 342 

III.  Aphthas  (Aphthous  Stomatitis) 343 

IV.  Thrush  (Soor.     Muguet)        .        .        . 344 

V.     Glossitis 345 

VI.     Noma  (Water-cancer.     Cancrum  oris) 347 

VII.     Parotitis  (Mumps) 348 

Idiopathic,  Primary  Parotitis 348 

Secondary,  Metastatic  Parotitis 349 

VIII.    Angina  Ludovici 349 

IX.    Anomalies  of  Dentition         . 350 

SECTION  II. 

DISEASES   OF   THE   SOFT   PALATE,   TONSILS,   PHARYNX,   AND  NASO-PHARYNX. 

I.    Sore  Throat  (Tonsillitis.    Angina) 351 

Catarrhal  Sore  Throat 352 

Follicular  Tonsillitis 353 

Tonsillar  Abscess  (Parenchymatous  Sore  Throat) 353 

Necrotic  Tonsillitis  (Necrotic  Sore  Throat) 354 

II.     Chronic  Hypertrophy  of  the  Tonsils 356 

HI.    Chronic  Pharyngitis 357 

Chronic  Catarrh  of  the  Naso-pharynx .  357 

Pharyngitis  Sicca 358 

Hypertrophic  Catarrh  of  the  Pharynx  and  Naso-pharynx 358 

IV.    Retropharyngeal  Abscess 360 


CONTENTS. 


Xlll 


SECTION  III. 


DISEASES   OF   THE   fESOPHAG  US. 


CHAPTER 

I. 

II 


Inflammation  and  Ulcer  of  the  Oesophagus 
Dilatation  of  the  Oesophagus 
Diffuse  Dilatation  . 
Diverticula     .... 

III.  Stenosis  of  the  Oesophagus  . 

IV.  Cancer  of  the  Oesophagus 
V.     Rupture  of  the  Oesophagus  . 

VI.    Neuroses  of  the  Oesophagus  . 
Spasm  of  the  Oesophagus 
Paralysis  of  the  Oesophagus 


PAOE 

.  301 
.  303 
.  303 
.  363 
.  366 
.  369 
.  371 
.  371 
.  371 
.  371 


SECTION  IV. 

DISEASES   OF   THE   STOMACH. 

I.     Acute  Gastric  Catarrh 372 

II.     Chronic  Gastric  Catarrh 374 

Appendix.    Hyperacidity  and  Hypersecretion  of  the  Gastric  Juice .        .        .  382 

III.  Phlegmonous  Gastritis 383 

IV.  Gastric  Ulcer  (Simple  or  Round  Ulcer  of  the  Stomach) 384 

Appendix.     Melsena  Neonatorum 390 

V.     Cancer  of  the  Stomach 391 

VI.    Dilatation  of  the  Stomach 396 

VII.    Nervous  Disorders  of  the  Stomach 400 


SECTION  V. 

diseases  of  the  intestines. 

1.     Intestinal  Catarrh  (Catarrhal  Enteritis) 403 

Different  Forms  of  Intestinal  Catarrh '      .         .         .  406 

II.     Cholera  Morbus  (Cholera  Nostras,  Cholera  Infantum) 410 

III.  Intestinal  Catarrh  of  Children  (Pedatrophy) 413 

IV.  Typhlitis  and  Perityphlitis  (Inflammation  of  the  Caecum) 418 

V.     Perforating  Ulcer  of  the  Duodenum .        .  423 

VI.    Tuberculosis  of  the  Intestines 423 

VII.     Syphilis  of  the  Rectum 425 

VIII.    Cancer  of  the  Intestines 426 

IX.    Haemorrhoids 428 

X.     Habitual  Constipation 430 

XI.     Stricture  and  Obstructions  of  the  Intestines         .        .        .        .        .        .        .  432 

XII.    Intestinal  Parasites         .        , 440 

Tape-worms  (Tasnia  and  Bothriocephalus) 440 

Round- worms  (Ascaris  lumbricoides) 445 

Oxyuris  vermicularis  (Seat-worms) 446 

Anchylostomum  duodenale  (Dochmius  s.  Strongylus  duodenalis)        .        .        .  448 
Trichocephalus  dispar  (Whip-worm) 448 


SECTION  VI. 

diseases  of  the  peritoneum. 

I.    Acute  Peritonitis 

II.     Chronic  Peritonitis.     Tubercular  Peritonitis 


449 
457 


xiv  CONTENTS. 

CHAPTER  PAGE 

III.  Ascites  (Hydroperitoneum) 460 

IV.  Cancer  of  the  Peritoneum 463 

SECTION  VII. 

DISEASES   OF  THE   LIVER,   BILE-DUCTS,   AND   PORTAL  VEIN. 

I.    Catarrhal  Jaundice  (Icterus  catarrhalis.     Gastro-duodenal  Catarrh  with  Jaun- 
dice)  464 

Appendix.    Acute  Febrile  Jaundice.     Weil's  Disease 469 

II.     Biliary  Calculi  (Hepatic  Colic.     Cholelithiasis) 470 

III.  Suppurative  Hepatitis  (Hepatic  Abscess) 476 

IV.  Cirrhosis  of  the  Liver  (Chronic  Diffuse  Interstitial  Hepatitis.    Laennec's  Cir- 

rhosis.    Gin-drinkers'  Liver) 478 

V.     Biliary  and  Hypertrophic  Cirrhosis  of  the  Liver 483 

VI.     Acute  Yellow  Atrophy  of  the  Liver 485 

Appendix.     Pernicious  Jaundice.     Chola?mia  and  Acholia        ....  489 

VII.     Icterus  Neonatorum  (Jaundice  of  the  Newborn) 490 

VIII.    Syphilis  of  the  Liver 490 

IX.    Cancer  of  the  Liver  and  Bile-ducts 492 

X.    Echinococcus  of  the  Liver 494 

XI.     Circulatory  Disturbances  in  the  Liver 496 

XII.    Atrophy,  Hypertrophy,  and  Degenerations  of  the  Liver 498 

XIII.  Anomalies  in  the  Shape  and  Position  of  the  Liver 499 

XIV.  Suppurative  Pylephlebitis  (Purulent  Inflammation  of  the  Portal  Vein  and  its 

Branches) 500 

XV.    Thrombosis  of  the  Portal  Vein  (Chronic  Adhesive  Pylephlebitis.     Pylethrom- 

bosis) 502 

Appendix.     Diseases  of  the  Pancreas 503 


Diseases  of  the  Nervous  System. 

/.     The  Diseases  of  the  Peripheral  Nerves. 

SECTION  I. 

DISEASES   OF  THE   SENSORY   NERVES. 

I,     General  Remarks  upon  the  Disturbances  of  Sensibility 505 

The  Different  Varieties  of  Cutaneous  Sensibility  and  the  Methods  of  testing 

them 505 

The  Sensibility  of  the  Muscles  and  Joints .        .  509 

II.    Anaesthesia  of  the  Skin 510 

Anaesthesia  of  the  Trigeminus 513 

III.  Neuralgia  in  General 515 

IV.  The  Individual  Forms  of  Neuralgia 521 

1.  Neuralgia  of  the  Trigeminus 521 

2.  Occipital  Neuralgia 523 

3.  Neuralgias  in  the  Region  of  the  Brachial  Plexus 524 

4.  Intercostal  Neuralgia 524 

5.  Neuralgias  in  the  Region  of  the  Lumbar  Plexus 526 

6.  Sciatica 526 

7.  Neuralgia  of  the  Genitals  and  the  Rectal  Region 528 

V.     Neuralgia  of  the  Joints 528 

VI.    Habitual  Headache 530 

VII.     Anomalies  of  the  Sense  of  Smell 532 

VIII.    Anomalies  of  the  Sense  of  Taste 533 


CONTENTS.  xv 

SECTION  II. 

DISEASES  OP  THE  MOTOR  NERVES. 
CHAPTER  PAGE 

I.    General  Remarks  upon  the  Disturbances  of  Motility 534 

1.  Paralysis 534 

2.  Symptoms  of  Motor  Irritation 539 

3.  Ataxia 542 

4.  General  Remarks  upon  testing  the  Reflexes  and  the  Condition  of  them         .  543 
Mechanical  Muscular  Irritability  and  Paradoxical  Contraction  ....  546 

5.  General  Remarks  upon  the  Changes  of  Electrical  Excitability  in  the  Motor 

Nerves  and  Muscles 546 

II.     The  Different  Forms  of  Peripheral  Paralysis 555 

1.  Paralysis  of  the  Ocidar  Muscles 555 

2.  Paralysis  of  the  Motor  Branch  of  the  Trigeminus 557 

3.  Facial  Paralysis 558 

4.  Paralyses  in  the  Region  of  the  Muscles  of  the  Shoulder 562 

5.  Paralyses  of  the  Muscles  of  the  Back 564 

6.  Paralyses  in  the  Region  of  the  Upper  Extremity 564 

Radial  (Musculo-spiral)  Paralysis 564 

Ulnar  Paralysis 566 

Median  Paralysis 566 

Combined  Paralyses  of  the  Arm 567 

7.  Paralysis  of  the  Diaphragm 568 

8.  Paralyses  in  the  Region  of  the  Lower  Extremity 568 

9.  Toxic  Paralyses 569 

Lead  Paralysis 569 

Arsenical  Paralysis. 571 

III.  The  Different  Forms  of  Localized  Spasms 571 

1.  Spasms  in  the  Motor  Distribution  of  the  Trigeminus 571 

2.  Clonic  Facial  Spasm 572 

3.  Spasm  in  the  Region  of  the  Hypoglossal  Nerve.    Lingual  Spasm  .        .        .  573 

4.  Spasms  in  the  Muscles  of  the  Neck 573 

5.  Spasms  in  the  Muscles  of  the  Shoulder  and  Arm 575 

6.  Spasms  in  the  Muscles  of  the  Lower  Extremity 575 

Saltatory  Reflex  Spasm 575 

Arthrogryposis 576 

Paramyoclonus  Multiplex 576 

Electrical  Chorea 576 

7.  Spasms  in  the  Respiratory  Muscles 576 

IV.  Writer's  Cramp  and  Allied  Professional  Neuroses 577 

V.    Simple  and  Multiple  Degenerative  Neuritis 579 

Clinical  History  of  the  Different  Forms  of  Neuritis 581 

1.  Secondary  Neuritis 581 

2.  Primary  Simple  Neuritis 582 

3.  Primary  Multiple  Degenerative  Neuritis 582 

4.  The  Chronic  Neuritis  of  Alcoholic  Subjects 584 

VI.    New  Growths  in  the  Peripheral  Nerves 585 

77.     Vasomotor  and  Trophic  Neuroses. 

1.    Preliminary  Remarks  upon  Vasomotor,  Trophic,  and  Secretory  Disturbances  .  587 

Acute  Angioneurotic  (Edema 588 

Myxcedema 589 

Acromegaly 589 

Hydrops  Articulorum  Intermittens 590 

II.    Hemicrania 591 


xvi  CONTENTS. 

CHAPTER  PAGE 

III.  Progressive  Facial  Hemiatrophy  ...........  594 

IV.  Exophthalmic  Goitre 595 

777.     The  Diseases  of  the  Spinal  Cobb. 

I.     Diseases  of  the  Spinal  Meninges 599 

1.  Acute  Inflammations  of  the  Spinal  Meninges 599 

2.  Chronic  Spinal  Leptomeningitis 601 

3.  Pachymeningitis  cervicalis  hypertrophica 602 

4.  Haemorrhages  of  the  Spinal  Meninges 603 

II.    Disturbances  of  Circulation,  Haemorrhages,  Functional  Disturbances,  and  Trau- 
matic Lesions  of  the  Spinal  Cord 604 

1.  Disturbances  of  Circulation       .  604 

2.  Spinal  Apoplexy.     Hsematomyelia 604 

3.  Functional  Disturbances 605 

4.  Traumatic  Lesions 606 

5.  Diseases  of  the  Spinal  Cord  after  a  Sudden  Reduction  of  the  Atmospheric 

Pressure  (Caisson  Disease) 608 

III.  The  Pressure  Paralyses  of  the  Spinal  Cord 608 

IV.  Acute  and  Chronic  Myelitis 615 

Localization  of  the  Functions  of  the  Segments  of  the  Spinal  Cord     .        .        .  624 

V.    Multiple  Sclerosis  of  the  Brain  and  Spinal  Cord 627 

VI.     Tabes  Dorsalis 632 

Appendix.     Hereditary  Ataxia.     Friedreich's  Form  of  Locomotor  Ataxia     .  648 

Ataxic  Paraplegia 649 

VII.     Amyotrophic  Lateral  Sclerosis       . 650 

VIII.    Progressive  (Spinal)  Muscular  Atrophy 653 

Appendix.     The  Primary  Myopathic  Forms  of  Muscular  Atrophy.        .        .658 

IX.    The  So-called  Spastic  Spinal  Paralysis 663 

X.    Acute  and  Chronic  Poliomyelitis 667 

1.  Spinal  Paralysis  of  Children 667 

2.  Acute  Poliomyelitis  of  Adults 671 

3.  Subacute  and  Chronic  Poliomyelitis          .        .        .         .   •     .        .        .        .  673 
XI.    Acute  Ascending  Spinal  Paralysis 674 

XII.    New  Growths  of  the  Spinal  Cord  and  of  its  Membranes 676 

XIII.  The  Formation  of  Cavities  and  Fissures  in  the  Spinal  Cord        ....  677 
Morvan's  Disease 679 

Appendix.    Spina  Bifida 679 

XIV.  Secondary  Degenerations  in  the  Spinal  Cord 680 

XV.     Unilateral  Lesion  of  the  Spinal  Cord    .        .        .    ■ 682 

IV.     The  Diseases  of  the  Medulla  Oblongata. 

I.    Progressive  Bulbar  Paralysis 685 

Appendix.    The  Rarer  Forms  of  Chronic  Bulbar  Paralysis,  and  Progressive 

Ophthalmoplegia 690 

II.    Acute  and  Apoplectiform  Bulbar  Paralysis 691 

1.  Haemorrhage  into  the  Medulla  Oblongata  and  the  Pons 691 

2.  Embolism  and  Thrombosis  of  the  Basilar  Artery 693 

3.  Acute  or  Inflammatory  Bulbar  Paralysis 694 

III.    Compression  of  the  Medulla 695 


CONTENTS.  xvii 


V.     The  Diseases  of  the  Brain. 
SECTION  I. 

DISEASES   OF  THE   CEREBRAL   MENINGES. 
CHAPTER  l-M.E 

I.     Hematoma  of  the  Dura  Mater 696 

II.    Purulent  Meningitis 698 

III.  Tubercular  Meningitis 702 

Tubercular  Meningitis  in  Children 705 

IV.  Thrombosis  of  the  Cerebral  Sinuses 707 

SECTION  II. 

DISEASES   OF   THE   BRAIN- SUBSTANCE. 

I.    Disturbances  of  Circulation  in  the  Brain 708 

II.  General  Preliminary  Remarks  upon  the  Localization  of  Cerebral  Diseases  (Top- 

ical Diagnosis  of  Cerebral  Lesions) 710 

1.  The  Motor  Region  of  the  Cortex  Cerebri 711 

2.  The  other  Parts  of  the  Cortex  Cerebri,  except  the  Center  for  Speech     .        .  715 

3.  The  Centers  of  Speech  and  the  Disturbances  of  Speech  (Aphasia  and  Allied 

Conditions) 716 

4.  The  Centrum  Ovale,  Internal  Capsule,  Central  Ganglia,  and  Region  of  the 

Corpora  Quadrigemina 720 

5.  The  Cerebellum 723 

General  Diagnostic  Principles 724 

III.  Cerebral  Haemorrhage 725 

IV.  Cerebral  Embolism  and  Thrombosis 737 

V.     Inflammation  of  the  Brain 741 

1.  Abscess  of  the  Brain  (Suppurative  Encephalitis) 741 

2.  Acute  and  Chronic  Non-suppurative  Encephalitis 743 

Idiopathic  Softening  of  the  Brain 744 

Curable  Form  of  Encephalitis 744 

Diffuse  Cerebral  Sclerosis 744 

The  Acute  Encephalitis  of  Children  (Cerebral  Paralysis  of  Children) .        .        .  744 

VI.    Insolation.     Sunstroke.    Heat  Prostration.     Thermic  Fever      ....  746 

VII.    Tumors  of  the  Brain 748 

Varieties  of  Cerebral  Tumor 748 

The  General  Symptoms  of  Cerebral  Tumors 749 

Tumors  in  the  Different  Parts  of  the  Brain.     Their  Focal  Symptoms         .        .  751 

General  Course  of  Cerebral  Tumors 754 

Appendix.     Hydatids  of  the  Brain 756 

VIII.    Cerebral  Syphilis 757 

IX.    Progressive  General  Paralysis  of  the  Insane  (Paralytic  Dementia)      .        .        .  760 

X.     Chronic  Hydrocephalus 767 

XI.    Meniere's  Disease 769 

VI.    Neuroses  without  Known  Anatomical  Basis. 

I.    Epilepsy 770 

Appendix.    Infantile  Convulsions 779 

II.     Chorea 780 

III.  Paralysis  Agitans 784 

IV.  Athetosis 787 

V.     Tetany 789 

VI.     Tetanus 791 

B 


xvüi  CONTENTS. 

CHAPTER  PAGE 

VII.     Congenital  Myotonia  (Thomsen's  Disease) 795 

VIII.     Catalepsy 796 

IX.    Hysteria 797 

X.    Neurasthenia 815 

XI.     The  Traumatic  Neuroses 819 


Diseases  of  the  Kidneys,  the  Pelvis  of  the  Kidney,  and  the  Bladder. 

SECTION  I. 

DISEASES    OF   THE   KIDNEYS. 

I.    General  Preliminary  Remarks  upon  the  Pathology  of  Renal  Disease  .        .        .  822 

1.  Albuminuria 823 

2.  Casts  and  other  Abnormal  Morphological  Constituents  of  the  Urine  in  Renal 

Disease 826 

3.  The  Dropsy  of  Renal  Disease 828 

4.  Ura?mia 829 

5.  The  Changes  in  the  Circulatory  Apparatus  in  Renal  Disease          .        .        .  834 
II.     Acute  Nephritis  (Acute  Bright's  Disease) 836 

III.  The  Subchronic  and  Chronic  Forms  of  Nephritis,  with  the  Exception  of  the 

Genuine  Contracted  Kidney 849 

IV.  Contracted  Kidney 856 

V.    Amyloid  Kidney 864 

VI.     Purulent  Nephritis  and  Perinephritis 868 

Perinephritic  Abscess 870 

VII.     Disturbances  of  Circulation  in  the  Kidneys 871 

1.  The  Congested  Kidney 871 

2.  Embolic  Infarction  in  the  Kidneys 871 

VIII.     New  Growths  in  the  Kidneys 872 

IX.     Parasites  of  the  Kidneys  and  of  the  Urinary  Passages.     Chyluria      .        .        .  874 

X.     Movable  Kidney  (Floating  Kidney.     Ren  Mobilis) 876 

Appendix.    The  Diseases  of  the  Suprarenal  Capsules  and  Addison's  Disease 
(Bronzed  Skin) 878 

SECTION  II. 

DISEASES   OF   THE   PELVIS   OF   THE   KIDNEY   AND   OF   THE  BLADDER. 

I.  Inflammation  of  the  Pelvis  of  the  Kidney.     Pyelitis 881 

II.  Nephrolithiasis 884 

III.  Tuberculosis  of  the  Genito-urinary  Apparatus 888 

IV.  Hydronephrosis 890 

V.  Cystitis  (Vesical  Catarrh) 893 

VI.    New  Growths  in  the  Bladder 897 

VII.     Enuresis  Nocturna  (Nocturnal  Incontinence  of  Urine) 898 


Diseases  of  the  Organs  of  Locomotion. 

I.    Acute  Articular  Rheumatism 900 

II.     Chronic  Articular  Rheumatism  (Chronic  Polyarthritis)  and  Arthritis  Defor- 
mans          911 

III.  Acute  and  Chronic  Muscular  Rheumatism 916 

Appendix.     Acute  Polymyositis 919 

IV.  Rachitis 920 

V.    Osteomalacia 925 


CONTENTS.  xix 

Diseases  affecting  the  Blood  and  Tissue-metamorphosis. 

(constitutional  diseases.) 

CHAPTER  PAGE 

I.    Anaemia  and  Chlorosis 928 

II.    Progressive  Pernicious  Anaemia 938 

III.  Leukaemia 945 

IV.  Pseudo-leukaemia 951 

V.    Haemoglobinaemia  and  Haemoglobinuria 953 

VI.  Scurvy 956 

VII.  Purpura.    Morbus  Maculosus  Werlhofii.     Peliosis 961 

VIII.  Haemophilia 903 

IX.  Diabetes  Mellitus 905 

X.  Diabetes  Insipidus 982 

XI.  Gout Ö84 

XII.  Obesity .992 

XIII.  Scrofula 999 

Appendix  I.    Summary  of  the  Symptoms  and  Treatment  in  Cases  of  Poisoning  1003 

Appendix  II.     Table  of  Weights  and  Measures 1011 

Index 1012 


LIST  OF  ILLUSTRATIONS. 


FIG.  PAGE 

1.  Typhoid  Bacilli 1 

2.  Temperatures  in  typhoid  fever 6 

3.  Example  of  the  temperature  curve  in  relapsing  fever         ......    33 

4.  Spirilli  of  relapsing  fever  in  the  blood 34 

5.  Example  of  a  normal  scarlet-fever  curve 38 

6.  Example  of  the  temperature  curve  in  measles 48 

7.  Example  of  the  temperature  curve  in  true  smallpox 55 

8.  The  cocci  of  erysipelas .62 

9.  Comma  bacilli 83 

10.  Quotidian  intermittent  fever 93 

11.  Tertian  intermittent  fever 93 

12  a,  12  b.  Anthrax  bacilli 118 

13.  Trichinae ....  122 

14.  Paralysis  of  left  vocal  cord 140 

15.  Bilateral  paralysis  of  the  posticus        . 141 

16.  Paralysis  of  both  internal  thyro-arytaenoid  muscles 141 

17.  Paralysis  of  the  arytaenoideus 142 

18.  Paralysis  of  the  thyro-arytaenoids  and  arytasnoideus 142 

19.  20.  Pediculated  fibromata 144 

21.  Crystals  of  fat  acids 156 

22.  Asthma  crystals  and  Curschmann's  spirals 169 

23.  Example  of  the  temperature  curve  in  croupous  pneumonia 199 

24.  Example  of  the  temperature  curve  in  "  intermitting  "  pneumonia    .        .        .        .199 

25.  Cholesterine  crystals 203 

26.  Elastic  fibers 7        ...„„.  219 

27.  Tubercle  bacilli  in  the  sputum     ...........  220 

28.  Masses  of  actinomyces 274 

29.  Pulse  curve  in  marked  mitral  stenosis 285 

30.  Pulse  curve  in  aortic  insufficiency 289 

31.  Pulse  curve  in  stenosis  of  the  aortic  orifice  .        . 291 

32.  Pulsus  bigeminus   ...  298 

33.  Plan  of  the  dentition ;        .        .        .        .        .        .        .  350 

34.  Sarcini  ventriculi  and  yeast-cells 376 

35.  Haemine  crystals 392 

36.  Stomach-tube  with  Hegar's  funnel 399 

37.  Head  of  taenia  solium 440 

38.  Head  of  Cysticercus  of  the  brain 440 

39.  Taenia  solium 440 

40.  Eggs  of  intestinal  parasites 441 

41.  Head  of  taenia  mediocanellata .        .        .  442 

42.  Taenia  mediocanellata 442 

43.  Head  of  bothriocephalus  latus 442 

44.  Bothriocephalus  latus 442 

(xxi) 


xxji  LIST  OP  ILLUSTRATIONS. 

FIG.  PAGE 

45.  Embryo  of  bothriocephalus  latus 443 

46.  Ascaris  lumbricoides 445 

47.  48.  Oxyuris  vermicularis 447 

49,  50.  Anchylostomum  duodenale 448 

51.  Trichocephalus  dispar 449 

52.  Leucine  and  tyrosine  crystals 488 

53.  Taenia  echinococcus 494 

54.  55.  Echinococcus  scolices 495 

56.  Echinococcus  booklets 495 

57,  58.  Distribution  of  the  sensory  cutaneous  nerves  in  the  head 513 

59,  60.  Distribution  of  the  sensory  cutaneous  nerves  in  the  trunk  and  upper  extremities  514 

61.  Detailed  distribution  of  the  nerves  to  the  dorsal  surface  of  the  fingers      .        .        .  514 

62,  63.  Distribution  of  the  sensory  cutaneous  nerves  to  the  lower  extremities         .        .  515 

64.  Horizontal  section  through  the  right  cerebral  hemisphere 534 

65.  Transverse  section  through  the  crura  cerebri  in  secondary  degeneration  .        .        .  535 

66.  Transverse  section  through  the  cervical  enlargement 535 

67.  Transverse  section  through  the  lumbar  enlargement 535 

68.  Motor  points  of  face 547 

69.  70.  Motor  points  of  arm 548,  549 

71.  Motor  points  of  thigh 550 

72,  73.  Motor  points  of  leg •        •  551,  552 

74.  Right  facial  paralysis 558 

75.  Trunk  of  the  facial 560 

76.  Paralysis  of  the  right  serratus 563 

77.  Position  of  the  hand  in  paralysis  of  the  radial  nerve 565 

78.  Claw- shaped  hand,  main  en  griffe 566 

79.  Spasm  of  the  right  splenius  capitis 574 

80.  Left  facial  hemiatrophy 594 

81.  Position  of  the  hand  in  pachymeningitis  cervicalis  hypertrophica     .        .        .        .602 

82.  Vertebral  displacement  in  spondylitis 609 

83.  Relations  of  the  vertebrae  to  the  spinal  segments 622 

84.  Areas  of  anaesthesia  at  various  levels  of  the  spinal  cord 623 

85.  Example  of  disease  of  the  cord  in  multiple  sclerosis 628 

86.  Distribution  of  the  sclerosed  nodules  on  the  surface  of  the  pons        .        .        .        .628 

87.  Transverse  section  through  the  lumbar  region  in  locomotor  ataxia   ....  634 

88.  Transverse  section  through  the  cervical  region  in  locomotor  ataxia  .      •  .        .        .  634 

89.  90.  Transverse  section  of  cord  in  beginning  locomotor  ataxia 634 

91.  Tabetic  arthropathy  of  the  right  knee  and  left  ankle  ......  644 

92.  Positions  of  a  child  with  pseudo-hypertrophic  paralysis  on  rising      .        .        .        .659 

93.  Pseudo-hypertrophy  of  the  muscles 660 

94.  Juvenile  myopathic  muscular  atrophy 662 

95.  Section  of  the  cord  in  anterior  poliomyelitis 667 

96.  Secondary  descending  degeneration  of  the  pyramidal  tracts 681 

97.  Secondary  ascending  and  descending  degeneration 682 

98.  Course  of  the  main  tracts  in  the  cord 683 

99.  Representation  of  the  chief  symptoms  in  unilateral  lesion 684 

100.  Diagram  of  focal  diseases  in  the  pons 692 

101,  102.  Lateral  aspect  of  the  brain 712,  713 

103.  Aspect  of  the  median  surface  of  the  cerebrum 713 

104.  Topographical  relations  between  the  surface  of  the  brain  and  the  skull    .        .        .714 

105.  Diagram  of  the  course  of  the  optic  fibers  in  the  chiasma 716 

106.  Examples  of  handwriting  in  general  paralysis 763 

107.  Characteristic  position  of  the  body  in  paralysis  agitans      .        .  .        .        .785 

108.  Example  of  the  position  of  the  fingers  in  the  movements  of  athetosis        .        .        .788 

109.  Hysterical  contracture '•  °"4 

110.  Hysterical  arc  de  cercle °®7 


LIST  OF  ILLUSTRATIONS. 


XX1U 


111.  Different  forms  of  casts 

112.  Acute  nephritis  (scarlatinal,  early  stage) 

113.  Distoma  haematobium   .... 

114.  Embryos  of  filaria         .... 

115.  Pelvic  renal  epithelium 

116.  Crystals  of  triple  phosphate  and  ammonic  urate 

117.  Deformity  of  the  hand  in  protracted  arthritis  deformans 

118.  Changes  in  the  red  blood-corpuscles  in  pernicious  anaemia 

119.  Anaemic  blood 


PAGE 

.  826 
.  837 
.  875 
.  876 
.  883 
.  895 
.  914 
.  943 


ACUTE    GENERAL   INFECTIOUS   DISEASES. 


CHAPTER  I. 

TYPHOID   FEVER. 

(Typhvs  abdominalis.    Enteric  Fever.     Ileotyphus.) 

iEtiology. — According  to  our  present  views,  the  cause  of  typhoid  fever  must  be 
sought  in  some  specific,  organized,  pathogenic  poison.  The  later  investigations 
in  bacteriology  have  apparently  revealed  what  this  poison  is.  Koch  and  Eberth 
were  the  first  to  point  out  a  clearly  specific  variety  of  short,  rod -shaped  bacteria 
(bacilli),  which  appear  in  this  disease  alone.  They  take  up  the  aniline  colors. 
Koch  and  Eberth,  and  later  W.  Meyer,  Friedländer,  and  Gaffky,  found  them  in 
the  intestine,  especially  in  its 
lymphatic  apparatus,  and  also 
in  the  mesenteric  glands,  the 
spleen,  liver,  and  kidneys.  The 
subjects  in  whom  these  bacteria 
were  detected  had  died  in  the 
beginning  or  during  the  fastigi- 
um  of  typhoid  fever. 

The  length  of  these  bacilli 
(see  Fig.  1)  is  about  one  third 
the  diameter  of  a  red  blood- 
globule,  and  their  breadth  equals 
one  third  their  length.  Their 
ends  are  rounded  off,  and  in 
their  interior  the  formation  of 
spores  can  sometimes  be  plainly 
recognized.  They  ai*e  found  for 
the  most  part  lying  together  in 
little  clumps  (foci  of  bacilli)  in 
the  organs.  They  have  also 
been  demonstrated  in  the  dejections  of  typhoid  patients,  and  sometimes  in  the 
blood  taken  from  rose-spots. 

That  these  typhoid  bacilli  are  specific,  is  shown,  however,  as  in  the  case  of 
many  micro-organisms,  less  by  their  external  form  than  by  their  peculiarities,  as 
observed  in  pure  cultures  of  them.  Gaffky,  who  first  succeeded  with  such  culti- 
vations, found  that  the  colonies  of  these  bacilli,  reared  in  a  mass  of  stiff  gelatin, 
are  made  up  of  very  minute,  brownish-yellow  clumps,  and  that  in  their  growth 
they  are  always  limited  to  the  spots  where  they  have  been  implanted,  and  never 
liquefy  the  jelly  in  which  they  grow.  The  growth  of  typhoid  bacilli  upon  the  cut 
1  (l) 


Fig.  1.— Typhoid  bacilli.    Section  of  the  spleen,  x  800. 
(After  Flügge.) 


2  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

surface  of  boiled  potatoes  is  also  very  characteristic.  The  bacilli  cover  the  entire 
surface  with  a  very  thin  though  tough  pellicle  scarcely  recognizable  to  the  naked 
eye.  Examined  in  water,  the  typhoid  bacilli  exhibit  quite  an  active  individual 
motion.  The  formation  of  spores  takes  place  only  when  the  temperature  is 
between  86°  and  108°  (30°-42°  C.),  ceasiug  at  lower  temperatures. 

Numerous  attempts  have  been  made  to  produce  typhoid  fever  artificially  by 
introducing  pure  cultures  of  the  typhoid  bacilli  into  the  bodies  of  animals,  but  the 
results  of  these  efforts  have  not  yet  proved  perfectly  harmonious.  The  main  cause 
of  the  discrepancy  is  probably  that  animals  are  in  general  very  slightly  susceptible 
to  the  disease.  At  any  rate,  the  attempts  at  artificial  infection  up  to  this  date  have 
proved  successful  only  in  cases  when  the  animals  subjected  to  the  experiment 
(rabbits,  guinea-pigs)  have  received  large  amounts  of  the  typhoid  bacilli  directly 
into  a  vein  or  into  the  abdominal  cavity  (E.  Fränkel,  Simmonds),  or  when  the 
bacilli  have  been  introduced  into  the  duodenum  (A.  Fränkel).  Probably,  how- 
ever, we  have  here  to  do  rather  with  the  intoxication  of  the  animals  caused  by  the 
poisonous  matters  generated  in  the  cultures  of  bacilli  than  with  an  actual  in- 
fection, for  the  pathological  changes  of  typhoid  fever  are  but  little  developed  in 
the  animals,  and  the  injected  bacilli  themselves  appear  to  be  for  the  most  part 
destroyed  within  the  body  of  the  animal  experimented  upon  (Flügge  and 
Sirotinin,  and  others).  Attempts  to  produce  the  disease  by  mixing  the  dejecta 
of  typhoid  patients  with  the  animal's  food  have  thus  far  proved  invariably  un- 
successful. Probably  the  bacilli  are  immediately  destroyed  by  the  hydrochloric 
acid  in  the  stomach. 

Investigation  of  the  aetiology  of  typhoid  fever  must  consequently  be  directed  to 
ascertaining  in  what  manner  and  through  what  channels  the  specific  typhoid 
bacilli  penetrate  *  into  the  human  body,  and  what  circumstances  are  then  essen- 
tial to  their  further  development  and  to  the  display  of  their  pathogenic  properties. 
It  must  be  confessed  that  the  ability  to  answer  these  questions  accurately  is  a  goal 
from  which  we  are  quite  distant. 

It  is  almost  universally  believed  that,  as  a  rule,  typhoid  bacilli  do  not  have  any 
permanent,  independent  existence  outside  the  human  body.  Often,  however,  the 
conditions  essential  to  an  abundant  development  of  the  bacilli  arise  in  certain 
places,  and  thus  make  it  possible  for  a  greater  or  less  number  of  persons  to  absorb 
the  pathogenetic  poison,  and,  as  a  result,  to  be  attacked  by  typhoid  fever.  In  this 
way  occur  the  numerous  greater  or  smaller  epidemics  of  typhoid  fever  in  contrast 
to  the  sporadic  cases,  which  are  likewise  possible,  and  are  not  infrequent.  If 
an  epidemic  of  typhoid  appears  in  a  place  till  then  entirely  free  from  the  disease, 
we  must  always  refer  it  to  an  importation  of  the  disease-germs,  and  seek  their 
source  in  some  previous  case  of  typhoid.  We  must,  therefore,  take  for  granted 
that  the  poison  of  typhoid  can  in  some  way  escape  from  the  body  of  the  patient 
into  the  outer  world.  If  wTe  believe  this,  we  shall  be  sure  to  think,  first  of  all,  of 
the  intestinal  discharges  as  the  source  of  infection.  These  discharges,  as  already 
stated,  are  known  to  contain  the  typhoid  bacilli  or  their  spores. 

As  to  the  exact  manner  of  infection,  views  are  still  widely  different.  Up  to 
the  present  time  there  are  chiefly  two  contrasted  theories,  called,  respectively,  the 
"  ground-soil  "  and  the  "  drinking-water  "  f  theories.  According  to  the  former, 
which  is  maintained  principally  by  Pettenkofer  and  his  pupils,  the  ground-soil  is 

*  Perhaps  it  is  not  useless  once  more  to  call  attention  expressly  to  the  fact  that  typhoid  fever  can 
result  only  from  an  infection  of  the  body  with  actual  typhoid  bacilli,  and  never  through  any  other 
bacteria,  through  the  products  of  decay  and  decomposition,  tainted  food,  and  the  like ;  nor  does  there 
yet  exist  the  slightest  proof  that  typhoid  bacilli  can  be  developed  from  any  other  micro-organisms. 

t  Compare  with  what  follows  the  statements  concerning  the  cetiology  of  cholera,  where  the  same 
disputed  points  are  considered. 


TYPHOID  FEVER.  3 

to  be  regarded  as  the  chief  place  of  development  for  the  schizomycetic  fungus  of 
typhoid  fever.  Whether  this  will  flourish  depends  chiefly  on  the  condition  of  the 
soil  (varying  at  different  times  and  in  different  places),  and  this  alone  should  ex- 
plain all  the  peculiarities  observable  in  the  spread  of  the  disease — e.  g.,  that  single 
houses,  streets,  or  wards  of  a  city  should  suffer.  According  to  Pettenkofer,  a  soil 
that  air  and  water  easily  penetrate — e.  g.,  one  made  up  of  alluvial  or  detrital  depos- 
its— is  most  favorable  for  the  spread  of  the  disease,  while  a  firm,  rocky  bottom 
makes  its  further  development  impossible;  and,  where  this  "tendency  of  the 
ground-soil  "  is  wanting,  the  disease  can  neither  be  introduced  nor,  if  brought  in, 
spread  any  further ;  for,  according  to  Pettenkofer,  the  typhoid  poison  is  seldom  if 
ever  transferred  directly  from  one  person  to  another.  The  poison  in  the  stools 
must  first  be  changed  by  the  soil  before  it  becomes  infectious.  The  "  ground-air," 
which  is  continually  rising,  carries  the  poison  not  only  into  the  open  atmosphere, 
but  into  the  air  of  dwelling-rooms,  and,  being  then  inhaled,  produces  infection. 
We  can  thus  understand  why  Pettenkofer  regards  typhoid  fever  as  not  directly 
contagious.  The  chief  support  of  the  ground-soil  theory,  beyond  the  results  of 
comparing  the  character  of  the  soil  with  the  extent  of  the  epidemics,  consists  in 
the  proof  which  Buhl  and  Pettenkofer  have  given  (taking  Munich  as  an  example; 
that  a  relation  exists  between  the  variations  of  the  standing  water  in  the  soil  and 
the  frequency  of  typhoid  cases.  It  appears  that,  when  the  water  stands  high  (near 
the  surface),  fewer  cases  occur,  and  when  it  falls  below  the  mean  height  cases  are 
more  numerous.  This  relation,  which  is  said  to  hold  true  also  for  Berlin  and  some 
other  places,  is  not  yet,  we  may  add,  explained  with  certainty. 

To  be  contrasted,  or  rather  compared,  with  the  soil-gas  theory  is  the  view  held 
by  many  physicians,  despite  the  vigorous  protest  of  Pettenkofer,  that  drinking- 
water  plays  an  important  role  in  the  origin  of  many  epidemics  of  typhoid.  In 
fact,  in  the  case  of  numerous  epidemics,  whose  extent  bears  an  unmistakable  rela- 
tion to  the  water-supply,  we  seem  perfectly  justified  in  supposing  that  the  typhoid 
germs  are  brought  into  the  body  by  means  of  water  used  in  chinking  or  otherwise. 
Even  then  we  are  by  no  means  wholly  to  disregard  the  character  of  the  soil,  for 
the  disease-producing  poison — not  to  speak  of  direct  pollution — is  probably  often 
communicated  to  the  well-water  from  the  soil.  The  possibility  of  this  will  be 
especially  great  if  the  wells  are  near  drains  or  cess-pools  containing  typhoid  dis- 
charges. In  epidemics  spread  by  drinking-water,  the  typhoid  bacilli  have  lately 
been  repeatedly  found  in  the  suspected  water. 

We  believe  the  idea  is  continually  gaining  ground  that  no  single  "  theory  " 
can  fully  explain  all  the  facts,  and  that  the  possibility  of  infection  occurring  in 
several  different  ways  must  be  considered.  Beside  the  possible  inhalation  of  the 
poison,  or  the  ingestion  of  polluted  water,  it  may  be  that  sometimes  the  disease 
is  conveyed  by  food.  For  example,  it  has  been  remarked  in  England,  and  lately 
in  Cologne,  that  the  fever  in  certain  epidemics  was  limited  to  individuals  who 
had  their  milk  from  one  common  source.  In  such  cases,  however,  the  probable 
cause  is  not  a  disease  in  the  cows,  but  a  pollution  of  the  milk  or  the  milk-cans 
by  water.  It  is  as  yet  doubtful  if  animals  can  have  typhoid  fever;  at  any  rate, 
all  attempts  at  artificial  inoculation  have  had  a  negative  result.  This  fact  makes 
it  uncertain  whether  the  illnesses  which  have  been  observed  to  follow  the  inges- 
tion of  the  flesh  of  diseased  calves  (e.  g.,  the  epidemic  of  Kloten)  are  actually 
to  be  considered  typhoid  fever,  although  the  pathological  changes  are  said  by 
Huguenin  to  be  very  similar  to  those  found  in  typhoid.  Finally,  it  seems  very 
probable  that  persons  who  come  into  direct  contact  with  typhoid  discharges  are 
thereby  exposed  to  the  danger  of  infection.  Many  deny  this  (vide  supra),  but 
it  would  explain  why  nurses  and  laundresses,  who  have  to  handle  clothing  soiled 
by  the  discharges  of  patients,  are  comparatively  often  attacked  by  typhoid  fever. 


4  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

Through  the  agency  of  dirty  linen,  utensils,  etc.,  the  poison  may  be  spread  even 
further. 

[It  is  not  probable  that  sewer-gas  in  itself  is  an  exciting  cause  of  typhoid  fever. 
Especially  in  large  cities  typhoid  dejections  are  constantly  finding  their  way  into 
the  sewers,  which  afford  all  the  conditions  favorable  to  the  further  growth  and 
development  of  the  poison.  If,  then,  the  drainage  of  any  house  is  defective,  the 
seeds  of  the  disease  can  readily  gain  access  to  the  interior  of  the  house  and  infect 
susceptible  individuals. 

One  of  the  most  instructive  epidemics  on  record  is  that  in  Plymouth,  Pennsyl- 
vania, a  town  of  eight  thousand  inhabitants.  In  the  spring  of  1885  a  disease,  at 
first  supposed  to  be  of  a  strange  character,  broke  out  in  the  place,  and,  before  it 
ceased,  affected  twelve  hundred  persons,  causing  one  hundred  and  thirty  deaths. 
It  was  soon  found  that  the  malady  was  typhoid  fever,  which  arose  from  one  case, 
briefly  in  this  wise:  In  January,  February,  and  March  there  was  a  case  of  typhoid 
in  a  house  on  a  hill  sloping  toward  a  water-supply  of  the  town.  The  dejec- 
tions were  thrown  out  on  the  snow,  under  which  the  ground  was  deeply  frozen. 
Ou  March  25th  a  sudden  and  great  thaw  occurred,  the  water  did  not  sink  into 
the  ground,  but  ran  immediately  into  the  natural  surface  channels,  and  on  April 
10th  the  epidemic  began.  There  were  reasons,  which  it  is  not  necessary  here  to 
detail,  why  the  above  source  of  water-supply  was  drawn  upon  to  an  unusual  de- 
gree just  at  that  time,  but  it  has  been  shown  that  those  who  derived  their  water 
from  other  sources  were  spared  by  the  disease.  The  original  case  came  from  Phil- 
adelphia.] 

In  almost  all  cases  the  intestine  seems  to  be  the  actual  gate  of  entrance  for  the 
typhoid  poison  into  the  human  system.  This  is  shown  by  the  fact  that  in  all 
cases  which  come  to  autopsy  in  early  stages  of  the  disease,  the  typhoid  bacilli  are 
mainly  confined  to  the  lymphatic  tissues  of  the  intestine.  The  typhoid  poison 
(bacilli  or  spores)  is  probably  swallowed,  either  directly  with  water  or  polluted 
food,  or  after  being  inhaled  or  in  some  other  way  introduced  into  the  mouth.  If 
not  destroyed  in  the  stomach,  it  passes  on  in  viable  condition  into  the  alkaline 
contents  of  the  intestine,  and  here  finds  the  conditions  essential  to  its  further 
development.  It  penetrates  at  first  into  the  follicles  and  Peyer's  patches,  and 
thence  goes  on  into  the  mesenteric  glands,  the  blood-current,  the  spleen,  and  other 
organs. 

As  in  the  case  of  most  other  infectious  diseases,  the  occurrence  of  infection  is 
dependent  not  only  on  outward  conditions,  but  also  on  an  individual  predisposi- 
tion. Details  of  the  circumstances  attending  this  latter  are  as  yet  not  at  all  accu- 
rately understood.  Even  in  the  worst  typhoid  centers,  where  the  possibility  of 
infection  must  be  universal,  many  escape  the  disease. 

Age  has  an  indubitable  influence  upon  the  liability  to  the  disease.  Typhoid  is 
especially  a  disease  of  youthful,  vigorous  individuals,  of  fifteen  to  thirty  years. 
Above  that  age  it  is  noticeably  less  frequent,  although  cases  do  occur  at  sixty  and 
even  seventy  years.  Formerly  it  was  often  said  that  young  children  were  never 
attacked ;  but  this  was  because  the  disease  was  not  recognized,  for  in  reality  it  is 
only  children  under  one  year  old  who  seem  to  be  seldom  infected.  At  a  later  age, 
cases  are  by  no  means  rare. 

Sex  can  not  be  shown  with  certainty  to  have  an  especial  predisposing  influence 
upon  the  frequency  of  typhoid  fever. 

Mental  excitement  and  gross  errors  in  diet  seem  to  predispose  to  the  disease. 
On  the  other  hand,  a  certain  immunity  has  been  alleged  to  be  given  by  many  cir- 
cumstances, especially  pregnancy,  the  puerperal  state,  and  other  diseases  already 
existing  (tuberculosis,  heart  disease).  Most  of  these  statements  are  shown,  how- 
ever, by  more  extended  experience,  to  be  very  doubtful.    It  does  seem  to  be  certain 


TYPHOID   FEVER.  5 

that  the  occurrence  of  typhoid  fever  gives  very  probable  though  not  absolute 
immunity  against  any  later  new  attack. 

Finally,  it  must  be  mentioned  that  the  necessary  conditions  for  an  abundant 
development  and  conveyance  of  the  typhoid  germs  are  beyond  doubt  dependent 
on  the  season.  According  to  statistics,  most  of  the  typhoid  epidemics  come  in  the 
months  from  August  to  November,  while  generally  the  number  of  cases  greatly 
diminishes  from  December  to  spring. 

General  Course  of  the  Disease.— Extended  experience  shows  that,  after  infection 
with  the  typhoid  poison  has  taken  place,  a  certain  time  must  elapse  before  the 
symptoms  of  the  disease  appear.  The  length  of  this  time,  the  "stage  of  incuba- 
tion," is,  unlike  that  of  many  other  infectious  diseases,  not  perfectly  definite.  On 
the  average,  it  lasts  two  to  three  weeks,  sometimes  less  time,  sometimes  longer. 
During  this  period  the  patient  either  feels  perfectly  well,  or  has  certain  slight 
symptoms,  to  which  he  pays  more  or  less  attention,  according  to  his  individual 
susceptibility.  These  prodromata  consist  of  languor,  disinclination  to  exertion, 
anorexia,  slight  headache,  pain  in  the  limbs,  etc.  Often  they  last  only  a  few  days. 
Not  infrequently  the  patients  state  afterward  that  they  had  felt  the  disease  coming 
on  for  weeks. 

The  transition  of  the  prodromata  into  the  regular  disease  takes  place  sometimes 
so  gradually  that  it  is  utterly  impossible  to  take  any  one  day  as  the  first  of  the 
illness,  in  order  to  reckon  from  it  its  duration.  It  is  usually,  however,  the  first 
symptoms  of  a  high  temperature,  chilliness,  feverishness,  and  the  accompanying 
increase  in  general  discomfort,  which  allow  one  to  fix,  with  at  least  some  accuracy, 
the  beginning  of  the  disease.  A  decided  initial  rigor  is  certainly  exceptional.* 
After  the  fever  begins,  most  patients  soon  take  to  their  beds,  although  it  happens 
often  enough  that  the  sick  feel  either  unable  or  unwilling  to  give  up,  and  keep  on 
at  work  for  days ! 

There  have  been  manifold  attempts  to  divide  the  whole  course  of  the  disease 
into  separate  periods.  The  most  natural  division  seems  to  be  into  the  three  stages 
of  development,  height  or  fastigium,  and  decline  {stadium,  incrementi,  s.  acmes,  s. 
decrementi) .  Usually,  however,  physicians  reckon  according  to  the  week  of  the 
disease.  The  first  week  corresponds  to  the  developmental  stage,  the  second,  and 
in  all  severer  cases  the  third  as  well,  to  the  fastigium,  the  fourth  (in  light  cases 
the  third)  to  the  decline.  The  course  of  the  disease  is  very  variable,  however,  and 
naturally  there  is  the  greatest  diversity  in  the  departures  from  this  general  plan. 

In  the  first  week,  the  initial  period,  the  general  symptoms  augment  rapidly. 
The  patients  become,  in  severe  cases,  very  languid  and  feeble,  have  generally  an 
intense  headache,  and  complete  anorexia,  with  great  thirst.  The  fever,  which  is 
all  the  time  gradually  rising,  is  recognizable  subjectively  by  alternating  sensations 
of  heat  and  cold,  and  objectively  by  the  hot,  dry  skin,  the  parched  lips,  and  the 
dry  and  coated  tongue.  The  sleep  is  disturbed.  For  the  most  part  there  are  no 
prominent  thoracic  or  abdominal  symptoms,  except  that  at  times  there  is  a  sense  of 
oppression  in  the  chest,  or  some  cough.  The  pulse  is  quickened,  sometimes  even 
now  dicrotic.  There  is  often  a  temporary  epistaxis.  The  belly  is  not  much 
swollen  as  a  rule,  and  but  little  if  at  all  tender.  There  is  generally  constipation. 
Usually  the  spleen,  even  at  this  time,  exhibits  a  swelling  that  can  be  easily 
demonstrated. 

Generally  the  fastigium  has  begun  before  the  end  of  the  first  week.  The 
severe  general  symptoms  persist  or  even  increase.  The  fever  maintains  constant- 
ly a  considerable  elevation.     The  patients  become  more  stupid.     Often  delirium 

*  According  to  the  representations  of  many  authors,  a  marked  initial  rigor  seems  to  occur  rather 
often  in  some  places.     In  Leipsic,  and  also  in  Erlangen,  it  is  very  rare. 


6  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

appears,  especially  at  night.  In  the  lungs  there  is  developed  a  more  or  less 
intense  and  extensive  bronchitis.  The  abdomen  becomes  more  swollen.  On  the 
skin  of  the  trunk  appear,  generally  at  the  beginning  of  the  second  week,  a  number 

of  small,  pale-red  spots,  roseolse.  In- 
3  stead  of  constipation,  there  is  a  moderate 
5      diarrhoea.     There  are  daily  about  two 

2  to  four  soft,  thin,  bright- yellow  dejec- 

3  tions. 

\  The  third  week,  during  which  in  the 

:  severe  cases  the  symptoms  already  men- 
3  tioned  persist,  is  the  chief  time  of  the 
I  numerous  complications  and  of  especial 
3  clinical  events,  about  which  we  shall 
3  speak  below  at  leugth.  If  the  disease 
f  takes  a  favorable  course,  there  comes  at 
!  the  end  of  the  third  week  a  decline  of 
|  the  fever ;  and  then  the  general  symp- 
!      toms  also   improve    as    a  rule.      The 

mind  becomes  clearer,  the  patient  sleeps 

!  better,  and  gains  some  appetite.     The 

I  pulmonary    and     digestive    symptoms 

1,  abate,     and     convalescence    gradually 

.  £  begins. 

S     II  ill  Siillili    |.S  This  short  sketch  of  the  course  of  the 

™  §  disease  corresponds  to  most  of  the  cases 

-o  '8  of  medium  severity.     There  are,  how- 

•g  §  a  ever,  besides  these,  so  many  forms  and 


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ssiiisiisiissg!!:: 

IEÜSSSSS8S 


»a    so  many  variations  from  the  usual  pict- 


2  &  ure,  that  it  seems  almost  impossible  to 

|  enumerate  completely  all  the  events  of 

^  typhoid  fever.    And  besides,  the  separate 

*  epidemics  vary  in  their  general  charac- 

a  ter  according  to  the  time  and  place  of 

5  their  occurrence.     In  many  epidemics 

«  the  cases  run  a  peculiar  course  and  have 

"2  certain  special  complications  not  seen 

h  in  others. 

k  We  will  begin  the  presentation  of 

J>  the  chief  peculiarities  by  speaking  of  the 

I«  course  of  the  fever. 

|  2  Course  of  the  Fever.— Observation  of 

-.Jf  £?  the  temperature  in  typhoid  is  so  abso- 

Jj  .3  lutely  essential   for  the   estimation  of 

|  each  individual  ca'-e  that  no  scientific 

■§  physician  ought  to  treat  a  case  without 

§  regular  measurement  of  the  tempera- 

.2  |  ture.      The    measurements    should    be 

-a  I  taken,  if  possible,  in  the  rectum.     Their 

.3  Ci.  frequency  must  of  course  be  modified 

§          §          T.           is  £  by  circumstances,  but  it  will  probably 

be  possible  to  have  three  or  four  meas- 
urements daily.  At  night,  especially  if  the  patients  are  asleep,  it  is  generally 
not  requisite  to  take  the  temperature.     A  general  idea  of  the  course  of  the  fever 


TYPHOID   FEVER.  7 

can  be  gained  only  by  representing-  the  separate  measurements  graphically  in  a 
continuous  "temperature  curve." 

The  typical  curve  of  typhoid  fever  (see  Fig.  2)  falls  naturally  into  three  or  four 
divisions.  The  first  division  is  the  initial  period,  or  the  pyrogenetic  stage,  and  is 
seldom  observed,  since  at  this  time  the  patients  are  generally  not  yet  under  the 
doctor's  care.  The  initial  period  of  the  fever  lasts,  as  a  rule,  some  three  or  four- 
days,  seldom  longer;  and  during  this  time  the  temperature  rises,  generally  by 
gi-adual  steps,  so  that  the  morning  as  well  as  the  evening  temperature  is  each  day 
2°  or  3°  (1°-1'5°  C.)  higher  than  on  the  day  before.  A  sudden  and  considerable  rise 
of  temperature,  such  as  occurs  in  many  other  diseases,  is  very  rarely  seen  in  the 
beginning  of  typhoid  fever. 

The  second  division  of  the  curve  represents  the  so-called  fastigium,  and  cor- 
responds to  the  height  of  the  disease.  During  this  time  the  fever  presents,  in  most 
of  the  severer  cases,  the  general  character  of  "febris  continua" — i.  e.,  the  spon- 
taneous remissions  of  the  fever  seldom  exceed  2°  (1°  C).  Almost  always  the  lower 
temperatures  come  in  the  morning  hours  and  the  higher  hi  the  evening.  In  cases 
of  average  severity  the  morning  remissions  touch  102°-103°  (390-39-5°  C),  and  the 
evening  exacerbations  104°-105°  (40°-40'5°  C).  Temperatures  which  reach  or 
exceed  106°  (41°  0.)  are  seen  only  in  very  severe  cases.  Considerable  morning 
remissions  are  always  a  favorable  symptom,  while  morning  temperatures  of  104° 
(40°  C.)  or  higher  generally  show  the  case  to  be  severe.  The  duration  of  the  fas- 
tigium varies  with  the  severity  and  obstinacy  of  the  case.  It  may  last  only  a  few 
days  or  one  and  a  half  to  two  weeks ;  in  violent  cases  still  longer. 

In  many  cases  of  slight  or  average  severity  the  period  of  decline  follows  directly 
on  the  fastigium;  but  in  severe  cases  there  frequently  intervenes  another  stage, 
which  Wunderlich  has  graphically  named  the  "  ambiguous  "  period.  The  temper- 
ature curve  becomes  irregular  and  more  variable.  The  morning  remissions  may 
be  great,  even  reaching  the  normal,  while  the  evening  temperatures  are  often  still 
very  high.  This  stage  has  accordingly  been  termed  the  "period  of  the  steep 
curves."  It  may  be  said  that  in  general  the  longer  a  case  of  typhoid  lasts  the 
more  irregular  will  be  the  course  of  the  fever. 

The  last  stage — i.  e.,  in  cases  of  slight  or  average  severity  the  third  stage,  and 
in  severe  cases  commonly  the  fourth — is  the  period  of  defervescence  or  recovery. 
The  peculiarity  of  this  period  in  typhoid  fever  is  that  the  fall  of  the  fever  is  never 
by  crisis,  but  always  gradually,  by  lysis.  Commonly  the  temperature  descends  by 
degrees,  so  that  on  each  new  day  the  morning  remissions  as  well  as  the  evening 
exacerbations  are  1°  to  2°  (0'5°-l°  C.)  lower.  The  zigzag  form  of  curve,  in  which 
thei'e  are  of  course  very  frequently  slight  irregularities,  must  be  taken  as  the  rule. 
The  duration  of  the  defervescence  generally  exceeds  that  of  the  initial  period. 
It  lasts  five  to  eight  days,  often  longer.  It  is  not  very  seldom  that  in  defervescence 
the  morning  remissions  become  from  the  first  very  marked,  even  reaching  the 
normal  temperature,  while  the  evening  exacerbations  become  daily  less  and  less, 
until  they  too  are  not  above  the  normal.  A  third  form  of  decline  is  much  less 
frequent,  in  which  the  morning  remissions  become  every  day  greater,  while  the 
evening  temperature  persists  for  some  days  at  about  the  same  height.  Several 
times  we  have  seen  the  fever  take  on  a  tertian  type  during  recovery. 

To  this  outline  must  be  added  a  number  of  observations  of  practical  importance. 

The  initial  period  does  not  exhibit  especial  variations  from  the  course  we  have 
stated.     Its  entire  duration  is  bounded  by  certain  relatively  narrow  limits. 

The  fastigium  presents,  as  already  mentioned,  the  greatest  varieties  in  its  dura- 
tion. In  light  cases  it  is  wholly  wanting,  so  that  these  consist  only  of  a  period  of 
gradually  rising  fever,  and  of  a  gradual  defervescence  almost  immediately  con- 
secutive to  the  rise.     The  entire  duration  of  such  light  cases  is  onlv  one  and  a  half 


8  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

to  two  weeks.  In  other  and  tolerably  frequent  cases,  which  are  often  tedious,  but 
still  for  the  most  part  are  light,  the  fever  is  not  continuous,  but  remittent.  We 
have  seen  in  Leipsic,  notably  in  the  autumn  epidemic  of  1878,  a  number  of  cases 
where  the  fever  was  even  perfectly  intermittent  during  almost  the  entire  illness, 
and  where  for  two  to  three  weeks  afternoon  elevations  reaching  104°  (40°  C.)  or 
more  daily  succeeded  normal  morning  temperatures.  Tbese  cases  had  the  general 
course  of  lig'ht  attacks. 

Various  influences,  not  to  speak  of  therapeutic  interference,  may  produce  a 
considerable  temporary  remission  of  temperature  in  the  course  of  the  fastigium. 
Such  a  remission  sometimes  occurs  spontaneously  from  the  seventh  to  tenth  day  of 
the  disease.  If  a  marked  intestinal  haemorrhage  occurs  (vide  infra),  the  tempera- 
ture generally  falls  several  degrees  centigrade,  and  the  less  frequent  instances  of 
severe  epistaxis  have  the  same  effect.  If,  in  female  patients,  abortion  or  prema- 
ture delivery  occurs,  we  often  observe  a  similar  considerable  fall  of  temperature, 
even  without  severe  attendant  haemorrhage.  Perforation  of  the  intestine  often 
causes  the  temperature  to  fall  rapidly.  At  times  the  occurrence  of  mental  dis- 
turbances effects  a  moderate  though  noticeable  lowering  of  temperature.  Those 
great  and  sudden  depressions  of  tempei'ature  remain  to  be  mentioned  which  are 
accompanied  by  a  very  small  but  exceedingly  rapid  pulse  and  general  prostration. 
Every  such  collapse,  if  severe,  is  a  most  dangerous  event,  and  demands  prompt 
and  energetic  medical  treatment  (vide  infra). 

The  occurrence  of  local  complications,  such  as  pneumonia  or  inflammation  of 
the  parotid  gland,  is  generally  accompanied  by  a  considerable  rise  of  temperature. 
The  fever  in  such  cases  often  becomes  more  irregular. 

The  period  of  defervescence  departs  most  frequently  from  its  typical  behavior 
by  being  lengthened  out  into  a  "  stage  of  retardation."  The  morning  temperature 
is  then  generally  normal,  wdiile  in  the  evening  slight  or  moderate  elevations  con- 
tinue. The  reason  for  this  long  continuance  of  the  fever  may  frequently  be  found 
in  some  not  yet  completely  healed  local  complication,  but  often  no  such  lesion 
can  be  demonstrated.  Then  we  are  commonly  inclined  to  surmise  sluggish  intes- 
tinal ulcers  which  will  not  heal,  or  trouble  in  the  mesenteric  glands,  etc.  This 
sluggish  fever  may  continue  for  weeks.  It  is  prone  to  follow  severe  cases,  but 
lighter  attacks,  especially  in  elderly  or  feeble  patients,  may  also  take  on  this  slug- 
gish character  at  a  relatively  early  period. 

Entrance  into  complete  convalescence  is  shown  with  far  greater  certainty  by 
the  absence  of  elevations  of  temperature  than  by  any  other  single  symptom. 
There  sometimes  come,  however,  temporary  elevations  of  temperature  during  con- 
valescence, following  some  error  in  diet,  long-continued  constipation,  or  mental 
excitement.  In  other  cases  the  new  fever  depends  on  some  local  sequela,  e.  g.,  a 
boil  or  a  glandular  abscess.  Often,  however,  the  most  accurate  investigation  fails 
to  demonstrate  a  cause.  Especially  in  the  beginning  of  convalescence  there  some- 
times comes  a  high  fever,  or  even  a  rigor,  which  may  recur  several  times,  but 
soon  gives  place  to  a  normal  temperature.  Generally  no  certain  cause  for  these 
brief  but  decided  elevations  of  temperature  can  be  pointed  out.  Perhaps  we  might 
consider  the  possibility  of  some  affection  of  the  mesenteric  lymph-glands.  These 
sudden  and  great  elevations  have  seldom  any  grave  significance. 

This  new  fever  which  we  have  just  described  is  best  termed  recurrent  fever- 
attack,  in  contrast  with  the  proper  typhoid  relapse.  That  is,  after  typhoid  fever 
has  ended,  the  whole  process  may  be  repeated  ;  and  this  occurrence  is  called  a 
relapse.  Particulars  as  to  the  behavior  of  the  fever  in  such  cases  will  be  consid- 
ered below,  in  connection  with  all  the  other  peculiarities  of  typhoid  relapses. 


TYPHOID  FEVER 


Phenomena  and  Complications  relating  to  the  Separate  Organs.* 

1.  Digestive  Organs. — We  think  it  best  to  begin  our  consideration  of  the  more 
special  symptoms  with  the  phenomena  referable  to  the  intestinal  canal,  for  the 
reason  that  the  anatomical  changes  in  the  intestine  are  pathognomonic.  Indeed, 
these  alterations  may  sometimes  become  of  surpassing  import  in  a  clinical  point 
of  view,  although  in  the  majority  of  cases  the  intestinal  symptoms  are  clinically 
not  nearly  so  prominent  as  the  general  symptoms  that  result  from  the  infection 
of  the  system  as  a  whole. 

The  characteristic  typhoid  lesion  of  the  intestine  consists  of  an  affection  of 
Peyer's  patches,  most  marked  in  the  lower  part  of  the  ileum.  In  the  first  week 
the  patches  swell  gradually  (stage  of  medullary  infiltration).  The  rest  of  the 
mucous  membrane  exhibits  at  the  same  time  more  or  less  marked  symptoms  of 
simple  catarrhal  inflammation.  In  the  second  week,  necrotic  crusts  form  on  the 
surface  of  the  patches,  which  are  cast  off  in  the  third  week,  leaving  behind  the 
typhoid  ulcers.  Toward  the  end  of  the  third  week  the  ulcers  clean  up,  and  then 
in  the  fourth  week,  if  the  case  takes  a  favorable  course,  the  ulcers  heal.  Smooth 
scars  are  formed,  often  diffusely  pigmented.  Experience  shows  that  these  scarcely 
ever  lead  to  stricture  of  the  intestine.  The  same  process  also  goes  on  in  a  greater 
or  less  number  of  the  solitary  follicles  as  well  as  in  the  Peyer's  patches  themselves. 
We  may  add  that  probably  in  lighter  cases  of  typhoid  {vide  infra)  there  is  often 
no  actual  ulceration.  The  swelling  of  the  lymphatic  tissue  subsides  in  this  case 
before  sloughing  occurs.  We  have  already  mentioned  the  occurrence  of  typhoid 
bacilli  in  Peyer's  patches  and  the  intestinal  follicles. 

The  number  and  extent  of  the  ulcers  formed  have  no  direct  relation  whatever 
to  the  severity  of  the  case.  Although  very  extensive  lesions  in  the  intestine  are 
often  found  in  cases  that  end  fatally,  yet,  on  the  other  hand,  we  observe  fatal 
cases  in  which  only  a  few  ulcers  are  found  in  the  intestine.  In  cases  with  exten- 
sive intestinal  lesions  we  often  see  follicular  ulcers  in  the  colon  as  well  as  in  the 
small  intestine  (colo-typhoid). 

The  clinical  symptoms  referable  to  the  intestinal  canal  are,  as  we  have  said, 
prominent  only  in  exceptional  cases.  In  the  beginning  of  typhoid  fever  there  is 
usually  constipation.  This  may  last  throughout  the  illness,  so  that  the  patients 
have  but  one  dejection  in  every  two  or  three  days,  or  often  none  at  all  unless  an 
enema  be  given.  As  a  rule,  a  moderate  diarrhoea  begins  during  the  second  week. 
There  are  two  to  four  stools,  or  sometimes  more,  each  day.  They  usually  have 
a  characteristic  bright-yellow  color.  On  standing,  they  divide  into  an  upper, 
cloudy,  and  quite  liquid  layer,  and  a  lower  layer  composed  of  yellow,  crumby 
masses.  They  have  generally  an  alkaline  reaction,  and  upon  microscopic  exami- 
nation they  are  found  to  contain,  besides  remnants  of  the  ingesta  and  granular 
detritus,  a  few  epithelial  cells,  round  cells,  many  crystals  of  triple  phosphate,  and 
numberless  bacteria.  Pfeiffer  and  other  investigators  have  been  able  frequently, 
although  not  invariably,  to  demonstrate  the  true  typhoid  bacilli  in  the  dejecta 
by  means  of  special  methods  of  cultivation. 

Severe  diarrhoea  (ten  to  twenty  stools  daily)  is  relatively  infrequent.  In  some 
severe  cases  we  have  seen  the  stools  take  on  a  dysenteric  character.  The  autopsy 
showed  in  these  cases  unusually  severe  lesions  of  the  colon  and  a  diphtheritic 
inflammation  of  its  mucous  membrane. 

Gaseous  distention  affecting  the  intestine,  and  especially  the  colon,  is  very 
frequent,  but  in  most  cases  it  is  not  excessive.     Indeed,  severe  cases  of  typhoid  are 

*  To  avoid  repetition,  we  have  in  what  follows  united  a  description  of  the  anatomical  changes  with 
the  presentation  of  the  clinical  symptoms. 


10  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

observed  in  which  the  abdomen  always  remains  concave.  Marked  tympanites  is 
always  an  unpleasant  complication.  We  saw  one  case,  which  ended  fatally,  with 
very  great  tympanites,  in  which  the  lesions  were  almost  exclusively  in  the  colon, 
and  it  was  the  enormous  distention  of  its  entire  length  which  had  so  swollen 
the  abdomen.  The  noise  that  can  often  be  produced  by  pressure  in  the  ileo-caecal 
region  (gurgling)  used  to  be  regarded,  but  probably  erroneously,  as  especially 
characteristic  of  typhoid  fever.  Abdominal  pain  is  often  entirely  absent.  Some 
patients,  however,  complain  of  abdominal  pain  during  almost  the  entire  illness. 
On  pressure,  the  belly  is  generally  somewhat  sensitive,  but  the  tenderness  is  sel- 
dom extreme.  It  is  more  apt  to  be  marked  when  there  is  constipation.  Often 
such  tenderness  is  due  to  a  participation  of  the  peritoneum  in  the  disease,  even 
when  thei*e  is  no  perforation  (vide  infra). 

There  still  remain  two  symptoms  of  the  greatest  practical  importance,  both  of 
which  have  a  direct  connection  with  the  intestinal  lesions  :  they  are  intestinal 
hemorrhage  and  perforation. 

Intestinal  haemorrhages  in  the  course  of  typhoid  are  almost  always  due  to  the 
erosion  of  the  walls  of  blood-vessels  in  connection  with  the  formation  and  throw- 
ing off  of  the  crusts  of  the  ulcers.  The  haemorrhages  occur,  therefore,  most  fre- 
quently toward  the  end  of  the  second  and  during  the  third  week.  The  blood  pours 
out  into  the  intestine,  and  is  passed  with  the  stools.  Its  amount  may  be  small,  or 
it  may  reach  to  one  or  two  pints,  or  even  more.  Its  color  is  generally  rather  dark. 
The  later  discharges  are  generally  tarry.  Liebermeister  states  that  he  has  observed 
intestinal  haemorrhages  in  7'3  per  cent,  of  typhoid  patients,  and  Griesinger  in  5*3 
per  cent.  We  have  ourselves  seen,  in  the  medical  clinique  at  Leipsic,  45  intes- 
tinal haemorrhages  in  472  cases,  i.  e.,  in  9 "5  per  cent.  In  individual  epidemics  the 
frequency  varies  greatly.     It  rose  in  1880  to  eighteen  per  cent. 

Intestinal  haemorrhage  is  always  a  grave  symptom.  Even  slight  haemorrhages 
deserve  consideration,  for  they  may  be  the  precursors  of  severer  ones.  And  yet 
intestinal  haemorrhage,  even  if  profuse,  is  not  necessarily  fatal.  Of  the  above 
forty-five  cases  of  typhoid  with  haemorrhage,  twenty-six  ended  in  complete  recov- 
ery. In  eight  cases,  death  occurred  as  the  immediate  result  of  the  loss  of  blood. 
Eleven  ended  fatally  after  a  time. 

After  every  considerable  intestinal  haemorrhage,  the  symptoms  of  general 
anaemia,  often  even  of  collapse,  appear.  The  fall  of  the  bodily  temperature  has 
been  already  mentioned.  The  haemorrhage  has  sometimes  a  favorable  influence 
on  severe  cerebral  symptoms,  for  consciousness  succeeds  to  the  previous  stupor 
or  delirium.  Often  the  haemorrhage  is  directly  followed  by  recovery  from  the 
disease. 

Much  more  ominous  than  the  intestinal  haemorrhage  is  the  occurrence  of  per- 
foration, as  a  result  of  the  breaking  through  of  a  typhoid  ulcer  into  the  abdominal 
cavity,  because,  almost  without  exception,  this  is  followed  by  a  purulent  or  even 
ichorous  peritonitis.  The  occurrence  of  perforation  is  sometimes  marked  by  a  vio- 
lent pain  suddenly  felt  by  the  patient;  but  it  may  also,  even  in  severe  cases,  take 
place  insidiously.  The  abdomen  is  generally  (not  always)  greatly  distended  and 
very  tender  on  pressure,  so  that  even  in  stupor  patients  groan  while  being  exam- 
ined. If  gas  has  entered  through  the  opening  into  the  peritoneal  cavity,  we  often 
observe  absence  of  the  ordinary  dullness  over  the  liver ;  but  this  symptom  is  to 
be  employed  cautiously  as  a  factor  in  diagnosis,  for  absence  of  hepatic  dullness 
may  also  result  from  distended  intestines  lying  in  front  of  the  liver.  When  per- 
foration has  occurred,  the  patient  soon  looks  collapsed,  with  cheeks  fallen  in  and 
sharp,  cool  nose.  Frequent  eructations  and  vomiting  often  follow.  The  pulse 
becomes  small  and  very  frequent.  The  temperature  generally  falls  as  the  peri- 
tonitis begins,  and  later  it  usually  undergoes  great  variations. 


TYPHOID  FEVER.  u 

Perforation  of  the  intestine  occurs  most  frequently  in  the  third  or  fourth  week 
of  the  disease.  In  sluggish  cases,  however,  we  can  not  be  without  apprehensions 
of  it  till  a  late  period.  The  perforation  generally  takes  place  in  a  coil  of  the  lower 
part  of  the  small  intestine,  and  with  marked  relative  frequency  in  the  right  side 
of  the  pelvis — seldom  in  the  vermiform  appendix  or  in  the  colon.  With  few 
exceptions,  death  comes  quickly,  after  a  few  days  at  latest.  Out  of  fifty -six  fatal 
typhoid  cases  in  the  Leipsic  medical  clinique  we  lost  five,  or  nine  per  cent.,  from 
peritonitis  following  perforation.  Here  and  there  a  case  of  recovery  has  been 
reported,  probably  resulting  from  a  limitation  of  the  peritonitis  through  speedy 
adhesion  of  the  intestines. 

It  should  be  mentioned  here  that  sometimes  in  typhoid  fever  a  local  or  general 
peritonitis  may  occur  through  direct  extension  of  the  process  to  the  serous  mem- 
brane without  actual  perforation.  We  have  seen  in  one  case,  as  a  result  of  the 
peritonitic  bands  and  false  membranes,  complete  occlusion  of  the  intestine  (ileus), 
and  death. 

Swelling  of  the  mesenteric  lymph-glands  (less  often  of  the  retro-peritoneal 
glands  as  well)  is  found  in  typhoid  almost  as  constantly  as  the  anatomical  changes 
in  the  intestine.  Sometimes  they  break  down,  i.  e.,  suppurate.  In  cases  that  have 
passed  through  the  disease  we  often  find  considerable  deposits  of  lime  in  the 
glands.  These  changes  have  a  certain  clinical  importance  ;  for,  as  already  men- 
tioned, we  may  often  venture  to  refer  a  more  or  less  tedious  recurrent  febrile  state 
which  has  no  other  demonstrable  cause  to  this  lesion  of  the  mesenteric  glands. 
In  some  rare  cases  a  general  peritonitis  has  been  observed  as  a  result  of  the  burst- 
ing of  a  suppurating  gland. 

The  swelling  of  the  spleen  (acute  splenic  tumor)  is,  in  typhoid  fever  as  well  as 
in  many  other  acute  infectious  diseases,  one  of  the  most  constant  symptoms.  The 
enlargement  of  the  spleen  can  often  be  demonstrated  as  early  as  the  end  of  the 
first  week,  and  is  therefore  of  considerable  diagnostic  importance  ;  but  percussion 
of  the  spleen  is  sometimes  decidedly  difficult  and  deceptive  in  this  disease  because 
of  the  existence  of  tympanites.  The  surest  demonstration  of  splenic  enlargement 
is  therefore  always  by  means  of  palpation,  which,  after  a  little  practice,  gives  a 
positive  result  in  the  majority  of  cases.  Absence  of  splenic  tumor  is  most  fre- 
quently observed  in  elderly  typhoid  patients.  The  spleen  may  also  diminish  con- 
siderably in  size  after  severe  intestinal  haemorrhage.  Pain  in  the  splenic  region, 
resulting  from  tearing  of  the  distended  capsule,  is  comparatively  rare.  The  splenic 
infarctions  which  sometimes  occur  may,  in  exceptional  cases,  prove  the  starting- 
point  of  a  peritonitis. 

Hepatic  symptoms  are  seldom  seen  in  typhoid  fever,  except  that  there  maybe  a 
moderate  swelling  of  the  organ.  The  anatomical  changes  of  "parenchymatous 
degeneration,"  and  the  frequent  formation  in  the  liver  of  the  small  lymph omata 
which  Wagner  discovered,  have  no  clinical  significance.  The  bile  secreted  is  gen- 
erally pale  and  scanty.  This  is  a  partial  explanation  of  the  light  color  of  the 
stools.  A  very  rare  complication,  which  we  ourselves  observed  in  one  case,  is 
acute  yellow  atrophy  of  the  liver. 

The  stomach  presents  no  especial  anatomical  changes  in  typhoid.  Anorexia 
is  an  almost  invariable  symptom  in  the  beginning  and  during  the  course  of 
all  severer  cases.  There  is  seldom  any  desire  for  food  till  recovery  begins;  but 
then,  if  convalescence  is  undisturbed,  the  appetite  soon  attains  an  enviable  keen- 
ness. Vomiting  in  the  beginning  or  course  of  the  disease  is  an  exception,  unless 
after  some  error  in  diet.  We  have  already  mentioned  it  as  a  symptom  of  perito- 
nitis. 

The  changes  in  the  mouth  and  throat  of  typhoid  patients  deserve  the  careful 
attention  of  the  physician.     The  lips  and  tongue  are  in  severe  cases  dry  and  fis- 


12  ACUTE  GENERAL  INFECTIOUS  DISEASES 

sured.  The  lips  are  often  covered  with  dry,  black  crusts,  sometimes  described  as 
a  "  fuliginous  coating. "  The  tongue  is  apt  to  be  thickly  coated  at  first,  but  later 
cleans  off  from  the  edges  and  tip.  In  severe  cases,  especially  if  the  mouth  is  not 
properly  cleansed,  a  rather  severe  stomatitis  may  occur  and  produce  superficial 
ulceration  of  the  buccal  mucous  membrane  and  of  the  edges  of  the  tongue.  The 
gums  sometimes  become  spongy,  and  are  apt  to  bleed,  as  if  scorbutic. 

Actual  sore  throat,  at  least,  according  to  our  experience  in  Leipsic,  occurs  but 
seldom  at  the  beginning  of  typhoid  fever.  The  difficulty  in  swallowing,  often 
complained  of  by  patients,  is  generally  due  to  dryness  of  the  pharynx.  In  certain 
epidemics,  however,  the  occurrence  of  sore  throat  at  the  beginning  of  the  illness 
has  been  frequently  observed.  It  may  even  happen  that  this  early  sore  throat  is 
accompanied  by  an  erythema  diffused  over  the  body,  so  that  at  first  suspicions  of 
scarlet  fever  arise.  In  rare  cases  (so-called  tonsillo-typhoid  or  pharyngo-typhoid) 
there  are  seen  upon  the  tonsils  peculiar  whitish  elevations,  which  later  ulcerate. 
These  are  probably  to  be  regarded  as  a  specific  typhoid  lesion  of  the  tonsils.  It 
should  also  be  mentioned  that  in  severe  cases  there  is  often  an  extensive  growth 
of  thrush  in  the  mouth  and  throat,  and  this  may  spread  quite  a  distance  down  the 
oesophagus. 

The  changes  in  the  mouth  and  throat  are  of  especial  interest,  for  the  reason 
that  they  may  be  directly  propagated  to  important  neighboring  organs.  Starting 
from  the  pharyngeal  cavity,  the  pathogenic  agent,  probably  in  most  cases  the 
staphylococcus,  may  penetrate  through  the  Eustachian  tube  into  the  middle  ear. 
Thus  arise  those  inflammations  of  the  middle  ear  which  are  not  very  rare  in  severe 
cases  of  typhoid,  and  which  lead  to  perforation  of  the  membrana  tympani  and 
to  purulent  discharges  from  the  ear.  The  not  infrequent  inflammation  of  the 
parotid  gland  is  also,  as  we  believe,  occasioned  in  a  similar  way,  the  inflammatory 
agent  reaching  the  parotid  gland  from  the  mouth  by  way  of  Steno's  duct.  We  do 
not  regard  the  otitis  and  parotitis  as  especial  localizations  of  tbe  typhoid  poison, 
but  as  genuine  complications  (secondary  disease),  for  the  occurrence  of  which 
typhoid  fever  merely  furnishes  the  occasion,  as  when  the  mouth  is  imperfectly 
cleansed.  The  parotitis  appears  most  frequently  in  the  third  week,  and  generally 
on  one  side,  though  sometimes  on  both.  It  almost  always  becomes  purulent,  and 
discharges  either  externally  or  into  the  external  auditory  meatus,  unless  there  is  a 
timely  incision. 

2.  Organs  of  Respiration. — Affections  of  the  lungs  are  among  the  most  frequent 
and  important  complications  of  typhoid  fever,  but  are  for  the  most  part  not  a 
direct  result  of  the  typhoid  infection.  The  bronchitis  very  often  found  in  severe 
cases,  and  especially  in  patients  who  do  not  come  till  late  under  proper  care,  cer- 
tainly is  chiefly  dependent  on  the  imperfect  expectoration  of  the  bronchial  secre- 
tions and  on  the  inhalation  of  inflammatory  agents  coming  from  the  mouth  and 
throat. 

Numerous  cases  of  typhoid  of  slight  or  average  severity,  under  proper  care, 
run  their  course  without  any  considerable  bronchitis.  In  many  other  cases,  and 
even  severe  ones,  the  bronchitis  remains  within  moderate  bounds,  especially  if 
the  patient  is  brought  promptly  under  proper  care  and  treatment;  but  in  severe 
cases,  where  marked  disturbances  of  the  nervous  system  arise,  and  the  patient  in 
his  stupor  expectorates  little,  swallows  things  the  wrong  way,  and  lies  all  the 
time  on  his  back,  passive  and  collapsed,  the  occurrence  of  a  sevei'e,  diffuse  bron- 
chitis, especially  in  the  lower  lobes  of  the  lungs,  can  hardly  be  avoided.  Nor  in 
such  cases  is  there  generally  a  mere  bronchitis,  but  a  more  or  less  extensive 
catarrhal,  lobular  pneumonia,  to  be  classed  therefore  under  the  so-called  inhala- 
tion pneumonias  (cf.  chapter  on  lobular  pneumonia).  What  was  formerly  termed 
"  hypostatic  pneumonia"  is  also  almost  invariably  to  be  put  in  this  group. 


TYPHOID  FEVEE.  13 

From  the  way  in  which  these  pulmonary  disorders  arise,  we  can  understand 
why  the  bronchitis  sometimes  takes  on  a  putrid  character,  and  why  the  lobular 
infiltrations  are,  in  severe  cases,  transformed  into  genuine  gangrene.  If  such  spots 
touch  the  pleura,  they  occasion  the  development  of  a  pleurisy  which  is  almost 
always  purulent.  In  rare  cases,  pneumothorax  may  arise  as  a  sequel  to  the  perfo- 
ration of  a  gangi'enous  infiltration  into  the  pleural  cavity.  Various  circumstances 
promote  the  occurrence  of  pulmonary  symptoms.  Thus  we  find  it  especially  easy 
for  a  severe  bronchitis  and  its  sequelae  to  be  developed,  in  the  case  of  elderly  per- 
sons, or  the  kyphoskoliotic,  or  the  corpulent,  or  patients  who  have  previously  suf- 
fered from  emphysema  or  cardiac  disease. 

The  subjective  thoracic  symptoms,  in  typhoid  patients  who  have  pulmonary 
complications,  are  generally  not  very  prominent.  It  is  only  occasionally  that 
patients  complain  in  the  early  stages  of  typhoid  fever  of  pain,  and  of  a  sense  of 
oppression  in  the  chest,  or  of  cough,  or  of  a  stitch  in  the  side ;  and  even  when 
such  symptoms  exist,  the  physical  examination  may  give  comparatively  insignifi- 
cant results.  The  severer  pulmonary  complications  are  seen  mainly  in  those 
whose  intelligence  is  more  or  less  blunted,  and  who,  therefore,  make  little  com- 
plaint, are  not  much  disturbed  by  the  dyspnoea,  and  cough  and  expectorate  little. 
A  careful  physical  examination  alone  can  enlighten  us  as  to  their  condition.  On 
auscultation,  sibilant  rhonchi  are  the  chief  signs  observed  in  the  milder  cases.  In 
the  severer  ones  there  are  moist,  fine,  and  coarse  rales,  especially  numerous  toward 
the  base  of  the  chest.  If  there  are  abundant  moist  rales,  we  may  infer  that  there 
is  a  lobular  pneumonia,  although  this  can  not  be  demonstrated  with  certainty  till 
the  separate  islets  of  infiltration  unite  into  a  more  extensive  solidification,  so  as  to 
afford  dullness  on  percussion. 

In  addition  to  the  pulmonary  lesions  already  mentioned,  genuine  croupous  or 
lobar  pneumonia  does  occur  in  typhoid  fever.  Probably  this  must  be  regained  as 
a  direct  result  (localization)  of  the  typhoid  poison,  although  this  croupous  pneu- 
monia is  not  anatomically  distinguishable  from  the  common,  genuine  pneumonia. 
It  often  appears  as  early  as  the  second  week,  and  attacks  the  lower  as  well  as  the 
tipper  lobes.  Liebermeister  states  that  he  has  sometimes  observed  it  during  con- 
valescence. 

Especial  interest  attaches  to  those  cases  of  typhoid  fever  which  begin  with  a 
lobar  pneumonia.  Often  there  is  at  first  not  the  slightest  suspicion  of  a  typhoid 
fever,  for  the  disease  is  regarded  as  an  ordinary  croupous  pneumonia;  but  it  is 
usually  to  be  noticed  that  the  illness  does  not  begin  suddenly  with  a  rigor,  but 
more  gradually,  and  that  from  its  incipiency  the  constitutional  symptoms,  the 
headache  and  splenic  tumor,  are  more  prominent  than  is  usually  the  case  in  pneu- 
monia. At  the  end  of  the  first  week's  illness  there  is  no  crisis,  but  persistent  fever. 
Now  the  pulmonary  symptoms  often  retreat  more  and  more  to  the  background, 
while,  on  the  contrary,  diarrhoea  and  rose-spots  appear.  The  spleen  is  enlarged. 
In  short,  the  clinical  picture  of  typhoid  is  developed.  It  is  not  unnatural  to  sup- 
pose, although  there  is  yet  no  absolute  proof  of  the  fact,  that  in  these  cases,  which 
are  fittingly  termed  "  pneumo-typhoid,"  the  infection  with  the  typhoid  bacilli  has 
taken  place  exceptionally  in  the  pulmonary  area,  and  that,  therefore,  the  first 
pathological  changes  are  developed  in  the  lungs. 

Laryngeal  Lesions. — The  same  causes  which  produce  the  bronchitis  result  also 
in  a  simple  catarrhal  laryngitis,  with  hoarseness.  This  is  in  severe  cases  accom- 
panied by  superficial  ulcers  on  the  vocal  cords  or  the  posterior  wall  of  the  larynx. 
Sometimes,  again,  the  lesion  is  due  to  mechanical  causes,  constituting  the  so-called 
"decubitus  laryngis.'''1  The  disorders  which  attack  the  less  superficial  structures 
of  the  larynx  are  fortunately  rare.  Chief  among  them  is  a  laryngeal  perichon- 
dritis of  the  arytenoid  cartilages.     This  complication  is  justly  regarded  as  of  bad 


14  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

omen,  and  may  lead  to  the  rapid  development  of  cedema  of  the  glottis,  with  great 
laryngeal  obstruction  and  threatening  suffocation.  These  severe  laryngeal  affec- 
tions in  typhoid  are  regarded  by  some  authorities,  especially  by  Klebs,  as  always 
the  direct  effect  of  the  infecting  poison ;  but  in  most  cases  they  are  probably  clue 
to  an  invasion  of  staphylococci  or  some  similar  microbes.  We  have  several  times 
seen  laryngeal  croup  in  typhoid  fever,  and  it  is  a  very  dangerous  symptom.  We 
are  inclined,  however,  to  the  belief  that  it  was  in  every  case  a  secondary  disease. 

Among  symptoms  referable  to  the  mucous  membrane  of  the  nose,  epistaxis  is 
important.  It  occurs  in  the  beginning  of  typhoid  with  tolerable  frequency,  and 
is  in  one  way  not  unfavorable,  for  it  often  mitigates  the  patient's  headache.  At  a 
later  period  uose-bleed  may  become  a  very  unpleasant  complication,  as  it  is  some- 
times very  difficult  to  check.  We  have  even  seen  one  fatal  case  due  to  persistent 
nose-bleed.  Other  nasal  symptoms  are  exceptional.  There  is  an  old  saying  that 
typhoid  never  begins  with  a  coryza. 

3.  Nervous  System. — The  old  term  "  nervous  fever,"  which  is  still  used  by  the 
laity,  shows  how  frequent  and  severe  are  the  nervous  derangements  which  occur 
in  typhoid.  In  cases  of  any  severity  there  is  almost  always  a  certain  dullness  of 
intellect,  often  amounting  to  apathy  and  somnolence.  The  patients  give  mono- 
syllabic and  incomplete  answers  to  all  questions,  and  their  statements  about 
their  previous  history  are  often  disordered  and  contradictory.  There  may  even 
be  sopor  or  a  deep  coma  in  the  worst  cases.  All  cases  of  this  sort  in  which 
there  was  a  condition  of  intellectual  enfeeblement  were  termed  by  the  old 
physicians  " febris  nervosa  stupida,"  in  contrast  to  the  "febris  nervosa  ver- 
satilis,"  that  form  in  which  abnormal  mental  activity  or  delirium  predominates. 
In  severe  cases  delirium  is  very  frequent.  It  is  generally  worse  at  night,  and  at 
times  when  the  patient  happens  to  be  left  alone.  Very  often  he  tries  to  leave  his 
bed,  because  of  his  delusions,  and  talks  of  persons  and  things  with  which  he  was 
formerly  familiar;  or  he  is  very  noisy  and  restless,  sometimes  shrieking  from 
groundless  fears.  We  may  add  that  these  diverse  nervous  symptoms  frequently 
succeed  one  another,  or  appear  in  combination.  Sometimes  a  soporose  patient 
may  be  heard  softly  whispering  to  himself  in  "  muttering  delirium." 

Certain  motor  disturbances  are  often  combined  with  considerable  impairment 
of  consciousness.  There  is  a  slight  twitching  of  the  muscles  of  the  face  and  ex- 
tremities. The  old  authorities  gave  the  name  subsultus  tendinum  to  the  sudden 
leaping  into  prominence  of  the  sinews  thus  caused.  It  is  best  seen  on  the  back 
of  the  hands.  In  severe  cases  the  patient  is  sometimes  observed  to  grind  the  teeth 
together;  this  is  due  to  a  cramp-like  condition  of  the  muscles  of  mastication,  and 
is  justly  regarded  as  ominous.  We  often  see  persistent  tremor  of  the  extremities 
and  lower  jaw ;  and  it  is  especially  in  these  cases,  as  we  have  demonstrated  upon 
numerous  patients,  that  the  tendon  reflexes  and  the  mechanical  excitability  of  the 
muscles  are  much  increased.  If  deep  coma  comes  on,  the  muscles  become  lax, 
the  motions  of  the  eye  are  not  co-ordinated,  and  reflex  excitability  diminishes,  or 
is  wholly  extinguished. 

Headache  is  one  of  the  most  constant  symptoms  in  the  beginning  of  the  dis- 
ease. It  is  usually  referred  to  the  forehead  or  temples.  The  pain  may  be  very 
violent,  and  sometimes  takes  on  almost  a  neuralgic  character.  It  almost  always 
subsides  in  the  second  week. 

If  we  seek  the  cause  of  these  nervous  symptoms,  which  are  often  so  severe,  we 
find  that  the  anatomical  changes  in  the  nervous  system,  including  the  brain,  bear 
no  relation  whatever  to  the  severity  of  the  symptoms  obseiwed  during  life.  We 
sometimes  meet  with  minute  haemorrhages  in  the  cerebral  meninges,  or  meningeal 
opacity  or  cedema,  or  a  moist  condition  of  the  cerebral  parenchyma ;  but  the  con- 
nection of  these  and  similar  changes  with  the  symptoms  of  the  disease  is  often 


TYPHOID  FEVER.  15 

more  than  doubtful.  Nor  can  the  microscopic  alterations  in  the  brain,  which 
have  been  reported,  be  regarded  as  important  and  authoritative.  It  is  only  in 
very  rare  cases  that  large  cerebral  haemorrhages  or  purulent  meningitis  have 
been  found.  As  to  this  last,  we  should  always  be  very  cautious  in  making  a  diag- 
nosis, as  symptoms  which  would  seem  to  be  most  conclusively  meningeal — such 
as  stiffness  of  the  neck,  rigidity  of  the  whole  spinal  column,  and  occipital  head- 
ache— may  appear  in  typhoid  patients,  and  yet  the  autopsy  show  no  trace  of 
meningitis. 

One  theory,  which  has  Liebermeister  for  its  chief  supporter,  and  which  has 
won  a  tolerably  wide-spread  acceptance  among  physicians,  is  that  the  nervous 
symptoms  are  chiefly  a  direct  result  of  the  febrile  temperature.  It  is  impossible, 
however,  for  us  to  regard  this  view  as  universally  true.  The  unprejudiced  con- 
sideration of  a  large  number  of  personal  observations  prevents  it.  Although  it  is 
undeniable  that  elevated  temperature  has  a  harmful  influence  on  the  nervous  sys- 
tem, yet  in  numerous  cases  there  is  no  relation  between  the  height  of  the  fever 
and  the  severity  of  the  nervous  derangements.  There  are  cases  in  which  the  fever 
remains  continuously  high  for  days,  while  the  patient  feels  perfectly  comfortable 
and  presents  no  symptoms  of  any  important  cerebral  disturbance.  The  opposite 
class  of  cases  is  still  more  numerous,  in  which  from  the  very  start  there  is  always 
a  low  temperature,  and,  notwithstanding,  the  most  severe  nervous  symptoms 
arise.     Fräntzel  has  published  very  striking  cases  of  this  sort. 

Hence  we  must  seek  for  some  other  special  cause  of  the  severe  nervous  symp- 
toms, and  according  to  our  present  views  this  cause  must  be  the  intoxication  re- 
sulting from  the  specific  infection.  We  know  that  all  bacteria  produce,  by  their 
own  tissue-metamorphosis  and  the  chemical  processes  which  they  excite  in  their 
neighborhood,  certain  chemical  matters  which,  especially  in  the  case  of  the 
so-called  "  pathogenic  bacteria,"  seem  to  be  similar  to  the  alkaloids  (''  ptomaines '' 
and  "toxines''),  and  exercise  a  decided  poisonous  influence  upon  the  body,  and 
especially  upon  the  nervous  system.  These  products  are  formed  by  the  typhoid 
bacilli,  enter  the  blood,  and  are  the  chief  cause  of  the  nervous  phenomena.  The 
difference  in  the  violence  of  the  latter  in  different  cases  probably  depends  mainly 
on  a  difference  in  the  amount,  and  perhaps  also  in  the  quality,  of  the  toxines 
produced  by  the  typhoid  bacilli,  and  probably  also  in  the  different  susceptibility  of 
individuals  to  the  poison.  The  reason  that  the  influence  of  these  poisons  is  not 
much  greater  than  it  is,  is  that  they  are  in  part  destroyed  within  the  body  and  in 
part  excreted  with  great  rapidity,  the  channel  of  exit  being  mainly  the  kidneys. 
Thus  is  explained  the  interesting  fact  discovered  by  Lepine,  Bouchard,  and  others, 
that  the  urine  of  typhoid  patients  possesses  poisonous  properties  not  present  in 
normal  urine. 

That  the  appearance  of  the  nervous  symptoms  is  dependent  not  only  on  the 
material  causes,  but  also  on  the  susceptibility  of  the  individual,  is  shown  by  the 
fact  that  certain  patients  are  especially  prone  to  exhibit  marked  nervous  phe- 
nomena; for  example,  hard  drinkers,  ''  nervous  ";  individuals,  and  also  those  who 
have  suffered  violent  emotional  disturbances  shortly  before  the  onset  of  the 
disease. 

Actual  insanity  is  not  very  infrequent  during  the  course  of  typhoid,  or  in  con- 
valescence. It  generally  takes  the  form  of  melancholia.  We  have  repeatedly 
seen  patients  in  such  a  state  that  they  would  lie  almost  motionless  in  bed,  with 
eyes  open,  and  perhaps  assert  that  they  were  dead!  In  other  cases  there  is 
mental  excitement,  sometimes  combined  with  hallucinations,  or  there  is  confu- 
sion of  ideas.  In  one  case,  in  a  girl  who  was  evidently  predisposed  to  nervous  dis- 
orders, we  saw  typical  hysterical  insanity  break  out  during  the  fever.  Sometimes 
the  mental  excitement  at  the  beginning  of  a  relapse  terminates  in  actual  insanity. 


16  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

Few  of  the  psychoses  which  arise  during  or  at  the  end  of  typhoid  outlast  con- 
valescence. 

We  have  still  to  mention  a  number  of  nervous  diseases  that  develop  in  the 
course  of  typhoid  or  after  its  decline.  Neuralgia  is  sometimes  seen,  as  well  at  the 
beginning  as  at  the  end  of  the  disease.  It  is  most  frequent  in  the  regions  supplied 
by  the  trigeminus  and  the  occipital  nerves.  Great  hyperesthesia  of  the  skin 
and  muscles  is  not  rare  during  convalescence.  It  attacks  the  lower  extremi- 
ties by  preference.  Paralysis  of  single  muscles  (e.  g.,  of  the  serratus  magnus),  or 
paralysis  of  a  single  extremity,  has  been  repeatedly  observed  as  a  sequela.  The 
paralysis  is  generally  of  the  atrophic  variety,  and  is  probably,  as  a  rule,  due  to 
neuritis.  Ataxia  and  spastic  paralysis  of  the  lower  extremities  are  rare  sequelae. 
Finally,  there  are  sometimes  developed,  either  in  the  course  or  at  the  conclusion  of 
typhoid  fever,  the  symptoms  of  a  localized  cerebral  disorder  (e.  g.,  hemiplegia  and 
aphasia),  the  anatomical  cause  of  which  varies.  There  may  be  a  haemorrhage  or 
an  embolism,  and  probably  in  still  other  cases  a  localized  encephalitis. 

4.  Circulatory  System. — Disturbances  of  the  heart  such  as  to  produce  striking 
anatomical  changes  are  very  rare.  Endocarditis  and  pericarditis  are,  however, 
possible.  The  slight  mitral  endocarditis  sometimes  found  at  the  autopsy  has  no 
clinical  significance.  On  the  other  hand,  great  weight  is  laid  by  some  authors 
upon  the  parenchymatous  or  fatty  degeneration  of  the  heart.  They  say  it  is  often 
the  cause  of  cardiac  failure.  We  can  not  admit  this,  for  experience  shows  that 
the  two  do  not  stand  in  any  constant  relation  to  each  other. 

The  pulse  is  almost  always  rapid,  although  often  not  so  much  so  as  the  height 
of  the  temperature  might  lead  one  to  expect.  It  averages  from  90  to  110,  and 
often  more.  When  it  keeps  at  140  or  higher,  in  adults,  it  is  always  an  unfavorable 
symptom.  This  abnormal  frequency  is  often  in  part  due  to  the  high  temperature; 
but  there  are  other  factors.  Temperature  and  pulse  do  not  correspond  in  all  cases. 
Sometimes  the  pulse  will  have  a  normal  or  even  subnormal  frequency  throughout 
the  entire  attack,  despite  the  fever.  Temporary  accelerations  are  easily  produced 
by  mental  excitement  or  bodily  exertion,  as  by  sitting  up  in  bed.  In  convalescence 
the  rate  is  frequently  subnormal. 

Slight  irregularities  of  the  pulse  are  not  rare,  either  in  the  acme  or  the  decline 
of  typhoid.  Marked  irregularity  is  always  a  grave  symptom,  although  in  many 
cases  it  passes  off  and  the  patient  recovers. 

Dicrotism  is  so  frequent  that  many  elderly  physicians  still  regard  it  as  charac- 
teristic of  the  disease.  It  is  often,  however,  equally  marked  in  other  acute  dis- 
eases.    Its  cause  is  diminished  arterial  tension. 

The  diminished  cardiac  activity  may  result  in  venous  thrombosis,  especially 
in  the  lower  extremities.  This  sometimes  causes  swelling  of  one  of  the  lower 
extremities  during  convalescence.  The  swollen  member  generally  regains  its 
normal  size  after  some  weeks.  In  other  cases  the  thrombosis  occurs  earlier,  and 
in  patients  who  are  still  too  vigorous  to  suffer  from  cardiac  weakness,  so  that  we 
are  forced  to  the  conclusion  that  there  is  some  local  specific  cause.  A  possible,  but 
fortunately  infrequent,  result  of  these  thrombi  in  the  lower  limbs  is  pulmonary 
embolism  and  sudden  death. 

In  severe  cases,  which  end  in  death,  cardiac  thrombi  are  sometimes  found,  with 
emboli  in  the  lungs,  spleen,  kidneys,  or  other  organs. 

(Edema  of  the  ankles  and  legs  is  very  often  seen  in  convalescents,  especially 
when  they  first  get  otit  of  bed.  It  is  due  to  the  weakness  of  the  heart  and  changes 
in  the  vascular  walls.  Once  we  saw  a  general  dropsy  develop  at  the  end  of  a 
severe  attack  in  a  girl  of  fourteen.  The  autopsy  disclosed  no  other  possible  cause 
for  it  than  the  extreme  atrophy  and  flabbiness  of  the  heart. 

5.  Skin. — The  eruption  seen  in  typhoid  fever  is  characteristic.     The  rose-spots 


TYPHOID  FEVER.  17 

appear  at  the  beginning  of  the  second  week,  usually  on  the  trunk,  and  chiefly  on 
the  abdomen.  The  number  varies  greatly.  Rarely  they  are  entirely  absent,  most 
often  in  elderly  persons.  Sometimes  they  are  very  abundant,  and  extend  to  the 
thighs,  the  arms,  and  even  to  the  neck  and  face.  Often  they  vanish  after  a  few 
days,  but  they  may  persist  much  longer.  In  the  latter  case  they  may  become  to 
a  very  slight  degree  petechial,  so  that  they  will  not  entirely  disappear  on  press- 
ure. They  often  occur  in  successive  crops.  We  have  even  seen  several  cases 
where  new  rose-spots  kept  coming  for  some  days  after  the  fever  had  disappeared. 

As  to  other  cutaneous  eruptions,  we  may  mention  first  of  all  that  herpes  la- 
bialis is  so  rare  in  typhoid  that  in  cases  of  doubtful  diagnosis  it  is  a  factor  in 
excluding  that  disease.  Miliaria,  urticaria,  and  superficial  pustules  are  sometimes 
observed.  Occsionally  little  bluish  spots  appear,  especially  on  the  trunk.  These 
used  to  be  called  "  taclies  bleuatres  "  (pelioma  typhosum) ;  but  later  observations 
show  that  they  are  not  connected  with  typhoid  fever  particularly.  They  are  due 
to  pediculi.  We  might  use  the  term  pelioma  typhosum  to  designate  the  kind  of 
vesicles  which  we  have  repeatedly  seen  on  the  abdomen  in  severe  cases.  They 
are  about  the  size  of  peas,  and  have  sero-heemorrhagic  contents.  Boils  and  super- 
ficial abscesses  are  frequent,  especially  as  disagreeable  sequelae  in  convalescence 
from  severe  cases.  There  are  often  abscesses  of  the  sweat-glands  in  the  skin  of  the 
axilla  during  convalescence.  All  these  and  similar  cases  of  suppuration  in  typhoid 
fever  do  not  depend  upon  the  original  cause  of  the  disease,  but  upon  secondary 
pathogenic  germs,  such  as  the  staphylococcus  or  streptococcus,  for  whose  entrance 
the  typhoid  process  has  merely  prepared  the  way.  Extensive  ecchymoses  are  very 
rare,  and  are  symptomatic  of  a  general  hsemorrhagic  diathesis.  Petechia?  are  fre- 
quent during  recovery.  They  are  generally  seen  in  the  follicles  of  the  skin  below 
the  knee.  There  have  been  a  few  cases  of  gangrene  in  the  lower  extremities, 
especially  in  the  toes.  We  saw  in  one  patient  an  extensive  gangrene  of  the  skin 
of  the  abdomen.     Its  cause  could  not  be  determined. 

Finally,  we  must  mention  that  bed-sores  are  prone  to  develop  in  severe  or 
neglected  cases.  The  localities  most  often  attacked  are  the  nates,  the  furrow  be- 
tween them,  and  the  heels.  A  bed-sore  may  be  so  extensive,  and  accompanied  by 
such  undermining  of  the  skin,  as  to  be  a  dangerous  or  even  fatal  complication. 

The  epidermis  often  scales  off  to  a  considerable  extent  during  convalescence 
after  a  severe  attack  of  typhoid.  Everybody  knows  how  the  hair  falls  out  after 
the  fever,  but  it  is  sure  to  grow  again.  The  nails  also  are  not  infrequently 
affected,  becoming  rough  and  brittle,  or  even  falling  off. 

6.  Muscles,  Bones,  Joints. — Zenker  has  discovered  a  degeneration  of  the  volun- 
tary muscles  which  occurs  in  typhoid  as  well  as  in  other  severe  diseases.  It  is 
called  the  "  granular  "  or  "  waxy  "  degeneration.  Whether  it  has  clinical  symp- 
toms can  not  be  determined.  Perhaps  it  may  explain  the  great  muscular  hyper- 
sesthesia  which  is  often  observed,  and  the  muscular  pains,  which  may  be  very 
trying.  Severe  cases  sometimes  have  haemorrhages  into  the  muscles,  particularly 
the  rectus  abdominis. 

Lesions  of  the  bones  and  joints  occur  but  seldom.  We  have  seen  periostitis  of 
the  tibia,  and  of  a  rib,  during  convalescence.  Swelling  of  the  joints  is  equally 
rare.  If  there  is  a  purulent  arthritis,  it  is  always  due  to  some  secondary  infection 
(vide  supra). 

7.  Genito-urinary  Apparatus. — Genuine,  acute,  haamorrhagic  nephritis  is  a  very 
rare  complication.  It  does  occur,  however,  and  has  even  given  rise  to  the  estab- 
lishment of  a  special  "  renal  form  of  typhoid  fever  "  (nephro-typhoid).  This  name 
applies  especially  to  those  cases  in  which  a  severe  acute  nephritis  is  the  predomi- 
nant symptom  at  the  start,  while  at  a  later  period  the  course  of  the  fever,  the 
intestinal   symptoms,  the  rose-spots,  etc.,  show  the  disease  to  be  typhoid  fever. 

2 


18  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

Nephro-typhoid  is  analogous  to  pneuino-typhoid  and  tonsillo-typhoid.  A  simple 
so-called  febrile  albuminuria  occurs  very  frequently  at  the  acme  of  typhoid,  and 
is  not  to  be  interpreted  unfavorably.  It  is  probably  the  result  of  that  slight  par- 
enchymatous degeneration  of  the  kidneys  which  occurs  in  typhoid  with  the  same 
frequency  as  in  most  of  the  other  severe  infectious  diseases.  There  does  not  seem 
to  be  a  direct  relation  between  the  albuminuria  and  the  fever,  although  some 
authors  assume  it  to  exist.  It  is  more  likely  that  the  renal  epithelium  is  injured 
by  the  noxious  products  which  have  been  formed  in  the  body  and  excreted  by  the 
kidneys.  In  other  respects  the  urine  presents  the  same  peculiarities  as  in  most 
other  severe  febrile  diseases  :  its  amount  is  diminished  ;  its  color  dark  ;  its  specific 
gravity  increased  ;  the  excretion  of  urea  greater  than  normal.  It  should  be  added 
that  the  urine  at  the  height  of  the  disease  presents  Ehrlich's  ''diazo-reaction"  in 
almost  all  cases.*  Cystitis  is  not  a  rare  development  toward  the  end  of  the  illness. 
It  is  probably  always  secondary. 

In  men,  orchitis  is  sometimes  observed.  Women  often  have  their  catamenia 
at  the  beginning  of  typhoid.  Later  in  the  course  of  the  disease,  and  in  convales- 
cence from  severe  attacks,  the  menses  are  often  absent  for  several  periods.  In 
pregnant  women  there  is  considerable  danger  of  abortion  or  miscarriage. 

Peculiarities  in  the  Course  of  the  Disease. 

The  above  statements  show  an  almost  inexhaustible  variety  in  the  possible  com- 
plications of  typhoid.  The  course  of  the  disease  as  a  whole  may  likewise  present 
many  diverse  forms  and  peculiarities.  We  shall  attempt  merely  to  cite  the  most 
essential. 

The  numerous  light  and  rudimentary  attacks  {typhus  levissimns)  are  first  to 
be  mentioned.  It  was  not  recognized  till  lately  that  they  belonged  to  typhoid 
fever  at  all  (Griesinger).  They  used  to  have  all  sorts  of  names  applied  to  them, 
the  favorite  term  being  "gastric  fever."  This  light  form  lasts  eight  to  fourteen 
days.  The  fever  is  moderate  and  often  decidedly  remittent.  There  is  almost  no 
proper  fastigium.  The  typhoid  symptoms  are  but  slightly  developed.  There 
are  no  severe  pulmonary  or  cerebral  symptoms.  There  is  generally  a  moderate 
diarrhoea,  the  spleen  is  plainly  enlarged,  and  often  rose-spots  can  be  found.  The 
diagnosis  of  these  cases  is  of  course  difficult  in  proportion  to  the  scanty  develop- 
ment of  typhoid  symptoms.  It  is  best  established  by  demonstrating  an  serological 
relation  between  these  cases  and  others  which  are  plainly  typhoid  fever. 

Abortive  typhoid  is  justly  distinguished  by  Liebermeister  from  typhus  levis. 
The  name  belongs  to  cases  which  begin  with  severe  symptoms  and  high  fever,  as 
if  they  were  going  to  be  grave,  but  in  which  these  violent  symptoms  disappear 
after  a  few  days  and  give  place  to  a  rapid  convalescence. 

On  the  other  hand,  there  are  cases  which  for  a  long  time  cause  so  little  subject- 
ive discomfort  that  the  patient  does  not  even  go  to  bed  (walking  typhoid).  It  is 
not  till  quite  late  that  there  occurs  a  sudden  change  for  the  worse,  or  some  severe 
complication.     Thus  it  has  happened  that  people  who  were  apparently  healthy 

*  This  reaction  consists  in  the  red  coloration  of  the  urine  upon  the  addition  of  Ehrlich's  reagent 
(chiefly  sulphanilic  acid)  and  ammonia.  For  particulars,  see  treatises  upon  chemical  analysis.  [Ehrlich's 
test  is  carried  out  as  follows :  Solution  1  consists  of  strong  hydrochloric  acid,  one  part,  mixed  with 
twenty  parts  of  a  saturated  aqueous  solution  of  sulphanilic  acid.  Solution  2  is  a  one-half-per-cent. 
solution  of  sodic  nitrite  in  water. 

A  test-tube  is  one-eighth  part  filled  with  solution  1,  and  five  to  ten  drops  of  solution  2  are 
added  to  this  ;  a  quarter  of  the  test-tube  of  urine  is  then  added,  aud,  lastly,  enough  ammonia  to  make 
it  strongly  alkaline.  The  deep-red  color,  which  appears  promptly,  is  not  so  characteristic  as  a  green 
precipitate  of  phosphates,  which  appears  at  the  bottom  of  the  tube  after  standing  for  twenty-four  hours.] 


TYPHOID  FEVER.  19 

have  suddenly  had  all  the  symptoms  of  a  severe  peritonitis  due  to  perforation  and 
have  died,  the  autopsy  disclosing  the  lesions  of  the  third  week  of  typhoid  fever. 

The  individual  circumstances  are  very  important  in  weighing  each  case,  for 
they  may  modify  the  disease  in  many  ways. 

In  children  it  is  a  remarkable  fact  that  typhoid  ulcers  are  much  less  frequent 
than  in  adults.  This  explains  why  intestinal  haemorrhage  and  peritonitis  are 
much  rarer  in  children.  Severe  cerebral  symptoms  are,  on  the  other  hand,  very 
frequent.  In  severe  cases  children  sometimes  exhibit  the  peculiar  symptom  of 
a  continuous  penetrating  screaming.  In  other,  mild,  cases  the  children  are  sop- 
orose. 

In  the  aged  the  diagnosis  of  typhoid  is  often  very  difficult,  since  the  course  of 
the  disease  is  frequently  irregular.  Generally  the  fever  is  not  very  high,  and  it 
very  seldom  exhibits  distinctly  the  type  described  above.  The  pulmonary  or  cere- 
bral symptoms  predominate  as  a  rule. 

In  the  corpulent,  typhoid  fever  is  often  very  severe,  so  that  our  prognosis  must 
always  be  rather  grave,  especially  if  pulmonary  symptoms  arise. 

Hard  drinkers  are  also  in  especial  peril  in  this  as  in  all  other  acute  diseases. 
Dangerous  cardiac  weakness  is  prone  to  appear.  Severe  cerebral  symptoms  are 
frequent.  It  is,  however,  surprising  that  true  delirium  tremens  is  relatively  infre- 
quent, although  so  common  in  pneumonia. 

The  influence  of  previous  strong  mental  excitement  and  of  certain  already  ex- 
isting diseases  (cardiac  disease,  emphysema,  kyphoskoliosis,  etc.)  has  been  already 
mentioned.  Finally,  we  repeat  that  often  the  different  epidemics  present  certain 
peculiarities.  For  instance,  in  one  the  type  of  the  disease  will  be  severe,  in 
another  mild.  In  one  epidemic  relapses  are  comparatively  frequent,  in  another 
exceptional.  The  same  is  true  with  regard  to  the  frequency  of  the  appeai'ance  of 
certain  symptoms,  such  as  intestinal  haemorrhage,  pneumonia,  or  nephritis.  In- 
deed, it  has  even  been  observed  that  those  cases  which  occur  during  a  given  epi- 
demic in  the  same  family  or  house  or  block  sometimes  present  striking  resem- 
blances to  one  another  (u  group  typhoid  "  of  E.  Wagner  and  others). 

Relapses  op  Typhoid  Fever. 

Typhoid  fever  exhibits  in  many  cases  the  peculiarity  of  repeating  itself  com- 
pletely after  having  run  its  entire  course  and  disappeared.  This  process  is  called 
a  relapse.  It  is  in  all  probability  the  result,  not  of  a  fresh  infection  of  the  system 
from  without,  but  of  a  renewed  development,  or  possibly  of  a  second  generation, 
of  the  infectious  germs  already  present.  A  typical  relapse  is  like  a  first  attack  in 
all  clinical  and  anatomical  particulars,  with  this  difference,  that  everything  is 
more  condensed,  and  lasts  a  shorter  time  than  in  the  first  attack.  The  interval 
between  the  two,  during  which  there  is  no  fever,  lasts  seven  to  ten  days.  It  may 
be  longer,  and  is  often  shorter.  Sometimes  the  relapse  follows  immediately  upon 
recovery.  Indeed,  it  may  even  happen  that,  before  the  patient  has  completely 
recovered,  his  temperature  begins  to  rise  again  in  the  characteristic  step-like  way. 
To  such  cases  as  this  last  the  term  recrudescence  is  applied.  Except  in  the  time  of 
its  beginning,  it  may  be  just  the  same  as  a  genuine  relapse.  In  the  interval  be- 
tween the  two  attacks  many  persons  are  perfectly  comfortable,  and  appear  to  be 
fully  convalescent.  There  is  often,  however,  a  slight  evening  rise  of  temperature. 
It  is  noticeable  that  the  splenic  tumor  does  not  completely  disappear  after  the  first 
attack  in  many  cases  which  are  followed  by  a  relapse. 

The  relapse  is  generally  briefer,  as  we  have  said,  than  the  first  attack,  seldom 
lasting  more  than  fifteen  to  eighteen  days.  The  temperature  rises  more  rapidly, 
perhaps  in  two  or  three  days.     The  fastigium  is  shorter,  the  decline  more  abrupt. 


20  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

The  absolute  height  of  the  temperature  may  be  very  considerable,  even  exceeding 
that  in  the  first  attack.  Rose-spots  appear  as  soon  as  the  third  or  fourth  day.  The 
stools  become  liquid,  the  spleen  enlarges  again,  and  all  sorts  of  complications  may 
arise.  The  danger  occasioned  by  a  relapse  may,  however,  be  overestimated.  On 
the  whole,  a  relapse  is  not  so  very  dangerous,  and  it  is  especially  noticeable  that 
the  subjective  symptoms,  such  as  headache,  are  often  slight.  A  severe  relapse 
may  follow  a  mild  case.  In  other  instances  the  relapse  may  prove  merely  rudi- 
mentary. 

The  frequency  of  relapses  varies  considerably  in  different  epidemics.  In  Leip- 
sic,  we  had  relapses  in  about  nine  per  cent,  of  all  cases,  but  in  separate  years  the 
percentage  varied  between  four  and  sixteen.  Out  of  about  five  hundred  cases 
we  have  seen  three  in  which  there  were  two  successive  and  typical  relapses. 

Diagnosis. — The  diagnosis  of  typhoid  fever  may  be  perfectly  easy,  but,  if  the 
case  be  anomalous,  or  come  under  observation  at  a  late  period,  it  may  be  ex- 
tremely obscure.  Inasmuch  as  a  search  for  the  specific  bacilli  is  too  difficult 
and  troublesome,  for  the  practicing  physician,  the  diagnosis  of  the  disease  must 
be  made  from  its  course  and  symptoms.  Important  factors  are  the  gradual  onset, 
then  the  height  and  course  of  the  fever,  with  no  demonstrable  localized  disease, 
and  the  rose-spots.  Less  characteristic,  but  still  of  value,  are  the  stools,  the  tym- 
panites, and  the  swelling  of  the  spleen.  ^Etiological  factors,  such  as  the  occur- 
rence of  undoubted  cases  of  typhoid  in  the  neighborhood,  are  of  great  diagnostic 
value  in  obscure  cases.  Sometimes  the  diagnosis  can  not  be  established  till  the 
appearance  of  certain  symptoms,  like  intestinal  hemorrhage,  a  characteristic 
mode  of  convalescence — viz.,  by  lysis — or  a  relapse.  It  is  an  important  rule  not 
to  make  a  diagnosis  of  typhoid  after  a  single  examination.  It  is  generally  neces- 
sary to  observe  the  case  accurately  for  several  days  before  the  diagnosis  can  be 
established.  The  differential  diagnosis  from  other  acute  diseases,  such  as  miliaiy 
tuberculosis,  acute  endocarditis,  meningitis,  etc.,  will  be  considered  in  discussing 
these  diseases. 

Prognosis. — A  perfectly  favorable  prognosis  should  never  be  made.  Cases 
which  seem  the  mildest  may  become  dangerous.  Yet,  if  there  are  good  nursing 
and  good  treatment,  typhoid  fever  is  not  a  particularly  dangerous  disease,  and  we 
may  hope  for  recovery  even  in  very  severe  attacks.  The  danger  lies,  first,  in  the 
severity  of  the  infection,  as  shown  chiefly  (though  not  wholly)  by  the  height  of  the 
fever  and  the  intensity  of  the  general  symptoms.  A  further  danger  is  the  appear- 
ance of  the  complications  already  enumerated  and  discussed.  Thirdly,  the  con- 
stitution and  condition  of  the  individual  are  important.  The  circumstances  com- 
ing under  this  head  have  likewise  been  repeatedly  mentioned  above.  All  these 
factors  must  be  carefully  estimated  before  we  decide  as  to  the  danger  in  each  case 
and  make  our  prognosis. 

The  mortality  in  typhoid  varies  greatly  in  the  separate  epidemics.  The  severe 
cases  are  undoubtedly  more  frequent  at  some  times  than  at  others.  This  renders 
it  difficult  to  give  statistics  which  are  universally  applicable.  We  may  in  general 
reckon  on  an  average  mortality  of  about  ten  per  cent.,  and  measure  the  severity 
of  separate  epidemics  by  this  standard.  Numerous  observers  agree  that  the  treat- 
ment now  in  vogue  has  decidedly  diminished  the  mortality.  It  was  formerly  not 
rare  for  it  to  reach  twenty  or  twenty-five  per  cent. 

Treatment. — A  specific  cure  for  typhoid — i.  e.,  some  remedy  to  destroy  the 
specific  cause  of  the  disease  within  the  system,  or  to  render  it  harmless — is  as  yet 
unknown.  Antiseptic  and  antizymotic  drugs,  such  as  quinine  and  antipyrine 
(vide  infra),  do  have  a  certain  influence  upon  the  fever,  but  they  are  not 
capable  of  essentially  modifying  the  course  of  the  disease  as  a  whole,  at  least 
not  in  such  doses  as  we  dare  admininister.     The  continued  internal  use  of  car- 


TYPHOID   FEVER.  21 

bolic  acid  (grains  five  to  ten,  gramme  O'SO-O'SO,  or  more,  in  the  course  of 
twenty-four  hours)  is  the  means  chiefly  recommended  lately  for  this  purpose; 
hut  we  doubt  if  it  is  of  much  benefit.  Liebermeister  ascribes  to  iodine  a  demon- 
strable, although  slight,  beneficial  influence.  Other  physicians  had  previously 
recommended  it.  Four  to  five  drops  of  the  following  solution  are  given  every 
two  hours  in  a  wineglass  of  water:  Iodine,  one  part;  iodide  of  potassium,  two 
parts;  distilled  water,  ten  parts.  We  have  had  no  personal  experience  with  this 
remedy. 

Calomel  is  also  said  to  have  a  specific  effect  on  typhoid.  Wunderlich  and 
others  have  noticed  that  if  a  few  rather  large  doses  of  calomel  be  given  at  the 
beginning  of  the  disease,  it  will  on  the  average  run  a  lighter  and  more  favorable 
course  than  otherwise  would  have  been  the  case.  Wunderlich  believed  that 
typhoid  fever  may  sometimes  be  aborted  by  this  method.  Although  we  can  hardly 
expect  this,  it  is  really  an  efficient  means  of  procedure,  which  we  have  often 
found  satisfactory,  to  give  two  or  three  powders,  of  five  grains  (0'30  gramme)  each, 
of  calomel,  as  the  first  prescription,  to  patients  who  come  under  treatment  in  the 
first  week  or  the  beginning  of  the  second.  As  there  is  generally  constipafion,  the 
laxative  effect  is  also  beneficial.  Moreover,  it  often  lowers  the  temperature  some- 
what. A  moderate  diarrhoea  is  not  a  contra-indication,  but,  if  the  bowels  be  very 
loose,  the  calomel  should  be  omitted. 

Ergotine  may  be  mentioned  as  another  drug  which  is  said  to  act  specifically. 
It  has  been  lately  used,  chiefly  by  French  physicians,  in  doses  of  twenty  to  forty- 
five  grains  (1*50-3  grammes)  in  twenty- four  hours.  Again,  subnitrate  of  bismuth 
is  used  (by  the  French  to  the  amount  of  four  to  eight  drachms — grammes  15-30 
pro  die),  and  naphthaline  in  single  doses  of  three  to  eight  grains  (0-l-0'5)  or  in 
the  course  of  the  day  seventy-five  grains  (5"0).  We  doubt  if  these  remedies  will  be 
popular  long. 

In  the  present  state  of  our  knowledge  the  treatment  of  typhoid  must  still  be 
chiefly  general  and  symptomatic,  and  in  one  sense  prophylactic.  We  must  fight 
the  symptoms  already  present,  and  further  seek,  as  far  as  possible,  to  defend  the 
patient  from  the  attack  of  certain  dangerous  secondary  disorders.  Starting  out 
with  this  view,  the  proper  treatment  of  typhoid  fever  is  a  task  of  the  highest  im- 
portance, and  by  no  means  a  thankless  one. 

We  will  begin  by  considering  the  general  treatment.  The  sick-room  must  not 
be  too  warm,  and  must  be  frequently  and  thoroughly  aired.  The  sick-bed  must 
be  well  cared  for.  If  pains  be  taken  to  prevent  bed-sores,  Ave  shall  obviate  one 
source  of  pain  and  danger  (vide  supra),  and  save  ourselves  and  the  nurse  much 
trouble.  Those  who  are  very  sick  should  therefore  be  laid  on  an  air-cushion,  or, 
if  possible,  a  water-bed.  The  patient  should  be  told  not  to  lie  always  upon  his 
back,  but  to  change  now  and  then  upon  his  side.  The  back,  the  region  of  the  sa- 
crum, and  the  heels  are  to  be  often  bathed  with  spirits  of  camphor  or  brandy.  The 
minutest  bed-sore  is  to  be  treated  carefully.  It  should  be  cleansed  twice  a  day 
(rinsed  off  with  a  weak  solution  of  salicylic  or  carbolic  acid),  and  done  up  with  an 
ointment  containing  Peruvian  balsam,  1-30.*  If  the  bed-sore  be  extensive,  dusting 
with  iodoform  is  very  efficient  treatment.  We  should  be  particularly  careful  not 
to  let  the  skin  be  undermined.  If  this  has  already  occurred,  we  must  be  prompt 
in  the  use  of  the  knife  or  drainage-tube. 

We  can  not  recommend  too  strongly  that  the  mouth  should  be  kept  clean.  In 
a  light  case  the  patient  can  see  to  this  himself,  but  otherwise  the  mouth  and 
tongue  must  he  frequently  cleansed  with  a  linen  cloth  wet  in  cold  water  or  a  solu- 

*  The  unguentum  balsami  peruviani  is  made  by  mixing  one  part  of  balsam  very  exactly  with  thirty 
parts  of  the  glycerite  of  starch  (B.  P.).     It  is  not  officinal  in  Germany. — Trans. 


22  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

tion  of  borax  (1  to  30).  Perhaps  we  need  hardly  repeat  the  reason  for  this  excess- 
ive cleanliness.  It  lies  in  the  causative  relation  between  stomatitis  and  inflam- 
mation of  the  parotid  gland,  and  of  the  middle  ear.  If  the  tongue  and  lips  be 
dry,  they  may  be  touched  with  glycerine. 

The  diet  must  be  at  once  liquid  and  nourishing.  Milk  is  excellent,  and  should 
always  be  ordered,  but  will,  unfortunately,  be  taken  by  very  few  patients  continu- 
ously. It  is  often  better  borne  if  coffee  or  a  little  brandy  be  added  to  it.  Cocoa 
made  with  milk  may  also  be  given  for  a  change.  In  severe  cases  Nestle's  food 
(Kindermehl)  has  been  often  employed  by  us  with  benefit.  Broth  and  soup,  thick- 
ened with  sago  or  rice,  are  also  good.  They  may  be  made  more  nourishing  by 
adding  an  egg  to  them.  If  the  patient  is  very  anxious  to  have  more  solid  food, 
as  often  happens,  we  need  not  hesitate  to  give  him  a  roll  or  rusk  (Zwieback) 
that  has  been  softened  by  soaking.  If  a  patient  becomes  exceedingly  enfeebled 
we  should  give  him  fine  shavings  of  raw  beef,  regardless  of  the  fever.  A  little 
dilute  hydrochloric  acid  might  be  given  with  the  meat.  Beef -tea  would  be  still 
better  than  the  raw  meat,  and  is  to  be  strongly  recommended.  The  various  prep- 
arations of  meat  which  are  now  made  (meat-solution,  meat-peptones,  etc.)  may  be 
sometimes  useful.  Where  the  fever  takes  a  sluggish  course,  we  must  often  begin 
to  give  stronger  nourishment  before  the  fever  has  ended.  The  best  drink  is  cold 
water,  which  the  patient  would  often  not  think  of  using  unless  we  offered  it  to 
him.  Lemonade  and  similar  preparations  generally  become  distasteful  in  time. 
Drinks  containing  carbonic  dioxide  are  to  be  avoided,  because  they  increase  the 
meteorism.  Cold  tea  with  milk  is  good.  In  severer  cases  we  should  give  some 
good  strong  wine,  such  as  port,  Malaga,  or  Hungarian  wine.  If  the  patient 
desires  beer,  we  need  not  hesitate  to  give  it  in  moderate  amount.  During  conva- 
lescence we  should  be  very  careful  about  diet,  since  errors  often  have  disagreeable 
consequences.  We  must  wait  till  there  has  been  no  fever  at  all  for  seven  to  ten 
days  before  we  allow  a  solid,  animal  diet,  and  return  by  degrees  to  common  sorts 
of  food. 

The  general  and  dietetic  treatment  which  we  have  thus  far  discussed  is  very 
important.  Outside  of  this,  it  is  our  opinion  that  there  is  only  one  method  of 
treatment  to  be  chiefly  considered — at  least  under  the  present  limitations  of  our 
therapeutic  ability.  This  method  consists  in  the  persistent  use  of  cool  baths,  as 
first  practiced  by  Brand  in  Stettin.  We  do  not  indeed  believe  that  the  indications 
for  this  method  of  treatment  are  exactly  what  its  original  promoter  held  them  to 
be,  and  we  think  some  of  the  minutiae  of  the  treatment  should  be  changed.  Yet 
there  is  at  present  no  other  single  method  of  treating  typhoid  fever  which  has  so 
numerous  and  evident  advantages  for  the  patient.  To  carry  it  out  in  private  prac- 
tice may  often  be  more  difficult  than  in  a  well-appointed  hospital.  However,  even 
in  private  houses  it  will  generally  be  possible  to  manage  it,  and  we  regard  it  as 
the  duty  of  every  physician  who  undertakes  to  treat  a  severe  case  of  typhoid  to 
try  his  best  to  have  the  baths  employed. 

The  great  advantages  of  the  treatment  by  baths  are:  1.  The  baths  diminish 
the  fever,  if  their  temperature  be  only  sufficiently  low,  by  direct  absorption  of 
heat.  The  baths  thus  obviate,  as  far  as  possible,  all  the  bad  effects  which  might 
result  from  a  rise  of  temperature.  2.  The  direct  influence  of  the  baths  upon  the 
nervous  system  is  still  more  important.  The  intellect  becomes  clearer,  the  apathy 
and  dullness  diminish.  In  fact,  if  baths  be  used,  we  do  not  see  nearly  so  often  as 
formerly  the  grave  "  typhoid  condition."  It  is  thus  evident  that  bathing  not  only 
causes  an  improvement  in  the  subjective  sensations  of  the  patient,  but  brings  in 
its  train  many  other  beneficial  effects.  The  patient  takes  his  nourishment  better, 
does  not  so  often  swallow  the  wrong  way,  coughs  more  effectively,  is  easier  to 
move,  and  his  body  and  his  mouth  can  be  better  cleansed.     3.  The  influence  of 


TYPHOID  FEVER.  23 

the  baths  upon  the  respiratory  organs  is  of  the  greatest  importance.  We  refer 
especially  to  the  stimulation  to  deeper  inspirations,  and  the  promotion  of  expec- 
toration. The  best  proof  of  the  benefit  of  this  influence  is  the  circumstance 
that,  if  patients  are  subjected  to  baths  from  the  start,  it  is  comparatively  a  ran; 
thing  for  severe  bronchitis,  atelectasis,  and  catarrhal  pneumonia  to  develop.  4. 
The  good  care  of  the  skin,  which  the  bathing  makes  possible,  is  not  to  be  despised. 
Since  this  treatment  has  been  introduced,  bed-sores  are  much  rarer  in  typhoid 
than  before.  5.  Lastly,  the  baths  are  sometimes  observed  to  have  a  diuretic 
effect. 

What  has  been  said  shows  that  the  height  of  the  fever  is  by  no  means  the  sole 
indication  for  the  employment  of  baths,  at  least  in  our  opinion.  The  condition 
of  the  nervous  system  and  of  the  respiratory  organs  is  also  to  be  considered.  It  is 
true  that  numerous  mild  cases  run  a  favorable  course  without  a  single  bath;  but 
we  should  always  remember  that  this  treatment  is  not  only  directed  against  the 
symptoms  already  existing,  but  has  also  a  prophylactic  importance,  since  it  tends 
to  prevent  any  severe  cerebral  or  pulmonary  manifestations. 

We  will  pass  on  to  the  special  method  of  carrying  out  balneo-therapeutics  in 
typhoid.  Full  baths  are  generally  employed,  immersing  the  patient  to  his  neck. 
The  tub  must  stand,  if  possible,  by  the  bedside.  In  hospitals,  where  there  are  beds 
on  rollers,  it  is  a  better  way  to  wheel  the  patients  into  the  bathroom.  All  who 
are  severely  ill  should  be  lifted  into  the  bath  and  there  held  and  supported,  to 
avoid  any  bodily  fatigue.  During  the  bath  the  skin  should  be  gently  rubbed. 
This  averts  unpleasant  sensations  of  chilliness.  The  temperature  of  the  water 
should  not  be  set  too  low,  especially  for  the  first  baths.  We  begin  at  85°  to  90° 
(24°  to  26°  R.),  or,  if  the  individual  be  elderly  or  sensitive,  and  timid,  at  even 
warmer  temperatures.  When  the  patient  has  become  accustomed  to  the  tempera- 
ture of  the  water,  we  can  cool  off  the  bath  still  further.  Baths  below  73°  (18°  to 
20°  R.)  have  scarcely  ever  been  used  by  us,  and  we  believe  that  they  are  seldom 
needed.  A  very  satisfactory  average  temperature  is  80°  to  85°  (20°  to  24°  R. ). 
A  bath  lasts  on  the  avei^age  ten  minutes.  If  the  patient  feels  very  cold  or  very 
uneasy  in  the  bath,  it  must  be  cut  short.  After  the  bath  the  patient  is  at  once 
lifted  into  bed,  wrapped  up  in  a  sheet  previously  made  ready,  and  wiped  dry,  with 
rather  vigorous  rubbing  of  the  extremities  and  back.  The  moist  sheet  is  then 
removed.  The  patient  is  covered  up  rather  warmly,  and  is  given  some  hot  broth 
or  a  sip  of  good  strong  wine.  The  effect  of  the  bath  upon  the  temperature  is 
measured  about  half  an  hour  later  by  the  rectum.  If  the  temperature  be  2°  to  3° 
(1°  to  2°  C.)  lower  than  before,  the  result  is  deemed  satisfactory.  Often  the  differ- 
ence is  greater,  but  in  severe  cases  the  fever  may  be  so  obstinate  that  the  tempera- 
ture remits  only  a  small  fraction  of  a  degree.  In  such  cases  it  is  sometimes  per- 
missible to  lower  the  temperature  of  the  bath  still  more,  or  continue  it  a  little 
longer.  If  cool  baths  are  ill-borne,  protracted  baths  of  lukewarm  water  are  some- 
times very  efficient  (Riess,  and  other). 

In  so  far  as  the  height  of  the  fever  furnishes  an  indication  for  baths,  we  may 
accept,  say  103 '6°  (39 '8°  C.)  in  the  rectum,  as  the  temperature  calling  for  a  bath. 
As  a  rule,  baths  should  not  be  given  offener  than  every  three  hours,  as  otherwise 
they  exhaust  the  patient.  In  many  cases  three  or  four  baths  a  day  are  enough. 
At  night  we  have  given  baths  very  seldom,  when  forced  to  by  extremely  high 
temperatures  or  other  bad  symptoms.  It  must  be  a  mistake  to  wake  a  patient 
who  is  quietly  sleeping,  and  put  him  into  cold  water,  even  if  his  temperature  is 
above  104°  (40°  O).  Likewise,  in  cases  where  the  temperature  shows  considerable 
spontaneous  remissions,  there  may  be  no  use  in  inflicting  a  cold  bath  upon  a 
patient  who  has  high  fever  only  temporarily.  On  the  other  hand,  even  if  the 
temperature  be  not  excessive,  or  even  if  it  be  normal,  there  is,  as  we  have  said,  no 


24  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

better  remedy  than  the  baths  for  severe  pulmonary  or  cerebral  symptoms.  In 
such  cases  we  often  raise  the  temperature  of  the  baths  a  little,  and  during  them 
we  have  colder  water  poured  upon  the  head  and  back.  If  we  do  this,  the  ears 
must  be  stopped  with  cotton-wool,  lest  the  cold  water  find  its  way  into  them. 

It  is  not  always  advisable  to  use  baths,  however  advantageous  this  treatment 
may  be,  in  typhoid  fever.  There  are  a  number  of  contra-indications  which  can 
not  be  disregarded.  First,  the  occurrence  of  intestinal  haemorrhage,  however 
slight,  and  likewise. the  suspicion  that  peritonitis  is  developing,  prohibit  bathing. 
In  these  cases  quiet  is  the  very  first  requirement  of  the  patient,  and  the  baths 
must  be  at  once  discontinued.  Further  contra-indications  are  great  weakness  or 
great  sensitiveness,  such  that  the  excitement  caused  by  the  bath  might  do  harm. 
Sometimes  baths  are  followed  by  severe  rheumatic  ("  rheumatoid  ")  pains  in  the 
limbs,  and  often  they  seem  to  promote  the  occurrence  of  furunculosis.  In 
such  cases  it  is  often  necessary  to  omit  the  baths,  or  at  any  rate  to  employ  them 
less  often  and  at  a  warmer  temperature.  The  same  is  true  if  a  severe  laryngeal 
affection  develops,  or  otitis  or  nephritis.  Nothing  seems  to  us  a  greater  mistake 
than  to  attempt  to  establish  a  scheme  for  the  treatment  of  typhoid  by  baths  that 
shall  be  always  applicable.  Here,  if  anywhere,  the  only  correct  way  is  to  treat 
each  individual  case  according  to  its  special  symptoms  and  circumstances. 

We  shall  now  pass  on  to  the  consideration  of  the  further  symptomatic  treat- 
ment of  typhoid.  The  first  question  is  whether  the  fever — that  is,  the  elevation  of 
bodily  temperature,  as  such — demands  special  consideration.  In  general,  we  are 
of  the  opinion  that  the  internal  antipyretics  are  seldom  indispensable.  It  is  true 
that  by  giving  quinine  (single  doses  of  fifteen  to  twenty  grains,  gramme  1  to 
1*50)  or  salicylate  of  soda  (in  amounts  of  a  drachm  or  a  drachm  and  a  half, 
grammes  4  to  6),  the  elevated  temperature  may  often  be  considerably  diminished; 
but  whether  the  patient  is  thereby  benefited  is  at  least  doubtful.  Certainly  the 
unpleasant  accessory  symptoms  caused  by  the  drugs  mentioned — viz.,  vomiting, 
ringing  in  the  ears,  vertigo,  and  profuse  perspiration  —  make  the  patient  feel 
decidedly  more  uncomfortable  than  he  was  before.  There  is  also  some  danger 
that  these  medicines  may  have  an  unfavorable  influence  upon  the  cardiac  activity. 
Decidedly  better  than  quinine  and  salicylic  acid  is  antipyrine.  This  substance 
was  synthetically  produced  by  L.  Knorr  from  Phenylhydrazin  and  acetacetic 
ether,  and  was  first  recommended  by  Filehne.  In  the  dose  of  fifteen  to  thirty 
grains  (grammes  1  to  2)  it  is  a  very  efficient  antipyretic.  It  may  be  given  in  wafers 
or  dissolved  in  water,  and  it  is  easy  to  take.  Exceptionally  there  are  disagreeable 
results,  such  as  vomiting,  an  eruption  resembling  measles,  or  a  rigor  followed  by 
a  return  of  fever.  In  severe  cases  the  dose  must  be  repeated  after  two  or  three 
hours.  More  than  eighty  or  ninety  grains  (grammes  5  to  6)  as  a  maximum  should 
not  be  given  in  one  day.  The  general  condition  often  improves  under  the  influ- 
ence of  antypyrine.  Especially  is  this  true  with  regard  to  headache,  restlessness, 
and  other  nervous  symptoms.  Another  very  efficient  antipyretic  is  acetanilide, 
which  was  lately  discovered  by  Cahn  and  Hepp,  and  has  already  been  largely 
introduced  into  medicine  under  the  name  of  antifebrin.  One  advantage  is  that  it 
is  far  cheaper  than  antipyrine.  It  is  given  in  doses  of  four  to  eight  or  even 
fifteen  grains  (gramme  0'25,  0*5,  1"0)  either  in  wafers  or  in  wine.  It  usually 
causes  a  decided  lowering  of  the  temperature,  and  seldom  with  any  unpleasant 
effect,  such  as  a  chill.  One  disadvantage,  however,  is  the  frequent  appearance  of 
a  peculiar  bluish  discoloration  of  the  skin,  which  is  probably  dependent  upon  a 
change  in  the  coloring  matter  of  the  blood,  similar  to  that  seen  in  poisoning  from 
aniline.  It  is  therefore  probable  that  caution  should  be  used  in  giving  the  drug. 
Numerous  other  antipyretics,  such  as  kairin  and  thallin,  have  been  proposed,  but 
have  not  become  popular.    It  is  also  improbable  that  a  continued  administration  of 


TYPHOID  FEVER.  25 

small  doses  of  thallin  (two  thirds  to  one  grain,  gramme  0"04, 0-0G)  every  hour  would 
have  a  favorable  influence  upon  the  course  of  the  disease,  although  this  has  been 
asserted.  The  newest  antipyretic  of  all  is  phenacetine,  which  was  recommended 
by  Kast  and  Hinsberg.     Its  dose  is  about  fifteen  grains  (gramme  \). 

After  all,  it  should  be  borne  in  mind  that  the  only  benefit  from  the  internal 
antipyretics  consists  in  the  lowering  of  the  temperature,  while  baths  not  only 
abate  the  fever,  but  possess  numerous  other  advantages,  as  has  been  already  shown. 
If  we  had  to  choose  whether  to  treat  typhoid  fever  exclusively  with  baths 
or  with  antipyrine,  and  the  like,  we  should  certainly  choose  the  baths.  We  do 
not  by  any  means  desire  to  banish  the  use  of  internal  antipyretics  from  the 
treatment  of  typhoid,  but  only  to  make  their  employment  more  limited  than 
has  often  been  the  case.  We  consider  that  they  are  actually  indicated  only 
where  the  fever  is  high  and  the  employment  of  baths  is  for  some  reason  impos- 
sible or  contra-indicated,  or  where  the  fever  remains  continuously  high,  despite 
bathing.  In  such  cases  it  is  often  advantageous  to  combine  the  bath-treatment 
and  the  internal  antipyretics,  especially  in  the  evening.  If  patients  with  a 
moderately  high  fever  are  made  to  take  large  doses  of  quinine  and  the  like, 
without,  any  satisfactory  reason  for  it,  we  regard  such  treatment  as  at  any  rate 
useless  and  often  really  injudicious.  This  is,  unfortunately,  a  common  practice, 
and  frequently  its  only  permanent  result  is  a  disordered  stomach. 

[Water  or  an  acid  drink  should  be  given  frequently  by  the  nurse  without  wait- 
ing for  the  patient  to  ask  for  it,  unless  the  mind  is  unusually  clear.  Phenacetine 
seems  to  have  proved  itself  less  depressing  to  the  heart  than  its  predecessors.  The 
antipyretic  dose  usual  in  this  country  is  five  grains.  A  strong  protest  should  be 
entered  against  the  routine  or  frequent  use  of  any  of  these  internal  antipyretics. 
If  the  temperature  seems,  in  itself,  to  cause  restlessness  and  discomfort,  an  oc- 
casional dose  may  be  given.  When  used  early  in  the  course  of  the  disease,  anti- 
pyretics may  seriously  embarrass  the  diagnosis  in  doubtful  cases.  The  method  of 
Brand  has  been  slowly  working  its  way  in  America  of  late  years,  and  perhaps 
would  have  spread  more  widely  and  rapidly  were  it  not  that  we  have  long 
been  in  the  habit  of  frequently  sponging  our  typhoid  patients  with  alcohol  and 
water.] 

Another  important  symptom  which  needs  special  treatment  is  intestinal 
haemorrhage.  It  has  been  already  mentioned  that  if  this  occurs,  the  baths  should 
cease  at  once.  Further  than  this,  the  chief  remedies  are  ice  and  opium.  Flat 
ice-bags  are  laid  upon  the  abdomen.  They  should  not  be  too  heavy,  and  should, 
if  possible,  be  suspended  from  a  hoop.  Internally,  the  patient  is  given  every  two 
hours  a  powder  of  one-half  grain  or  one  grain  (gramme  0-03  to  0'05)  of  opium, 
either  pure  or  combined  with  acetate  of  lead  (opii,  gr.  ss.,  grm.  0*03;  plumbi  ace- 
tatis,  gr.  j,  grm.  0-05 ;  sacchari  albi,  gr.  j,  grm.  0"05).  The  object  of  the  opium  is  to 
check  peristalsis,  and  thus  promote  the  formation  of  a  clot  in  the  bleeding  vessel. 
Liquor  ferri  chloridi  (five  to  ten  drops  in  water  every  hour)  is  often  employed, 
but  is  of  extremely  doubtful  value.  The  baths  can  not  be  resumed  till  there  has 
been  no  bleeding  for  at  least  three  or  four  days — and  then  only  cautiously. 

If  peritonitis  occurs,  the  treatment  is  much  the  same.  Above  all,  opium 
must  he  used  in  still  larger  doses,  but,  unfortunately,  as  a  rule,  in  vain.  Per- 
haps surgical  treatment  is  destined  eventually  to  be  useful,  viz.,  incision, 
cleansing,  and  drainage  of  the  peritoneum.  Its  results  thus  far  are  not  very 
encouraging. 

If  there  is  considerable  diarrhoea,  we  can  give  mistura  gummosa  [P.  G.,  gum 
arabic  and  sugar,  each  15  parts  ;  water,  170  parts],  tannin,  subnitrate  of  bismuth, 
or  small  doses  of  opium.  Constipation  at  the  beginning  of  the  disease  is  over- 
come by  calomel  (vide  supra).     In  later  stages  Ave  always  try  enemata  first,  to 


26  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

produce  an  operation.  If  this  does  not  succeed,  then  we  must  employ  rhubarb  or 
castor-oil.  Great  tympanites  may  be  diminished  by  laying  cold  wet  cloths  or 
ice-bags  upon  the  belly.  Considerable  amounts  of  gas  may  often  be  removed  by 
introducing  a  long  rectal  tube.  As  to  puncturing  the  greatly  inflated  intestines, 
a  method  practiced  by  some  physicians,  we  have  no  personal  experience. 

If  there  are  severe  pulmonary  symptoms,  baths  and  pouring  on  cool  water 
are,  as  we  have  said,  the  best  remedies.  Internally  we  may  try  liquor  ammonii 
anisatus  [P.  G.,  olei.  anisi,  1  part;  aquae  destillatoe,  24  parts;  aquaa  ammonia?,  5 
parts]  and  benzoic  acid  (grains  ij  to  iij,  gramme  0-l  to  0"2,  in  powder).  If  the 
pulse  be  very  rapid,  we  can  put  an  ice-bag  over  the  heart.  If  at  the  same  time 
the  pulse  is  small  and  weak,  we  give  stimulants,  of  which  the  best  is  camphor' 
(vide  infra).  Digitalis  (one-half  grain  of  the  leaves,  gramme  0'03,  two  or  three 
times  daily)  may  also  be  employed  if  the  pulse  be  rapid ;  but  it  should  be  used 
with  great  caution. 

For  nervous  symptoms  the  baths  and  douching  are  the  most  effective  reme- 
dies. The  head  is  meanwhile  co veiled  by  an  ice-bag.  If  there  be  great  excite- 
ment, as  shown  by  excessive  restlessness  or  delirium,  small  doses  of  morphine  are 
often  very  useful. 

The  conditions  of  collapse  and  cardiac  failure,  which  sometimes  appear  rather 
suddenly,  demand  prompt  and  energetic  treatment.  Stimulants  to  be  given  in- 
ternally are  some  stronger  kind  of  wine,  camphor  (two  to  five  grains,  gramme 
0-10  to  0*30,  in  the  form  of  a  powder),  musk  (one  half  grain  to  one  grain,  gramme 
0"03  to  0*05  at  each  dose),  or  spiritus  aetheris  [P.  G.,  aether,  one  part;  alcohol, 
three  parts].  Subcutaneous  injections  act  quicker  and  are  much  more  conven- 
ient. We  may  use  either  ether  or  camphor  (one  part  camphor  to  four  parts  olive- 
oil,  seven  to  fifteen  minims,  c.  c.  0-5  to  l-0,  every  one  to  two  hours).  To  start  up 
respiration,  the  best  means  is  to  pour  cold  water  on  the  back  of  the  neck.  Artifi- 
cial respiration  also  succeeds,  in  many  cases,  in  reviving  the  breathing  when  it 
is  about  to  stop. 

The  numerous  other  complications  aud  sequela?  which  may  occur,  but  which 
can  not  all  be  mentioned  here,  should  be  treated  on  general  principles. 

The  prophylactic  measures  to  avoid  the  spreading  of  the  disease  can  be  only 
briefly  referred  to.  Of  chief  importance  is  careful  disinfection  of  the  excreta, 
which  can  be  accomplished  by  pouring  upon  the  stools  a  not  too  small  amount  of 
five-per-cent.  carbolic  solution.  We  should  also  take  care  that  bed-pans,  bed- 
clothes, linen,  etc.,  are  handled  by  other  persons  as  little  as  possible.  If  there 
seems  reason  to  suspect  that  the  disease  ai'ose  from  bad  water,  of  course  the  source 
of  such  suspected  water  must  be  cut  off. 

[Recent  experiments  tend  to  show  that  the  above  solution  of  carbolic  acid  does 
not  kill  spores  except  after  prolonged  contact. 

The  following  are  the  measures  of  disinfection  recommended  by  the  American 
Public  Health  Association.  It  will  be  observed  that  they  apply  to  all  infectious 
diseases,  and  it  seems  well  to  give  them  here  nearly  in  extenso,  as  the  directions 
for  disinfection  in  most  text-books  are  far  too  vague. 

Disinfection  of  Excreta,  etc. — The  infectious  character  of  the  dejections  of 
patients  suffering  from  cholera  and  from  typhoid  fever  is  well  established;  and 
this  is  true  of  mild  cases  and  of  the  earlier  stages  of  these  diseases  as  well  as  of 
severe  and  fatal  cases.  It  is  probable  that  epidemic  dysentery,  tuberculosis,  and 
perhaps  diphtheria,  yellow  fever,  scarlet  fever,  and  typhus  fever,  may  also  be 
transmitted  by  means  of  the  alvine  discharges  of  the  sick.  In  cholera,  diphtheria, 
yellow  fever,  and  scarlet  fever,  all  vomited  material  should  also  be  looked  upon 
as  infectious;  and  in  tuberculosis,  diphtheria,  scarlet  fever,  and  infectious  pneu- 
monia, the  sputa  of  the  sick  should  be  disinfected  or  destroyed  by  fire.     It  seems 


TYPHOID   FEVER.  27 

advisable  also  to  treat  the  urine  of  patients  sick  with  an  infectious  disease  with 
one  of  the  disinfecting  solutions  below  recommended. 

Chloride  of  lime,  or  bleaching-  powder,  is,  perhaps,  entitled  to  the  first  place 
for  disinfecting- excreta,  on  account  of  the  rapidity  of  its  action.  The  following- 
standard  solution  is  recommended  : 

Standard  Solution  No.  1. 

Dissolve  chloride  of  lime,  of  the  best  quality,*  in  pure  water,  in  the  proportion 
of  four  ounces  to  the  gallon.  Use  one  quart  of  this  solution  for  the  disinfection 
of  each  discharge  in  cholera,  typhoid  fever,  etc.  Mix  well  and  leave  in  vessel  for 
at  least  one  hour  before  throwing  into  privy- vault  or  water-closet.  The  same 
directions  apply  for  the  disinfection  of  vomited  matters. 

Standard  Solution  No.  2. 

Dissolve  corrosive  sublimate  and  permanganate  of  potash  in  pure  water,  in  the 
proportion  of  two  drachms  of  each  salt  to  the  gallon.  This  is  to  be  used  for  the 
same  purposes  and  in  the  same  manner  as  Standard  Solution  No.  1.  It  is  equally 
effective,  but  must  be  left  a  longer  time  in  contact  with  the  material  to  be  disin- 
fected— at  least  four  hours.  The  only  advantage  this  solution  has  over  No.  1  con- 
sists in  the  fact  that  it  is  odorless.  It  costs  about  two  cents  a  gallon.  It  is  very 
poisonous,  and  will  injure  lead  pipes  if  passed  through  them  in  considerable 
quantities.  Solutions  of  corrosive  sublimate  should  not  be  placed  in  metal  re- 
ceptacles. 

Disinfection  of  the  Person. — The  surface  of  the  body  of  a  sick  person,  or  of 
his  attendants,  when  soiled  with  infectious  discharges,  should  be  at  once  cleansed 
with  a  suitable  disinfecting  agent.  For  this  purpose  solution  of  chlorinated  soda, 
diluted  with  three  parts  of  water,  or  Standard  Solution  No.  1,  diluted  with  three 
parts  of  water,  may  be  used.  A  two-per-cent.  solution  of  carbolic  acid  is  also 
suitable  for  this  purpose,  and,  under  proper  supervision,  the  use  of  a  solution  of 
corrosive  sublimate  (1-1,000)  is  to  be  recommended. 

In  diseases  like  small-pox  and  scarlet  fever,  in  which  the  infectious  agent  is 
given  off  from  the  entire  surface  of  the  body,  occasional  ablutions  with  solution 
of  chlorinated  soda,  diluted  with  twenty  parts  of  water,  will  be  more  suitable  than 
the  stronger  solution  above  recommended. 

In  all  infectious  diseases  the  body  of  the  dead  should  be  enveloped  in  a  sheet 
saturated  with  Standard  Solution  No.  1,  or  with  a  five-per-cent.  solution  of  car- 
bolic acid,  or  a  1-500  solution  of  corrosive  sublimate. 

Disinfection  of  Clothing. — Boiling  for  half  an  hour  will  destroy  the  vitality 
of  all  known  disease-germs,  and  there  is  no  better  way  of  disinfecting  clothing  or 
bedding  which  can  be  washed  than  to  put  it  through  the  ordinary  operations  of 
the  laundry.  No  delay  should  occur,  however,  between  the  time  of  removing 
soiled  clothing  from  the  person  or  bed  of  the  sick  and  its  immersion  in  boiling 
water,  or  in  one  of  the  following  solutions ;  and  no  article  should  be  permitted  to 
leave  the  infected  room  until  so  treated. 

Standard  Solution  No.  3. 

Dissolve  four  ounces  of  corrosive  sublimate  and  one  pound  of  sulphate  of 
copper  in  a  gallon  of  water.  Two  fluid  ounces  of  this  standard  solution  to  the 
gallon  of   water  will  make  a  suitable  solution  for  the  disinfection  of  clothing. 

*  Good  chloride  of  lime  should  contain  at  least  twenty-five  per  cent,  of  available  chlorine.  The  cost 
of  the  solution  is  less  than  one  cent  a~2;allon.     The  sediment  does  no  harm. 


23  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

The  articles  to  be  disinfected  must  be  thoroughly  soaked  with  the  disinfecting 
solution,  and  left  in  it  for  at  least  two  hours,  after  which  they  may  be  wrung  out 
and  sent  to  the  wash. 

Clothing  may  also  be  disinfected  by  immersing  it  for  four  hours  in  a  two-per- 
cent, solution  of  carbolic  acid.  Soiled  mattresses,  pillows,  feather  beds,  and  articles 
of  this  nature  can  not  be  effectually  disinfected  by  sulphur  fumigation,  owing  to 
the  fact  that  the  gas  does  not  penetrate  to  their  interior  in  sufficient  amount. 
For  articles  of  this  kind,  and  in  general  for  articles  of  little  value,  which  have 
been  soiled  by  the  discharges  of  the  sick,  destruction  by  fire  will  be  advisable. 

Disinfection  of  the  SicJc-Room. — No  disinfectant  can  take  the  place  of  free 
ventilation  and  cleanliness,  and  it  is  impracticable  to  disinfect  an  occupied  apart- 
ment.    Neutralizing  bad  odors  is  not  disinfection. 

All  surfaces  should  be  thoroughly  washed  with  Standard  Solution  No.  1,  diluted 
with  three  parts  of  water,  or  with  a  1-1,000  solution  of  corrosive  sublimate. 
Standard  Solution  No.  3,  diluted  in  the  proportion  of  four  ounces  to  the  gallon  of 
water,  may  be  used. 

The  walls  and  ceiling,  if  plastered,  should  be  brushed  over  with  one  of  these 
solutions,  and  subsequently  washed  over  with  a  lime-wash. 

Especial  care  must  be  taken  to  wash  away  all  dust  from  window  ledges  and 
other  places  where  it  may  have  settled,  and  thoroughly  to  cleanse  crevices  and 
Out-of-the-way  places.  After  this  application  of  the  disinfecting  solution,  and  an 
interval  of  twenty-four  hours  or  longer  for  free  ventilation,  the  floors  and  wood- 
work should  be  well  scrubbed  with  soap  and  hot  water,  and  this  should  be  followed 
by  a  second  more  prolonged  exposure  to  fresh  air,  admitted  through  open  doors 
and  windows. 

As  an  additional  precaution,  fumigation  with  sulphurous-acid  gas  is  to  be 
recommended,  especially  for  rooms  which  have  been  occupied  by  patients  with 
small-pox,  scarlet  fever,  diphtheria,  typhus  fever,  and  yellow  fever.  All  apertures 
into  the  room  should  be  carefully  closed,  and  not  less  than  three  pounds  of  sul- 
phur for  each  thousand  feet  of  air-space  should  be  burned.  To  secure  complete 
combustion,  the  sulphur,  in  powder  or  small  fragments,  and  moistened  with 
alcohol,  should  be  placed  in  a  shallow  iron  pan,  and  this  should  be  placed  on 
bricks  in  a  tub  partly  filled  with  water  to  guard  against  fire.] 


CHAPTER  II. 

TYPHUS  FEVER. 

(Spotted  Fever.    Ship  Fever.) 

Typhus  fever  is  an  acute  infectious  disease,  perfectly  distinct  from  typhoid 
fever,  but  formerly  often  confounded  with  it.  The  similarity  of  the  two  diseases, 
which  led  to  their  similar  names,  consists  only  in  the  grave  general  condition, 
with  fever,  and  in  a  number  of  complications,  which  may  appear  in  botb.  There 
is,  however,  an  essential  difference  in  the  whole  course  of  the  diseases,  and  espe- 
cially in  the  circumstance  that  the  intestinal  lesion  which  is  characteristic  of 
typhoid  is  never  seen  in  typhus.  The  chief  distinction  between  the  two  affections, 
which  must  undoubtedly  lie  in  the  difference  in  their  causes,  can  not  yet  be  dem- 
onstrated. We  do  not  yet  know  the  organized  pathogenic  agents  of  typhus 
fever,  although  it  must  be  presupposed  that  they  exist. 

iEtiology. — As  to  the  way  in  which  infection  occurs,  we  have  much  less  infor- 
mation even  than  in  relation  to  typhoid.     We  regard  it  as  an  established  fact  that 


TYPHUS  FEVER.  2D 

the  disease  never  arises  spontaneously,  and  that  its  appearance  in  a  place  previ- 
ously free  from  the  disease  is  always  to  he  referred  to  an  importation  of  the  patho- 
genic poison.  It  is  likewise  determined,  through,  numerous  observations,  that 
typhus  is  one  of  the  contagious  diseases — that  is,  that  the  specific  poison  can  be 
directly  transferred  from  the  patient  to  others  around  him.  How  it  is  transferred 
we  have  no  certain  knowledge.  Perhaps  the  poison  is  contained  in  the  expired 
air;  or,  as  is  still  more  probable,  in  the  scales  of  epidermis;  or,  perhaps,  in  the 
other  excretions  and  secretions  of  the  patient.  We  are  equally  ignorant  through 
what  channel  the  infectious  agent  enters  the  system — whether  it  is  inspired  or 
swallowed.  It  is  certain  that  the  poison  may  be  transferred  in  the  clothes,  etc., 
of  the  patient  (fomites). 

Favorable  hygienic  surroundings  decidedly  diminish  the  contagiousness  of 
typhus  fever.  For  example,  in  the  well-ventilated  pavilions  of  the  Leipsic  hos- 
pital there  have  rarely  been  cases  of  transfer  of  the  disease  to  physicians,  nurses, 
or  other  patients.  On  the  other  hand,  if  the  hygienic  influences  be  unfavorable, 
typhus  fever  may  appear  in  very  widespread  epidemics.  Those  terrible  epidemics 
which  have  been  described  under  the  names  of  "  famine  fever,"  "camp  fever" 
(Hungertyphus,  Kriegstyphus),  etc.,  were  for  the  most  part  typhus  fever.  In  the 
smaller  epidemics  it  is  often  possible  to  trace  the  disease  to  some  wretched,  over- 
filled tenement-house. 

At  present  typhus  fever  appears  constantly  in  Great  Britain.  Ireland  has  been 
notorious  for  many  years  as  a  breeding-place  of  the  disease.  It  is  also  frequent  in 
the  eastern  part  of  Germany  (Posen,  East  Prussia  and  West  Prussia,  Silesia),  in 
Poland,  Galicia,  Russia,  and  in  parts  of  southern  Europe.  The  isolated  cases 
which  occur  every  year  here  and  there  in  central  Germany,  though  more  or  less 
numerous,  are,  almost  without  exception,  to  be  referred  to  an  importation  of  the 
disease. 

Typhus  fever  attacks  by  preference  young  adults  of  twenty  to  forty  years ;  but 
it  occurs  in  children,  and  is  comparatively  frequent  in  elderly  persons.  There  is 
no  marked  dependence  of  the  epidemics  upon  any  particular  season  of  the  year. 
As  in  the  case  of  typhoid  fever,  a  person  who  has  once  had  the  disease  seems  to 
enjoy  immunity  from  any  fresh  attack. 

[The  practical  acquaintance  of  American  physicians  with  typhus  fever  is,  fortu- 
nately, limited.  Many  of  the  outbreaks  which  have  occurred  were  traceable  to  im- 
migrants, especially  from  Ireland. 

During  our  civil  war  the  disease  broke  out  neither  among  the  armies  in  the 
field  nor  among  the  prisoners  of  war.  A  number  of  cases  were  reported  at  the 
time,  but  great  doubt  has  since  been  thrown  upon  the  correctness  of  the  diag- 
nosis.] 

Course  and  Symptoms  of  the  Disease.— If  we  try  to  sketch  the  characteristic 
behavior  of  typhus  fever,  especially  as  contrasted  with  typhoid,  we  may  say  that 
the  disease  begins  much  more  abruptly  and  rapidly,  and  that  the  fever  quickly 
becomes  very  high  and  the  general  disturbance  very  severe,  but  the  illness  lasts 
a  shorter  time,  seldom  more  than  two  weeks,  and  generally  passes  by  crisis  into 
recovery. 

The  length  of  incubation  seems  to  vary.  Murchison  thinks  it  is  usually 
more  than  nine  days.  Sometimes,  though  not  invariably,  slight  prodromata 
precede  by  some  days  the  actual  outbreak  of  the  disease.  These  are  languor, 
anorexia,  headache,  and  pain  in  the  limbs.  Then  the  regular  illness  begins,  as  a 
rule,  rather  suddenly,  and  often  with  a  pronounced  rigor.  With  this  the  tem- 
perature rises  quickly,  and  may  on  the  very  first  evening  reach  104°  or  105° 
(40°-40"5°  C).  Vomiting  is  not  rare,  and  may  be  repeated.  A  grave  general 
condition,  wTith  fever,  is  developed  in  a  few  days.     The  patient  feels  exhausted. 


30  ACUTE  G-ENEKAL  INFECTIOUS  DISEASES. 

There  is  often  violent  pain  in  the  loins  and  extremities.  Nervous  symptoms 
soon  appear:  persistent  and  intense  headache,  vertigo,  spots  before  the  eyes, 
ringing  in  the  ears,  and  in  many  cases  quickly  increasing  stupor  and  delirium. 
In  severe  cases  the  fever  often  reaches  106°  (41°  C),  and  may  be  even  higher,  and 
it  is  almost  constant,  with  but  slight  morning  remissions.  The  skin  is  hot  and 
dry,  the  tongue  dry  and  thickly  coated,  the  respiration  moderate,  the  pulse  very 
rapid.  We  very  frequently  find  in  the  chest  the  signs  of  an  extensive  bronchitis. 
Nasal  catarrah  and  conjunctivitis  also  occur.  Serious  intestinal  symptoms  are 
generally  absent,  although  there  may  be  slight  tympanites  or  diarrhoea.  The 
spleen  is  almost  always  greatly  enlarged.  Only  in  a  few  epidemics  is  the  splenic 
tumor  said  to  have  been  wanting  (?).  The  urine  is  concentrated  and  scanty,  and 
sometimes  has  a  trace  of  albumen. 

On  the  third  to  the  seventh  day  of  the  disease  the  characteristic  eruption  ap- 
pears. To  this  the  disease  owes  its  name  of  "spotted  fever."  The  eruption  con- 
sists of  rose-spots,  generally  very  numerous  and  widespread,  upon  the  trunk  and 
extremities,  often  also  on  the  face.  Sometimes  the  spots  are  larger,  and  may  then 
bear  great  resemblance  to  a  fresh  eruption  of  measles.  The  skin  between  the  sep- 
arate rose-spots  is  not  infrequently  diffusely  reddened.  After  two  or  three  days 
the  roseola?  become  haemorrhagic,  and  change  into  lighter  or  darker  petechias. 
It  is  commonly  only  in  the  lighter  cases  that  the  rose-spots  fade  away  without 
first  becoming  petechial.  In  rare  though  well-substantiated  cases  the  eruption  has 
been  scanty,  or  even  wholly  wanting.     Herpes  does  occur,  but  only  seldom. 

The  fever  begins  to  abate  in  light  cases  as  early  as  the  second  week,  coin- 
cidently  with  an  improvement  in  the  general  symptoms.  Often  this  change  is 
indicated  about  the  seventh  day  by  a  considerable  remission  in  the  temperature. 
On  the  other  hand,  in  severe  cases,  all  the  symptoms  grow  worse.  The  weakness 
increases.  The  nervous  derangement  reaches  the  extreme  of  a  severe  "typhoid 
state,"  expressed  either  by  marked  stupor,  which  sometimes  passes  into  complete 
coma,  or  by  violent  delirium.  Lobular  pneumonia  attacks  the  lungs,  and  the 
fever  continues  with  unabated  violence.  These  symptoms  may  end  with  death, 
but  in  favorable  cases  they  decline  rapidly.  Sometimes  this  decline  is  preceded 
by  a  great  rise  in  temperature  (perturbatio  critica)  on  the  fourteenth  to  seven- 
teenth day,  rarely  a  few  days  earlier  or  later.  In  such  cases  the  temperature  is 
apt  to  fall  by  crisis,  sinking  in  a  day  or  two,  with  but  slight  interruption,  down  to 
the  normal  level.  Even  in  those  cases  in  which  the  descent  is  by  gradations  it  is 
always  decidedly  more  abrupt  than  in  typhoid.  The  eruption  quickly  fades,  the 
patients  gradually  improve,  and,  as  a  rule,  become  completely  and  permanently 
convalescent.  It  is  true  that  some  observers  have  seen  relapses,  but  they  are,  at 
least  in  our  present  epidemics,  extremely  rare. 

Complications  and  Varieties  in  the  Course  of  the  Disease. — From  what  we  have 
said  of  its  course,  it  is  evident  that  the  symptoms  are  essentially  those  of  an  intense 
general  infection  of  the  system.  The  sole  demonstrable  local  lesion  which  is 
almost  invariably  present  is  the  characteristic  eruption,  and  this  has  evidently  no 
causal  relation  to  the  severe  symptoms  of  the  disease.  It  is  likewise  extremely 
probable  that  most  of  the  complications,  which  not  infrequently  arise  in  severe 
cases,  are  secondary,  and  occur  in  the  way  already  described  with  considerable 
detail  in  the  preceding  chapter.  They  are  just  such  complications  as  are  possible 
in  every  severe  general  disease,  and  embrace  otitis,  parotitis,  extensive  lobular 
pneumonia,  more  rarely  gangrene  of  the  lungs,  and  pleurisy ;  also  f urunculosis, 
purulent  cellulitis,  bed-sores,  dysentery,  icterus,  etc.  Whether  some  of  the  local 
lesions  which  are  observed  may  not  be  direct  results  of  the  pathogenic  poison, 
we  can  not  at  present  decide.  Among  these  would  come,  first  of  all,  the  rare 
cases  of  lobar  pneumonia  and    nephritis.      Sequelae  are,   on  the  whole,  rare, 


RELAPSING  FEVER.  31 

though,  sometimes  there  is  a  tedious  anaemic  condition,  or  neuralgia,  paraly- 
sis, etc. 

The  separate  epidemics  of  typhus  present  considerable  variety,  not  only  as 
regards  the  occurrence  of  individual  complications,  hut  more  especially  in  the 
general  course  and  character  of  the  cases.  For  instance,  some  epidemics  are  dis- 
tinguished by  the  greater  frequency  of  light  attacks  (typhus  exanthematicus 
levissimus,  unsuitably  termed  by  some  "  febricula  ").  Here  the  entire  attack  runs 
its  course  in  five  to  eight  days.  The  fever  is  generally  comparatively  moderate; 
there  are  no  severe  general  symptoms,  and  complications  are  exceptional. 

Diagnosis. — It  may  be  very  difficult  for  a  time  to  distinguish  typhus  from 
typhoid.  The  following  factors  are  of  chief  importance:  1.  The  onset  is  much 
more  abrupt  in  typhus  than  in  typhoid,  and  is  often  accompanied  by  a  pronounced 
rigor.  2.  In  typhus,  the  nervous  disturbaiices  usually  appear  earlier  and  are  more 
severe  than  in  typhoid.  3.  The  rash  is  seldom  so  extensive  in  typhoid  as  in  ty- 
phus, and  in  typhoid  it  hardly  ever  becomes  petechial.  4.  In  typhus  the  pains  in 
the  loins  and  limbs  are  generally  much  more  pronounced.  5.  If  we  still  find  it 
hard  to  decide,  the  manner  of  recovery  will  almost  always  settle  the  question. 
Recovery  in  severe  cases  of  typhoid  is,  on  the  average,  much  more  tardy  and 
gradual,  by  lysis.  In  typhus  it  occurs  generally  by  the  seventeenth  day,  and  by 
crisis. 

The  prognosis  is  chiefly  determined  by  the  severity  of  the  fever  and  of  the 
nervous  symptoms.  Extensive  lobular  pneumonia  is  the  most  frequent  dangerous 
complication.  The  mortality  varies  greatly  in  the  separate  epidemics.  It  is  some- 
times only  six  or  seven  per  cent.,  but  may  rise  to  twenty  per  cent. 

Treatment  is  based  on  the  same  principles  as  in  typhoid  fever.  There  is  no 
specific  remedy.  Besides  good  nursing,  a  judicious  employment  of  baths  is  cer- 
tainly our  chief  reliance  for  lessening  the  severity  of  many  of  the  symptoms,  such 
as  febrile,  nervous,  and  pulmonary  disturbances,  as  well  as  for  averting  many 
dangerous  complications.  For  all  details  of  treatment  we  may  refer  to  the  pre- 
ceding chapter. 


CHAPTER  III. 


RELAPSING  FEVER. 

(Relapsing  Typhus — Febris  recurrens.) 

iEtiology.— This  disease  was  first  named  by  English  pathologists  relapsing 
fever,  and  by  Griesinger  febris  recurrens.  It  has  a  peculiar  course,  made  up  of 
separate  attacks,  and  is  further  of  great  interest  because  it  is  one  of  the  first  infec- 
tious diseases  in  which  the  specific  pathogenic  organisms  became  known,  and, 
being  easily  demonstrable  in  each  separate  case,  were  utilized  for  the  speedy  and 
certain  diagnosis  of  the  disease.  Obermeier  discovered  in  Berlin,  in  the  year  1873, 
that  in'  relapsing  fever  the  blood,  at  certain  times,  invariably  contains  peculiar, 
thread-like  micro-organisms.  This  discovery  has  since  been  universally  con- 
firmed ;  and  it  may  be  maintained  that  if  once  the  presence  of  these  "  spirilli  "  be 
demonstrated  in  the  blood,  we  are  justified  in  making  an  absolute  diagnosis  of 
relapsing  fever. 

In  Germany  the  disease  did  not  become  epidemic  till  the  year  1868.  In  1872 
and  1873  there  were  considerable  epidemics  in  Breslau  and  Berlin.  Its  last  exten- 
sive appearance  was  in  1879  and  1880,  when  it  spread  over  most  of  northern  and 
central  Germany,  and  was  accurately  studied  by  numerous  observers.     People  of 


32  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

the  poorer  classes  were  almost  exclusively  attacked,  and  especially  the  "  tramps." 
The  uncleanly  dens  where  these  people  lodge  were  found  everywhere  to  be  the 
chief  centers  of  infection. 

The  precise  manner  of  infection  is  as  yet  almost  wholly  unknown.  All  ob- 
servers agree  that  the  disease  is  directly  contagious ;  but  it  can  not  be  very  con- 
tagious if  the  hygienic  influences  be  good.  At  least  the  results  of  our  late  epi- 
demics would  imply  this.  In  the  Leipsic  hospital,  where  over  two  hundred  and 
fifty  cases  were  treated,  and  isolation  could  not  be  at  all  perfectly  carried  out,  not 
one  case  of  infection  occurred.  It  is  certain  tbat  the  disease  can  be  transmitted 
by  direct  inoculation  with  the  blood  of  patients.  This  has  been  established  by  a 
Russian  physician  by  the  experimental  inoculation  of  healthy  persons.  Doctors 
have  been  repeatedly  inoculated  at  the  autopsy  of  those  who  have  died  of  relaps- 
ing fever.  The  disease  may  likewise  be  transferred  by  inoculation  to  monkeys, 
while  other  mammals  seem  to  enjoy  an  immunity  from  it. 

[The  first  cases  of  relapsing  fever  observed  in  this  country  were  in  Irish  immi- 
grants coming  over  in  the  same  vessel  in  the  year  1844.  At  several  periods  since 
then  more  or  less  limited  outbreaks  traceable  to  immigration  have  occurred,  but 
the  disease  has  never  acquired  any  foothold  with  us,  and  comparatively  few  physi- 
cians have  ever  seen  it.  So  far  as  I  can  learn,  only  one  case  has  ever  been  seen  in 
Boston,  and  that  was  in  the  person  of  a  physician  from  another  city,  who  brought 
the  disease  with  him  and  passed  through  it  in  the  Massachusetts  General  Hospital.] 

Clinical  History. — The  stage  of  incubation  lasts  about  five  to  eight  days.  It  is 
only  exceptionally  that  some  slight  prodromal  symptoms  present  themselves  just 
before  the  outbreak  of  the  disease  proper.  As  a  rule,  it  begins  suddenly,  with  a 
more  or  less  pronounced  chill  and  intense  constitutional  symptoms.  There  are 
violent  headache,  great  languor,  anorexia,  and  especially  marked  pains  in  the  loins 
and  extremities.  The  temperature  rises  rapidly,  reaching  generally  106°  (41°  C.) 
or  higher  as  early  as  the  first  or  second  day.  The  skin  is  hot  and  dry,  and  usually 
quickly  assumes  a  very  characteristic  dirty-yellowish  color.  In  Leipsic,  we  often 
saw  herpes  labialis,  which  seems,  however,  to  have  been  rarer  in  epidemics  else- 
where. The  tongue  becomes  dry  and  thickly  coated.  Sometimes  there  is  vomit- 
ing. The  bowels  are  constipated,  or  there  is  a  slight  diarrhoea.  The  spleen  be- 
comes rapidly  enlarged,  being,  as  a  rule,  even  larger  than  in  typhoid  or  typhus. 
The  liver  is  slightly  enlarged.  The  chest  presents  the  signs  of  a  bronchitis,  gener- 
ally moderate,  but  in  exceptional  instances  severe.  The  pulse  is  much  quickened. 
It  is  seldom  that  there  are  severe  cerebral  symptoms  beyond  a  certain  apathy  and 
stupor.  "We  have  seen  delirium  tremens  sometimes,  in  drunkards.  A  very  char- 
acteristic symptom,  already  mentioned,  is  the  marked  hyperesthesia  of  the  mus- 
cles, especially  in  the  calves. 

After  these  symptoms,  accompanied  by  persistent  and  generally  very  high 
fever,  have  lasted  five  days  to  a  week,  there  is  a  critical  decline  of  temperature, 
with  profuse  sweating.  The  patient  now  improves  so  rapidly  and  decidedly  that 
he  thinks  himself  completely  cured,  and  generally  gives  little  credence  to  the 
physician's  prophecy  of  a  relapse.  In  rare  but  well-attested  cases  there  has  been 
really  but  one  attack.  The  rule  is  that,  after  about  a  week,  a  second  attack  occurs, 
often  a  third  after  that,  and,  infrequently,  even  a  fourth  and  fifth.  In  each  of 
these,  the  above-mentioned  symptoms  are  repeated  more  or  less  completely  and 
violently.  As  the  only  certain  and  constant  sign  of  the  recurring  attacks  (the 
so-called  relapses)  is  a  fresh  rise  of  temperature,  it  will  be  well  to  consider  their 
peculiarities  at  the  same  time  that  we  describe  the  course  of  the  fever.  During 
the  intervals  of  normal  temperature  the  other  objective  symptoms  of  disease  are 
usually  absent,  except  an  evident  splenic  tumor,  and,  not  infrequently,  the  pecul- 
iar pale-yellow  hue. 


RELAPSING  FEVER. 


33 


Course  of  the  Fever  (see  Fig.  3). — The  beginning-  of  the  fever  in  the  first 
attack  is,  as  we  have  said,  almost  always  sudden,  so  that  it  may  even  in  a  few 
hours  reach  a  considerable  height.  The  fever  lasts,  as  a  rule,  five  to  seven  days, 
but  not  infrequently  as  short  a  time  as  three  or  four  days,  or  as  long  as  ten  or 
twelve  days.  During  this  time  it  may  keep  a  tolerably  uniform  height,  but 
oftener  there  are  considerable  remissions,  which  may  even  come  to  deserve  the 
name  of  pseudo-crises.  In  such  cases  the  temperature  sinks  in  the  morning  to 
normal  or  even  lowei*,  so  that  we  might  believe  the  fever  ended ;  but  in  the  even- 
ing the  temperature  rises  again  to  its  former  level.  These  pseudo-crises  are  most 
frequent  toward  the  end  of  the  attack,  but  do  occur  sometimes  in  the  very  first 
days.  The  absolute  height  of  the  fever  is,  as  a  rule,  very  considerable.  Tempera- 
tures between  105"5°  and  lOö^ö0  (41°  and  41-5°  C.)  are  very  often  observed,  and  in 
themselves  are  not  especially  ominous  in  relapsing  fever.  The  highest  tempera- 
ture we  have  observed  was  107'"°  (42'2°  C).  Sometimes  the  temperature  is  more 
moderate  (between  102°  and  104°,  39°  and  40°  C).  The  fever  almost  always  ends 
at  the  close  of  the  attack  by  crisis,  only  rarely  by  a  rapid,  gradual  decline.  The 
crisis  is  often  preceded  by  an  especially  great  rise  the  evening  before  (perturbatio 
critica) ;  so  that  the  subsequent  fall  of  temperature  is  very  considerable.  It  gen- 
erally occurs  at  night,  and  is  accompanied  by  profuse  perspiration.  The  fall  may 
amount  to  9°  or  10°  (5°  to  6°  C).  The  temperature  sinks  almost  always  below 
normal,  often  as  low  as  95°  (35°  C.)  or  thereabouts.  Once  we  saw  it  fall  to  92"1° 
(33-4°  C). 

To  the  first  attack  succeeds  an  interval  during  which  there  is  no  fever  (apy- 
rexia),  which  lasts  on  the  average  about  a  week,  sometimes  a  less  time,  and  often 
a  greater.     The  longest  interval  we  have  ever  observed  lasted  seventeen  days. 


12      3      4 


9      10    11     12     13    14    15    16    17    18    19    20     21     22    23    24 


42-0° 
41-0° 
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39-0° 
38-0° 
37-0° 
36-0° 
35-0° 


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Fig.  3.— Example  of  the  temperature  curve  in  relapsing  fever. 


During  this  interval  the  temperature,  which,  as  a  rule,  is  at  first  subnormal,  rises 
to  normal,  and  then  generally  remains  there.  Exceptionally  there  are  slight 
evening  exacerbations  to  above  100'5°  (38°  C).  These  may  have  no  demonstrable 
cause,  or  may  result  from  some  complication,  such  as  otitis,  or  a  furuncle.  Then 
comes  another  change,  and  generally  a  sudden  one,  ushered  in  with  a  chill,  and  a 
new  rise  of  temperature,  the  beginning  of  the  second  attack  or  first  relapse. 
During  this  attack  the  fever  has  the  same  general  peculiarities  as  in  the  first  at- 
tack. Generally  the  first  relapse  is  briefer  by  a  day  or  two  than  the  first  attack ; 
but  the  reverse  is  sometimes  true.  We  will  add  that  we  have  observed  not  infre- 
3 


3± 


ACUTE  GENERAL  INFECTIOUS  DISEASES. 


quently  a  rather  high  evening  temperature  (say  101"5°,  S8'5°  C.)  for  one  or  two 
days  before  the  second  attack  began,  as  also  before  the  third. 

Relapsing  fever  seems  in  many  epidemics  to  have  been  made  up  of  two  attacks, 
so  that  not  more  than  one  tenth  of  the  cases  had  a  third  attack.  On  the  other 
hand,  the  majority  of  the  cases  in  the  last  epidemic  had  two  relapses.  And  in 
these  cases  the  rule  was  for  the  interval  between  the  second  and  third  attacks  to 
be  one  or  two  days  longer  than  the  first  apyrexia ;  but  earlier  epidemics  seem  to 
have  had  the  second  apyrexia,  if  there  was  one  at  all,  briefer  than  the  first.  The 
third  attack  is  set  down  in  all  reported  cases  as  decidedly  shorter  than  either  of  its 
predecessors.  It  lasts  generally  two  or  three  days.  Exceptionally  we  have  seen 
it  persist  for  four  or  even  six  days. 

A  fourth  and  even  a  fifth  attack  may  occur,  but  only  exceptionally.  If  they 
do  happen,  they  are  usually  imperfectly  developed,  and  often  are  limited  to  a  fever 
of  one  day's  duration.  The  more  accurately  and  persistently  we  take  the  tem- 
perature during  convalescence,  the  offener  do  we  find  slight  rises  of  temperature 
occurring  at  intervals  late  in  the  history  of  the  case.  These  are  probably  to  be 
interpreted  as  final,  rudimentary  attacks. 

The  Spirilli. — The  number  of  cases  of  relapsing  fever  in  which  no  spirilli  can 
be  demonstrated  in  the  blood,  if  the  examination  be  accurate,  has  become  so  small 
that  it  can  be  disregarded  when  we  compare  it  with  the  much  greater  number  of 
cases  where  such  demonstration  is  made  with  ease  and  certainty.  The  best  way  is 
to  get  a  drop  of  blood  by  pricking  the  skin,  and  examine  it  as  it  is,  without  mixing 
anything  with  it.  There  is  no  need  of  an  immersion  lens.  With  a  good  Hartnack 
No.  8  [about  330  to  440  diameters,  according  to  eyepiece]  the  spirilli  are  seen  with 
perfect  distinctness.  We  have  often  seen  them  plainly  with  a  No.  7  [250  to  340 
diameters].  It  requires  a  little  practice  to  make  them  out;  but  this  is  easily  ob- 
tained. Often  the  attention  is  first  caught  by  little  jogglings  and  motions  of  the 
red  blood-corpuscles,  and  then  we  see  the  delicate,  narrow  threads.  Their  length 
equals  about  three  to  six  times  the  diameter  of  the  red  globules  (Fig.  4).  They 
exhibit  an  active  and  almost  continuous  motion,  like  snakes.  Often  the  whole 
thread  bends  upon  itself,  and  then  stretches  out  again.  They  are  partly  separate 
and  partly  tied  up  in  knots  composed  of  four  to  twenty  individuals.  The  whole 
number  visible  in  one  field  varies  greatly  in  individual  cases,  and  has  no  direct 

relation  to  the  severity  of  the  case.  Often 
it  requires  long  searching  to  find  a  few, 
while  in  other  cases  there  may  be  twenty 
or  more  in  the  field  at  once.  A  very  inter- 
esting fact  is  that  their  appearance  in  the 
blood  depends  upon  the  attacks  of  fever. 
On  the  first  day  of  the  attack  we  rarely  find 
spirilli,  and  then  only  one  or  two.  Upon 
succeeding  days  their  number  increases. 
Shortly  before  the  end  of  the  attack — that 
is,  before  the  crisis— they  generally  disap- 
pear entirely;  but  even  after  the  crisis  they 
have  been  found,  exceptionally  and  in  very 
small  numbers.  They  have  very  often  been 
found  by  the  author  as  well  as  other  ob- 
servers during  the  pseudo-crisis  described 
above,  so  that,  after  the  temperature  has  be- 
come normal,  the  presence  of  spirilli  makes  it  very  probable  that  another  rise  of 
temperature  is  impending.  The  spirilli  have  thus  far  been  found  in  the  blood  only, 
in  the  catamenia,  in  bloody  urine,  or  in  blood  coughed  up  from  the  lungs,  and 


Fig.  4.— Spirilli  of  relapsing  fever  in  the  blood. 


RELAPSING  FEVER.  35 

never  in  the  organs  or  secretions  (urine,  milk,  sweat,  contents  of  herpetic  vesicles). 
There  can  hardly  be  any  doubt  that  the  spirilli  which  appear  in  tin;  separate  at- 
tacks are  to  be  regarded  as  separate  generations.  As  to  their  manner  and  place  of 
development  we  have  as  yet  no  knowledge.  In  the  final,  rudimentary  attacks,  we 
find  few  if  any.  If  the  patient  dies  during  an  attack,  they  are  to  be  found  in  the 
blood  after  death.  Artificial  cultivations  have  not  been  very  successful ;  nor  have 
pure  cultures  of  them,  to  our  knowledge,  ever  succeeded.  Albrecht  states  that 
they  will  subsequently  develop  in  blood  taken  from  a  patient  during  the  interval 
when  he  has  no  fever. 

The  blood  is  otherwise  modified  during  relapsing  fever.  We  very  often  find  a 
slight  increase  in  the  white  corpuscles.  There  is  often  a  noticeable  abundance  of 
very  small  bodies,  so-called  granular  elements  (Körnchenbildungen).  The  signifi- 
cance of  these  (the  remains  of  white  corpuscles  ?)  is  still  doubtful.  There  are, 
finally,  peculiar  cells,  rather  large,  with  fat-granules.  They  were  demonstrated 
by  Ponfick  in  the  venous  blood,  and  are  said  to  come  from  the  spleen.  We  also 
find  fatty-degenerated  endothelium  in  the  blood. 

Complications  are  on  the  whole  rare,  and  mostly  secondary.  Important  among 
these  are  troublesome  ophthalmic  disturbances,  especially  iritis  and  iridochoroid- 
itis.  Sometimes  parotitis,  laryngitis,  and  pneumonia  occur.  Epistaxis  is  a  not 
infrequent  complication.  It  is  usually  profuse  and  persistent,  and  may  even  be 
dangerous.  Sometimes  there  has  been  rather  severe  dysenteric  trouble.  In  one 
case  which  ended  fatally  we  observed  a  very  peculiar  intestinal  lesion,  consisting 
of  hsemorrhagic-necrotic  foci  in  the  colon  and  lower  ileum.  In  severe  cases  acute 
haemorrhagic  nephritis  occurs  with  comparative  frequency.  At  the  autopsy  an 
important  and  characteristic  phenomenon  is  the  wedge-shaped  white  spots  which 
occur  in  the  spleen,  like  infarctions.  They  have  a  clinical  interest,  as  they  may 
become  the  starting-point  of  pysemic  conditions  or  of  peritonitis.  Splenic  ab- 
scesses have  been  observed  in  a  few  cases. 

Variations  in  the  course  of  the  disease  occur  in  this,  as  in  all  other  acute  infec- 
tious diseases.  First  there  are  mild,  abortive  cases,  in  which  the  attacks  are  few 
and  brief.  Then  cases  have  been  described  resembling  intermittent  fever.  Of 
chief  importance  is  that  severe  variety  of  relapsing  fever  first  observed  in  Egypt 
by  G-riesinger,  and  described  as  "bilious  typhoid."  There  is  no  longer  any  doubt 
about  the  proper  classification  of  this  disease,  for  spirilli  have  been  proved  to 
appear  in  it,  and  it  has  even  been  shown  that  its  inoculation  upon  another  per- 
son ( ! )  produces  a  common  case  of  relapsing  fever.  Bilious  typhoid  fever  occa- 
sions successive  attacks,  like  those  of  relapsing  fever.  The  type  is  much  more 
severe.  As  a  rule,  there  appear  marked  icterus,  grave  nervous  symptoms,  haemor- 
rhages into  the  skin  and  mucous  membranes,  and  the  termination  is  frequently 
fatal.  The  autopsy  shows  a  greatly  enlarged  spleen,  often  containing  infarctions 
and  abscesses,  and  in  some  cases  hepatic  abscesses,  septic  nephritis,  and  similar 
lesions.  . 

The  prognosis  of  ordinary  relapsing  fever  is  on  the  whole  very  favorable.  In 
the  last  epidemics  the  usual  mortality  was  only  two  to  four  per  cent.  The  fatal 
cases  could  some  of  them  be  laid  to  wretched  nursing  In  the  remaining  portion 
death  resulted  from  complications,  such  as  pneumonia  and  nephritis. 

The  treatment  must  as  yet  be  purely  symptomatic.  Antipyretic  treatment  is 
generally  needless,  since  the  fever  is  relatively  brief  and  often  quite  intermittent. 
Moreover,  most  patients  can  not  well  endure  cold  baths,  because  the  muscles  are 
so  painful.  As  a  rule,  good  nursing  and  proper  food  amply  suffice.  If  the  mus- 
cular pains  are  very  violent,  we  may  order  chloroform  liniment  as  an  embroca- 
tion.    Complications  are  to  be  treated  on  general  principles. 

We  are  not  acquainted  with  any  remedy  that  can  influence  the  disease  itself 


36  ACUTE  GENEEAL  INFECTIOUS  DISEASES. 

or  avert  the  relapses.  Large  doses  of  quinine,  salicylic  acid,  etc.,  have  heen  fre- 
quently employed  for  this  purpose,  but  never  with  success.  Lately  there  has 
been  ascribed  to  calomel  a  favorable  influence  upon  the  general  course  of  the  dis- 
ease, and  its  use  is  said  to  diminish  the  number  of  attacks.  We  must  await  fur- 
ther evidence  in  support  of  this  statement. 


CHAPTER  IV. 

SCARLET   FEVER. 

{Scarlatina.) 

We  now  begin  the  consideration  of  those  acute  infectious  diseases  which  are 
usually  embraced  under  the  name  of  the  "  acute  exanthemata."  In  this  group  are 
reckoned,  besides  scarlet  fever,  measles,  rötheln,  small-pox,  varicella,  and  some- 
times also  facial  erysipelas.  The  point  which  these  diseases  have  in  common  is 
tbat  in  all  of  them  is  developed  a  characteristic  eruption,  of  slight  clinical  signifi- 
cance in  itself,  in  most  cases,  but  of  thoroughly  characteristic  appearance  in  each 
disease,  and  hence  of  essential  importance  in  diagnosis.  A  number  of  the  acute  ex- 
anthemata have  this  further  point  of  mutual  resemblance  that  they  appear  chiefly 
in  children.     These  diseases  are  scarlet  fever,  measles,  rötheln,  and  varicella. 

iEtiology. — Infection  with  the  specific  scarlatinal  poison  occurs  almost  always 
by  contagion,  which  takes  place  very  readily.  A  single  approach  to  a  patient  ill 
with  scarlet  fever  may  suffice  to  communicate  the  disease.  There  is  no  doubt  that 
the  disease  may  be  transferred  by  objects  which  the  patient  has  touched,  such  as 
linen,  clothing,  furniture,  or  toys.  Persons  who  have  been  with  the  sick  may  be 
the  means  of  transmitting  the  disease,  although  themselves  unaffected.  In  Eng- 
land it  has  been  thought  that  the  contagium  may  be  carried  by  milk. 

Numerous  observations  show  that  the  scarlatinal  poison  is  with  great  difficulty 
destroyed,  and  may  keep  its  contagious  powers  for  months  ("tenacity  ").  We  can 
thus  see  how  difficult,  how  impossible,  it  may  be  in  an  individual  case  to  point  out 
the  source  of  contagion.  Scarlet-fever  patients  can  communicate  the  disease  cer- 
tainly as  late  as  the  end  of  the  desquamative  period. 

Details  as  to  the  manner  of  contagion,  or  as  to  the  specific  poison  itself,  are  as 
yet  unknown.  There  have  been  repeated  statements  about  the  presence  of  bacteria 
in  the  blood  and  in  the  tissues  of  scarlatinal  patients;  but  it  is  very  improbable 
that  the  specific  poison  of  scarlet  fever  has  been  observed.  This  poison  must,  how- 
ever, be  contained  in  the  blood,  and  in  the  contents  of  the  miliary  vesicles,  of 
scarlet-fever  patients,  for  the  disease  has  repeatedly  been  artificially  produced  in 
healthy  persons  by  inoculation  with  these  fluids. 

Predisposition  to  scarlet  fever  is  far. less  universal  than  is  predisposition  to 
measles  or  small-pox.  In  families  with  several  children  often  only  one  or  two  fall 
sick,  while  the  rest  escape,  although  equally  exposed.  As  age  increases,  liability 
to  the  disease  greatly  diminishes,  although  there  are  cases  of  scarlet  fever  among 
adults.  The  majority  of  patients  are  between  two  and  ten  years  of  age.  Scarlet 
fever  is  rare  during  the  first  year  of  life.  It  is  an  interesting  fact  that  children 
with  fresh  wounds,  either  accidental  or  surgical,  are  especially  liable  to  scarlet 
fever.  An  analogous  and  familiar  fact  is  that  women  after  delivery  have  a  strong 
tendency  to  the  disease.*  With  very  few  exceptions  a  person  is  attacked  but  once, 

*  In  puerperal  cases  genuine  scarlet  fever  and  septic  diseases  were  formerly  often  confounded. 
(See  Chapter  XVIII.) 


SCARLET  FEVER.  37 

so  that,  after  the  disease  is  over,  an  immunity  from  contagion  is  enjoyed ;  hut  there 
are  exceptions  to  this  rule. 

Scarlet  fever  is  now  spread  over  the  entire  globe.  Here  in  Germany  there  are 
almost  always  some  sporadic  cases  in  the  larger  towns,  while  from  time  to  time, 
especially  in  autumn,  there  are  more  or  less  extensive  epidemics  in  one  place  or 
another.  There  is  considerable  variation  in  the  diffei-ent  epidemics  of  scarlet 
fever,  as  in  many  other  infectious  diseases,  in  the  general  character  of  the  disease, 
and  above  all  in  the  prevailing  mildness  or  severity  of  the  cases. 

Clinical  History. — The  period  of  incubation  is  about  four  to  seven  days,  or  is 
sometimes  apparently  shorter.  There  are  hardly  ever  any  decided  prodromata 
The  disease  begins  rather  suddenly,  with  fever,  often  introduced  by  chilliness,  and 
sometimes  by  a  well-marked  rigor.  There  is  almost  invariably  a  painful,  scar- 
latinal sore  throat.  A  further  symptom,  in  all  cases  of  any  severity,  is  cerebral 
disturbance,  generally  rather  intense.  There  may  be  headache,  dullness,  uneasy 
sleep,  delirium,  and,  in  smaller  children,  sometimes  even  convulsions.  A  very 
frequent  and  characteristic  early  symptom  is  vomiting,  which  may  be  repeated. 

The  characteristic  rash  usually  appears  as  early  as  the  close  of  the  first  day,  or 
on  the  second,  and  begins  on  the  neck  and  on  the  chest  and  face,  soon  becoming 
almost  universal.  The  eruption  consists  at  first  of  numberless  small  red  points, 
crowded  thickly  together  and  soon  united  into  a  diffuse,  intense,  scarlet-colored 
erythema.  The  small  and  somewhat  elevated  points  almost  always  correspond  to 
the  swollen  hair-follicles.  The  diffuse  redness  is  the  result  of  an  excessive  hyperae- 
mia  of  the  skin,  and  vanishes  completely  on  pressure.  The  back  usually  presents 
the  most  vivid  tint.  In  the  face  there  is  generally  pallor  of  the  lips  and  chin,  pre- 
senting a  very  striking  and  characteristic  contrast  to  the  bright-red  cheeks.  If 
some  object  like  the  end  of  a  pen-holder  be  drawn  over  the  red  skin,  there  soon 
arise  corresponding  white  lines,  due  to  contraction  of  the  blood-vessels.  It  is  pos- 
sible thus  to  make  letters  or  pictures  upon  the  back  of  the  patient.  We  should 
"add,  however,  that  this  is  not  a  peculiarity  of  the  scarlatinal  eruption,  being  seen 
in  other  erythematous  eruptions. 

The  rash  persists  for  some  three  or  four  days,  at  first  even  increasing  somewhat 
in  vividness.  It  often  appears  more  intense  by  artificial  light  than  in  the  daytime. 
Meanwhile  the  severe  general  symptoms  continue — the  fever,  the  usually  excess- 
ively rapid  pulse,  the  cerebral  symptoms,  and  the  throat  trouble.  The  spleen  is 
often  somewhat  swollen,  though  seldom  very  large.  Then  the  eruption  begins  to 
fade,  the  fever  gradually  ceases  by  lysis,  the  general  condition  and  the  difficulty 
in  swallowing  improve.  With  the  end  of  the  first  week  or  the  beginning  of  the 
second,  the  cases  which  run  the  typical  course  become  fully  convalescent.  When 
the  rash  disappears,  the  epidermis  usually  begins  to  peel  off,  in  a  very  characteristic 
way,  in  pieces  of  considerable  size.  The  exfoliation  upon  the  hands  and  feet  is 
especially  pronounced,  and  the  little  convalescents  often  amuse  themselves  by 
peeling  off  the  epidermis  in  strips.  Cases  which  are  apparently  the  mildest  and 
most  benign  may  have  their  convalescence  interrupted  by  the  occurrence  of  a 
secondary  scarlatinal  nephritis.     There  is  no  certain  prophylaxis  against  this. 

We  will  now  pass  on  from  this  general  summary  to  a  more  complete  considei-a- 
tion  in  detail  of  general  and  local  symptoms.  And  we  shall  see  how  manifold 
are  the  clinical  phenomena  presented  by  scarlet  fever. 

1.  Fever  (see  Fig.  5). — Although  in  a  few  undeveloped  cases  there  is  no  fever, 
or  scarcely  any,  almost  all  cases  of  any  importance  have  high  fever.  It  is  only 
exceptionally  that  severe  cases  are  observed  where  the  bodily  temperature  is  little 
if  at  all  elevated.  As  a  rule,  the  fever  rises  rapidly  upon  the  very  first  day,  cor- 
responding to  the  sudden  onset  of  all  the  symptoms,  to  about  104°  or  105°  (40°- 
40-5°  C).     The  next  day  it  often  becomes  a  little  higher  still,  and  then  persists 


39-0° 


38-0° 


370< 


38  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

with  but  slight  variations,  as  a  rule,  so  long  as  the  eruption  is  at  its  height.     Dur- 
ing this  period  a  temperature  of  105°  or  more   (40'5°-41°  C.)   is  not  infrequently 

observed.  When  the  eruption  fades, 
and  the  other  symptoms  decline,  defer- 
vescence occurs.  This  happens  but 
rarely  by  crisis,  and  that  in  the  slight 
attacks.  It  is  almost  always  by  pro- 
longed lysis,  as  in  typhoid,  only  more 
irregularly  and  more  rapidly.  If  the 
fever  lasts  into  the  second  week  of  the 
disease,  it  is  almost  always  (though  not 
without  exceptions)  caused  by  demon- 
strable complications.  The  most  fre- 
quent causes  are  the  persistence  of  a 
severe  sore  throat,  the  occurrence  of  in- 
flammatory changes  in  the  cervical 
glands,  or  a  purulent  otitis  media.  In 
Fig.  5.— Example  of  a  normal  scarlet-fever  curve.       closing  what  we  have  to  say  about  the 

fever  in  this  disease,  we  would  empha- 
size the  fact  that  the  pulse  is  often  very  rapid,  even  considering  the  height  of  the 
temperature. 

2.  The  Throat.— The  throat  presents  the  most  constant  local  lesion  of  scarlet 
fever.  Sore  throat  is  only  in  the  rarest  cases  wholly  absent;  but  its  form  and 
intensity  may  vary  extremely.  The  mildest  variety  is  a  simple,  erythematous 
catarrh,  without  much  swelling,  but  exhibiting  a  more  or  less  intense  reddening  of 
the  soft  palate  and  tonsils,  frequently  associated  with  enlargement  of  the  little 
mucous  follicles.  Sometimes  minute  haemorrhages  take  place  into  the  mucous 
membrane.  In  other  cases  the  scarlatinal  affection  of  the  throat  is  from  the  start 
associated  with  considerable  swelling  of  the  parts,  and  especially  of  the  tonsils, 
justifying  the  term  "parenchymatous  sore  throat."  Not  infrequently  small 
abscesses  form  in  the  lacunae  of  the  tonsils  or  superficial  spots  of  necrosis  develop 
which  leave  behind  them  larger  or  smaller  ulcers,  and  sometimes  occasion 
considerable  haemorrhage.  There  may  even  be  a  circumscribed  gangrene  of  the 
tonsils. 

By  far  the  most  important,  because  it  is  also  the  most  dangerous,  of  the  affec- 
tions of  the  throat  resulting  from  scarlet  fever  is  the  so-called  scarlatinal  diph- 
theria—that is,  a  diphtheritic  inflammation  of  the  tonsils  and  soft  palate.  This 
usually  develops  on  the  third,  fourth,  or  fifth  day  of  the  disease,  replacing  a  simple 
inflammatory  condition  of  the  parts.  Whitish,  dirty-colored  spots  develop  on  the 
tonsils,  the  arches  of  the  palate,  and  the  uvula.  These  rapidly  increase  in  size, 
and  cause  a  dry  necrosis  of  the  mucous  membrane  and  subsequent  ulceration. 
The  process  is  a  truly  diphtheritic  one — that  is,  there  is  an  inflammation  combined 
with  an  extension  into  the  diseased  tissues  of  a  fibrinous  exudation. 

It  is  especially  characteristic  of  scarlatinal  diphtheria  that  there  is  almost 
invariably  a  considerable  swelling  of  the  cervical  lymph-glands,  except  in  those 
cases  which  die  very  quickly.  It  is  true  that  the  glands  are  usually  somewhat 
enlarged  in  the  milder  forms  of  pharyngitis  accompanying  scarlet  fever,  but  they 
seldom  attain  the  size  observed  in  the  true  diphtheritic  process.  In  this  there  is 
an  inflammatory  and  cedematous  infiltration  affecting  often  not  only  the  glands 
themselves,  but  also  the  surrounding  connective  tissue,  so  that  in  severe  cases  the 
whole  cervical  region  and  the  floor  of  the  buccal  cavity  presents  a  firm  and 
usually  a  very  painful  enlargement.  It  should  be  added  that  the  severity  of  the 
throat  symptoms  and  the  extent  of  the  glandular  swelling  are  not  always  com- 


SCARLET  FEVER.  39 

mensurate.  Almost  always  the  scarlatinal  diphtheria  is  associated  with  a  marked 
stomatitis,  and  very  often  also  with  a  severe  purulent  or  even  diphtheritic  rhinitis. 
At  the  alse  of  the  nose  and  the  corners  of  the  mouth  there  are  often  superficial 
ulcers  from  this  cause.  Otitis  is  also  a  frequent  complication  of  scarlatina  (vide 
infra).  The  swelling  of  the  lymph  glands  in  the  throat  very  often  terminates  in 
suppuration.  The  influence  upon  the  general  condition  of  the  patient  of  the 
scarlatinal  diphtheria  is  apt  to  be  considerable,  apart  from  the  marked  local  dis- 
comfort. The  constitutional  symptoms  are  often  as  severe  as  in  septicaemia  or 
pyaemia.  Many  cases  end  fatally  in  a  few  days,  while  others  pursue  a  more 
tedious  course,  lasting  perhaps  several  weeks  before  death  comes.  These  are 
often  associated  with  pyaemic  processes  in  other  parts  of  the  body. 

With  regard  to  the  pathogenesis  of  the  throat  troubles  seen  in  scarlet  fever,  the 
more  simple  forms  are  in  all  probability  directly  associated  with  the  scarlatinal 
process — that  is,  they  are  direct  sequences  of  the  affection.  As  relates,  however,  to 
the  severer  forms,  and  in  especial  the  diphtheritic  variety,  it  is  at  least  very 
probable  that  these  are  not  a  direct  result  of  the  scarlatinal  poison,  but  are  due  to 
some  secondary  infection  which  takes  place  at  the  spot  of  the  primary  scarlatinal 
angina.  But  we  are  almost  obliged  to  suppose  that  there  is  some  intimate  con- 
nection between  the  two  varieties  of  infection,  else  why  should  this  peculiar 
secondary  disease,  the  scarlatinal  diphtheria,  be  so  often  conjoined  with  scarlet 
fever?  Yet  the  fact  deserves  emphasis  that  the  diphtheria  seen  in  scarlet  fever  has 
no  aetiological  connection  with  genuine  primary  diphtheria  (see  the  chapter  on  this 
latter  disease),  although  the  pathological  anatomy  is  almost  the  same  in  both 
diseases.  From  a  clinical  standpoint  the  two  present  several  important  points  of 
difference.  In  particular  the  scarlatinal  diphtheria,  in  contrast  with  the  primary 
form  of  the  disease,  seldom  spreads  to  the  larynx.  Laryngeal  croup  is  therefore 
but  rarely  seen  in  scarlet  fever,  and  perhaps  when  it  does  occur  it  is  to  be  ex- 
plained by  an  actual  complication  of  the  scarlatina  with  genuine  diphtheria.  The 
severe  dyspnoea  which  sometimes  develops  in  the  course  of  scarlet  fever  is 
probably  caused  by  an  inflammatory  oedema  of  the  glottis.  Another  important 
clinical  distinction  between  genuine  and  scarlatinal  diphtheria  is  that  paralysis  of 
the  soft  palate,  the  ocular  muscles,  and  other  parts  is  scarcely  ever  a  sequel  of 
scarlatinal  diphtheria. 

The  definitive  answer  to  the  question  of  the  primary  and  the  secondary 
varieties  of  infection  in  scarlet  fever  must  be  postponed  until  the  individual  germs 
corresponding  to  the  same  are  accurately  known.  At  present  we  have  but  a 
single  noteworthy  item  of  information,  which  is  that  there  is  present  in  scarlatinal 
diphtheria  a  peculiar  "  chain-forming  micrococcus,"  discovered  by  Löffler  in  the 
necrotic  mucous  membrane,  the  lymph -glands,  and  even  in  the  blood.  This,  per- 
haps, is  the  occasion  of  the  secondary  disease. 

It  may  be  added  that,  in  puerperal  scarlet  fever,  affections  of  the  throat  are 
noticeably  infrequent  or  trivial,  but  the  same  question  arises  whether  here  scarlet 
fever  and  other  diseases  have  not  been  confounded. 

In  addition  to  the  redness  there  is  often  a  variable  degree  of  swelling.  These 
latter  cases  form  a  connecting  link  between  the  ordinary  variety  and  those  cases 
of  parenchymatous  sore  throat  where  the  tonsils  are  intensely  swollen  and  the 
soft  palate  and  uvula  are  more  or  less  cedematous.  There  may  be  small  suppurat- 
ing spots  in  the  crypts  of  the  tonsils,  or  these  organs  may  suffer  from  larger 
abscesses,  necrosis,  or  even  gangrene.  When  the  necrosed  portions  slough  off, 
there  may  in  rare  cases  occur  a  considerable  haemorrhage  from  the  tonsils. 
Often  chronic  hypertrophy  of  the  tonsils  remains  after  these  severer  forms  of 
inflammation. 

These  graver  varieties  are  almost  always  accompanied  by  swelling  of  the  sub- 


40  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

maxillary  lymph-glands.  The  neighboring  connective  tissue  will  then  often 
present  diffuse  infiltration  and  cedematous  swelling.  This  swelling  may  in  severe 
cases  involve  the  floor  of  the  mouth  and  the  entire  neighborhood  of  the  throat. 
The  severity  of  the  trouble  in  the  throat  does  not  always  correspond  to  that  in  the 
lymph-glands.  Very  frequently  the  swelling  of  the  lymph-glands  and  the  neigh- 
boring structures  ends  in  the  formation  of  abscesses. 

The  croupous  and  diphtheritic  inflammations  of  the  throat  are  the  most  impor- 
tant and  justly  the  most  feared.  We  believe  that  it  is  a  mistake  to  speak  of  a 
'•  complication  of  scarlatina  with  diphtheria."  The  diphtheria  of  scarlet  fever  has, 
from  an  setiological  point  of  view,  no  relation  to  the  common  genuine  diphtheria. 
It  is  a  throat  trouble  having  a  direct  connection  with  the  scarlatinal  process  as 
such.  It  can,  indeed,  from  its  outward  appearance,*  be  distinguished  with  diffi- 
culty, if  at  all,  from  the  primary,  genuine  variety  (q.  v.);  and  therefore,  from  an 
anatomical  point  of  view,  it  must  be  termed  a  croupous  or  diphtheritic  inflam- 
mation. 

Scarlatinal  diphtheria  may  be  united  with  any  of  the  above  varieties  of  angina, 
either  appearing  at  the  very  beginning  of  the  illness,  especially  in  very  severe 
cases,  or  not  till  later,  at  the  end  of  the  first  or  even  in  the  beginning  of  the  second 
week.  It  is  almost  always  the  sign  of  a  severe  attack,  and  is  therefore  generally 
associated  with  high  fever  and  grave  general  symptoms.  The  secondary  swelling 
of  the  cervical  lymphatic  glands  and  the  surrounding  connective  tissue  generally 
attains  a  severe  grade,  and  it  is  often  very  painful.  Here,  as  in  the  other  varieties 
of  severe  angina,  there  is  almost  always  a  simultaneous,  intense  stomatitis,  and  fre- 
quently a  purulent  coryza.  There  are  often  superficial  ulcers  on  the  alas  nasi  and 
at  the  corners  of  the  mouth.  This  form  of  diphtheria  has  one  peculiarity  of  great 
interest  and  clinical  importance.  Unlike  primary  diphtheria,  it  seldom  extends 
to  the  larynx,  so  that  it  is  only  in  rare  cases  of  scarlet  fever  that  there  are  symp- 
toms of  laryngeal  croup.  A  further  important  clinical  difference  between  these 
two  forms  of  diphtheria  is  that  in  scarlet  fever  there  is  scarcely  ever  any  subse- 
quent paralysis  of  the  soft  palate  or  of  the  muscles  of  the  eye.  A  dangerous,  but 
fortunately  a  rare,  complication  is  oedema  of  the  glottis.  This  may  quickly  cause 
death  from  suffocation.  We  may  finally  mention  that  puerperal  scarlatina  is 
said  to  have  in  many  cases  extremely  slight  throat  complications,  or  none  what- 
ever. 

3.  We  proceed  by  a  natural  sequence  to  the  consideration  of  the  affections  of 
certain  parts  adjacent  to  the  throat,  troubles  which  must  be  regarded  as  chiefly 
the  result  of  direct  extension,  or  of  a  conveyance  of  the  inflammatory  process  from 
the  throat. 

The  stomatitis  we  have  already  mentioned,  as  well  as  the  disturbance  in  the 
neighboring  lymph-glands  f  and  the  surrounding  tissue.  Parotitis  is  not  rare  in 
severe  cases.  Of  especial  importance  is  the  scarlatinal  inflammation  of  the  middle 
ear,  which  often  results  in  permanent  deafness. 

This  inflammation  usually  arises  at  the  time  of  desquamation,  but  it  may  occur 
earlier.  It  is  either  a  simple  catarrh  of  the  middle  ear,  or,  in  severe  cases,  an 
actual  diphtheritic  process.  The  deafness  and  earache  are  easily  overlooked,  as 
the  other  symptoms  of  the  patient  occupy  the  attention,  so  that  the  ear  trouble  is 
first  recognized  by  the  occurrence  of  perforation  of  the  tympanum  and  subsequent 
purulent  otorrhcea.     After  this  declines  there  very  often  remains  behind,  as  we 

*  In  microscopic  preparations,  however,  according  to  Heubner's  investigations,  there  arc  evident 
differences  between  genuine  primary  diphtheria  and  that  of  scarlet  fever. 

t  It  should  be  remarked  that  not  infrequently  there  is  also  in  scarlet  fever  a  slight  universal  swell- 
ing of  the  lymph-glands  (back  of  the  neck,  axilla,  groins,  etc.). 


SCAKLET  FEVER.  41 

have  said,  permanent  deafness.  Statistics  have  shown  that  four  or  five  per  cent, 
of  all  cases  of  deafness  are  referable  to  an  attack  of  scarlet  fever  in  childhood. 
The  otitis  is  seldom  immediately  dangerous,  but  yet  cases  of  purulent  meningitis 
have  been  observed  to  follow  it. 

We  have  already  spoken  of  the  purulent  or  even  diphtheritic  rhinitis  which 
almost  always  accompanies  the  scarlatinal  sore  throat.  In  rare  cases  then;  may 
also  occur  a  purulent  conjunctivitis,  which  is  most  probably  the  result  of  a  direct 
conveyance  of  inflammatory  secretions. 

The  tongue  in  scarlet  fever  deserves  special  mention.  The  first  coating  cleans 
off,  and  then  the  tongue  usually  presents  a  very  characteristic  appearance.  It  is 
diffusely  reddened  and  covered  with  little  elevations  corresponding  to  swollen 
papillae  (strawberry  tongue,  scarlatinal  tongue). 

4.  The  characteristic  eruption,  as  developed  in  the  great  majority  of  cases,  has 
been  described  above.  It  remains  to  describe  certain  variations  from  the  usual 
appearances. 

First,  the  eruption  may  be  rudimentary.  It  is  then  not  pronounced,  and  visible 
only  on  a  limited  portion  of  the  body  (face,  trunk,  or  extremities). 

Variations  from  the  type  are  not  rare ;  sometimes  the  papules  are  more  strongly 
developed  {scarlatina  papulosa) ;  very  frequently  there  are  little  vesicles  {scarla- 
tina miliaris).  This  latter  form  of  the  eruption  appears  by  preference  upon  the 
trunk,  but  it  also  may  come  upon  the  extremities,  and  is  often  brought  out  by  ex- 
cessive perspiration,  or  by  wrapping  up  the  patient  too  warmly.  Many  epidemics 
are  noticeable  from  the  frequent  appearance  of  this  miliary  form.  More  rarely 
the  rash  has  a  spotted  look,  resembling  the  eruption  of  measles  {scarlatina  varie- 
gata).  There  may  be  minute  ecchymoses,  which  ai'e  not  ominous.  Well-devel- 
oped cases  of  haämorrhagic  scarlatina  are,  however,  very  dangerous,  because  here 
the  general  infection  of  the  system  is  almost  always  exceedingly  severe ;  and  there 
is  besides,  as  a  rule,  a  general  heemorrhagic  diathesis.  Other  cutaneous  lesions, 
especially  herpes  and  urticaria,  are  not  so  very  unusual  in  connection  with  the 
scarlatinal  eruption.  Furunculosis  has  been  repeatedly  observed  after  the  rash 
fades. 

Desquamation  generally  begins  as  soon  as  the  rash  has  completely  disappeared, 
but  may  not  occur  till  a  few  days  or  even  one  or  two  weeks  later.  Its  extent 
corresponds  in  general  to  the  severity  of  the  eruption,  although  extensive  desqua- 
mation may  follow  a  rudimentary  eruption.  It  is  seldom  bran-like  or  furfura- 
ceous,  as  in  measles.  The  rule  is  for  it  to  be  in  lamellae,  so  that,  as  we  have  stated, 
quite  large  strips  of  epidermis  may  be  detached  entire. 

In  rare  cases  an  oedema  of  the  skin  appears  after  scarlet  fever,  which  can  not 
be  shown  to  depend  upon  nephritis  {vide  infra),  but  may  perhaps  be  due  to  an 
abnormal  permeability  of  the  walls  of  the  cutaneous  blood-vessels  following  the 
eruption  {hydrops  scarlatinosus  sine  nephritide). 

Kidneys. — Next  to  the  severer  forms  of  throat  trouble,  the  most  important  and 
dangerous  complications  are  located  in  the  kidneys.  They  may  appear  as  early 
as  the  acme  of  the  disease,  as  in  many  other  infectious  diseases.  The  urine  has  a 
trace  of  albumen.  In  rare  cases  the  amount  of  albumen  may  be  considerable. 
The  appearance  of  the  urine  is  generally  not  much  changed,  and  the  microscope 
reveals  but  few  abnormal  constituents.  There  are  some  white  and  red  blood- 
globules,  a  few  hyaline  casts,  sometimes  one  or  two  renal  epithelial  cells.  This 
initial  albuminuria  very  rarely  gives  cause  for  alarm. 

The  genuine  scarlatinal  nephritis  scarcely  ever  develops  much  before  the  end 
of  the  second  or  the  beginning  of  the  third  week.  Sometimes  it  comes  even  later. 
In  one  case  under  our  own  observation  it  did  not  begin  till  the  thirty-third  day  of 
the  disease.     It  may  therefore  be  regarded  to  a  certain  degree  as  a  localized  re- 


43  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

lapse.  It  may  be  so  mild  as  to  cause  no  subjective  symptoms  whatever,  and 
would  be  unnoticed  if  the  urine  were  not  carefully  examined.  On  the  other 
hand,  it  may  be  accompanied  by  the  gravest  symptoms,  and  soon  terminate  fa- 
tally. It  may  follow  either  severe  cases  or  the  mildest,  so  that  the  rule  should  be 
to  examine  the  urine  in  every  case  of  convalescence  from  scarlet  fever  as  often  and 
as  accurately  as  possible.  No  exact  statement  can  be  made  as  to  the  frequency  of 
this  complication,  for  it  is  much  more  common  in  some  epidemics  than  in  others. 

The  development  of  nephritis  is  often  marked  by  a  fresh  rise  of  temperature. 
The  elevation  may  be  slight  or  it  may  reach  104°  (40°  O).  According  to  our  own 
experience,  the  fever  often  comes  a  day  or  two  earlier  than  the  changes  in  the 
urine.  As  the  nephritis  goes  on,  it  is  very  often  accompanied  by  a  moderate 
fever  with  remissions.  This  fever  may  be  almost  wholly  absent,  especially  in 
mild  cases.  The  pulse  generally  becomes  harder,  and  is  sometimes  quickened; 
but  in  many  cases  it  will  be  slow,  and  it  is  sometimes  irregular.  Among  other 
objective  symptoms,  the  first  to  excite  notice  is  generally  a  slight  pufhness  of  the 
face,  which  is  usually  pale.  The  eyelids,  particularly,  present  an  evident  oedema. 
In  the  milder  cases  this  oedema  remains  limited,  while  in  others  it  gradually 
increases  in  extent  and  degree,  involving  first,  as  a  rule,  the  dependent  parts  of 
the  trunk,  and  later  the  extremities.  Severe  cases  develop  a  pronounced  ana- 
sarca. There  are  then,  usually,  effusions  into  the  serous  cavities,  especially  ascites 
and  hydrothorax.  The  hydrothorax  is  frequently  combined  with  severe  bron- 
chitis, and  then  may  occasion  extreme  dyspnoea. 

The  urine  exhibits  the  most  important  changes.  These  may  be  insignificant  in 
the  milder  cases,  but  are  very  pronounced  in  the  severe  ones.  The  amount  is 
much  diminished.  Sometimes  there  will  be  for  several  days  almost  complete 
anuria.  In  cases  of  any  severity  the  urine  is  turbid,  dark,  often  evidently  bloody, 
with  increased  specific  gravity  (about  1015  to  1025),  and  containing  a  large 
amount  of  albumen.  The  sediment  is  generally  abundant,  and  exhibits  numerous 
hyaline  casts  of  various  lengths  and  diameters.  To  these  may  be  attached  red  or 
white  blood-corpuscles,  detritus,  granules  of  haematoidin,  or  bacteria,  In  cases 
of  some  duration  the  casts  are  often  moderately  fatty.  Very  frequently  there  are 
found  noticeably  long  and  broad  waxy  casts,  which  are  opaque  and  yellow.'  In 
many  cases  of  scarlatinal  nephritis  the  urine  is  peculiar  in  having  very  many 
white  blood-corpuscles,  either  isolated  or  adhering  to  the  casts.  These  un- 
doubtedly originate  for  the  most  part  in  the  kidneys.  Red  globules,  some  of  them 
in  the  form  of  colorless  rings,  are  found.  They  are  usually  present  in  small 
numbers,  but  may  become  more  abundant,  especially  for  a  day  at  a  time.  Renal 
epithelium  is  frequently  seen,  but  not  invariably  nor  in  very  large  amount.  It 
must  be  mentioned,  in  conclusion,  that  in  some  rare  instances  the  autopsy  dis- 
closes quite  a  marked  nephritis,  although  the  urine  was  apparently  normal  during 
life,  or  at  least  was  not  very  abnormal. 

Uraemic  symptoms  are  not  infrequent.  They  may  be  of  all  degrees  of  severity. 
They  will  be  described  in  detail  under  diseases  of  the  kidney  {vide  infra).  The 
uraemia  may  be  so  severe  as  to  cause  convulsions,  coma,  and  death;  but  it  is 
remarkable  with  what  frequency  children  recover  from  what  seems  to  be  the 
most  pronounced  uraemia. 

The  duration  of  scarlatinal  nephritis  varies  greatly  according  to  its  severity. 
In  cases  which  run  a  favorable  course,  the  urine  is  generally  abnormal  for  two  to 
four  weeks,  or  e^en  longer.  Death  may  be  due  either  to  uraemia  or  to  dyspnoea. 
The  latter  cause  is  the  more  frequent  one,  and  may  depend  upon  the  ascites  and 
hydrothorax,  or  upon  pneumonia  {vide  infra).  Sometimes  death  comes  from 
cardiac  failure,  which  may  now  and  then  be  very  suddenly  developed.  The 
nephritis  may  go  on  into  chronic  renal  disease,  but  this  is  rare. 


SCAKLET  FEVER.  43 

Pathologically,  the  kidneys  present,  in  a  more  or  less  pronounced  degree,  the 
lesions  of  ordinary  acute  hemorrhagic  nephritis  (vide  infra).  It  is  sometimes 
astonishing  to  see  how  apparently  insignificant  the  lesions  are,  in  spite  of  the 
grave  clinical  symptoms.  In  such  cases  there  is  usually  a  so-called  glomerulo- 
nephritis (Klebs),  in  which  the  lesions  are  chiefly  confined  to  the  walls  of  the 
capillaries  and  to  the  epithelium  of  the  glomeruli.  If  the  nephritis  has  been  of 
some  weeks'  duration,  we  generally  find  that  well-marked  hypertrophy  of  the  left 
ventricle  has  already  developed,  as  was  first  pointed  out  by  Friedländer.  We 
have  ourselves  observed  it,  and  have  even  been  able  to  demonstrate  it  repeatedly 
during  life. 

6.  Joints. — When  desquamation  begins,  or  even  earlier,  pain  and  swelling 
may  attack  a  certain  number  of  the  joints.  This  trouble  was  formerly  called 
scarlatinal  rheumatism,  but  now  is  usually  known  as  scarlatinal  synovitis.  It  is 
generally  mild  and  quite  temporary.  The  articular  inflammation  may,  however, 
be  severe  and  even  purulent.  This  is  usually  a  part  of  a  general  pyaemia,  as 
evinced  by  such  other  lesions  as  empyema  and  subcutaneous  abscesses;  and  they 
all  seem  to  be  caused  by  the  above-mentioned  "  chain-forming "  micrococcus, 
which  swarms  in  the  pus  found  in  all  the  affected  parts. 

We  have  seen  a  few  instances  of  excessive  pain  in  the  muscles  of  the  thighs, 
accompanied  by  a  moderate,  diffuse  swelling. 

7.  Another  important  complication  of  scarlet  fever  is  pneumonia.  In  severe 
cases  lobular  pneumonia  sometimes  appears  as  early  as  the  first  stage  of  the  dis- 
ease; but  it  occurs  more  frequently  in  connection  with  the  nephritis.  The 
respiration  may  be  very  seriously  interfered  with  by  it.  Inflammations  of  serous 
membranes  in  the  chest — viz.,  endocarditis,  pericarditis,  and  pleurisy — are  more 
rare.  They  may  or  may  not  be  accompanied  by  disturbances  in  the  joints  (vide 
supra).  Quite  severe  intestinal  symptoms,  such  as  diarrhoea,  may  appear. 
These  are  generally  the  result  of  a  catarrhal  inflammation  of  the  intestinal 
follicles.  Dysentery  is  less  frequent.  The  enlargement  of  the  spleen  has  been 
already  mentioned.  The  liver  is  also  sometimes  found  to  be  considerably  en- 
larged. 

Variations  in  the  Course  of  the  Disease. — The  diversities  of  the  clinical  picture 
in  different  cases  of  scarlatina  will  be  understood  when  we  consider  the  variety 
and  number  of  the  disturbances  thus  far  cited.  It  is  to  be  added  that  the  general 
course  of  the  disease  may  exhibit  numerous  peculiarities,  of  which  it  is  hardly 
possible  to  give  an  exhaustive  presentation.  We  will  content  ourselves  with  a 
cursory  statement  of  the  most  important  deviations  from  the  typical  course. 

1.  Rudimentary  Forms. — To  this  class,  in  which  the  disease  does  not  reach  a 
perfect  development,  belong  first  the  cases  of  simple  sore  throat  with  no  erup- 
tion, or  at  most  an  extremely  faint  and  partial  one  (scarlatina  sine  exanthe- 
mate).  Sometimes  even  the  sore  throat  is  hardly  to  be  seen,  and  there  is  noth- 
ing but  a  brief  and  slight  fever  with  mild  symptoms  of  general  disturbance.  The 
recognition  of  these  cases  as  scarlatinal  is  possible  only  when  we  consider  their 
etiological  relation  to  other  undoubted  cases  of  scarlet  fever.  We  had  an  excel- 
lent opportunity  to  observe  them  when  the  disease  broke  out  in  the  children's 
wards  of  the  hospital  at  Leipsic.  The  diagnosis  is  sometimes  confirmed  by  a 
slight  though  evident  desquamation,  affecting  the  hands,  feet,  legs,  and  back,  or 
by  an  acute  nephritis,  which  may  follow  the  mildest  attacks  of  this  sort.  Many 
cases  of  acute  nephritis,  though  apparently  wholly  spontaneous  and  primary, 
must  be  regarded  as  astiologically  scarlatinal. 

2.  Rudimentary  but  Pernicious  Forms. — Under  this  head  belong  those  attacks 
of  scarlet  fever  where  the  eruption  is  scanty  or  absent,  while  from  the  very  start  the 
most  violent  general  symptoms  appear.     There  is  a  very  high  fever,  enormously 


4J.  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

rapid  pulse,  and  delirium.  Such  cases  must  be  the  result  of  an  uncommonly  severe 
general  infection.  They  usually  end  in  speedy  death.  Other  cases,  ending  fatally 
in  a  few  days,  have  a  well-developed  rash  without  other  localized  disturbances. 

3.  Severe  Forms  icith  a  more  Protracted  Course. — In  these  cases  the  long 
duration  is  not  the  exclusive  result  of  especial  complications,  but  is  likewise  due 
to  the  severity  of  the  intoxication.  One  variety  is  the  so-called  typhoid  form  of 
scarlatina,  with  persistent  high  fever  and  severe  constitutional  symptoms.  An- 
other variety  is  the  •  hemorrhagic  form  briefly  mentioned  above,  in  which  there 
are  extensive  haemorrhages  into  the  skin  and  into  the  mucous  and  serous  mem- 
branes. This  form  may  run  an  extremely  acute  course.  Further,  in  ail  pernicious 
forms,  there  may  be  severe  local  complications,  particularly  diphtheritic  or  gan- 
grenous sore  throat,  inflammations  of  serous  membranes,  etc.  Attacks  of  this 
sort  are  often  not  produced  by  the  poison  of  scarlet  fever  alone,  but  by  secondary 
complicating  processes.  While  speaking  of  scai-latinal  diphtheria  it  has  already 
been  pointed  out  that  secondary  infection  of  the  body  may  result,  principally 
originating  from  the  diseased  throat,  and  occasioning  sometimes  a  grave  septic 
condition  of  the  whole  body,  sometimes  local  disease  of  distinct  parts. 

4.  In  extremely  rare  cases  relapses  do  occur.  After  the  first  illness  a  fresh 
eruption  breaks  out  with  all  the  other  symptoms  of  scarlet  fever.  In  anomalous 
cases,  running  a  severe  course,  there  is  sometimes,  at  an  advanced  stage,  a  fresh, 
imperfect  eruption  (generally  in  spots),  which  Thomas  has  termed  a  pseudo-relapse. 

Diagnosis. — The  diagnosis  of  scarlet  fever  is  made  in  most  cases  from  the  char- 
acteristic eruption  taken  in  connection  with  the  other  symptoms.  We  should, 
however,  bear  in  mind  that  exceptionally  other  eruptions  appear  which  exhibit  the 
closest  resemblance  to  that  of  scarlet  fever.  1.  After  the  use  of  certain  drugs, 
especially  atropine  (belladonna),  quinine,  antipyrine,  morphine,  chloral  ;  and  like- 
wise after  the  ingestion  of  crabs,  fish,  etc.  2.  As  a  symptom  of  other  infectious 
diseases,  such  as  typhoid  fever,  small-pox ;  and,  above  all,  in  septic  diseases  (vide 
infra).  In  an  anomalous  case  factors  of  importance  for  diagnosis  are  the  aetiology 
and  the  occurrence  of  desquamation  or  of  a  secondary  nephritis. 

The  prognosis  must  in  every  case  be  guarded.  From  what  has  been  said  of  the 
course  of  the  disease,  it  is  evident  that,  even  in  cases  which  are  at  first  appar- 
ently the  most  favorable,  dangerous  complications  may  appear  later,  particularly 
nephritis. 

Treatment. — The  majority  of  those  cases  of  scarlet  fever  which  take  a  typical 
course  will  recover  completely  without  our  aid.  In  these  the  task  of  the  physi- 
cian, so  far  as  treatment  is  concerned,  consists  in  arranging  the  details  of  hygiene 
and  the  general  care  of  the  patient.  The  sick-room  should  be  cool,  and  the  diet 
rather  strict,  consisting  mainly  of  milk.  Broths  and  eggs  may  also  be  allowed. 
We  should  see  that  the  skin  and  the  mouth  are  kept  clean.  To  change  the  linen 
frequently,  if  done  with  proper  precaution,  is  not  only  permissible,  but  very  desir- 
able. The  favorite  practice  of  rubbing  the  skin  with  fat  pork  has  some  merit, 
and  is  especially  to  be  recommended  if  the  skin  be  harsh  and  dry  after  the  erup- 
tion has  faded. 

[From  the  moment  that  the  disease  is  declared  the  patient  should  be  thoroughly 
anointed  daily  with  carbolized  vaseline,  lard,  or  the  like;  and  this  should  be  kept 
up  until  desquamation  has  ceased.  Not  only  is  the  comfort  of  the  patient  pro- 
moted, but  the  danger  of  the  spread  of  the  infection  is  thereby  greatly  lessened.] 

The  scarlatinal  disease  of  the  throat  must  be  treated  with  the  greatest  attention, 
the  main  duty  of  the  physician  in  this  regard  being  to  prevent,  if  possible,  the 
ingress  of  the  above-mentioned  secondary  infection.  It  is  therefore  our  opinion 
that  in  every  case  of  scarlet  fever  the  greatest  pains  should  be  taken  from  the 
very  commencement  of  the  disease  to  maintain  complete  disinfection  of  the  mouth 


SCARLET  FEVER.  45 

and  throat.  Larger  children  may  use  a  gargle  (two-per-cent.  solution  of  chlorate 
of  potash,  one- or  two-per-cent.  solution  of  carbolic  acid).  Inhalation  of  carbolic- 
acid  spray  is  also  to  be  recommended  where  practicable.  If  there  is  prostration, 
or  if  the  child  be  young  or  willful,  we  must  cleanse  the  mouth  and  throat  at  short 
intervals,  by  means  of  a  spray-apparatus,  with  disinfectants,  such  as  carbolic  acid 
or  permanganate  of  potash  in  solution.  Sometimes  it  is  a  good  plan  to  let  the 
patient  swallow  slowly  a  half-teaspoonful  of  a  solution  of  potassic  chlorate  (about 
1  to  40)  every  half-hour  or  oftener,  with  the  object  of  contributing  to  the  local 
disinfection  of  the  throat.  If  scarlatinal  diphtheria  nevertheless  develops  and 
the  cervical  lymph-glands  begin  to  increase  further  in  size,  there  is  reason  to 
hope,  according  to  the  experience  of  Taube  and  Heubner,  that  parenchymatous 
injections  into  the  tissue  of  the  tonsils  or  the  palatine  arches  may  yet  check  the 
spread  of  the  secondary  infection.  About  6  minims  (a  Pravaz  syringe  half  full) 
of  a  three-per-cent.  solution  of  carbolic  acid  may  be  injected  twice  daily  upon 
each  side  by  means  of  a  long  hollow  needle  and  a  subcutaneous  syringe. 

If  the  nose  be  likewise  affected,  the  chief  thing  to  do  is  frequent  cleansing  and 
syringing  while  the  head  is  bent  forward.  "We  should  be  on  the  watch  for  the 
possible  occurrence  of  otitis.  In  this  particular  the  physician  is  often  guilty  of 
sins  of  omission.  Much  harm  may  be  averted  by  a  prompt  cleansing  of  the  ears, 
or,  if  need  be,  by  insufflation  of  air  into  the  middle  ear,  or  paracentesis  of  the 
membrana  tympani. 

Inflammation  of  the  glands  in  the  neck,  if  severe,  is  prone  to  pass  on  to  sup- 
puration, and  must  then  be  treated  surgically.  When  the  swelling  has  just  begun, 
or  is  still  moderate,  we  may  try  to  cure  it  by  rubbing  in  iodoform  ointment  (1  to 
15)  two  or  three  times  a  day.  Ice  is  generally  not  so  well  borne  as  warm  applica- 
tions (poultices  or  warm  bran-cushions). 

If  there  be  continuous  high  fever,  accompanied  by  rather  severe  constitutional 
symptoms,  a  moderate  employment  of  the  cold-water  treatment  is  strongly  to  be 
recommended.  The  baths  seldom  need  to  be  cooler  than  81°  to  88°  (22°-25°  R.), 
and  are  to  be  employed  two  or  three  times  daily,  or  oftener  in  severe  cases.  If  the 
nervous  disturbance  be  serious,  or  if  the  respiration  be  impaired,  the  patient  should 
be  douched  with  cold  water  during  the  bath.  At  the  same  time  wine  or  strong 
coffee  is  to  be  given  as  a  stimulant,  or,  if  cardiac  failure  and  signs  of  collapse 
appear,  the  best  remedy  is  subcutaneous  injections  of  camphor.  We  are  con- 
vinced that  internal  antipyretics,  such  as  antipyrine,  may  usually  be  dispensed 
with,  although  in  private  practice  we  may  be  obliged  to  employ  them. 

If  the  pulse  is  abnormally  rapid,  and  there  is  clanger  of  cardiac  failure,  we  can 
employ,  besides  stimulants,  an  ice-bag  placed  over  the  heart.  Digitalis  may  also 
be  tried  cautiously. 

The  scarlatinal  inflammation  of  the  joints  is  sometimes  improved  by  salicylate 
of  soda  (forty-five  to  sixty  grains,  grm.  3  to  4,  in  one  dose  [!]).  Sometimes,  how- 
ever, this  remedy  has  failed  us. 

We  know  of  no  means  to  avert  the  nephritis.  In  justice  to  himself,  the  physi- 
cian must  always  at  the  start  point  out  the  possibility  of  its  occurrence,  and  must 
avoid  as  far  as  possible  errors  in  diet  or  exposure  to  cold  on  the  part  of  his  pa- 
tient. He  may  thus  escape  blame.  For  the  treatment  of  the  nephritis  and  its 
results,  see  the  section  on  renal  diseases.  We  must  likewise  refer  the  reader  to 
the  appropriate  chapters  for  the  treatment  of  other  possible  complications  of  scar- 
let fever. 

The  patient  must,  as  a  rule,  keep  his  bed  three  or  four  weeks,  even  if  convales- 
cence be  uninterrupted. 

[This  injunction  is  rather  extreme.  Nephritis  is  as  likely  to  follow  a  mild  as  a 
severe  case,  and  occurs  sometimes  in  spite  of  every  precaution.     The  physician 


46  ACUTE  GENERAL  INFECTIOUS   DISEASES. 

should  use  his  discretion  as  to  the  length  of  time  the  patient  is  kept  in  bed,  care- 
fully guarding  against  exposure  to  cold  and  imprudence  in  diet.] 

The  disease  is  so  dangerous  that,  whenever  a  case  occurs  in  a  family,  isolation 
is  absolutely  demanded,  and,  if  possible,  all  the  other  children  should  be  sent 
away.  If  this  advice  be  disregarded,  we  can  reject  all  responsibility  for  any 
further  cases  and  their  results. 

[Scarlet  fever  is  a  disease  at  once  so  highly  contagious  and  so  common  that  it 
may  be  taken  as  the  type  of  its  class.  Its  hygienic  treatment  and  the  measures 
needful  to  prevent  its  spread  consequently  deserve  more  minute  detail. 

The  sick-room  should  be  at  the  top  of  the  house,  if  possible,  and  exposed  to  the 
south ;  every  unnecessary  article  of  furniture  and  all  ornaments  should  be  re- 
moved beforehand,  carpets,  curtains,  and  stuffed  or  upholstered  furniture  being 
included.  A  window  should  be  kept  open  constantly,  top  and  bottom ;  in  cool 
weather  a  fire  should  be  burning ;  in  warm  weather  ventilation  is  furthered  by 
placing  a  gas-burner  or  large  kerosene  lamp  near  the  throat  of  the  chimney. 
Outside  the  door  of  the  sick-room  a  sheet  moistened  with  a  disinfectant  solution 
should  be  carefully  hung.  Only  those  whose  presence  is  absolutely  necessary  are 
to  be  allowed  in  the  sick-room,  and  the  physician,  when  his  visit  is  completed, 
should  pass  directly  out  of  the  house. 

A  convalescent  should  be  kept  away  from  all  who  are  liable  to  contract  or  con- 
vey the  disease  until  desquamation  has  entirely  ceased.  Several  warm  soap-baths 
should  be  given  before  the  child  emerges  into  every-day  life,  and  it  should  finally 
be  dressed  in  uncontaminated  clothing. 

For  further  directions  as  to  the  disinfection  of  the  room,  the  clothing,  and  the 
excreta,  see  pages  26,  27.] 


CHAPTER  V. 

MEASLES. 

{Morbilli.) 

.ffitiology. — In  contrast  with  the  malignancy  of  scarlet  fever  is  the  compara- 
tively benign  nature  of  measles,  a  disease  of  childhood  which  is  but  little  feared 
even  by  mothers.  It  is  so  wide-spread,  and  the  susceptibility  to  it  is  so  universal, 
that  measles  passes  for  an  almost  unavoidable  but  comparatively  insignificant  an. 
noyance.  Indeed,  few  escape  it ;  and  probably  the  reason  that  adults  have  mea- 
sles so  much  less  frequently  than  children  is  simply  that  most  adults  have  already 
suffered  from  it  in  childhood.  A  second  attack  of  measles  in  the  same  individual 
may  occur,  but  it  is  certainly  extremely  rare. 

[In  highly  civilized  countries  measles  has  prevailed  so  long  that  it  would  seem 
that  a  relative  resistance  against  the  poison  has  been  acquired.  The  frightful  rav- 
ages of  the  disease  when  it  was  planted  in  virgin  soil,  as  among  the  Fiji  Islanders 
not  many  years  ago,  apparently  bear  out  this  view.  The  susceptibility  to  measles 
is  greater  and  more  widespread  than  is  that  to  scarlet  fever — that  is  to  say,  fewer 
individuals  reach  adult  life  without  having  experienced  an  attack  of  the  former 
than  of  the  latter.] 

Measles  generally  comes  in  epidemics.  Sporadic  cases  are  exceptional.  In 
this  respect  measles  differs  decidedly  from  scarlet  fever.  The  rapid  spread  of  the 
disease  when  it  has  once  broken  out  is  a  result  of  its  great  contagiousness.  If  one 
child  in  a  family  is  attacked,  the  others  almost  always  take  the  disease.  The  in- 
fection may  be  transferred  even  by  well  people  and  by  means  of  articles  with 
which  the  sick  have  come  in  contact.     We  are  not  yet  acquainted  with  the  spe- 


MEASLES.  47 

cific  poison  of  measles,  although  its  existence  is  to  be  taken  for  granted,  nor  with 
the  details  of  its  transmission.  Still  it  seems  most  probable  that  the  poison  is 
inhaled  through  the  mouth  and  nose,  and  that  this  is  the  reason  why  its  effects 
are  usually  first  developed  in  the  respiratory  passages  (vide  infra).  The  disease 
can  be  artificially  produced  by  inoculation  of  healthy  children  with  the  blood  or 
liquid  secretions  of  those  suffering  from  it. 

Clinical  History.— The  length  of  the  stage  of  incubation  is  tolerably  uniform. 
It  is  ten  days  to  the  beginning  of  the  first  symptoms,  and  thirteen  or  fourteen 
days  to  the  breaking  out  of  the  eruption.  These  figures  have  been  established  by 
the  observations  of  Panum,  the  opportunity  having  been  afforded  upon  the  first 
introduction  of  the  disease  into  the  Faroe  Islands.  As  a  rule,  there  are  no  espe- 
cial prodromata  during  the  period  of  incubation  except  some  slight  elevations  of 
temperature.  At  the  end  of  ten  days  the  initial  stage  *  begins,  generally  suddenly, 
and  with  an  abrupt  rise  of  temperature  to  102°  or  104°  (39°-40°  C).  At  the  same 
time  the  characteristic  catarrhal  symptoms  appear:  nasal  catarrh  (coryza),  to 
be  recognized  by  the  abundant  nasal  secretion,  the  frequent  sneezing,  sometimes 
also  by  nose-bleed ;  more  or  less  severe  conjunctivitis,  recognizable  by  the  photo- 
phobia, the  reddening  of  the  eyes,  and  the  increased  flow  of  tears;  and,  lastly, 
symptoms  of  a  catarrh  of  the  upper  part  of  the  respiratory  tract,  usually  moderate, 
but  nevertheless  causing  hoarseness  and  a  slight  cough.  With  all  this  the  gen- 
eral condition  is  disturbed,  the  children  are  restless,  have  headache,  and  eat  little. 
Symptoms  of  a  mild  sore  throat  are  not  infrequent,  but  are  very  far  from  being  so 
prominent  as  in  scarlet  fever. 

These  initial  symptoms  last,  as  we  have  said,  three  or  four  days.  Then  the 
eruption  begins  (stage  of  eruption).  This  is  very  often  preceded  for  a  day  or 
two  by  a  peculiar,  usually  spotted,  reddening  of  the  hard  and  soft  palates,  termed 
"eruption  upon  the  mucous  membrane."  The  true  eruption  of  measles  begins 
almost  always  in  the  face,  on  the  cheeks,  forehead,  and  around  the  mouth  (con- 
trasting with  the  characteristic  pallor  of  the  chin  in  scarlet  fever),  and  spreads 
from  there  rapidly  downward  over  all  the  rest  of  the  body.  The  eruption  consists 
at  first  of  little  papilla?,  corresponding  to  the  follicles.  These  are  soon  surrounded 
by  a  pale-red,  slightly  elevated  border,  and  in  many  cases  become  confluent.  Per- 
fectly flat  elevations,  of  various  sizes  and  of  extremely  irregular,  dentated,  round- 
ish, or  angular  shape,  develop.  These  are  often  so  thickly  crowded  together  as  to 
touch  one  another,  but  usually  limited  portions  of  normal  skin  intervene  between 
them.     Within  each  raised  spot  the  little  follicular  papilke  remain  visible. 

With  the  beginning  of  the  eruption  the  fever  rises,  having  been,  as  a  rule, 
slight  during  the  last  days  of  the  initial  stage.  It  attains  about  104°  or  105°  (40°- 
40'5°  C).  In  thirty-six  to  forty-eight  hours  the  eruption  reaches  its  full  devel- 
opment and  its  greatest  extent.  The  fever  and  the  catarrhal  symptoms  also  per- 
sist for  the  same  length  of  time.  Sometimes  we  find  a  slight  swelling  of  all  the 
lymph-glands.  Then  follows  a  decline  of  the  fever,  usually  rapid,  and  indeed 
almost  by  crisis,  while  the  eruption  after  a  short  period  of  full  development  begins 
gradually  to  fade  during  the  two  or  three  days  following.  At  the  same  time  the 
catarrhal  symptoms  diminish.  A  more  or  less  extensive  desquamation  of  the 
epidermis  begins,  scarcely  ever  in  large  pieces  as  in  scarlet  fever,  but  in  little 
scales,  "like  bran."  After  eight  or  ten  days,  if  the  disease  runs  a  normal  course, 
the  patient  is  fully  convalescent. 

*  We  consider  the  term  "initial  stage"  more  correct  than  "prodromal  stage."  The  "prodromal 
symptoms  "  are  the  first  slight  symptoms  which  occur  during  the  time  of  incubation  of  an  infectious 
disease,  while  the  symptoms  presented  by  measles  before,  the  breaking  out  of  the  eruption  are  a  part 
of  the  already  developed  disease. 


4S 


ACUTE  GENERAL  INFECTIOUS  DISEASES. 


40-0° 


390° 


38-0' 


37-0° 


awiwmmi 
mwmmmmi 

1MB     IRMIiHl! 

"in  mwBir 

MMHKAVJI 


IL 
111! 

Ill 


After  this  brief  description  of  the  usual  course,  we  must  consider  more  closely 
some  of  the  symptoms  and  possible  complications. 

Tbe  fever  (see  Fig.  6)  of  measles  exhibits,  as  has  been  already  implied,  a  tolera- 
bly typical  course.  It  begins  with  a  rather  marked  and  rapid  rise  upon  the  com- 
mencement of  the  disease.  On  the  morning  of  the  second  day  there  is  usually  a 
marked  remission,  often  to  normal.  In  the  last  two  days  of  the  initial  stage  the 
fever  is  moderate,  very  rarely  being  so  high  as  at  the  beginning.  With  the  erup- 
tion there  is  a  new,  rapid  rise,  usually  higher  than  the  initial  one,  so  that  we  may 
well  divide  the  fever  into  two  periods — the  prodromal  fever  and  the  eruptive  fever. 
This  latter  is  but  brief  and  does  not  persist,  as  in  scarlet  fever,  during  the  entire 
duration  of  the  eruption.  It  falls  by  crisis  when  the  rash  has  attained  full  de- 
velopment. There  may,  to  be  sure,  be  slight  elevations  of  temperature  during  the 
next  day  or  two ;  but,  if  the  fever  is  considerable  and  persistent,  it  is  always  a  sign 
that  complications  have  arisen,  probably  in  the  respiratory  apparatus. 

The   eruption  usually  assumes  the 
l        2345678         form  described  above,  but  may  present 

manifold  varieties.  Sometimes  its  de- 
velopment is  rudimentary.  Sometimes 
it  does  not  begin  in  the  face,  but  on 
some  other  part  of  the  body.  This  is 
generally  regarded  as  a  sign  that  the 
case  will  be  anomalous  in  other  ways  as 
well.  The  individual  spots  may  be 
smaller  than  usual,  and  may  remain  en- 
tirely separate  from  each  other  (mor- 
billi papulosi).  In  other  cases  the 
eruption  is  so  confluent  (morbilli  con- 
fluentes)  that  it  resembles  the  eruption 
of  scarlatina.  The  formation  of  vesi- 
cles (morbilli  vesiculosi)  also  occurs,  but 
much  more  rarely  than  in  scarlet  fever. 
Hsemorrhagic  measles  are  also  observed, 
but  usually  only  in  the  form  of  small, 
capillary  bleeding,  and  in  cases  that 
otherwise  run  a  perfectly  favorable 
course.  Very  rare  cases  have  indeed  been  described,  with  a  general  hemorrhagic 
diathesis  and  bad  symptoms,  resembling  hemorrhagic  scarlatina.  It  is  doubtful 
whether  the  "  black  measles  "  of  the  old  writers  was  actually  measles  at  all.  In 
addition  to  the  proper  eruption  of  measles,  other  eruptions  sometimes  develop — 
among  others,  vesicles,  wheals,  and  pustules. 

The  complications  of  measles  are  for  the  most  part  exaggerations,  or  abnormal 
varieties  and  extensions,  of  those  troubles  which  are  observed  during  the  usual 
mild  course  of  the  fever.  As  in  scarlet  fever  (vide  supra),  we  often  have  to  deal 
with  the  effects  not  of  the  original,  but  of  secondary  infection.  Compared  with 
the  great  majority  of  mild  attacks  taking  the  typical  course,  cases  presenting  com- 
plications of  any  severity  are  rare,  and  much  less  frequent  than  in  scarlet  fever. 
Epidemics  are  only  now  and  then  distinguished  by  unusual  severity. 

Often  quite  grave  eye  diseases  are  developed,  particularly  blennorrhagic  con- 
junctivitis, keratitis,  and  iritis. 

Marked  inflammation  of  the  mucous  membrane  of  the  nose,  throat,  and  lar- 
ynx may  prolong  the  course  of  the  disease.  These  are  often  merely  exaggera- 
tions of  the  usual  catarrh.  Otitis  media  likewise  sometimes  occurs.  A  laryngitis 
of  marked  intensity,  with  considerable  swelling  of  the  parts  involved,  may  pro- 


■«■■■■ 
!!■■■■■ 

JiiiiiiBi! 

SSSBSSSSSSSSSSSI 

sesiss 

■illll 


Initial  Fever. 


Eruptive  Fever. 
Eruption. 


Fig.  6.— Example  of  the  temperature  curve  in 
measles. 


MEASLES.  40 

duce  much  discomfort,  or  even  symptoms  of  stenosis  ("false  croup").  Actual 
croupous  and  diphtheritic  lesions  of  the  throat  and  larynx  also  occur  (diphtheria 
of  measles).  This  last  is  indeed  much  rarer  than  scarlatinal  diphtheria,  hut  may 
have  the  same  unhappy  termination.  It  is  worth  mentioning  that  sometimes 
genuine  laryngeal  croup  is  observed  in  measles,  unaccompanied  by  lesions  of  the 
pharynx. 

It  is,  however,  in  the  lungs  that  the  most  frequent  and  important  of  all  compli- 
cations in  measles  occur.  The  usual  mild  bronchitis  becomes  very  intense,  ex- 
tends into  the  bronchioles  (capillary  bronchitis),  and  then  results,  for  the  most 
part,  in  a  more  or  less  extensive,  lobular,  catarrhal  pneumonia  (q.  v.).  This  is 
almost  always  to  be  suspected  when  moist  rales  are  heard  in  abundance  over  a 
large  part  of  the  chest,  and  when  there  is  at  the  same  time  persistent  fever  and  pro- 
nounced difficulty  in  respiration,  with  cough  or  dyspnoea.  We  get  decided  dull- 
ness on  percussion  only  when  the  separate  centers  of  infiltration  are  more  than 
usually  confluent.  Genuine  lobar,  croupous  pneumonia  appears  much  less  often 
than  the  lobular  variety.  It  attacks  one  lobe,  or  several,  is  attended  by  high  fever, 
and  may  end  with  a  well-marked  crisis. 

The  foregoing  pulmonary  symptoms  usually  appear  at  the  height  of  the  dis- 
ease, and  persist  after  the  eruption  fades.  They  may  delay  convalescence  for 
weeks.  In  other  cases  measles  will  seem  at  the  start  to  run  a  normal  course,  the 
temperature  will  have  already  fallen,  and  then  come  new  fever  and  the  appear- 
ance of  decided  pulmonary  disturbance.  This  is  always  to  be  regarded  as  a  grave 
complication;  and  especially  in  feeble  children  it  may  lead  to  death,  with  the 
symptoms  of  impaired  respiration,  or  of  constitutional  exhaustion. 

Marked  intestinal  symptoms  sometimes  appear,  particularly  an  excessive  diar- 
rhoea, due  to  intestinal  catarrh.  It  is  characteristic  of  measles  that  in  severe  cases 
such  a  diarrhoea  may  assume  a  pronounced  dysenteric  character,  indicated  by  blood 
and  slime  in  the  dejections,  symptoms  which  usually  depend  upon  the  develop- 
ment of  follicular  colitis  with  ulcerations. 

Now  and  then  still  other  complications  may  present  themselves,  of  which  a  full 
enumeration  is  impossible.  Nephritis  does  occur,  but  far  less  often  than  in  scar- 
let fever.  A  simple  albuminuria  during  the  acme  of  the  disease  is  not  infrequent, 
but  as  a  rule  has  no  especial  clinical  significance.  We  should  mention  gangrene 
of  the  cheek,  the  so-called  noma,  as  a  complication,  which  is  very  rare  but  appar- 
ently characteristic. 

Peculiarities  in  the  course  of  the  disease  are  much  rarer  in  measles  than  in 
scarlet  fever.  Yet  we  see,  on  the  one  hand,  unusually  mild  or  rudimentary 
cases,  in  which  either  the  rash  or  the  other  local  symptoms  are  remarkably  slight, 
and  on  the  other  hand,  abnormally  severe  cases.  These  latter  are  distinguished 
by  the  unusual  height  or  persistence  of  the  fever,  by  the  severe  constitutional  and 
nervous  symptoms,  and  further  by  the  early  appearance  of  complications.  Such 
cases  have  been  termed  "typhoid  measles."  We  have  already  mentioned  the 
severe  form  of  hemorrhagic  measles. 

We  should  notice  the  clinical  relation  which  measles  bears  to  some  other  in- 
fectious diseases — to  whooping-cough  and  tuberculosis.  Measles  and  pertussis 
(q.  v.)  may  follow  each  other  in  the  same  individual  at  a  short  interval,  some- 
times one  and  sometimes  the  other  taking  the  initiative;  epidemics  of  the  two  dis- 
eases prevail  with  comparative  frequency  at  the  same  time.  Tuberculosis  is  like- 
wise to  be  mentioned  as  an  important  sequela  of  measles.  Its  frequent  appearance 
at  the  close  of  measles  is  of  course  to  be  explained  by  supposing  either  that,  in 
children  who  are  already  the  victims  of  tubercle,  the  further  extension  of  the  tu- 
berculosis is  favored  by  measles,  or  that  the  catarrhal  inflammation  due  to  measles 
leaves  behind  it  an  especial  predisposition  to  infection  with  the  tubercular  poison. 
4 


50  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

The  diagnosis  of  measles,  as  of  the  other  acute  exanthematous  diseases,  is  based 
chiefly  upon  the  eruption.  Personal  experience  does  more  to  sharpen  the  percep- 
tion than  can  the  fullest  descriptions.  We  can  merely  suspect  the  disease  during 
the  initial  stage  unless  an  epidemic  prevails.  If,  beside  the  characteristic  catarrhal 
symptoms,  the  above-mentioned  eruption  on  the  mucous  membrane  of  the  palate 
exists,  the  diagnosis  becomes  tolerably  certain.  We  should  consider  that  erup- 
tions similar  to  that  of  measles  appear  in  other  diseases,  more  especially  in  rötheln, 
scarlet  fever,  typhus  fever,  in  the  beginning  of  small-pox,  and  in  syphilis. 
Furthermore,  we  need  to  exclude  eruptions  due  to  such  drugs  as  antipyrine,  tur- 
pentine, and  balsam  of  copaiba.  In  doubtful  cases  we  shall  be  enabled  to  form  a 
decided  opinion  by  the  other  symptoms,  and,  above  all,  by  the  further  course  of 
the  disease. 

Prognosis.— We  have  already  remarked  how  favorable  in  general  the  prog- 
nosis is,  but  we  must  here  repeat  that  all  epidemics  do  not  exhibit  the  same 
benign  character,  and  that  in  every  case  the  physician  must  bear  in  mind  the  pos- 
sibility of  complications,  and  particularly  the  danger  of  severe  pulmonary  dis- 
turbances. 

Treatment.— The  patient  should  in  general  be  kept  somewhat  warmer  than  in 
scarlet  fever.  Even  in  what  seem  to  be  the  mildest  cases  the  child  should  be 
kept  in  bed  till  desquamation  is  over.  The  sick-chamber  is  to  be  somewhat  dark- 
ened, on  account  of  the  photophobia  which  usually  exists  at  first.  In  this  way, 
normal  cases  run  on  favorably  without  any  especial  therapeutic  interposition. 
The  catarrhal  symptoms,  however,  should  always  be  heeded,  since  to  disregard 
them  may  lead  to  their  becoming  aggravated.  The  chief  requisite  is  cleanliness. 
At  regular  intervals  the  eyes,  the  nasal  cavity,  and  the  mouth  should  be  washed 
out  with  lukewarm  water. 

If,  despite  all  this,  certain  disturbances  appear  in  a  worse  form  than  usual,  or 
if  complications  develop,  these  must  receive  especial  attention.  Severe  eye 
troubles  should  be  treated  according  to  the  usual  ophthalmological  practice ;  and 
here  unguentum  hydrargyri  oxidi  flavi  (I  to  100)  [U.  S.  P.  is  40  to  420]  and  atro- 
pine are  chiefly  employed.  The  treatment  of  croupous  trouble  in  the  throat  or 
larynx  will  be  fully  described  in  a  later  chapter.  For  the  pulmonary  troubles, 
lukewarm  baths,  combined  if  need  be  with  rather  cool  douches,  constitute  the 
most  effectual  remedy,  which  we  should  employ  if  it  is  in  any  way  possible.  We 
thus  evoke  deeper  inspirations  and  promote  expectoration,  and  thereby  contribute 
largely  to  preventing  the  development,  or  the  aggravation,  of  severe  lung  trouble. 
Inhalations  of  steam  or  of  medicated  fluids  are  often  advantageously  combined 
with  the  baths.  To  substitute  the  cold  pack  for  the  baths  is  in  general  justifiable 
only  when  the  baths  are  not  practicable.  Still,  the  pack  does  good.  If  em- 
ployed, it  should  be  kept  up  for  three  hours  at  a  time,  two  or  three  times  a  day. 
The  breathing  will  be  improved,  and  usually  the  child  will  go  quietly  to  sleep. 
We  are  not  acquainted  with  any  internal  remedies  for  the  lung  troubles  which 
are  at  all  reliable.  In  rare  instances  the  excessive  accumulation  of  mucus  in  the 
bronchi  requires  the  administration  of  an  emetic.  As  expectorants  we  may  try 
ipecac,  liquor  ammonii  anisatus,  or  benzoin.  If  considei'able  intestinal  disturb- 
ance arises,  we  must  employ  small  doses  of  opium,  or  calomel,  or  subnitrate  of 
bismuth.  We  hardly  need  to  say  that,  whatever  else  is  done,  the  strength  of  the 
patient  should  be  kept  up  as  much  as  possible  by  giving  wine,  broths,  milk,  eggs, 
etc.  For  at  least  two  or  three  weeks  after  the  disease  has  ended,  the  child  must  be 
very  carefully  watched. 

As  the  disease  is  usually  so  mild,  prophylaxis  is  not  very  strenuously  attempted. 
If  one  child  in  a  family  is  attacked,  it  is  probably  already  too  late  to  isolate  the 
others,  and  it  is  even  an  advantage  to  the  family  to  have  all  the  children  finish  at 


EÖTHELN.  51 

once  what  they  will  hardly  he  able  eventually  to  avoid.  We  would  make  an  ex- 
ception in  favor  of  isolation  if  the  disease  prevailed  in  a  severe  form. 

[It  is  not  customary  with  us  to  insist  so  strongly  upon  isolation  and  thorough 
disinfection  as  in  scarlet  fever.  But  the  tendency  of  the  present  day  is  toward  a 
wide  application  of  the  principles  of  preventive  medicine.  It  is  certainly  of  no 
advantage  to  a  child  to  contract  the  measles.  Delicate  children,  especially  those 
with  tubercular  predisposition,  should  be  carefully  guarded  against  it;  and,  even 
if  it  is  decided  that  it  is  not  worth  while  to  attempt  to  confine  the  disease  to  one 
member  of  a  family,  every  precaution  should  be  taken  against  infecting  other 
families.  Under  suspicious  circumstances,  consequently,  children  are  to  he  kept 
away  from  school  and  from  contact  with  others. 

If  there  is  any  reason  to  fear  the  development  of  tuberculosis,  every  possible 
hygienic  means  should  be  employed  in  order  that  full  vigor  may  be  regained.] 


CHAPTER  VI. 

RÖTHELN. 

( German  Measles.) 

RÖTHELN  is  a  disease  similar  to  measles,  but  distinct  from  it,  although  formerly 
often  confounded  with  it,  and  perhaps  with  scarlet  fever  as  well.  The  observa- 
tions of  Steiner,  Thomas,  and  others  leave  now  no  room  to  doubt  that  these  dis- 
eases are  distinct,  for  epidemics  occur  in  which  all  cases  present  the  characteristic 
peculiarities  ascribed  to  rötheln.  But  the  best  proof  is  that  children  who  have  had 
rötheln  are  not  infrequently  attacked  by  genuine  measles  later.  It  may  indeed 
be  very  difficult  in  an  individual  case  to  decide  which  disease  is  present ;  but  that 
rötheln  does  exist,  as  an  independent  form  of  disease,  can  be  denied  by  those 
alone  who  have  never  seen  it. 

After  an  incubation  of  about  two  or  three  weeks  the  disease  begins  with  the 
appearance  of  the  eruption.  Initial  symptoms  preceding  the  eruption  are  either 
wholly  absent  or  at  most  last  for  half  a  day.  The  eruption  is  decidedly  like  that 
of  measles,  but  its  individual  spots  are  smaller.  They  are  seldom  larger  than 
small  peas  and  circular,  being  only  exceptionally  as  dentated  and  irregular  in 
outline  as  are  the  macula?  of  measles.  They  appear  on  the  whole  face,  the  head, 
the  trunk,  and  the  extremities,  are  pale  red  (sometimes  deep  red),  but  slightly 
elevated,  and  are  not  apt  to  become  confluent.  In  rare  instances,  small  vesicles 
develop  upon  the  macules.  The  soft  palate  sometimes  exhibits,  as  in  measles,  a 
faint  macular  eruption  at  the  beginning  of  the  disease.  After  two  to  four  days 
the  eruption  fades.     There  is  usually  no  decided  desquamation. 

Other  symptoms  of  disease  than  this  eruption  are  slight.  Fever  in  many  cases 
appears  to  be  entirely  absent.  As  a  rule,  there  is  for  a  day  or  two  a  slight  eleva- 
tion of  temperature,  reaching  102°  (39°  C.)  at  most.  Tokens  of  a  moderate  catarrh 
of  the  conjunctiva,  the  nasal  mucous  membrane,  the  throat,  and  the  larynx  are 
also  observed — viz.,  photophobia,  nasal  discharge,  and  cough.  Often,  the  cervical 
lymph-glands  are  more  or  less  swollen.  The  constitutional  disturbance  is  gener- 
ally so  slight  that  the  child  can  hardly  be  kept  in  bed.  Important  complications 
hardly  ever  occur. 

The  prognosis  of  rötheln  is  therefore  perfectly  favorable,  and  the  employment 
of  any  special  treatment  is  needless. 


52  ACUTE  GENEEAL  INFECTIOUS  DISEASES. 

CHAPTER  VII. 

SMALL-POX. 

( Variola.     Varioloid.) 

JEtiology.— Sin  all-pox  has  been  known  for  centuries,  although  formerly  often 
confounded  with  other  diseases.*  It  is  one  of  the  most  dreaded  acute  infectious 
diseases,  and  in  earlier  times  it  has  destroyed  thousands  in  its  pestilential  progress. 
It  was  the  discovery  of  the  possibility  of  prophylactic  inoculation,  and  the  ever- 
increasing  spread  of  this  pi^ecautionary  measure,  which  first  robbed  the  disease  of 
some  portion  of  its  terrors. 

Numerous  statements  have  been  made  about  the  occurrence  of  micro-organisms 
in  the  variolous  eruptions  on  the  skin  and  mucous  membranes,  but  we  are  com- 
pelled to  say  that  we  are  not  yet  acquainted  with  the  specific,  organized  poison  of 
small-pox,  however  strongly  justified  we  may  be  in  assuming  its  existence.  Bac- 
teria can  in  fact  easily  be  demonstrated  in  the  eruption  of  variola,  but  most  of 
them  come  from  the  surrounding  atmosphere,  and  have  no  relation  to  the  specific 
variolous  processes.  The  foci  of  bacteria  found  in  the  internal  organs  (liver, 
spleen,  kidneys)  are  also  due,  as  their  discoverer,  Weigert,  himself  supposed,  to  the 
secondary  ingress  of  other  varieties  of  micro-organisms,  and  are  not  directly  asso- 
ciated with  the  variolous  process,  the  diseased  condition  of  the  skin  furnishing  a 
ready  entrance  for  infectious  matter. 

Predisposition  to  variola,  except  as  diminished  by  vaccination  {vide  infra),  is 
universal.  The  disease  may  appear  at  any  age,  even  in  utero.  Women  are 
believed  to  be  especially  liable  to  it  during  pregnancy  and  child-bed.  It  is  said 
that  persons  ill  with  another  acute  infectious  disease,  such  as  scarlet  fever, 
measles,  or  typhoid  fever,  are,  for  the  time  being,  tolerably  secure  from  infection 
with  small-pox;  but  this  rule  has  exceptions.  The  same  individual  rarely  takes 
the  disease  a  second  time. 

A  case  of  variola  is  always  the  result  of  transmission  of  the  poison  to  a  healthy 
person  from  one  who  is  already  ill  with  it.  The  specific  poison  certainly  is  most 
abundant  in  the  diseased  portions  of  the  body  and  in  the  pus  of  the  suppurating 
pocks,  as  well  as  the  crusts  and  scales  which  are  left  when  these  have  dried  up ; 
but  the  disease  is  also  contagious  in  its  earlier  stages,  before  the  pustules  develop, 
and  even,  according  to  a  few  observations,  during  the  stage  of  incubation.  Cer- 
tainly the  variolous  poison  is  very  volatile — that  is,  it  is  prone  to  disseminate  itself 
through  the  air  in  the  neighborhood  of  the  patient.  In  order  to  catch  the  disease 
it  is  not  necessary  to  touch  the  patient,  but  merely  to  remain  in  his  vicinity.  In 
many  cases  we  can  not,  however,  determine  with  exactness  the  mode  of  trans- 
mission, since  the  contagion  may  either  be  direct  or  by  means  of  objects  and 
utensils  with  which  a  patient  has  come  in  contact — for  example,  the  soiled  linen. 
The  dead  body  is  capable  also  of  transmitting  the  disease.  In  general,  numerous 
instances  point  to  a  considerable  "  tenacity  "  in  the  poison.  The  precise  manner 
of  infection  is  not  yet  known.  It  is  most  probable  that  the  poison  is  drawn  into 
the  lungs  with  the  inspired  air. 

It  has  been  demonstrated  that  the  disease  can  be  transmitted  to  healthy  persons 
by  direct  inoculation  of  the  contents  of  the  variolous  pustules.  It  is  stated  that 
monkeys  and  other  animals  may  be  successfully  inoculated  in  the  same  way. 
Whether  inoculations  with  the  blood  of  the  sick  will  reproduce  the  disease  is  not 


*  The  very  name  small-pox  (petite  veröle)  is  significant  of  its  confusion  with  syphilis,  which  was 
termed  the  "  great  pox." 


SMALL-POX. 


53 


yet  settled.  The  secretions  (saliva,  sweat,  urine,  and  milk)  do  not  apparently  con- 
tain the  infectious  matter. 

Course  of  the  Disease,  Variola  and  Varioloid.— The-  stage  of  incubation  lusts 
some  ten  to  fourteen  days,  often  a  somewhat  shorter  time,  seldom  longer.  During 
this  period  prodromal  symptoms  are  absent  or  insignificant. 

The  disease  itself  begins  suddenly  with  what  are  usually  very  characteristic 
initial  symptoms — rigor,  fever,  headache,  and  intense  pain  in  the  loins.  It  is  only 
in  comparatively  few  cases  that  one  or  another  of  these  symptoms  is  slight  or 
wanting.  The  constitutional  symptoms  may  be  very  severe — a  dry  tongue,  stupor, 
wakefulness,  delirium.  The  fever  continues  intense  for  some  days.  The  pulse  is 
much  quickened.  There  is  almost  total  anorexia,  and  often  there  is  vomiting. 
There  is  constipation,  or,  more  rarely,  diarrhoea.  Frequently  there  is  a  slight  sore 
throat,  and  sometimes  a  slight  bronchitis.  The  spleen  is  enlarged  in  most  of  the 
severe  cases,  and  the  urine  often  has  a  trace  of  albumen.  In  women,  menstruation 
occurs  in  a  remarkably  large  number  of  cases.  The  proper  variolous  eruption 
does  not  at  once  appear,  but  from  the  second  day  other  characteristic  efflores- 
cences are  not  rare.  These  are  termed  the  initial  rash  of  small-pox.  We  may 
find  either  a  diffuse  or  macular  erythema,  extending  in  varying  degree  over  the 
trunk  and  extremities,  or  a  hasmorrhagic  eruption  with  small  spots  appearing  by 
preference  upon  the  hypogastrium  and  the  inner  surface  of  the  thighs  (in  the  so- 
called  femoral  triangle  of  Simon).  It  is  noteworthy  that  this  particular  region  is 
said  often  to  remain  free  from  the  proper  variolous  eruption.  The  erythema  soon 
vanishes,  but  the  petechiae  remain  visible  for  some  time. 

The  initial  stage,  just  pictured,  lasts  usually  three  days.  Severe  symptoms 
occurring  at  this  time  do  not  exclude  the  possibility  that  the  further  course  of  the 
disease  may  prove  favorable,  while  mild  symptoms  are  of  good  omen. 

At  the  end  of  the  third  or  on  the  fourth  day  the  temperature  makes  a  decided 
fall,  and  the  regular  variolous  eruption  begins  to  be  developed  upon  the  skin — the 
stadium  eruptionis.  During  this  period  an  evident  difference  among  the  separate 
cases  becomes  manifest.  This  distinction  can  not  indeed  be  always  drawn  with  a 
narrow  line,  but  it  is  noticeable  enough  to  justify  the  establishment  of  two  types 
of  variolous  disease.  We  refer  to  the  division  into  a  severe  form  (variola  vera), 
and  another,  mild  form  (varioloid).  The  variola  proper  has  a  well -developed 
eruption  with  many  pustules,  and,  as  a  result  of  this,  a  second  stage  of  fever 
(stadium  suppurationis) .  Varioloid  has  a  much  more  scanty  eruption,  and  little 
or  no  suppurative  fever.     We  must  now  discuss  these  two  forms  separately. 

Variola  Vera. 

The  eruption  almost  always  begins  in  the  face  and  upon  the  hairy  scalp,  ap- 
pearing somewhat  later  on  the  trunk  and  arms,  and  last  of  all  upon  the  legs. 
It  begins  in  the  form  of  little  red  dots  and  spots,  which  develop  in  about  two  days 
to  small  papules  (stadium  floritionis) .  If  the  hand  be  passed  over  thickly  set  and 
well -developed  papules  of  variola,  a  peculiar  soft,  satin-like  feeling  is  perceived. 
On  the  points  of  these  papillae  a  little  vesicle  forms.  This  keeps  growing  larger 
and  larger,  its  contents  become  turbid  and  purulent,  till  at  last,  on  the  sixth  day 
of  the  eruption  and  the  ninth  of  the  disease,  the  development  of  the  genuine  pust- 
ule of  variola  is  complete  (stadium  suppurationis).  The  pustule  usually  presents 
upon  its  summit  a  little  dimple  ("  Pocken-nabel "),  and  is  surrounded  by  a  red 
border  or  "halo."  Where  the  pocks  are  especially  close  together,  as  in  the  face, 
the  skin  between  them  is  diffusely  swollen,  and  the  consequent  burning  and  pain 
are  excessive.  The  countenance  becomes  much  disfigured.  Often  the  eyes  can  not 
be  opened  because  of  the  oedema.     The  hands  also  are  apt  to  be  intensely  affected. 


54  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

especially  the  back  of  the  hands,  and  also  all  parts  which  have  previously  been 
injured  in  any  way  (pressure  or  friction  of  clothing,  etc.).  The  immunity  of  the 
skin  in  the  so-called  femoral  triangle  has  been  already  mentioned. 

At  the  same  time  with  the  eruption  upon  the  skin,  or  even  somewhat  earlier,  a 
perfectly  analogous  efflorescence  develops  upon  the  mucous  membranes.  The 
chief  places  for  its  appearance  are  the  mouth  and  throat,  the  tongue,  the  soft  pal- 
ate, the  nasal  cavity,  also  the  larynx,  the  trachea,  and  the  upper  part  of  the  oesopha- 
gus. In  the  vagina  and  rectum  it  is  rare  and  scanty.  In  this  mucous  efflores- 
cence, however,  there  are  no  proper  pustules,  but  small,  superficial  ulcers.  These 
result  from  the  maceration  of  the  uppermost  layers  of  the  mucous  membrane. 
They  sometimes  become  confluent.  The  annoyance  produced  by  this  eruption  in 
the  mouth  and  throat  is,  of  course,  very  great.  The  pocks  in  the  larynx  manifest 
themselves  by  hoarseness,  and  occasionally  by  symptoms  of  stenosis. 

As  we  have  said,  the  beginning  of  the  eruption  is  the  signal  for  a  noticeable 
fall  in  the  temperature.  But  in  true  variola  the  fall  does  not  reach  the  normal, 
or  only  temporarily.  The  other  symptoms  likewise  remit,  especially  the  head- 
ache and  lumbar  pain.  When,  however,  the  suppuration  begins,  the  fever  rises 
once  more,  and  there  are  fresh  symptoms  of  constitutional  disturbance.  This  is 
the  time  for  the  dreaded  attacks  of  delirium,  during  which  the  patient  must  be 
vigilantly  watched,  lest  some  untoward  event  happen.  Now,  too,  complications 
may  arise  {vide  infra). 

On  the  twelfth  or  thirteenth  day  of  the  disease  the  pustules  begin  to  dry  up 
(stadium  exsiccationis).  The  purulent  contents  of  the  pustules,  part  of  which 
have  burst,  form  yellow  crusts,  the  swelling  of  the  skin  subsides,  and,  a  few 
days  later,  the  crusts  and  scabs  begin  to  fall  off.  With  the  beginning  of  desic- 
cation, the  fever  declines  ;  the  local  as  well  as  the  constitutional  symptoms 
become  daily  slighter,  and  convalescence  follows.  The  healing  of  the  pustules  is 
frequently  accompanied  by  an  extremely  troublesome  itching.  After  the  scabs 
have  been  cast  off,  the  skin  presents  pigmented  spots,  which  persist  for  months. 
Wherever  the  cutis  vera  has  itself  been  destroyed  by  the  suppuration,  a  scar  is 
inevitable.  Thus  arise  the  familiar  scars  of  small-pox,  which  continue  visible 
through  life.  Very  often,  after  the  end  of  the  disease,  there  is  almost  complete 
alopecia.     The  hair  often  grows  again,  but  not  always. 

Varioloid. 

The  distinction  between  varioloid  and  variola  vera  is  not  in  kind,  but  in  de- 
gree. Varioloid  is  only  a  milder  form  of  variola.  There  is,  as  we  have  already 
said,  no  sharp  boundary-line  between  the  two.  Varioloid  is  most  often  observed 
in  those  whose  susceptibility  to  the  variolous  poison  has  been  diminished  by 
vaccination  (vide  infra). 

As  above  mentioned,  the  behavior  of  the  disease  during  its  initial  stage  will 
not  permit  us  to  decide  positively  whether  variola  or  varioloid  will  be  developed. 
It  is  true  that  if  the  symptoms  be  especially  mild,  we  may  guess  that  it  will  be 
varioloid  ;  and,  likewise,  the  appearance  of  the  initial  erythema  already  spoken  of 
is  regarded  as  a  favorable  omen. 

Shortly  after  the  pocks  begin  to  appear,  the  decision  can  almost  always  be 
made  with  certainty.  In  varioloid  the  eruption  is  rather  scanty.  It  is  often 
irregular,  and  does  not  by  any  means  always  begin,  like  that  of  variola,  in  the 
face,  but  often  on  the  trunk.  The  individual  pocks  are  in  no  way  different  from 
those  of  variola  ;  but  it  often  happens  that  they  do  not  pass  through  all  the  regu- 
lar stages  to  full  suppuration,  but  undergo  resolution  before  this  occurs.  Such 
cases,  where  there  is  nothing  beyond  papillae  or  vesicles,  are  sometimes  spoken  of 


SMALL -POX.  55 

as  variolois  verrucosa  seu  miliaris.  The  scantiness  of  the  eruption  and  the 
limited  amount  of  suppuration  have  for  their  corollary  an  absence,  or  at  least  a 
very  slight  development,  of  the  suppurative  fever. 

When  the  eruption  appears  the  temperature  usually  falls  hy  crisis  to  the 
normal  level  and  remains  there.  The  desiccation  may  begin  as  early  as  the 
eighth  or  tenth  day  of  the  disease,  so  that  the  whole  duration  of  varioloid  is  con- 
siderably shorter  than  that  of  variola.  Grave  complications  are  very  exceptional. 
The  pocks  may  develop  upon  the  mucous  membranes,  but  here,  too,  they  are 
scanty  and  not  very  vigorous. 

Course  of  the  Fever,  Symptoms  presented  by  Separate  Organs,  and  Com- 
plications. 

1.  Fever  {vide  Fig.  7). — In  the  initial  stage,  as  we  have  said,  the  temperature 
rises  rapidly  as  a  rule,  with  a  pronounced  rigor;  and  during  the  first  days  it  very 
often  reaches  104°  to  106°  (40°-41°  C).  It  sinks  on  the  third  to  the  sixth  day, 
when  the  first  papilla?  develop,  and  now,  in  the  case  of  varioloid,  falls  rapidly  to 
normal,  and  remains  there.  In  variola  the  decline  is  slower  and  less  complete ; 
and  with  the  beginning  of  suppuration  the  temperature  begins  to  rise  again.  The 
violence  of  this  suppurative  fever  is  usually  in  direct  proportion  to  the  severity  of 
the  eruption.     It  has  manifold  fluctuations,  but  seldom  lasts,  in  severe  cases,  less 


2         3         4  5  6  7  8  9        10        11        12        13        14        15        16        17        18 


40-0° 


39-0° 


38-0° 


37  0C 

Initial  Fever.  Suppurative  Fever. 

Eruption. 

Fig.  7. — Example  of  the  temperature  curve  in  true  small-pox. 

than  a  week.  Temperatures  of  104°  (40°  C.)  and  higher  are  common.  The  fever 
declines  by  lysis.  In  case  of  approaching  death,  the  temperature  may  be  ex- 
tremely high,  even  reaching  108°  or  109°  (42°-43°  C). 

2.  Skin. — We  have  already  described  the  macroscopic  appearance  of  the  erup- 
tion. It  remains  to  mention  briefly  the  histological  phenomena.  The  first  de- 
monstrable changes  are  in  the  cells  of  the  deeper  layers  of  the  rete  Malpighi.  As 
a  result  of  the  variolous  infection,  the  cells  perish,  are  swollen  by  the  lymph 
which  escapes  from  the  papillary  blood-vessels,  and  are  transformed  into  flaky > 
homogeneous  masses  without  nuclei  ("  coagulation  necrosis  "  of  Weigert).  The 
lymph  becomes  more  and  more  abundant,  and  crowds  the  cells  farther  and  far- 
ther apart.  These  are  thereby  finally  changed  into  threads  and  membranes, 
forming  a  distinct  net-work  in  the  vesicle.  This  explains  why,  if  such  a  vesicle 
be  pricked,  its  entire  contents  are  never  discharged  at  once.  Great  numbers  of 
white  corpuscles  escape,  along  with  the  lymph,  from  the  blood-vessels,  and  finally 
render  the  contents  of  the  original  vesicle  purulent.     Proliferative  processes  occur 


56  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

in  the  surrounding  epithelial  cells,  which  are  still  intact,  and  thus  the  margin  of 
the  vesicle  becomes  elevated,  while  the  dead  portion  in  the  center  sinks  in.  Thus 
the  pock  becomes  umbilicated.  If  a  portion  of  the  papilla  itself  suppurates,  a  scar 
must  be  left  on  healing.  If  the  process  remains  limited  to  the  epithelium,  complete 
regeneration  takes  place,  and  the  skin  reassumes  its  normal  appearance. 

Certain  secondary  complications,  which  sometimes  attack  the  skin,  remain  to 
be  mentioned  ;  abscess,  phlegmon,  erysipelas,  gangrene,  and  bed-sores.  None  of 
these  are  directly  due  to  the  specific  variolous  intoxication. 

3.  Respiratory  Organs. — The  disturbances  here  are  in  part  symptoms  of  the 
specific  process  of  the  diseaso,  and  in  part  secondary.  The  frequent  occurrence  of 
secondary  symptoms  in  small-pox  is  easy  to  understand  (compare  the  chapter  on 
lobular  pneumonia).  Of  the  primary  symptoms,  we  should  mention  genuine  pocks 
in  the  larynx,  the  trachea,  and  the  larger  bronchi.  As  sequels  to  these,  more  or  less 
severe  secondary  disorders  are  very  frequent  :  laryngeal  ulcerations,  which  may 
even  lead  to  laryngeal  perichondritis  and  oedema  of  the  glottis  ;  diffuse  bron- 
chitis ;  lobular  pneumonia,  often  of  great  extent,  due  to  the  inhalation  of  solid 
matter  into  the  lungs,  and  frequently  accompanied  by  pleurisy.  It  should  be 
especially  noticed  that  lobar,  croupous  pneumonia  is  not  rare.  Whether  this  be 
likewise  secondary  or  a  direct  result  of  the  variolous  poison  is  not  yet  known. 

4.  Digestive  System. — The  genuine  pocks  often  develop,  as  stated,  in  the 
mouth  and  pharynx,  and  likewise  in  the  upper  part  of  tbe  oesophagus.  They  are 
not  observed  in  the  mucous  membrane  of  the  stomach  or  intestines.  The  active 
diarrhoea  sometimes  seen  depends  upon  catarrh  of  the  intestine.  Dysentery  is 
rare.  The  eruption  in  the  mouth  and  throat  may  result  in  severe  secondary  trou- 
bles, purulent  otitis,  parotitis,  pharyngeal  diphtheria,  etc.  The  spleen  is  almost 
always  considerably  enlarged,  and  often  the  liver,  but  in  a  less  degree. 

5.  Circulatory  System. — Pathological  changes  in  the  heart  are  rare,  if  we 
except  the  slight  parenchymatous  degeneration  of  its  muscular  fibers,  common  to 
almost  all  severe  infectious  diseases.  Sometimes  there  is  a  slight  endocarditis 
(q.  v.),  which  is  probably  secondary.     Pericarditis  is  rather  more  frequent. 

6.  Organs  of  Special  Sense. — Genuine  variolous  pustules  occur  upon  the  eye- 
lids and  the  conjunctiva.  Later  in  the  disease  there  may  be  keratitis,  iritis,  or 
choroiditis. 

We  have  already  mentioned  the  relative  frequency  of  aural  disturbances,  par- 
ticularly purulent  otitis  media. 

7.  Articular  swelling  may  appear  in  the  suppurative  stage.  The  shoulders  and 
knees  are  most  apt  to  be  attacked.     Periostitis  also  occurs. 

8.  Nervous  System. — We  find  no  pathological  changes  corresponding  to  the 
severe  nervous  derangements  manifested  during  the  disease.  After  the  small-pox 
is  over,  spinal  diseases  sometimes  occur,  with  either  paralysis  or  ataxia.  Westphal 
has  demonstrated  as  their  cause,  in  some  cases,  numerous  disseminated  centers  of 
inflammation  in  the  spinal  cord. 

9.  Albuminuria  is  quite  frequent  in  severe  attacks,  but  gemiine  nephritis  is  a 
very  rare  complication. 

Anomalies  in  the  course  of  the  disease  are  manifold.  We  do  not  speak  of 
the  two  typical  forms  already  considered.  There  are  abnormally  mild  cases,  with 
scarcely  any  initial  symptoms,  or  with  an  obscure  eruption,  or  with  no  eruption  at 
all  (febris  variolosa  sine  exanthemate).  In  such  cases  a  correct  diagnosis  is  pos- 
sible only  at  the  time  an  epidemic  prevails,  and  by  the  aid  of  the  attendant  etio- 
logical circumstances.  There  are  also  abortive  cases  in  which  the  first  symptoms 
are  severe,  but  which  recover  with  remarkable  rapidity. 

The  abnormally  severe  cases  are  more  important.  First,  there  is  the  confluent 
variety.     This  is  merely  the  typical  process  in  its  completest  development.     The 


SMALL-POX.  57 

initial  symptoms  are  themselves  generally  very  severe,  and  are  followed,  without 
any  considerable  remission  of  the  fever,  by  the  eruption  of  hundreds  of  pustules. 
The  skin  of  the  face  and  hands  is  one  continuous  area  of  suppuration.  The  local 
discomfort  is  extreme,  as  is  also  the  intensity  of  the  fever  and  of  the  constitutional 
symptoms.  The  nervous  system  suffers  most.  There  is  at  the  same  time  an  un- 
usually abundant  eruption  upon  the  mucous  membranes.  The  occurrence  of  the 
above-mentioned  complications  affecting-  the  various  organs  of  the  body  is  fre- 
quent. Death  is  a  common  result;  or,  if  recovery  takes  place,  it  may  be  delayed 
by  tedious  sequelae. 

Hsemorrhagic  small-pox  is  the  woi'st  anomalous  form.  The  name  is  applied 
to  several  different  varieties.  In  the  first  place,  any  variolous  eruption  may  be- 
come more  or  less  haemorrhagic,  and  yet  the  general  course  of  the  disease  not 
be  essentially  altered.  Such  cases  are  more  common  among  elderly  people,  cachec- 
tic persons,  and  drunkards.  Secondly,  there  is  a  very  severe  form  of  small-pox, 
which  is  generally  quickly  fatal.  The  initial  stage  is  marked  by  the  unusual 
severity  of  the  symptoms.  The  •  abundant  eruption  soon  becomes  hemorrhagic, 
and  there  are  also  ecchymoses  in  the  mucous  membranes  and  the  internal  organs. 
This  has  been  called  black  small-pox,  and  by  Curschmann  variola  hcemorrhayica 
pustulosa. 

There  is  another  form  of  hsemorrhagic  variola,  different  from  these  but  linked 
to  them  by  transitional  varieties.  In  it  the  acute  hsemorrhagic  diathesis  develops 
during  the  initial  stage.  Death  almost  always  occurs  before  the  regular  variolous 
eruption.  This  most  frightful  form  is  usually  termed  purpura  variolosa.  That  it 
is  small-pox  is  proved  by  its  setiological  relations  alone.  Otherwise  it  would  be 
impossible  to  distinguish  it  from  certain  other  acute  septic  disorders.  It  is  prone 
to  attack  the  youthful  and  vigorous.  Chills,  headache,  and  pain  in  the  loins  are 
the  first  symptoms,  just  as  in  ordinary  cases.  Cutaneous  ecchymoses  appear  as 
early  as  the  second  or  third  day.  They  increase  in  area  so  rapidly  that  one  can 
almost  see  them  grow.  They  are  most  extensive  in  the  hypogastric  region.  There 
are  also  ecchymoses  in  the  eyelids,  the  conjunctiva,  the  mouth  and  pharynx,  and, 
as  the  autopsy  discloses,  many  in  the  internal  viscera.  The  constitutional  symp- 
toms are  most  severe,  and  the  patient  seldom  survives  the  fifth  or  sixth  day  of  the 
disease. 

Diagnosis. — The  certainty  with  which  we  can  make  the  diagnosis  of  small-pox  in 
any  well-developed  case  is  equaled  by  the  difficulty  of  deciding  about  it  during  the 
beginning  of  the  disease,  or  even  during  the  beginning  of  the  eruption.  At  this 
period  diagnosis  may  be  impossible.  When  the  variolous  eruption  is  in  process 
of  development,  it  may  be  confounded  with  typhus  fever,  with  that  form  of  mea- 
sles in  which  the  papillae  are  prominent,  with  syphilitic  eruptions,  and  with  cer- 
tain forms  of  erythema  exsudativum,  just  breaking  out.  We  can  not  here  fully 
discuss  all  the  factors  which  should  be  considered  in  making  this  diagnosis.  It  is 
important  not  to  regard  the  cutaneous  appearances  alone,  but  to  note  all  the  other 
symptoms  besides.  But  it  is  often  necessary  to  watch  a  doubtful  case  for  some 
time  before  a  diagnosis  can  be  established. 

Prognosis. — The  facts  which  are  of  greatest  weight  in  prognosis  have  already 
been  emphasized.  We  may  repeat  that  during  the  initial  stage  the  prognosis  of 
any  individual  case  can  seldom  be  determined.  If  the  first  symptoms  are  mild, 
or  if  the  initial  erythema  appears,  the  case  is  regarded  hopefully.  The  abundance 
of  the  eruption  has  an  influence  upon  the  severity  of  the  disease.  Circumstances 
peculiar  to  the  individual  are  also  important — e.  g.,  age,  constitution,  or  alcoholic 
habits.  We  have  already  called  attention  to  the  danger  of  confluent  small-pox, 
and  to  the  almost  absolutely  fatal  prognosis  in  the  genuine  haemorrhagic  variety. 
The  mortality  varies  greatly  in  different  epidemics ;  on  the  average  it  may  be  taken 


58  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

at  about  fifteen  to  thirty  per  cent.  Beyond  doubt,  the  introduction  of  vaccination 
has  decidedly  lessened  the  fatality  of  the  disease  by  diminishing  the  frequency  of 
the  severe  forms. 

Treatment. — 1.  Prophylaxis — Vaccination. — As  in  ail  contagious  diseases, 
isolation  is  of  little  avail  unless  complete.  This  fact  has  led  to  tbe  erection  in  late 
years  of  small-pox  hospitals.  All  utensils  used  by  the  patient,  and  his  clothing, 
bedding,  and  the  like,  should  be  most  carefully  disinfected.  The  best  method  is  to 
employ  a  high  degree  of  heat— viz.,  240°  to  250°  (115°-120°  C). 

Tbese  precautionary  measures  are  employed  in  many  other  diseases  as  well,  but 
for  small-pox  we  are  acquainted  with  a  peculiar  method  of  prophylaxis.  It  is 
founded  upon  a  fact  which  is  at  once  the  most  remarkable  and  inexplicable,  and 
the  most  beneficent,  within  the  domain  of  the  infectious  diseases.  We  refer  to 
vaccination.  It  must  long  ago  have  been  remarked  that  a  person  who  has  had  the 
disease  once,  enjoys,  to  a  large  degree,  immunity  from  any  fresh  infection.  This 
suggested  the  idea  of  exposing  children  purposely  to  contagion,  so  as  to  insure 
them  from  small-pox  for  the  rest  of  their  lives.  The  actual  inoculation  of  small- 
pox is  said  to  have  been  long  practiced  in  India  and  Chiua.  In  the  year  1717  it 
was  employed  by  Laxly  Montague,  of  England,  upon  her  own  son,  and  with  suc- 
cess. Unfortunately,  however,  the  inoculated  small-pox  proved  fatal  in  many 
instances ;  and,  being  itself  contagious,  it  served  to  spread  the  disease  still  further. 
Then  appeared  an  article  written  by  the  English  surgeon,  Edward  Jenner,  in  1798. 
This  informed  the  medical  profession  of  a  fact  already  known  to  the  rural  popu- 
lation of  his  native  place,  but  which  Jenner  first  established  scientifically,  and 
recognized  in  all  its  importance.  There  sometimes  occurs  a  disease  similar  to 
small-pox  upon  the  teats  and  udder  of  the  cow,  called  variola  vaccina.  It  is  appar- 
ently a  local  trouble,  and  can  easily  be  inoculated  upon  the  skin  of  human  beings. 
Vaccine  pustules  will  be  developed  upon  the  spot  inoculated.  These  almost  invari- 
ably heal  without  any  great  constitutional  disturbance ;  but  the  person  vaccinated 
possesses  the  same  immunity  from  small-pox  as  if  he  had  had  small-pox  itself. 
This  statement  of  Jenner's  was  soon  confirmed  upon  every  side.  The  result  is 
the  continually  spreading  custom  of  prophylactic  vaccination.  In  some  coun- 
tries it  is  enforced  by  law,  and  it  can  be  opposed  only  by  ignorance  or  by  lament-: 
able  prejudice. 

To  explain  how  vaccination  can  protect  against  small-pox  in  this  way  is  still 
utterly  beyond  our  powers.  We  have  lately  gained  this  much  help  in  understand- 
ing it,  that  it  is  no  longer  an  isolated  fact;  for  analogies  have  been  discovered  in 
the  case  of  other  acute  infectious  diseases  (cf.  the  chapters  on  hydrophobia  and 
malignant  pustule).  We  are  likewise  in  the  dark  as  to  the  relation  between  small- 
pox and  vaccinia.  Many  authors  regard  the  virus  of  vaccinia  as  merely  a  modifi- 
cation of  the  variolous  poison,  while  others  assume  that  there  is  a  specific  differ- 
ence between  the  two.  As  yet,  the  infectious  material  of  neither  has  been  exhib- 
ited in  a  pure  state;  and  we  must  for  the  present  therefore  leave  this  question  un- 
decided. A  statement  in  support  of  the  essential  unity  of  the  two  infectious 
agents  can  be  adduced.  The  inoculation  of  cows  with  small-pox  is  said  to  pro- 
duce vaccinia,  which,  inoculated  in  its  turn  upon  children,  will  result  in  vaccinia 
and  not  in  small-pox.  This  statement  rests  on  doubtful  evidence.  Careful  ex- 
periments made  in  1865  in  Lyons  had  a  different  result,  showing  that  the  in- 
oculation of  cows  with  the  contents  of  variolous  pustules  produces  an  eruption 
different  from  that  of  vaccinia.  Children  inoculated  from  these  cows  had  ti*ue 
variola;  while  no  case  of  small -pox  has  ever  resulted  from  genuine  vaccine 
lymph. 

We  can  mention  only  the  most  important  of  the  details  relating  to  vaccination 
and  the  method  of  its  performance.     The  inoculation  is  made  either  with  animal 


SMALL-POX.  59 

virus,  direct  from  the  cow,  or  with  humanized  virus,  obtained  from  persons  previ- 
ously vaccinated.  The  lymph  taken  from  a  vaccine-pustule  can  be  kept  a  long 
time,  either  pure  or  mixed  with  glycerine,  without  deteriorating.  It  is  kept  in 
small  glass  tubes,  hermetically  sealed,  or  in  a  dried  form  between  glass  plates 
which  have  been  thoroughly  disinfected  and  cemented  together,  [or  else  upon 
little  "  points  "  made  of  bone].  The  most  common  mode  of  vaccination  now  in  use 
is  to  make  three  shallow  incisions,  3  or  4  ctm.  apart,  in  the  skin  of  the  upper  arm, 
and  to  introduce  the  vaccine-lymph  into  them.  Tbe  surrounding  tissue  becomes 
swollen  in  three  or  four  days.  In  seven  or  eight  days  the  vaccine  vesicles  are  well 
developed,  if  the  disease  takes  its  normal  course.  Next  they  become  purulent,  and 
then  dry  up,  and  finally,  on  healing  leave  the  familiar  scar  behind.  The  whole 
process  occupies  about  three  weeks.  If  the  vaccination  fails,  or  is  but  partially 
successful,  it  must  be  repeated  after  a  few  months.  The  protective  power  of 
vaccination  does  not  last  indefinitely,  and  therefore  re-vaccination  is  necessary 
every  five  or  six  years.  The  first  vaccination  of  children  usually  takes  place  when 
they  are  three  or  four  months  old.  If  they  are  feeble  we  wait  longer,  unless  small- 
pox is  prevalent. 

It  must  be  confessed  that  vaccination  is  not  without  its  dangers.  The  little 
cutaneous  wound  made  by  it  may  lead,  like  any  other,  to  sepsis  or  to  erysipelas. 
The  latter  has  been  called  vaccination-erysipelas.  But  such  misfortunes  are  ex- 
tremely rare.  The  "  vaccine  roseola  "  deserves  especial  mention.  It  appears  first 
upon  the  arm  vaccinated,  and  spreads  over  the  rest  of  the  body ;  but  it  is  not  a 
serious  matter.  It  is  of  course  possible  that  other  diseases,  among  which  syphilis 
is  of  chief  importance,  may  be  inoculated  along  with  vaccinia ;  but  this  is  a  very 
rare  occurrence — much  more  so  than  the  enemies  of  vaccination  pretend.  If  the 
physician  exercise  proper  care  in  the  selection  of  the  person  from  whom  to  take 
humanized  virus,  it  can  be  entirely  avoided.  The  exclusive  employment  of  ani- 
mal virus  in  vaccination  does  away  with  a  number  of  dangerous  possibilities,  and 
for  this  reason  it  is  constantly  growing  in  popularity. 

[The  incubation  stage  of  vaccinia  being  shorter  than  that  of  small-pox,  the 
prompt  vaccination  of  an  unprotected  individual  who  has  been  exposed  to  infec- 
tion should  always  be  practiced,  if  possible;  oftentimes  the  severe  disease  may 
thus  be  prevented.] 

2.  The  treatment  of  small-pox  is  purely  symptomatic.  When  the  disease  has 
once  begun  it  is  too  late  for  vaccination  to  have  any  influence  upon  its  further 
course.  During  the  initial  period  we  may  advantageously  employ  cool  baths  to 
diminish  the  fever  and  alleviate  the  constitutional  symptoms.  An  ice-bag  will 
relieve  the  headache.  We  must  not  let  the  lumbar  pains  lead  us  to  any  but  a 
cautious  use  of  local  irritants,  for  the  pocks  come  out  in  greater  abundance  upon 
such  portions  of  the  skin  as  have  been  in  any  way  irritated.  If  the  disease  proves, 
during  the  stage  of  eruption,  to  be  varioloid,  there  will  be  no  further  need  of 
special  treatment.     Good  nursing  and  proper  food  will  suffice. 

The  true  smallpox,  on  the  other  hand,  demands  the  interposition  of  the  physi- 
cian. He  must  strive  to  guard  the  regular  course  of  the  disease  in  the  skin  and  in 
those  portions  of  the  mucous  membrane  which  are  accessible  from  being  disturbed 
by  secondary  inflammations.  For  we  have  no  doubt  that  the  ruptured  pustules 
furnish  a  most  easy  ingress  to  septic  impurities  from  the  surrounding  atmosphere, 
so  that  later,  when  there  is  extensive  suppuration  of  the  skin,  or  analogous  and 
severe  disturbance  in  the  mucous  membrane,  it  is  impossible  to  discriminate 
between  the  effects  of  the  small-pox  itself  and  those  due  to  the  secondary  suppura- 
tion. If  we  were  able  to  have  the  whole  process  go  on  "  antiseptically  "  we 
should  certainly  have  made  an  important  advance  in  therapeutics.  Indeed,  the 
methods  of  treatment  which  have  been  up  to  this  time  recommended  fulfill  this 


60  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

indication  up  to  a  certain  point,  e.  g.,  painting  the  skin  with  tincture  of  iodine,  or 
with  a  strong  solution  of  nitrate  of  silver — methods  formerly  much  in  vogue. 
Schwimmer's  suggestion  seems  still  better.  He  recommends,  from  the  beginning 
of  the  eruption,  the  use  of  a  paste  made  as  follows  :  Acid,  carbol.,  parts  4  to  10; 
ol.  olivae,  40;  creta?  pra?parat.,  60.  M.  et  ft.  pasta  mollis.  This  is  spread  on  pieces 
of  old  linen  and  laid  upon  those  parts  where  the  eruption  is  apt  to  be  worst — viz., 
the  forearm,  hand,  and  leg.  The  face  is  covered  with  a  mask,  having  holes  corre- 
sponding to  the  mouth,  nose,  and  eyes.  The  applications  are  changed  every 
twelve  hours.  Under  this  treatment  the  local  distress  is  said  to  be  diminished, 
suppuration  slight,  and  healing  comparatively  rapid.  The  pain  and  sense  of  ten- 
sion in  the  skin  are  often  relieved  by  cold  applications,  or  by  simple  ointment  or 
oil.  Under  Hebra,  in  Vienna,  continuous  warm  baths  were  employed  in  severe 
cases  with  great  success. 

The  treatment  of  the  affected  mucous  membrane  in  small-pox  must  also  meet 
the  indication  above  mentioned.  The  most  thorough  disinfection  of  the  mouth 
and  pharynx  must  be  aimed  at.  The  means  to  be  used  are  careful  washing  and 
gargling  with  solutions  of  chlorate  of  potash  (1  to  30),  carbolic  acid,  borax,  per- 
manganate of  potash,  or  liquor  ferri  chloridi.  The  eyes,  if  they  need  it,  must  also 
be  appropriately  treated.  As  to  all  other  complications,  cool  baths  are  relatively 
the  most  useful  remedy.  They  can  be  given  without  difficulty.  The  chief  indica- 
tions for  them  are  severe  pulmonary  or  nervous  symptoms,  or  continuous  high 
fever.  Internal  antipyretics,  such  as  quinine  or  antipyrine,  are  also  employed. 
Violent  nervous  disturbances,  such  as  delirium,  sometimes  require  the  cautious 
use  of  narcotics.  There  is  nothing  to  add  as  to  the  treatment  of  malignant  hsemor- 
rhagic  small-pox,  for,  as  we  have  said,  such  cases  are  unfortunately  almost  hope- 
less. 


CHAPTER  VIII. 

VARICELLA. 

(  Chicken-pox.) 

Varicella  is  truly  one  of  the  children's  diseases.  Adults  very  rai'ely  have  it. 
It  is  contagious,  and  often  comes  in  epidemics. 

The  stage  of  incubation  does  not  last  over  thirteen  to  seventeen  days.  The 
disease  begins  with  the  appearance  of  vesicles,  the  size  of  a  pea  or  a  little  larger, 
usually  having  a  small  red  areola,  and  varying  in  number  from  ten  to  one  hun- 
dred  or  more.  The  trunk  usually  bears  the  greater  part  of  the  vesicles,  while  the 
extremities  have  few.  The  face  is  frequently  the  seat  of  a  considerable  number, 
and  sometimes  there  are  a  few  upon  the  hairy  scalp.  There  may  be  a  vesicle  here 
and  there  upon  the  mucous  membrane  of  the  mouth  or  palate.  There  are  seldom 
any  prodromata.  Slight  symptoms  of  fever  may  attend  the  eruption  itself.  The 
eruption  is  usually  over  in  a  few  days,  although  there  may  be  repeated  crops,  so 
that  we  often  see  fresh  vesicles  by  the  side  of  others  which  are  drying  up.  Each 
separate  vesicle  heals  quickly,  and  the  pustulation  seen  in  small-pox  is  here  excep- 
tional. The  course  of  the  disease  is  completed  in  a  week  or  ten  days.  Most  chil- 
dren feel  perfectly  well  the  whole  time,  although  there  may  be  in  rai'e  cases  pain 
in  the  limbs,  anorexia,  and  a  slight  coryza.  A  severe  complication  is  hardly  ever 
seen.     An  unusual  event  is  a  mild  nephritis. 

Exceptionally,  the  disease  may  be  rudimentary,  with  a  varicelloid  roseola  and 
no  formation  of  vesicles.  On  the  other  hand,  some  cases  present  quite  severe  con- 
stitutional symptoms  and  a  high  fever,  even  reaching  105°  (41°  C.)  temporarily. 


ERYSIPELAS.  61 

In  most  cases,  however,  as  we  have  said,  the  child  is  so  slightly  disturbed  that  a 
physician  is  hardly  thought  necessary. 

The  diagnosis  is  almost  always  easy.  Formerly  varicella  was  often  con- 
founded with  small-pox,  and  to  this  day  the  followers  of  Hehra,  in  Vicuna,  for 
some  inconceivable  reason,  maintain  the  identity  of  the  two.  That  they  are  essen- 
tially distinct  is  shown  (1)  by  the  epidemics  of  the  two  appearing  entirely  separate 
from  each  other,  (2)  by  the  fact  that  having  one  does  not  give  immunity  from  the 
other,  and  (3)  by  the  uniform  failure  of  attempts  to  produce  varied  a  by  inoculating 
varicella,  or  vice  versa.  Still,  we  must  bear  in  mind,  in  order  to  avoid  mistakes, 
that  many  dermatologists  class  the  mildest  cases  of  small-pox  as  varicella.  Those 
who  devote  themselves  to  general  diseases  are  probably  all  now  convinced  that 
varicella  is  a  separate  disease. 

The  prognosis  is  perfectly  good.  There  is  usually  no  special  treatment  ne- 
cessary, but  young  children  should  be  kept  in  bed  till  the  eruption  has  dried  up. 


CHAPTER  IX. 

ERYSIPELAS. 

(St.  Anthony's  Fire.) 


JEtiology. — Erysipelas  is  an  inflammation  of  the  skin,  excited  by  the  presence 
of  a  specific,  pathogenic  micrococcus  (vide  infra),  and  recognized  by  redness, 
swelling,  and  pain.  It  has  the  peculiarity  of  spreading  gradually,  by  direct  exten- 
sion, from  its  point  of  origin  over  a  larger  or  smaller  portion  of  the  skin.  There 
are  two  varieties  commonly  recognized — an  idiopathic,  or  exan thematic,  and  a 
traumatic.  The  latter  may  follow  any  cutaneous  wound  if  it  be  infected  with  the 
specific  virus  of  erysipelas.  Traumatic  erysipelas  is  therefore  a  surgical  disease, 
and  will  not  be  further  considered  here;  nor  shall  we  treat  of  puerperal  erysipelas, 
a  possible  sequence  to  injuries  inflicted  upon  the  female  genital  organs  during  par- 
turition ;  nor  of  the  erysipelas  of  the  new-born,  which  usually  has  its  origin  in 
the  navel  or  in  small  fissures  of  the  anus. 

The  so-called  idiopathic  erysipelas  appears  almost  exclusively  in  the  face,  or  at 
least  it  starts  there.  As  it  goes  on  it  very  frequently  spreads  to  the  hairy  scalp, 
and  not  infrequently  it  also  extends  down  upon  the  trunk.  The  clinical  manifes- 
tations are  perfectly  characteristic.  It  is,  however,  a  question  whether  idiopathic 
erysipelas  is  essentially  different  from  the  traumatic  variety.  There  is  good  reason 
to  suppose  that  facial  erysipelas  is  really  traumatic  in  every  case,  having  its  origin 
in  injuries  of  the  skin  or  mucous  membrane,  which  are  so  small  as  to  be  over- 
looked. This  view  not  only  seems  a  priori  very  probable,  but  is  supported  by  nu- 
merous cases.  We  see,  for  example,  erysipelas  taking  its  origin  in  excoriations  of 
the  nose  or  the  borders  of  the  nostrils,  or  in  excoriations  or  fissures  of  the  lobe  of 
the  ear.  Quite  often  coryza  precedes  the  eiwsipelas,  and,  in  that  case,  the  first  in- 
flammatory swelling  of  the  skin  is  at  the  nose.  The  probable  explanation  of  this 
fact  is  that  the  nasal  catarrh  is  apt  to  cause  slight  erosions  of  the  mucous  mem- 
brane, and  that  these  furnish  an  opportunity  for  infection  with  erysipelas.  On 
the  other  hand,  it  can  not  be  denied  that  there  are  cases  of  facial  erysipelas  where 
it  is  absolutely  impossible  to  make  out  any  cutaneous  excoriation,  and  where  there 
is  an  initial  stage  with  feverish  symptoms  preceding  the  localized  trouble  in  the 
skin  (vide  infra).  Such  cases  suggest  the  thought  that  erysipelas  is  like  the  acute 
eruptive  diseases,  and  that  it  is  at  least  possible  that  infection  may  take  place  in 
some  other  way  than  the  one  mentioned. 


62 


ACUTE  GENERAL  INFECTIOUS  DISEASES. 


Fig.  8.— The  cocci  of  erysipelas.     x700. 
Section  through  a  lymph- vessel  in  the  skin 


The  specific  virus  of  erysipelas  has  been  brought  to  our  knowledge  chiefly 
through  the  researches  of  Fehleisen.  He  has  demonstrated  a  characteristic 
"chain-forming  micrococcus"    (streptococcus  erysipelatos,   vide  Fig.    8)   in  the 

lymphatic  vessels  and  serous  canaliculi  of  the 
diseased  skin.  This  micrococcus  is  distin- 
guished by  its  peculiar  behavior  in  pure  gela- 
tine cultures,  and  invariably  causes  erysipelas 
in  the  rabbits  and  the  human  beings  that  are 
inoculated  with  it. 

Facial  erysipelas  is  most  apt  to  attack  the 
young,  and   seems  to  be  somewhat  more  fre- 
quent in  women  than  in  men.     The  laity  erro- 
neously regard  catching  cold  and  getting  f  right- 
W&\..  -^0P  ened  as  frequent  causes  of  the  disease.     If  we 

except  the  predisposing  causes  above  mentioned 
— viz.,  coryza,  slight  scratches,  cuts,  etc. — we 
usually  find  no  cause  of  which  we  can  feel  cer- 
tain. Often  endemic  influences  are  important. 
It  has  been  long  known  that  traumatic  erysipe- 
las can  get  so  secure  a  footing  in  particular  hos- 
pitals or  wards  that  every  wounded  person 
treated  in  them  is  in  danger  of  this  disease. 
But  the  apparently  idiopathic  variety  is  sometimes  remarkably  frequent  in  partic- 
ular places.  Likewise  several  members  of  one  family  may  have  facial  erysipelas 
simultaneously.  In  nearly  all  such  cases  the  sufferers  are  infected  from  some 
common  source,  for  direct  contagion  is  certainly  exceptional.  Direct  inoculation 
can,  however,  as  has  been  proved,  convey  the  disease  from  a  patient  to  other  per- 
sons or  to  animals. 

In  contrast  with  the  behavior  of  the  acute  eruptive  diseases,  erysipelas  is  pecul- 
iarly apt  to  attack  the  same  individual  over  and  over  again.  There  are  persons 
who  have  facial  erysipelas  about  every  one  or  two  years.  Often  the  explanation 
of  this  appai-ently  lies  in  some  chronic  disease — e.  g.,  chronic  ozsena — which  makes 
infection  easy,  but  in  other  cases  no  cause  can  be  discovered.  Marasmus  seems  to 
predispose  to  erysipelas.  At  least  we  have  observed  that  erysipelas  occurred  with 
relative  frequency,  in  the  Leipsic  hospital,  in  patients  suffering  from  the  last  stages 
of  phthisis  or  cancer,  or  similar  diseases. 

Clinical  History. — In  many  cases  the  first  subjective  symptoms  are  simultane- 
ous with  the  cutaneous  swelling,  and  these  are  chiefly  local.  There  is  pain  and  a 
sense  of  tension  in  the  skin.  Soon  subjective  symptoms  of  fever  also  appear,  such 
as  general  malaise,  anorexia,  and  headache.  In  other  cases  the  disease  starts  with 
more  violent  constitutional  symptoms  :  there  is  an  initial  rigor,  with  violent  head- 
ache and  great  languor.  Almost  at  the  same  time,  or  sometimes  two  or  three  days 
later,  the  patient  notices  that  the  face  is  swollen.  In  rare  instances  the  disease 
begins  with  sore  throat.  We  saw  three  almost  simultaneous  cases  of  facial  ery- 
sipelas in  one  family,  where  a  severe  sore  throat  lasted  for  four  or  five  days  pre- 
ceding the  appearance  of  the  cutaneous  disorder. 

The  erysipelatous  process  in  the  skin  is  almost  always  circumscribed  at  first, 
It  usually  starts  on  the  nose,  less  often  upon  the  cheek,  the  ears,  or  the  hairy  scalp. 
The  skin  becomes  considerably  swollen,  grows  red,  smooth,  and  shiny,  and  feels 
hot.  The  redness  and  swelling  keep  spreading.  There  is  usually  a  sharp,  elevated 
ridge,  perceptible  to  sight  and  touch,  separating  the  diseased  from  the  still  healthy 
portion  of  the  skin.  As  long  as  the  erysipelas  is  spreading,  we  see  stretching  out 
from  its  border,  or  somewhat  removed  from  it,  small  red  streaks  and  spots  which 


ERYSIPELAS.  63 

gradually  increase  in  area  and  intensity,  and  finally  coalesce.  Any  decided  fold  in 
the  skin  may  hinder  for  a  time  the  extension  of  the  disease.  The  naso-labial  folds 
are  particularly  apt  to  limit  it.  The  border  of  the  hairy  scalp  frequently  forms  a 
terminal  line;  but  the  whole  scalp  may  be  attacked,  the  inflammation  stopping 
only  when  it  reaches  the  nape  of  the  neck.  It  is  only  in  a  relatively  small  num- 
ber of  cases  that  it  spreads  farther  yet,  attacking  the  back,  the  arms,  and  the  an- 
terior surface  of  the  trunk,  or  even  extending  to  the  feet.  This  is  known  as  ery- 
sipelas migrans.  The  facial  erysipelas  may  be  healed  long  before  the  disease 
ceases  to  extend  over  the  other  parts  of  the  body.  When  the  spreading  process  is 
about  to  cease,  the  inflammation  usually  becomes  decidedly  milder,  appears  only 
in  isolated  spots,  and  finally  stops  completely.  In  most  cases,  only  the  face,  the 
ears,  and  a  part  of  the  scalp  are  attacked. 

It  is  not  a  rare  thing  for  vesicles  or  bullaa  to  form  in  the  portions  of  skin  at- 
tacked. Such  cases  are  called  erysipelas  vesiculosum  or  erysipelas  bullosum.  The 
serum  may  change  to  pus  in  these  blisters,  and  then  we  have  erysipelas  pustulo- 
sum.  Exceptionally  the  infiltration  of  the  skin  becomes  so  intense  as  to  result  in 
a  localized  necrosis  or  gangrene— erysipelas  gangraenosum.  The  parts  most  apt 
to  be  attacked  by  this  are  the  eyelids. 

Microscopic  examination  of  the  skin  shows  a  marked  hyperasmia  of  all  the 
blood-vessels  and  a  very  considerable  infiltration  of  both  the  skin  and  the  subcu- 
taneous connective  tissue  with  serum  and  cells.  In  those  parts  where  vesicles  are 
formed  there  are  many  dead  and  disintegrated  epithelial  cells  in  the  rete  Malpighii. 
The  presence  of  great  numbers  of  the  specific  chains  of  micrococci  has  been  already 
mentioned. 

The  inflammation  in  any  one  spot  usually  ends  four  or  five  days  after  it  has 
made  its  appearance  there.  There  is  usually  much  attendant  desquamation.  The 
face  is  often  left  with  a  finer  complexion  than  it  had  before. 

The  other  symptoms,  of  which  the  constitutional  disturbance  and  the  fever  are 
chief,  correspond  pretty  closely  to  the  severity  and  extent  of  the  cutaneous  lesion. 
It  is  comparatively  seldom  that  this  correspondence  does  not  exist. 

The  fever  in  facial  erysipelas  usually  rises  rapidly  at  first,  and  to  a  considerable 
height.  We  have  seen  but  few  cases  where  the  high  fever  was  delayed  till  a  day 
or  two  after  the  skin  was  attacked.  The  temperatures  observed  in  erysipelas  are 
often  extreme  :  106°  (41°  C.)  is  not  at  all  rare.  The  highest  we  ever  saw  was 
107'2°  (41  "8°  C).  While  the  erysipelas  continues  or  is  spreading,  the  fever  is  sel- 
dom continuous,  nor  are  the  remissions  insignificant.  Pronounced  intermissions, 
even  down  to  normal,  are  very  frequent,  but  are  followed  again  by  a  rapid  and 
great  rise  of  temperature.  The  fever  may  terminate  with  a  genuine  crisis.  In  in- 
tense cases  of  considerable  extent,  or  in  erysipelas  migrans,  the  termination  is 
more  apt  to  be  by  a  more  or  less  gradual  lysis.  We  have  seen  the  cutaneous  in- 
flammation in  erysipelas  migrans  still  extend  itself  a  little,  in  a  rudimentary 
form,  after  the  fever  had  completely  ceased. 

The  headache  is  often  intense,  and  seems  to  result  not  merely  from  the  inflam- 
mation of  the  scalp,  but  from  disturbances  of  the  circulation  in  the  underlying 
parts.  Other  severe  cerebral  symptoms  are  also  relatively  frequent.  The  patient 
may  be  very  restless,  excited,  and  wakeful.  At  night  there  may  be  mild  or  even 
violent  delirium  ;  or  there  may  be  decided  stupor.  All  these  symptoms  are  in 
chief  part  due  to  the  constitutional  infection,  or,  to  speak  more  accurately,  to  the 
intoxication  caused  by  the  infection  ;  but  they  also  justify  a  surmise,  as  we  have 
said,  that  there  is  a  circulatory  derangement  in  the  meninges  and  the  brain  itself, 
resulting  from  the  inflammation  of  the  scalp.  In  drunkards,  delirium  tremens  is 
not  infrequent. 

One  of  the  most  constant  symptoms  in  facial  erysipelas  is  gastric  find  intestinal 


64  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

disturbance.  There  is  usually  complete  anorexia.  The  tongue  is  thickly  coated. 
Vomiting  is  frequent,  not  only  at  the  beginning  but  during  the  course  of  the  dis- 
ease. There  is  constipation ;  or  there  may  be  quite  severe  diarrhoea.  There  is  no 
pathological  lesion  known  corresponding  to  these  clinical  symptoms. 

The  entire  duration  of  the  disease  varies  greatly  in  different  cases.  A  very 
light  case  may  get  well  in  a  few  days.  Most  cases  of  average  severity  last  a  week 
or  ten  days.  Erysipelas  migrans  may  continue  for  many  weeks.  We  have  sev- 
eral times  seen  a  relapse  come  on  after  a  number  of  days  of  complete  apyrexia. 
Either  the  face  would  be  once  more  attacked,  or  some  portion  of  the  skin  which 
had  previously  escaped. 

Local  complications  are  comparatively  rare  in  erysipelas.  The  lymphatic 
glands  of  the  throat  and  back  of  the  neck  are  very  frequently  somewhat  swollen, 
but  seldom  attain  great  size.  Bronchitis  and  lobular  pneumonia  may  develop  in 
severe  cases,  but  are  not  at  all  characteristic.  Some  observers  call  attention  to  the 
occurrence  of  pleurisy,  endocarditis,  and  pericarditis ;  but  these  complications  also 
are  probably  secondary.  The  spleen  is  usually  slightly  swollen.  Sometimes  there 
is  an  icteroid  hue.  The  urine  frequently  contains  a  small  amount  of  albumen, 
and  in  severe  cases  of  erysipelas  acute  hasmorrhagic  nephritis  is  not  so  very  rare. 
Swelling  of  the  joints  has  been  repeatedly  observed.  It  is  more  frequent  in  the 
severe  surgical  forms  of  erysipelas,  which  are  combined  with  universal  septic  and 
pyaemic  conditions  of  the  system.  Purulent  meningitis  may  complicate  an  ery- 
sipelas located  in  the  head,  but  it -is  very  rare.  "We  should  be  exceedingly  cautious 
about  asserting  its  existence  even  when  the  cerebral  symptoms  are  very  pro- 
nounced. 

Cutaneous  complications  are  relatively  frequent.  We  have  seen  herpes  labialis 
quite  often,  and  a  number  of  cases  of  urticaria.  Of  much  greater  importance  are 
the  cutaneous  abscesses  which  occur  in  severe  cases.  These  are  due  to  a  phleg- 
monous or  even  gangrenous  inflammation  of  the  connective  tissue.  Their  most 
f requent  seat  in  the  face  is  the  eyelids,  as  already  stated ;  and  in  that  case  the  eye 
may  itself  be  endangered.  At  the  close  of  severe  cases  of  eiysipelas  migrans, 
numerous  abscesses  may  develop  in  the  skin  of  the  trunk  and  extremities,  delay- 
ing convalescence. 

The  diagnosis  of  erysipelas  is  almost  always  easy  when  once  the  cutaneous 
lesion  has  developed.  Phlegmonous  inflammation  of  the  skin  and  lymphangitis 
are  to  be  eliminated;  but  this  is  always  possible,  with  proper  care.  After  a  single 
examination,  we  may  confound  it  with  acute  facial  eczema  of  great  severity,  or 
even  with  a  marked  urticaria.  Chief  attention  should  be  paid  to  the  characteristic 
border  of  erysipelas  and  to  its  manner  of  extension. 

The  prognosis  of  facial  erysipelas,  when  it  attacks  a  healthy  person,  is  very 
favorable.  In  drunkards  a  severe  case  may  be  complicated  by  delirium  tremens, 
and  the  issue  be  unfavorable.  We  saw  one  case  end  fatally  because  of  gangrene 
in  the  eyelids,  followed  by  purulent  inflammation  of  the  orbital  connective  tissue. 
Erysipelas  migrans  may  so  exhaust  the  powers  of  feeble  patients  as  to  become 
dangerous.  The  prognosis  of  surgical  erysipelas  is  relatively  more  unfavorable, 
but  can  not  be  considered  here. 

Treatment. — In  a  case  of  not  more  than  average  severity  no  special  treatment 
is  needed.  To  lessen  the  local  discomfort,  we  usually  cover  the  skin  with  pow- 
dered starch,  or  anoint  it  with  olive-oil,  carbolized  oil,  or  vaseline.  An  ice-bag 
on  the  head  is  agreeable  to  most  patients.  If  we  wish  to  prescribe  something,  we 
may  choose  an  acid  mixture,  as  follows:  Acid,  muriat.  dil.,  parts  8;  syrup,  15; 
aquse,  120.     M. 

In  severe  cases,  however,  the  high  fever  and  the  nervous  symptoms  may 
demand  our  interference.     The  remedy  to  be  chiefly  recommended  is  cold  baths, 


DIPHTHERIA.  65 

of  which  two  or  three  may  be  given  in  a  day,  and  which  most  patients  bear  very 
well.  The  exhibition  of  quinine,  antipyrine,  or  antifebrin  is  seldom  called  for,  as 
there  is  a  tendency  to  great  spontaneous  intermissions  in  the  fever.  If  the  facial 
inflammation  proves  to  be  part  of  an  erysipelas  migrans,  the  chief  indication  for 
treatment  would  be  to  check  the  unceasing  advance  of  tne  disease;  but,  unfortu- 
nately, the  means  recommended  for  this  purpose  too  often  fail.  It  used  to  be 
customary  to  cauterize  the  skin  along  the  border  of  the  erysipelas  with  nitrate  of 
silver,  but  this  has  been  almost  entirely  abandoned  as  useless.  Hueter  recom- 
mends the  injection  of  a  two-per-cent.  solution  of  carbolic  acid  beneath  the  skin 
at  a  little  distance  from  the  border  of  the  inflammation.  Although  this  is  cer- 
tainly a  rational  method  of  treatment,  we  have  seldom  seen  any  brilliant  results 
from  it.  Of  more  benefit  seems  to  be  the  newly  recommended  scarification  of  the 
diseased  surface,  followed  by  the  application  of  a  solution  of  corrosive  sublimate. 
For  internal  use  we  mention  first  PirogofFs  camphor  treatment.  The  patient 
takes  every  hour  or  two  three  grains  (0*15  grm.)  of  powdered  camphor  and  drinks 
large  quantities  of  hot  tea,  to  promote  perspiration.  In  severe  cases  this  method 
deserves  a  trial.  Numerous  other  internal  remedies  have  been  recommended ;  but 
we  need  not  enumerate  them.  "We  have  not  seen  any  influence  upon  the  ex- 
tension of  the  disease  exerted  by  large  doses  of  salicylic  acid  or  benzoate  of  soda. 
In  England  a  prominent  remedy  is  liquor  ferri  chloridi  (in  the  form  of  tr.  ferri 
chlorid.),  given  to  the  amount  of  drachms  jss.-ijss.  in  the  course  of  the  day  (6-10 
grm.).  In  the  severe  cases  the  main  point,  after  all,  is  to  maintain  the  patient's 
strength  by  nursing  and  food.  If  cutaneous  abscesses  form,  they  should  be  opened 
promptly,  when  they  usually  soon  heal. 


CHAPTER  X. 


DIPHTHERIA. 

(Diplitluritis.     Croup.     Cynanche  contagiosa.) 

iEtiology  and  General  Pathology.— Clinically,  "  diphtheria  "  means  a  certain 
well-characterized,  specific,  acute,  infectious  disease,  the  chief  visible  lesion  of 
which  is  a  croupous-diphtheritic  inflammation  of  the  pharynx  and  upper  air-pas- 
sages. In  a  purely  pathological  sense,  however,  the  terms  ''  croupous  "  and  "  diph- 
theritic "  have  a  broader  meaning.  They  denote  a  certain  form  of  inflammation 
which  may  occur  in  the  mucous  membrane  of  almost  any  part  of  the  body.  It  is 
frequent  in  the  intestine  and  bladder.  There  is  great  diversity  in  the  causes  which 
may  produce  it. 

The  pathological  characteristic  of  croupous-diphtheritic  inflammation  consists 
in  the  formation  of  a  fibrinous  exudation.  This  may  either  be  a  croupous  mem- 
brane, which  is  grayish  white,  rather  firm,  elastic,  and  can  be  lifted  off  with  com- 
parative ease  from  the  mucous  membrane  upon  which  it  rests,  or  it  may  be  a 
diphtheritic  infiltration  with  necrosis  of  the  tissues.  Here  the  exudation  is  more 
or  less  deeply  imbedd.ed  within  the  proper  structure  of  the  mucous  membrane 
itself.  There  is  no  essential  difference  between  croup  and  diphtheria ;  diphtheritic 
inflammation  is  the  severer  form  of  the  disease,  croupous  inflammation  the  milder. 
In  diphtheria  the  fibrinous  exudation  is  preceded  by  a  necrosis  of  the  epithelium 
and  of  the  underlying  tissues  of  the  mucous  membrane  as  well,  while  in  the  case 
of  croupous  exudation  the  necrosis  is  limited  to  the  epithelium.  The  croupous 
membrane  never  rests  upon  an  intact  mucous  surface,  but  replaces  the  epithelium, 
which  has  already  been  totally  or  in  very  large  part  destroyed.  Flaky  remnants 
5 


66  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

of  the  epithelium,  no  longer  nucleated,  are  sometimes  found  in  the  meshes  of  the 
fibrin.  The  preceding  destruction  of  the  epithelium  is  essential  to  the  occurrence 
of  fibrinous,  croupous  inflammation.  The  fibrinous  exudation  can  be  formed  in 
those  places  only  where  the  cause  which  excites  the  inflammation  kills  the  epithe- 
lium at  the  same  time.  Apparently  the  epithelial  cells  have  little  if  any  share  in 
the  formation  of  the  exudation.  It  is  more  probable  that  the  material  for  the 
fibrin  comes  from  the  fibrinogen  of  the  inflammatory  matter  which  transudes 
through  the  walls  of  the  vessels,  and  also  from  the  disintegrated  migratory  white 
blood-globules.  These  last  are  abundant  throughout  the  deposit  itself,  and  still 
more  numerous  in  the  entire  tissue  of  the  mucous  membrane  beneath  the  croupous 
or  diphtheritic  exudation.  If  recovery  takes  place  in  croup,  all  that  is  needed 
after  the  exudation  has  been  cast  off  is  the  renewal  of  the  epithelium,  which  can 
be  accomplished  through  the  exclusive  agency  of  the  remnants  of  epithelium  left 
along  the  borders  of  the  diseased  spot.  In  diphtheria,  however,  the  entire  necrotic 
portion  of  mucous  membrane  must  slough  off,  a  line  of  demarkation  being  formed, 
and  cicatricial  tissue  replaces  the  necrosed  portion. 

The  above  is  a  bare  outline  of  the  present  views  about  croupous  and  diph- 
theritic inflammations.  They  have  been  reached  gradually  through  the  labors  of 
E.  Wagner,  Weigert,  and  others.  We  have  not  yet  touched  upon  the  serological 
factors;  but  what  precedes  renders  it  evident  how  manifold  they  may  be,  for 
many  causes  which  destroy  the  epithelial  layer  of  the  mucous  membrane,  and  at 
the  same  time  promote  inflammation,  may  excite  croup.  We  have  mechanical 
causes,  such  as  impacted  faeces,  gall-stones,  renal  calculi ;  chemical  irritants,  caus- 
tics, like  ammonia  and  the  acids;  and,  Anally,  a  number  of  specific,  infectious,  dis- 
ease-producing poisons.     Among  these  is  the  specific  poison  of  diphtheiia  proper. 

Beyond  a  doubt  the  diphtheritic  poison  is  organized.  To  demonstrate  this, 
however,  has  been  thus  far  extremely  difficult,  for  there  are  in  the  diseased  spots 
a  great  number  of  diverse  micro-organisms,  originating  in  the  mouth  and  throat, 
and  really  secondary  to  the  diphtheritic  process ;  but,  although  they  of  course  are 
entirely  different  from  the  specific  "  diphtheritic  bacteria,"  it  is  very  hard  to  sepa- 
rate them.  The  latest  systematic  investigations  of  Löffler  have  made  us  acquainted 
with  a  bacillus  which  can  be  found  in  most  cases  of  diphtheria,  while  at  other 
times  it  is  very  rarely  found  in  the  mouth.  Löffler's  bacilli  are  little  cylinders 
with  a  peculiar  club-like  swelling  at  their  ends.  In  croupous  membranes  they  are 
found  in  colonies.  Inoculated  upon  animals,  they  have  a  decidedly  pathogenic 
power,  and  produce  a  disease  similar  to  diphtheria.  That  they  constitute  the 
long-sought  diphtheritic  poison  is  therefore  probable,  but  it  is  by  no  means  con- 
clusively proved. 

Diphtheria  is  chiefly  a  disease  of  childhood.  It  is  much  less  frequent  in  those 
over  ten  years  of  age  than  in  earlier  life.  In  the  larger  towns  sporadic  cases  are 
occurring  all  the  time,  but  now  and  then  the  cases  become  so  numerous  as  to  be 
endemic  or  epidemic.  As  to  the  precise  way  in  which  a  human  being  becomes 
infected  the  opinions  of  physicians  differ.  We  think  it  most  probable  that  the 
poison  reaches  the  pharynx  along  with  the  inspired  air  or  in  some  other  way,  and 
here  penetrates  into  the  mucous  membrane.  It  is  very  rare  for  the  larynx  to  be 
the  point  of  entrance  (vide  infra).  It  first  excites  a  local  disturbance,  to  which 
the  general  infection  of  the  system  (vide  infra)  is  only  a  sequel.  At  the  same 
time  secondary  infection  plays  often  an  important  part  in  diphtheria,  just  as  in 
many  other  infectious  diseases.  The  seat  of  the  primary  diphtheritic  process 
promotes  and  perhaps  gives  the  first  opportunity  for  a  colonization  of  other 
varieties  of  micro-organisms ;  and  these  change  for  the  worse  the  original  character 
of  the  disease.  It  is  especially  probable  that  many  cases  of  so-called  "  septic  diph- 
theria "  (vide  infra)  are  due  to  a  complication  of  the  primary  simple  diphtheria 


DIPHTHERIA.  $>j 

with  a  septic  infection.  A  confirmatory  and  remarkable  fact  has  been  discovered 
by  Löffler.  He  has  found  in  the  diseased  tissues  of  the  throat,  and  also  in  the  in- 
ternal viscera,  in  severe  cases  of  diphtheria,  the  same  "  chain-building  micrococcus  " 
with  which,  as  the  cause  of  certain  severe  forms  of  scarlatinal  angina  (sec  \>.  :','.)). 
we  have  already  become  acquainted.  According  to  A.  Fränkel,  this  organism  is 
identical  with  the  streptococcus  pyogenes. 

The  original  source  of  the  infectious  material  is  probably  always  some  other 
case  of  diphtheria.  Sometimes  a  direct,  immediate  transmission  of  the  poison 
(contagion)  is  extremely  probable — e.  g.,  due  to  coughing,  or  to  sucking  out  bits  of 
membrane  after  tracheotomy.  The  latter  is  a  comparatively  frequent  cause  of  the 
disease  in  physicians  and  nurses.  The  infection  is  often  spread  by  some  person 
who  may  himself  escape  the  disease,  or  by  fomites,  playthings  and  other  objects, 
to  which  the  poison  is  adherent.  The  potency  of  the  infectious  matter  is  not 
easily  destroyed  by  such  external  influences  as  desiccation  or  changes  of  tempera- 
ture. In  other  words,  it  possesses  great  "  tenacity."  As  to  what  extent  the  diph- 
theritic poison  may  have  a  power  of  independent  reproduction  outside  the  body — 
e.  g.,  in  the  ground,  or  in  the  floor  of  dwellings — we  remain  in  complete  igno- 
rance. Finally,  we  should  notice  that  of  late  attention  has  been  called  to  the 
possibility  of  catching  diphtheria  from  diseased  animals.  Poultry,  doves,  and 
calves  have  diseases  that  are  at  least  similar  to  diphtheria. 

[While  it  seems  in  the  highest  degree  probable  that  the  poison  is  usually  purely 
local  at  the  start,  cases  occur  which  suggest  that  constitutional  infection  through 
the  pulmonary  blood-vessels  may  precede  the  local  manifestations.  Infection 
through  the  alimentary  canal  is  not  probable,  though  its  occurrence  can  not  be 
positively  denied. 

There  are  still  points  in  the  aetiology  and  pathology  of  this  affection  which  are 
involved  in  obscurity.  Much  has  been  said  and  written  in  this  country  and  in 
England  about  the  relations  of  filth  and  diphtheria.  That  filthy  surroundings 
contribute  a  soil  favorable  to  the  development  of  the  poison,  and  at  the  same  time 
diminish  the  resisting  power  of  the  human  organism,  can  not  be  doubted ;  but,  as 
long  as  the  parasitic  theory  of  infectious  diseases  prevails,  sewer-gas  and  the  like 
must  be  classed  among  the  predisposing  or  accessory  causes. 

Some  of  the  frightfully  virulent  epidemics  of  diphtheria  in  sparsely  settled 
country  districts  and  on  the  Western  plains  are  difficult  to  explain  under  the 
theory  that  each  case  is  mediately  or  immediately  the  result  of  a  previous  case ; 
these  difficulties  will,  however,  doubtless  be  cleared  away  in  time.] 

Clinical  History. — The  incubation  is  rather  brief,  seldom  exceeding  two  to  five 
days.  The  disease  itself  almost  always  begins  with  general  malaise,  headache, 
fever,  and  pain  on  swallowing.  Little  children,  however,  often  do  not  complain 
of  this  last  symptom,  and  in  older  children  the  sore  throat  may  not  be  very 
troublesome  at  first.  It  is  therefore  a  very  important  rule  for  the  physician  to 
examine  the  throat  carefully  in  every  child  who  presents  ill-defined  general  symp- 
toms. If  diphtheria  is  beginning,  we  find  redness  of  the  soft  palate,  and  more  or 
less  swelling  of  the  tonsils.  Upon  the  inner  surface  of  the  latter,  and  perhaps 
upon  the  arch  of  the  palate  and  the  uvula  also,  are  spots  covered  with  a  grayish- 
white  coating,  which  is  quite  firmly  adherent  to  the  mucous  membrane.  They  are 
loss  frequent  upon  the  posterior  wall  of  the  pharynx  and  the  hard  palate.  Their 
extent  varies  greatly  in  different  cases.  In  the  mildest  they  are  chiefly  confined 
to  the  tonsils,  attacking  the  soft  palate  or  the  tonsillar  surface  of  the  tivula  but  lit- 
tle if  at  all.  In  severer  attacks  the  spread  of  the  false  membrane  during  the  first 
days  of  illness  is  rapid.  Almost  invariably  there  is  a  very  early  and  consider- 
able swelling  of  the  lymph-glands  at  the  angle  of  the  jaw.  The  constitutional 
symptoms  persist.     The  children  are  restless.     There  is  complete  anorexia,  and 


68  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

frequently  vomiting.  The  temperature-curve  is  not  typical.  It  is  irregular,  but 
is  often  rather  elevated,  reaching  104°  (40°  C.)  or  more.  On  the  other  hand,  fever 
may  he  slight  or  almost  absent,  even  in  the  worst  cases.  The  pulse  is  very  rapid. 
The  urine  may  have  a  trace  of  albumen. 

In  mild  cases  the  local  and  constitutional  symptoms  remain  moderate ;  and  at 
the  end  of  a  week  or  ten  days  there  is  decided  improvement,  with  rapid  convales- 
cence. In  severe  cases,  however,  dangerous  symptoms  appear,  perhaps  early;  the 
croupous  inflammation  involves  neighboring  organs,  or  a  severe  constitutional 
infection  is  developed. 

The  diphtheria  very  frequently  extends  into  the  nose.  This  "diphtheritic 
coryza,"  though  not  in  itself  dangerous,  is  usually  a  sign  that  the  case  is  a  severe 
one.  The  inflammation  of  the  nasal  mucous  membrane  may  be  simply  muco- 
purulent, but  it  may  also  be  croupous.  It  is  betrayed  by  the  abundant  purulent 
discharge.  Excoriations  and  superficial  ulcers  are  usually  soon  produced  at  the 
edge  of  the  nostrils.     There  may  be  nose-bleed. 

A  much  more  dangerous  complication  is  the  extension  of  the  process  into  the 
larynx.  This  creates  a  mechanical  hindrance  to  respiration,  which  proves  fatal  in 
a  great  many  cases,  as  the  child's  larynx  is  so  small.  Formerly  "croup" — i.  e., 
croupous  inflammation  of  the  larynx — was  regarded  as  a  different  disease  from 
diphtheria.  Many  specialists  in  children's  diseases  still  maintain  this  view ;  but 
it  is  in  direct  opposition  to  the  teachings  of  pathological  anatomy  as  well  as  of  the 
clinical  symptoms.  We  grant  that  there  are  cases  where  the  pharynx  is  slightly 
affected,  while  the  croujjous  inflammation  of  the  larynx  is  extreme;  and  once  in 
a  great  while  the  diphtheritic  infection  results  in  croupous  laryngitis  and  trache- 
itis alone,  the  pharynx  escaping  disease.  Still  the  proposition  that  there  are  two 
distinct  diseases,  "  croup  "  and  "  diphtheria,"  is  absolutely  untenable.  In  the  over- 
whelming majority  of  cases  the  throat  is  first  affected  and  then  the  larynx.  We 
should  also  consider  how  easily  slight  lesions  in  the  pharynx  might  be  over- 
looked, especially  if  located  upon  the  posterior  surface  of  the  soft  palate  or  upon 
the  epiglottis.  Cases  of  what  is  called  "  ascending  croup,"  in  which  the  laryngeal 
affection  precedes  the  appearance  of  the  disease  in  the  pharynx,  are,  to  say  the 
least,  very  exceptional. 

Usually  hoarseness  is  the  first  indication  that  the  diphtheria  has  attacked  the 
larynx.  Then  follows  the  peculiar,  harsh,  ringing,  "croupy  cough,"  so  dreaded  by 
the  parents,  and,  finally,  there  are  signs  of  beginning  laryngeal  stenosis.  Respira- 
tion is  not  much  accelerated,  but  is  labored,  and  the  accessory  muscles  of  respira- 
tion are  called  more  and  more  into  action.  The  child  becomes  more  restless  and 
anxious.  Its  face  grows  pale  and  livid.  The  chief  cause  of  the  dyspnoea  is  un- 
doubtedly the  mechanical  stenosis  due  to  the  croupous  deposit.  Paralysis  of  the 
laryngeal  muscles  may  perhaps  be  a  factor.  If  portions  of  the  false  membrane 
become  partially  detached,  they  may  act  like  valves,  being  sucked  in  at  each 
inspiration,  and  pushed  aside  by  the  current  of  expired  air.  If  stenosis  occurs, 
respiration  becomes  noisy,  resembling  snoring.  Inspiration,  particularly,  is  pro- 
longed and  "  sawing,"  and  is  attended  by  marked  depression  of  the  larynx  toward 
the  sternum.  An  important  diagnostic  point  is  the  drawing  in  during  inspiration 
of  the  supra-sternal  region,  the  epigastrium,  and  the  lower  part  of  the  sides  of  the 
thorax.  This  is  the  direct  result  of  the  obstructed  flow  of  air  into  the  lungs.  As 
the  lungs  do  not  expand  enough  to  correspond  to  the  inspiratory  dilatation  of  the 
thorax,  the  parts  mentioned  are  forced  in  by  atmospheric  pressure.  The  degree  of 
dyspnoea  may  vary  at  different  times.  The  false  membrane  may  be  loosened  and 
coughed  up,  rendering  respiration  easier  for  a  time,  till  fresh  exudations  or  dis- 
placements of  membrane  cause  renewed  distress.  Recovery  is  still  possible.  The 
membrane  may  be  expectorated  and   no  more  be  formed.     Unfortunately,  this 


DIPHTHERIA.  (;<) 

happy  termination  rarely, occurs.  In  most  cases  the  symptoms  of  suffocation  in- 
crease more  and  more,  respiration  grows  quicker  and  more  superficial,  and  the 
child  becomes  more  and  more  stupefied  by  the  excess  of  carbonic  dioxide  in  the 
blood.  The  pulse  gets  very  small,  rapid,  and  irregular.  There  are  mild  convul- 
sions and  then  death. 

The  autopsy  in  these  cases  discloses  usually  that  the  croupous  inflammation 
has  extended  into  the  larger  bronchi  or  even  into  the  smaller.  The  lumen  of  the 
bronchioles  may  be  almost  completely  occluded  by  false  membrane.  There  is 
also  sometimes  a  genuine  croupous  inflammation  of  the  pulmonary  parenchyma. 
Lobular  pneumonia  in  the  lower  lobes  is  much  more  frequent,  however.  It  is 
probably  secondary  and  to  be  regarded  as  a  pneumonia  from  inhalation.  During 
life  the  pulmonary  complications  may  be  suspected,  but  can  hardly  be  diagnosti- 
cated. If  we  hear  abundant  moist  rales  over  the  lower  lobes  we  are  usually  justi- 
fied in  supposing  that  lobular  infiltration  exists,  even  if  there  be  no  dullness  on 
percussion.  The  croupous  bronchitis  as  such  gives  rise  to  no  especial  auscultatory 
signs.  If  it  is  very  extensive  and  reaches  into  the  smaller  bronchi,  it  may  prove 
fatal,  even  if  there  be  no  laryngeal  stenosis.     This  is  more  apt  to  occur  in  adults. 

Another  danger  from  diphtheria  is  through  the  general  infection  of  the  system, 
which  may  cause  a  fatal  result.  Although  diphtheria  does  seem  to  start  as  a  local 
disease,  yet  infectious  matter  (or  poisonous  substances)  are  certainly  absorbed  from 
the  primary  lesion  into  the  general  system.  These  exert  their  deleterious  influ- 
ences mainly  upon  the  nervous  system.  We  have  already  pointed  out  (p.  66) 
that  the  exact  interpretation  of  these  phenomena  is  rendered  difficult  by  our 
inability  as  yet  to  distinguish  between  the  effects  of  the  primary  and  of  the 
secondary  infection  of  the  body.  Of  especial  practical  importance  are  those  cases 
in  which  we  see  the  child  sink  into  somnolence,  and  finally  into  complete  sopor; 
its  pulse  becomes  weaker  and  weaker,  and  more  and  more  rapid,  reaching  200  or 
more,  and  at  last  there  is  "paralysis  of  the  heart"  and  death.  All  this  occurs 
without  any  great  degree  of  laryngeal  stenosis.  Such  cases  of  severe  constitu- 
tional infection,  or  "septic  diphtheria,"  are  most  frequent  when  the  local  disorder 
in  the  pharynx  is  of  unusual  intensity,  and  the  croupous  exudation  is  replaced  by 
deeper- reaching,  necrotic,  or  even  gangrenous  inflammation  within  the  mucous 
membrane.  This  has  been  called  "gangrenous  diphtheria."  In  such  cases,  also, 
the  cervical  lymph-glands  are  usually  intensely  inflamed.  It  must  be  noted  that, 
exceptionally,  a  comparatively  mild  local  disorder  may  co-exist  with  the  worst 
general  symptoms.  A  question  of  great  interest,  but  which  can  not  yet  be 
answered,  here  presents  itself.  It  is  whether  the  constitutional  symptoms  are  in 
every  case  directly  dependent  upon  the  diphtheria,  or  whether  the  diphtheria  is 
not  re-enforced  by  a  peculiar,  secondary,  septic  infection,  proceeding  from  the 
diphtheritic  ulcerations.  We  regard  the  latter  view  as  probable.  In  adults  the 
constitutional  infection  is  a  prime  factor  of  danger,  for  in  them  laryngeal  stenosis 
is  less  apt  to  occur,  as  the  parts  are  so  much  larger  than  in  children. 

As  to  the  part  which  the  other  organs  play  in  diphtheria,  we  should  mention 
that  the  process  may  extend  not  only  into  the  nose  and  larynx,  but  into  the  Eu- 
stachian tube  and  the  middle  ear.  It  may  also  attack  the  anterior  portion  of  the 
mouth,  the  gums,  and  the  lips,  or  it  may  travel  through  the  nose  and  the  nasal 
ducts  to  the  conjunctivae.  Very  exceptionally  the  croupous  process  extends  into 
the  oesophagus.  The  infectious  matter  may  be  transferred,  by  the  finger  or  in 
some  similar  way,  to  excoriations  or  accidental  lesions  of  the  skin,  and  excite  diph- 
theritic exudations  upon  them.  The  frequent  cases  of  inflammation  of  the  eyes 
probably  originate  in  the  same  manner,  and  also  the  diphtheria  of  the  external 
genitals  seen  in  children.  With  regard  to  other  organs,  it  should  be  mentioned 
that  there  is  not  infrequently  a  splenic  tumor.     Intestinal  complications  (diar- 


70  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

rhcea)  are  generally  rare ;  nor  is  swelling  of  the  joints  frequent.  The  heart  and 
kidneys,  however,  always  need  watching.  It  has  already  heen  stated  that  in 
sevei'e  cases  of  diphtheria  the  pulse  becomes  remarkably  small  and  rapid.  It  is 
also  often  irregular.  Further,  even  in  cases  that  otherwise  seem  mild,  sudden 
cardiac  failure  may  occur,  ushered  in  by  excessive  rapidity  of  the  pulse,  and  often 
proving  quickly  fatal.  This  misfortune  often  happens  at  a  time  when  con- 
valescence seems  to  be  fully  established.  Small  islets  of  myocarditis  are  fre- 
quently found  in  diphtheria,  but  it  is  probable  that  the  collapse  is  not  so  much  due 
to  them  as  to  derangement  of  the  cardiac  nerves,  particularly  the  vagus  {vide 
infra).  Renal  disturbance  betrays  itself  through  the  greater  or  less  degree  of 
albuminuria  existing  in  most  of  the  severe  cases.  It  usually  appears  when  the 
disease  is  at  its  height,  less  often  at  a  later  period.  We  often  find  a  few  casts  in 
the  urine,  but  seldom  much  blood.  GEdema  is  rare.  At  the  autopsy  there  is 
generally  little  macroscopic  alteration  of  the  kidneys.  The  microscope  reveals 
the  ordinary  degenerative  changes  of  acute  nephritis  {vide  infra). 

The  Nervous  Sequelae  of  Diphtheria.— The  convalescent  from  diphtheria"  is 
liable  to  be  attacked  by  certain  nervous  sequelae.  Of  these,  diphtheritic  paralysis 
is  the  most  important.  It  appears  about  one  or  two  weeks  after  the  throat  trouble 
ceases,  or  perhaps  earlier,  and  it  is  quite  as  likely  to  follow  mild  cases  as  severe 
ones.  It  attacks  the  soft  palate  by  preference.  The  tone  becomes  nasal  and 
deglutition  difficult.  The  naso-pharynx  is  imperfectly  cut  off  during  the  act  of 
swallowing,  and  with  each  attempt  liquid  regurgitates  through  the  nose.  Usually 
the  pharyngeal  mucous  membrane  is  anaesthetic  at  the  same  time,  and  depiived  of 
its  reflex  excitability.  There  may  also  be  paralysis  of  the  vocal  cords  upon  one 
or  both  sides,  and  this  again  is  frequently  combined  with  anaesthesia  of  the 
mucous  membrane  of  the  throat.  There  may  be  paralysis  of  the  ocular  muscles, 
of  which  those  controlling  accommodation  are  most  apt  to  be  affected,  rendering 
the  vision  for  near  objects  imperfect.  Paralysis  of  the  muscles  of  the  trunk  and 
extremities  is  least  frequent,  but  it  may  be  very  extensive.  Sometimes  several  of 
these  parts  are  paralyzed  simultaneously.  Thus  we  see  quite  often  paralysis  of  the 
soft  palate  and  of  the  muscles  of  accommodation  combined.  In  some  cases  there 
is  well-marked  ataxia  of  the  lower  limbs  with  or  without  paresis.  This  renders 
the  gait  very  uncertain  and  tottering,  the  tendon  reflex  is  almost  always  abolished, 
while  sensation  is  affected  slightly  if  at  all.  Very  rarely  diphtheria  is  followed 
by  contracture  of  the  hands  or  other  parts,  by  difficulty  in  articulation  and  paresis 
of  the  bladder.  A  paralysis  of  the  pharynx  is  sometimes  left  behind,  so  that  the 
children  have  to  be  fed  for  weeks  through  an  oesophageal  tube.  It  is  a  remark- 
able fact  that  not  only  in  almost  every  case  of  the  nervous  disorders  which  we 
have  mentioned,  but  often  also  in  individuals  who  have  entirely  escaped  them, 
there  is  no  patellar  reflex  after  diphtheria  for  weeks  or  even  months.  With 
regard  to  the  pathological  state,  it  is  probably  a  degenerative  condition  of  the 
corresponding  peripheral  nerves,  not  only  in  the  post-diphtheritic  paralysis,  but 
also  in  the  cases  of  post-diphtheritic  ataxia.  This  harmonizes  with  the  usually 
favorable  termination  of  the  nervous  sequelae  of  diphtheria.  But  there  is  one 
paralysis  which  is  highly  dangerous — that  of  the  heart,  as  already  mentioned. 
It  may  occur  suddenly  during  convalescence.  Probably  it  is  analogous  to  the 
other  nervous  derangements,  and  the  result  of  degeneration  in  the  fibers  of  the 
pneumogastric. 

Diagnosis. — The  physician  will  seldom  mistake  a  case  of  actual  diphtheria  if 
be  pays  proper  attention.  The  characteristic  deposit  aud  the  severe  general  and 
local  symptoms  make  the  diagnosis  certain.  It  is  much  more  common  to  take 
other  forms  of  sore  throat,  particularly  in  adults,  for  diphtheria.  The  most  decep- 
tive are  follicular  and  necrotic  tonsillitis  {vide  infra).     We  must  not  suppose  that 


DIPHTHERIA.  71 

every  white  spot  upon  the  tonsils  is  diphtheritic.  The  above-mentioned  forms  of 
sore  throat  are,  however,  frequent  during  epidemics  of  diphtheria,  and  even,  as 
we  have  often  observed  of  late  years,  in  families  where  there  arc;  simultaneously 
cases  of  genuine  diphtheria;  so  that  the  thought  is  suggested  that  they  may 
serologically  have  some  relation  to  true  diphtheria.  It  is  at  any  rate  advisable 
not  to  omit  proper  precautionary  measures,  especially  if  there  are  children  about. 

[When  the  membranes  are  confined  to  the  nose,  the  diagnosis  may  be  more  or 
less  difficult;  but  it  is  especially  in  cases  in  which  the  nasal  mucous  membrane  is 
involved  that  we  encounter  great  swelling  of  the  glands  at  the  angles  of  the  jaw. 
There  is  also  apt  to  be  a  thin,  acrid,  bloody,  or  sero-purulent  discharge. 

Jacobi  states  that  while  diffuse  pharyngeal  injection  may  or  may  not  point  to 
imminent  diphtheria,  marked  local  congestion  is  either  traumatic  or  dix>htheritic. 
An  examination  of  the  urine  should  never  be  neglected  in  doubtful  cases:  in  diph- 
theria a  trace  of  albumen  is  very  common ;  in  simple  or  follicular  sore  throat 
albumen  is  very  rare,  if  indeed,  it  occurs  at  all.] 

Prognosis. — The  unfavorable  prognosis  of  the  disease  is  universally  known, 
even  by  the  laity.  The  very  fact  that  the  best  developed  and  healthiest  children 
so  often  fall  victims  to  it  associates  the  name  diphtheria  with  the  saddest  mem- 
ories. There  are  indeed  many  mild  cases  which  recover  in  a  week  or  two,  and 
severer  ones  which  end  happily  in  three  or  four  weeks ;  but  in  most  cases,  where 
the  process  extends  into  the  larynx,  or  the  symptoms  of  a  severe  constitutional  in- 
fection occur,  medical  interference  has,  unfortunately,  no  power  to  control  the 
unfavorable  issue.  What  the  dangers  are,  and  how  recognized,  can  be  well 
enough  inferred  from  the  preceding  description  of  the  symptoms.  We  will  only 
remind  the  reader  how  carefully  the  physician  should  watch  the  behavior  of  the 
heart,  since  danger  is  apt  to  arise  from  this  source,  even  when  the  case  seems 
otherwise  to  be  taking  a  favorable  course. 

Treatment. — If  we  take  the  ground  that  diphtheria  begins  as  a  merely  local 
process,  then  local  treatment  of  it  certainly  seems  rational,  at  least  at  first.  Un- 
fortunately, the  practical  result  bears  out  the  theory  very  imperfectly.  An  actual 
and  complete  destruction  of  the  croupous  exudation  is  but  seldom  possible;  and 
the  attempt  to  accomplish  this  in  a  struggling  child  is  so  difficult  and  disagreeable 
that  to-day  most  physicians  have  entirely  abandoned  the  application  with  a  brush 
of  caustics  or  other  substances  to  the  throat.  If  it  does,  nevertheless,  seem  de- 
sirable to  try  enei'getic  local  measures  at  the  commencement  of  the  disease,  the 
best  agents  to  choose  are  a  concentrated  solution  of  argentic  nitrate  (1-10),  or  a 
solution  of  corrosive  sublimate  (1-1,000),  or  a  mixture  containing  equal  parts  of 
carbolic  acid  and  alcohol.  If  the  disease  has  already  made  some  progress,  we  may 
well  spare  the  patient  needless  torture  and  consider  that,  by  destroying  the  mucous 
membrane  and  by  wiping  off  the  exudation,  we  are  likely  to  contribute  to  a  fur- 
ther extension  of  the  diphtheritic  process.  The  author  has  not  used  energetic  local 
treatment  for  years,  regarding  it  as  a  useless  disturbance  of  the  patient. 

We  do  not,  therefore,  regard  active  local  interference  as  justifiable  except  at 
the  very  beginning  of  the  disease ;  but  we  do  believe  that  both  then  and  at  a  later 
period  it  is  extremely  desirable  to  disinfect  the  mouth  and  throat  as  thoroughly 
as  possible.  Although  this  has  little  effect  upon  the  diphtheria  itself,  it  is  at  least 
a  factor  in  preventing  secondary  septic  infection,  and  thus  of  great  therapeutic 
importance.  Adults  and  older  children  should  rinse  the  mouth  and  gargle  fre- 
quently, using  disinfectant  solutions,  e.  g.,  of  potassic  chlorate  or  carbolic  acid. 
Often,  however,  gargling  proves  painful.  Inhalations  are  very  appropriate. 
They  are  usually  well  borne  when  either  lime-water  (diluted  with  equal  parts  of 
distilled  water)  or  simple  salt  solution  is  used,  while  the  stronger  disinfectants, 
such  as  a  one-per-cent.  or  two-per-cent.  solution  of  carbolic  acid,  often  cause  a 


72  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

burning  sensation.  Nevertheless,  it  is  advisable  to  keep  up  a  carbolic  spray  in 
the  neighborhood  of  the  patient.  We  may  sometimes  try  rinsing  out  the  mouth 
with  a  fountain  syringe,  using  for  the  purpose  a  weak  solution  of  salicylic  acid  or 
some  similar  antiseptic.  The  frequent  introduction  of  a  few  teaspoonf uls  of  cold 
water  into  the  nose  has  also  been  recommended  as  an  appropriate  treatment — 
"cold  nasal  bath." 

We  shall  mention  only  a  few  of  the  numerous  other  remedies  which  have 
been  recommended.  -  There  is  another  local  remedy,  papayotin,  which  is  obtained 
from  the  milky  juice  of  a  certain  plant,  and  has  the  property  of  digesting  albu- 
men. If  a  diphtheritic  exudation  be  frequently  touched  with  a  five-per-cent.  solu- 
tion of  this,  it  will  sometimes  disappear  rapidly ;  but  the  drug  can  not  be  shown 
to  have  an  active  influence  upon  the  disease  itself.  Of  internal  remedies,  we 
should  mention  potassic  chlorate,  which  has  been  much  vaunted  as  a  specific, 
when  given  internally  in  rather  large  doses.  We  recommend  it,  but  it  should  be 
used  as  follows:  a  half-teaspoonful  of  a  two-  or  three-per-cent.  solution  should  be 
slowly  swallowed  about  every  half-hour.  The  aim  is  to  obtain,  not  a  constitu- 
tional, but  a  local  antiseptic  action.  It  should  not  be  given  in  larger  amounts 
than  drachm  j-jss.  (grin.  5-6)  in  twenty-four  hours,  lest  it  cause  hsemoglobinuria 
or  other  toxic  symptoms.  Several  physicians  have  lately  recommended  spirits  of 
turpentine  very  highly,  one  half  to  one  teaspoonful  being  given  several  times  a 
day.  It  has  not  become  popular.  The  same  may  be  said  of  the  internal  use  of 
potassic  iodide.  Injections  of  pilocarpine  have  also  been  praised.  They  are 
said  to  promote  the  detachment  of  the  false  membrane;  but  their  efficacy  is 
doubtful. 

[The  tincture  of  the  chloride  of  iron  is  much  used  in  this  country  in  the  treat- 
ment of  diphtheria,  and  appears  to  be  of  real  service ;  but  it  must  be  given  in  large 
doses.  The  following  prescription  is  recommended  by  Jacobi,  whose  experience 
has  been  very  large,  for  a  child  of  two  years : 

1$  Tinct.  ferri  chloridi 3  ij ; 

Potas.  chlorat gr.  xx ; 

Glycerin,  pur ?  j ; 

Aquae §  v. 

M.  S. :  Teaspoonful  every  fifteen,  twenty,  or  thirty  minutes. 

Turpentine  is  better  as  an  inhalation  than  by  the  stomach;  a  teaspoonful  or  two 
of  the  oil  can  be  poured  in  water  kept  at  the  boiling  point  by  an  alcohol-lamp. 
The  whole  air  of  the  room  is  thus  charged  with  the  remedy.  No  drag  should  be 
used  which  disorders  the  stomach.  Tablet  triturates  containing  one  one  thou- 
sandth of  a  grain  of  corrosive  sublimate  can  be  allowed  to  melt  in  the  mouth  with 
the  greatest  freedom,  and  seem  sometimes  to  exert  a  distinctly  beneficial  local 
action.  The  dose  is,  however,  too  small  to  secure  the  systemic  effects  of  the  drug 
unless  the  case  is  a  mild  one  and  free  from  notable  dysphagia.] 

If  the  larynx  is  attacked,  and  the  consequent  laryngeal  stenosis  threatens  to 
cause  suffocation,  tracheotomy  is  our  only  resort.  It  is  never  indicated  by  the 
disease  itself  nor  by  the  severity  of  the  case,  but  only  by  persistent  obstruction  of 
the  larynx.  It  is  therefore  not  invariably  easy  to  decide  whether  tracheotomy  is 
called  for  in  any  particular  case.  If  the  general  condition  be  bad  and  respiration 
already  impaired,  it  may  be  very  difficult  to  determine  whether  laryngeal  stenosis 
exists.  Tracheotomy  will  be  of  no  avail  if  the  croup  has  already  extended  to  the 
bronchi,  or  if  the  dangerous  condition  of  the  patient  is  due  to  the  severity  of  the 
constitutional  infection  or  to  incipient  paralysis  of  the  heart.  This  explains  why 
the  results  of  tracheotomy  are  not  remarkably  brilliant.     On  an  average,  only 


DIPHTHERIA. 


73 


about  one  third  or  one  fourth  of  the  cases  operated  upon  get  well;  but  even  this 
number  is  enough  to  make  us  prize  the  operation  very  highly.  How  it  is  per- 
formed, and  in  what  the  after-treatment  consists,  must  be  learned  in  the  text-hooks 
on  surgery. 

The  attempt  to  expel  the  false  membrane  from  the  larynx  by  inducing  vomit- 
ing is  still  often  made,  but  seldom  succeeds,  and  tortures  and  exhausts  the  child. 
Warm  baths  with  cold  douches  may  prove  very  beneficial.  They  excite  deep  res- 
piration and  more  vigorous  coughing,  and  also  tone  up  the  whole  nervous 
system.  The  wet  pack  is  also  often  employed,  and  sometimes  with  great  benefit. 
Outward  applications  upon  the  throat  are  of  little  use.  In  general,  we  prefer  the 
cold,  wet  compress  to  the  ice-bag  and  ice-poultice,  which  are  likewise  often  em- 
ployed. 

[Dr.  Geo.  W.  Gay  says  ("  Phila.  Med.  Times,"  1884):  "Not  a  single  case  of 
pseudo-membranous  laryngitis  has  ever  recovered  in  the  Boston  City  Hospital 
without  operation."  In  twenty  years  tracheotomy  has  been  done  one  hundred 
and  eighteen  times  with  thirty-nine  recoveries. 

Four,  if  not  five,  successful  cases  were  practically  moribund  at  the  time  of 
operation. 

Lovett  and  Munro  bring  the  Boston  City  Hospital  statistics  down  to  Jan.  1, 
1887.  Tracheotomy  for  croup  was  done  three  hundred  and  twenty -seven  times, 
all  the  cases  but  thirty  dating  from  1880.  There  was  recovery  in  ninety-five,  or 
29  "05  percent.  "  The  following  table  shows  the  recovery  rate  incases  operated 
upon  within  one,  two,  three,  and  four  days  after  the  beginning  of  the  obstructed 
respiration  " : 


Day  of  operation. 


Number  of  cases. 


123 
86 
33 

7 


Recovery. 


40 
24 


Per  cent,  of  recovery. 


32  5 

28-0 
25-3 
14-0 


"Since  Dr.  Gay's  article  was  written  there  have  been  two  recoveries  from 
moderate  dyspnoea  without  operation.  ...  Of  forty-two  patients  under  two  years 
of  age  only  three  recovered." 

Intubation,  as  devised  by  Dr.  O'Dwyer,  is  a  procedure  which  makes  a  distinct 
advance  in  the  treatment  of  laryngeal  stenosis.  In  permitting  the  free  access  of 
air  to  the  trachea,  intubation  may  save  life  without  resort  to  the  serious  operation 
of  tracheotomy ;  or  it  may  tide  over  a  time  until  tracheotomy  becomes  absolutely 
necessary  or  until  the  consent  of  the  parents  can  be  obtained  to  the  use  of  the 
knife.  In  hopeless  cases  it  may  promote  euthanasia.  Of  eight  hundred  and  six 
cases  collected  and  analyzed  by  Dillon  Brown  two  hundred  and  twenty-one  re- 
covered, 27 "4  per  cent.] 

In  most  cases  of  septic  diphtheria,  treatment  usually  proves  completely  futile. 
We  must  seek  to  avert  cardiac  paralysis  as  well  as  we  can  by  stimulants,  such  as 
wine,  camphor,  and  strophanthus,  and  endeavor  to  improve  respiration  and  the 
condition  of  the  nervous  system  by  lukewarm  baths  combined  with  douches. 
Finally,  we  repeat  that  the  physician  should  never  neglect  to  maintain  the 
patient's  strength,  as  far  as  possible,  by  proper  nourishment. 

The  nervous  sequelae  of  diphtheria  are  best  treated  with  the  constant  current. 
As  an  internal  remedy,  iron  is  good,  and  also  nux  vomica  or  strychnine.  The  last 
may  be  given  subcutaneously,  if  desired,  in  doses  of  gr.  ^V-sV  (grm.  0-001-0-002). 

[Diphtheria  is  a  disease  which  involves  commonly  much  exhaustion,  and  too 
much  stress  can  hardly  be  laid  on  the  importance  of  administering  the  maximum 


74  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

amount  of  nourishment  in  the  most  assimilable  and  easily  swallowed  forms  from 
the  start. 

It  is  also  important  to  give  stimulants  early  in  most  cases,  not  waiting  for 
signs  of  exhaustion.  Enormous  quantities  of  brandy  can  often  be  given  to  small 
children  without  the  slightest  toxic  effect.  No  general  rule  can  be  laid  down; 
the  requirements  of  each  case  roust  be  studied  and  met. 

When  painful  deglutition  interferes  with  nutrition,  peptonized  milk,  eggs, 
brandy,  and  the  like,  must  be  given  by  the  rectum.  Rectal  alimentation  and 
stimulation  are  also  to  be  resorted  to  in  cases  of  post-diphtheritic  paralysis  of  the 
oesophagus.] 


CHAPTER  XI. 

INFLUENZA. 

{La  Gri'ippe.) 


Influenza  is  a  specific,  acute,  infectious  disease  which  is  especially  dis- 
tinguished by  the  enormous  extent  of  its  epidemics.  While  often  years  and 
decades  pass  without  any  especial  attention  being  called  to  the  disease,  suddenly 
cases  of  it  will  appear  with  such  frequency  that  the  largest  part  of  the  population 
are  attacked,  and  the  disease  may  better  be  described  as  pandemic  than  epidemic. 
Pandemics  of  influenza  can  be  traced  back  with  certainty  into  the  sixteenth 
century.  In  the  present  century  the  influenza  during  the  years  1830-33  traversed 
almost  all  ot  Asia  and  of  Europe,  then  later  there  appeared  numerous  smaller 
epidemics,  but  these  aroused  general  attention  so  little  that  the  disease,  upon  its 
last  pandemic  appearance  in  the  winter  of  1889-'90  was  almost  unknown. 

iEtiology. — Although  we  have  every  reason  to  suppose  that  the  true  cause  of 
influenza  is  the  infection  of  the  body  with  a  specific,  organized  pathogenic  germ, 
yet  this  latter  has  as  yet  evaded  discovery.  It  is  evident  that  we  have  to  do  with 
some  micro-organism  which  at  certain  times  appears  over  an  immense  territory, 
the  spores  of  which  are  probably  scattered  by  the  wind  over  large  areas  and  are 
inspired  with  the  atmospheric  air  by  human  beings.  Many  observations  upon 
the  appearance  of  the  disease  in  isolated  institutions  (convents  and  the  like)  ren- 
der it  quite  probable  that  the  poison  may  also  be  carried  by  a  person  suffering 
from  the  influenza  to  regions  previously  unaffected.  Nevertheless,  this  contagious 
manner  of  spreading  plays  no  great  role  in  comparison  with  the  direct  infection 
from  the  outer  woidd,  this  latter  mode  being  everywhere  possible  during  an  epi- 
demic of  influenza. 

There  is  scarcely  any  reason  for  speaking  of  especial  predisposing  causes  of 
influenza,  inasmuch  as  at  the  time  of  a  well-marked  epidemic  the  overwhelm- 
ing majority  of  the  population  are  attacked,  both  the  healthy  and  the  diseased,  the 
vigorous  and  the  feeble.  Sex  certainly  makes  no  difference,  and  age  only  to  this 
extent,  that  the  disease  is  seen  more  rarely  in  little  children  under  one  year  old 
than  in  older  children  and  adults.  That  catching  cold  has  no  special  serological 
significance  is  evident  from  the  fact  that  influenza  often  appears  in  patients  who 
are  already  sick  in  bed. 

It  should  finally  be  mentioned  that  animals  also,  and  in  particular  horses,  may 
be  attacked  by  the  influenza ;  but,  nevertheless,  it  is  as  yet  a  doubtful  question 
whether  all  the  diseases  in  animals  which  are  described  under  this  name  are  actu- 
ally identical  with  genuine  influenza. 

Symptoms  and  Clinical  History.— The  best  general  idea  of  the  extremely  mani- 
fold symptoms  of  the  disease  is  to  be  obtained  if  we  bear  in  mind  that  the  influ- 


INFLUENZA.  75 

enza  causes  both  a  marked  infectious  (or  toxic)  general  constitutional  disturbance 
of  the  body,  and  also  certain  local  lesions  with  local  symptoms.  The  clinical 
picture  therefore  varies  greatly  according  to  the  predominance  of  one  or  the 
other  group  of  symptoms,  and  also  according  to  the  special  form  of  the  local 
disease. 

The  onset  of  influenza  is  generally  rather  sudden.  As  a  rule  the  marked  cases 
begin  with  rather  high  fever,  ushered  in  with  a  chill,  violent  headache,  marked 
constitutional  depression,  and  usually  considerable  pain  in  the  back  and  loins. 
The  weakness  of  the  patient  may  be  so  great  that,  even  if  a  vigorous  individual, 
he  will  at  once  take  to  his  bed.  Severe  nervous  symptoms,  such  as  stupor  and  de- 
lirium, are  exceptional.  Sometimes,  but  not  very  often,  there  is  initial  vomiting. 
The  pains  in  the  back  are  often  associated  with  pains  in  the  muscles  and  joints. 
Oppressive  pain  in  the  eyes  is  quite  characteristic  also.  This  is  particularly  felt 
upon  moving  the  eyeballs,  and  therefore  is  probably  located  in  the  external 
muscles.  The  spleen  is  sometimes  somewhat  swollen,  but  any  great  increase  in  its 
size  is  exceptional. 

If  the  clinical  symptoms  as  the  case  progresses  are  mainly  limited  to  the  above- 
named  constitutional  symptoms — fever,  languor,  headache,  pain  in  the  muscles, 
we  may  speak  of  a  typhoid  form  of  the  disease.  Usually,  however,  certain  local 
symptoms  put  in  an  early  appearance,  and  it  is  especially  the  respiratory  appa- 
ratus which  is  attacked.  The  precise  symptoms  vary  considerably  in  different 
cases.  Sometimes  the  upper  portion  of  the  respiratory  tract,  the  nose,  larynx,  and 
trachea  are  involved ;  sometimes,  from  the  start,  the  smaller  bronchi.  In  the  first 
instance  there  is  marked  coryza  or  hoarseness,  in  the  other  case  there  is  cough 
due  to  a  dry  bronchitis,  which  can  be  easily  detected  upon  auscultation,  and  which 
involves  especially  the  lower  portion  of  the  lungs.  If  these  local  symptoms  out- 
weigh the  constitutional,  the  case  is  described  as  belonging  to  the  "catarrhal  form 
of  influenza." 

Sometimes  the  influenza  is  localized  in  the  digestive  apparatus.  This  "  gastro- 
intestinal form  "  is  much  rarer  than  the  catarrhal.  In  this  case,  in  addition  to  the 
more  or  less  strongly  characterized  constitutional  symptoms,  there  is  marked  dis- 
turbance of  the  stomach  and  intestines,  as  shown  particularly  by  nausea  with  per- 
sistent vomiting,  diarrhoea,  abdominal  pain,  etc.  In  one  case  we  observed  jaun- 
dice. We  may  also  mention  in  this  connection  the  appearance  of  an  initiatory 
pharyngitis. 

The  already  mentioned  pains  in  the  back,  loins,  and  extremities  may  persist 
with  unusual  violence,  and  this  peculiar  form  of  the  disease  is  known  as  the 
"rheumatoid."  Probably  the  muscles  and  the  muscular  attachments  are  the  chief 
seat  of  these  pains,  which  may  be  so  violent  that  the  patient  does  not  know  how 
to  lie,  and  sometimes  keeps  up  a  continual  moaning.  The  loins,  in  particular, 
may  be  the  seat  of  most  acute  pain,  also  the  upper  arms,  the  knees,  the  thighs,  and 
the  eyes.  Objective  changes  in  the  painful  parts,  such  as  swelling  of  the  joints, 
are  scarcely  ever  seen,  nor  are  the  nerve-trunks  as  a  rule  especially  sensitive  to 
pressure.     The  painful  muscles  are  usually  weaker  than  normal. 

The  grouping  of  the  clinical  varieties  of  influenza  under  the  four  forms  already 
named  renders  it  easier  to  obtain  a  general  idea  of  the  manifold  symptoms  of  the 
disease,  but  this  division  into  separate  forms  must  not  be  carried  out  too  strenu- 
ously, for  in  reality  numerous  cases  of  the  disease  occur  which  present  transition 
forms  and  combinations  of  the  various  groups  of  symptoms.  Moreover,  in  all  the 
forms  a  distinction  must  be  made  between  mild  and  severe  attacks,  for  in  influ- 
enza, just  as  in  most  other  infectious  diseases,  there  are  numerous  rudimentary 
and  mild  cases  as  well  as  the  fully  developed  ones,  and  some  could  not  be  properly 
interpreted  but  for  the  presence  of  the  epidemic. 


76  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

The  duration  of  the  disease  is  hest  determined  by  the  duration  of  the  fever.  In 
the  very  mildest  cases  there  may  be  no  fever  whatever,  or  simply  a  slight  evening 
rise  of  temperature.  As  a  rule,  there  is  a  moderate  fever,  say  between  101  "5°  and 
103°  F.  (38-5°  and  39-5°  C),  although  higher  temperatures  even  to  104°  F.  (40°  C.) 
and  more  are  not  infrequent.  In  the  beginning  of  every  severe  attack  the  fever 
rises  abruptly.  After  a  duration  of  several  days,  say  four  to  seven,  it  may  fall 
again  in  a  manner  approaching  a  crisis.  More  frequently,  especially  when  there 
exists  diffuse,  catarrhal  trouble  in  the  lungs,  the  fever  ends  by  lysis.  With  com- 
parative frequency  there  are  found  to  be  noticeable  deviations  in  the  temperature 
curve;  thus,  for  example,  the  high  fever  of  the  onset  sinks  on  the  second  or  third 
day,  to  be  followed  by  an  almost  afebrile  period  of  one  or  two  days,  whereupon  a 
marked  rise  of  temperature  ensues.  With  this  change  in  the  temperature  there 
are  usually  also  corresponding  variations  in  other  symptoms. 

We  see,  then,  that  the  duration  of  simple,  uncomplicated  influenza  is  in  the  mild 
cases  about  three  or  four  days,  in  the  severer  cases  about  seven  to  ten  days.  To  be 
sure,  we  should  also  consider  in  this  connection  that  convalescence  is  often  sur- 
prisingly slow,  so  that  the  after-pains  (as  it  were)  of  the  disease  are  felt  for  weeks. 
These  consist,  for  instance,  in  a  certain  degree  of  debility,  and  in  painfulness  of 
the  muscles.  Sometimes  also  there  are  complete  relapses,  so  that  directly  or  a 
short  time  after  the  disease  has  ended  the  symptoms  begin  anew.  The  special 
form  of  the  disease  may  change  in  this  case,  so  that,  for  example,  the  relapse  of  an 
influenza  with  predominant  constitutional  symptoms  assumes  the  pronounced 
catarrhal  form.  Again,  during  the  same  epidemic  it  is  not  very  rare  for  a  patient 
to  suffer  from  two  attacks  of  influenza  separated  by  a  considerable  interval  of 
time. 

Complications  and  Sequelae. — While  all  the  symptoms  of  influenza  which  we 
have  thus  far  described  are  the  direct  effects  of  the  original  pathogenic  cause,  the 
majority  of  the  frequent  complications  are  undoubtedly  dependent  upon  the  in- 
gress of  secondary  infection.  The  system  when  attacked  by  influenza  is  greatly 
exposed  to  these  secondary  influences,  and  almost  all  the  dangerous  and  tedious 
cases  of  influenza  become  such  only  because  of  a  mixed  infection  of  this  sort. 
This  is  particularly  true  of  the  lungs,  in  which  secondary  disease  occurs  most  fre- 
quently— sometimes  even  in  the  first  days  of  illness,  but  also  in  other  cases  later. 
The  conditions  here  are  similar  to  those  seen  in  measles  and  whooping-cough. 
The  simple,  mild  catarrh  belongs  to  the  original  disease;  the  severe  pulmonary 
affections  are,  however,  invariably  secondary  complications  occasioned  by  new 
pathogenic  influences.  These  influences  are  not  always  the  same.  According  to 
the  investigations  of  Ribbert,  Finkler,  and  others  it  is  chiefly  the  pneumonia  dip- 
lococcus  and  the  streptococcus  which  are  the  true  excitants  of  the  secondary  pneu- 
monia seen  in  influenza.  These  cases  of  pneumonia  are  either  extensive  catarrhal 
pneumonia  especially  affecting  the  lower  lobes,  or  more  rarely  croupous  pneu- 
monia with  its  characteristic  sputum.  The  whole  picture  is  then  overshadowed 
by  the  pulmonary  affection.  The  patient  is  oppressed  for  breath,  has  a  severe 
cough,  looks  pale  and  cyanotic,  and  suffers  from  high  fever.  These  symptoms 
persist  for  two  or  three  weeks,  and  then  gradually  abate.  It  is  in  this  way  that 
influenza  becomes  dangerous  for  elderly  and  feeble  or  sickly  persons.  With 
noticeable  frequency,  pleurisy  with  effusion  is  conjoined  with  the  influenza  pneu 
monia.     The  exudation  is  generally  serous,  but  exceptionally  it  is  purulent. 

Complications  in  other  organs  are  less  frequent.  We  should  mention  chiefly 
purulent  otitis  media  and  keratitis  and  other  severe  diseases  of  the  ej^e.  We  have 
several  times  observed  cases  of  acute  nephritis,  but  this  has  always  pursued  a  mild 
course.  Among  cutaneous  eruptions  herpes  labialis  is  a  frequent  phenomenon  in 
all  forms  of  influenza,  even  the  milder.     Other  exanthems,  such  as  urticaria  and 


DYSENTERY.  77 

roseola,  are  much  less  frequent.  Many  of  the  complications  named  may  continue 
even  after  the  fever  and  all  other  symptoms  have  ceased,  so  that  they  must  be  re- 
garded as  sequelae.  This  is  particularly  time  of  the  diseases  of  the  car  and  eye  and 
of  persistent  bronchitis,  but  only  rarely  of  a  pneumonia  assuming  the  chronic 
form.  An  important  and  for  the  patient  a  troublesome  and  painful  sequel  is 
furunculosis,  especially  if  the  separate  boils  are  located  in  the  axilla  or  near  the 
anus.  Very  often  neuralgic  pains  in  the  distribution  of  the  trigeminus  or  in  the 
course  of  the  sciatic  or  other  nerves  will  persist  for  a  considerable  time  after  the 
influenza  has  ceased.  But  these  pains  may  sometimes  be  located  i  11  the  muscles; 
thus,  for  example,  the  frequent,  persistent,  and  troublesome  pain  in  the  eyes. 

Diagnosis.— The  diagnosis  of  influenza  is  in  general  not  difficult  if  one  has  to 
deal  with  a  well-marked  case.  The  characteristic  initial  symptoms  of  fever,  head- 
ache, and  pain  in  the  loins  are  to  he  considered  first  of  all.  Their  onset  is  much 
more  rapid  than,  for  example,  in  typhoid  fever.  Later  on  the  pain  in  the  various 
muscles  as  well  as  the  catarrhal  symptoms  are  the  most  characteristic  phenomena. 
The  diagnosis  is  very  uncertain  in  many  mild  rudimentary  cases.  Often  it  is 
merely  the  fact  of  the  prevailing  epidemic  that  justifies  one  in  calling  these  influ- 
enza. Nevertheless,  one  should  be  very  careful  not  to  make  a  diagnosis  too 
quickly,  and  it  is  indubitable  that  during  the  time  of  an  epidemic  many  cases  are 
wrongly  called  influenza. 

Prognosis. — For  an  individual  who  is  healthy  and  vigorous,  influenza  is  not  a 
dangerous  disease,  even  in  its  severer  forms ;  for  elderly  persons  or  invalids  it  may, 
however,  be  a  serious  affection.  Patieuts  with  heart  disease  or  pulmonary  disease, 
or  those  suffering  from  chronic  nervous  troubles,  sometimes  succumb  to  it;  so  that 
the  general  mortality  at  the  time  of  a  great  epidemic  of  influenza  is  always  con- 
siderably increased.  The  above-enumerated  pulmonary  complications  are  by  far 
the  most  dangerous ;  less  often  is  a  fatal  termination  caused  by  general  or  cardiac 
weakness. 

Treatment. — No  specific  remedy  for  the  disease  is  known.  Many  physicians 
maintain  that  the  exhibition  of  calomel  at  the  beginning  of  the  attack  decidedly 
shortens  its  course,  but  confirmatory  experience  is  wanting.  In  general  we  must, 
therefore,  pursue  a  purely  symptomatic  method  of  treatment.  For  the  initiatory 
fever,  the  headache,  and  the  pain  in  the  loins,  antipyrine  is  sometimes  a  good 
remedy,  and  the  same  may  be  said  also  of  quinine,  phenacetine,  and  antifebrin. 
These  drugs  are  also  prescribed  for  the  persistent  pains  in  the  muscles  which  come 
on  later.  Soothing  liniments  and  ointments  may  be  employed,  with  friction,  for 
the  same  purpose.  The  treatment  of  the  pulmonary  complications  is  according  to 
the  established  methods.  Morphine  is  mainly  used  for  the  troublesome  cough. 
Apomorphine,  senega,  and  other  expectorants  may  be  employed,  and,  if  indicated 
external  remedies  such  as  an  ice-bag  or  dry  cupping.  If  the  patient  becomes  very 
feeble,  stimulants  such  as  champagne  and  strophanthus  are  demanded. 


CHAPTER  XII. 
DYSENTERY. 

iEtiology. — By  "  dysentery  "  is  meant  a  disease  of  the  colon,  which  appears 
sporadically,  but  more  often  in  epidemics;  it  is  excited  by  infection  with  an 
organized  pathogenic  poison,  about  which  we  have  as  yet  no  further  knowl- 
edge; and  the  infection  is  probably  at  first  a  local  one.  The  true  home  of 
dysentery  is  in  warmer  and  tropical  countries,  where  the  disease  is  much  more 


7S  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

violent  and  wide-spread  than  here.  For  example,  the  mortality  among  the  soldiers 
of  the  Anglo-Indian  army  due  to  dysentery  is  said  to  be  thirty  per  cent,  of  the 
entire  number  of  deaths.  In  our  climate  most  of  the  epidemics  occur  at  the  end 
of  summer  and  in  autumn.  Endemic  influences  are  certainly  important.  The 
condition  of  the  soil  in  some  places  is  evidently  very  favorable  for  the  develop- 
ment and  dissemination  of  dysenteric  germs,  and  that  of  other  places  is  equally 
unfavorable.  There  can  be  no  other  explanation  of  the  immunity  of  some 
localities  contrasting  with  the  great  prevalence  of  the  disease  in  others.  How 
infection  occurs  we  do  not  yet  know.  Dysentery  does  not  seem  to  be  directly 
contagious;  but  that  it  can  be  spread  through  the  medium  of  the  faecal  dejections 
of  the  sick — e.  g.,  from  privies,  chamber-vessels,  and  bed-linen — is  very  probable. 
Many  cases  were  formerly  referred  to  catching  cold  or  to  some  error  in  diet ;  but 
we  must,  of  course,  regard  these  merely  as  predisposing  influences. 

The  objective  pathological  lesion  of  the  colon,  in  all  severe  cases,  consists  in 
a  pronounced  croupous-diphtheritic  inflammation.  The  remarks  as  to  the  general 
pathology  of  such  inflammations  made  in  the  preceding  chapter  are  equally  ap- 
plicable to  the  analogous  dysenteric  inflammation.  In  this  case,  too,  there  is  first 
a  destruction  of  the  epithelium  and  then  the  formation  of  a  fibrinous  exudation 
occupying  its  place,  and  penetrating  down  into  the  tissue  of  the  mucous  mem- 
brane itself.  At  the  same  time  there  is  an  intense  purulent  infiltration  of  the 
mucous  and  submucous  tissue,  accompanied  by  extensive  ecchymoses.  In  the 
most  virulent  cases  the  macroscopic  appearances  are  marked  thickening  of  the 
whole  wall  of  the  intestine,  congestion  of  the  serous  layer,  and  the  conversion  of 
the  inner  surface  into  a  mottled,  dark-red,  irregularly  roughened  area  of  ulcera- 
tion. The  disease  may  be  confined  to  the  rectum  and  the  sigmoid  flexure,  but  in 
severer  cases  it  involves  the  entire  colon  as  far  as  the  ileo-caecal  valve,  or  even 
extends  to  the  lower  portion  of  the  ileum.  Besides  this  severe  form  of  diph- 
theritic or  even  gangrenous  dysentery,  there  is  a  mjlder  variety,  termed  catarrhal 
dysentery.  In  this  the  mucous  membrane  is  found  in  a  state  of  intense  purulent 
inflammation,  with  ecchymoses.  Even  here  little  masses  of  croupous  exudation, 
which  can  be  torn  off,  have  replaced  the  epithelium;  but  they  never  form  con- 
tinuous layers  of  great  extent.  There  is  no  sharp  boundary-line  between  the  two 
forms,  the  milder  catarrhal-croupous  and  the  severer  diphtheritic  dysentery. 
Numerous  transitional  and  combined  varieties  exist. 

We  must  remark,  in  conclusion,  that  precisely  the  same  anatomical  changes 
as  are  presented  in  true  dysentery  may  result  from  other  causes.  Important 
among  these  is  persistent  faecal  impaction  in  the  rectum,  which,  by  a  purely  me- 
chanical effect  upon  the  epithelium,  may  excite  a  diphtheritic  inflammation  in  the 
mucous  membrane.  And  any  severe  constitutional  disease  whatsoever,  such  as 
typhoid  fever,  measles,  small-pox,  septicaemia,  or  phthisis,  may  be  attended  by  a 
so-called ''secondary  dysentery.''  This  is  most  frequent  in  hospitals.  Whether 
it  has  the  same  aetiology  as  genuine  dysentery  is  uncertain. 

Clinical  History. — Throughout  the  entire  illness  the  most  prominent  symptoms 
are  intestinal.  There  may  be  first  of  all  some  slight  irregularity  of  the  bowels  for 
a  few  days,  and  then  appears  a  moderate  diarrhoea.  The  stools  are  at  first 
feculent,  although  thin,  and  number  two  to  six  daily.  After  a  few  days  the  dis- 
charges increase  in  frequency,  and  become  extremely  characteristic. 

The  stools  are  very  frequent,  occurring  ten  to  twenty,  and  even  sixty  or  more, 
times,  in  twenty-four  hours.  In  severe  cases  there  may  be  a  distressing  and  almost 
constant  desire  to  evacuate  the  bowels.  After  every  operation,  and  to  some  extent 
during  it,  there  is  tenesmus  attended  by  intense  burning  pain  in  the  anus.  The 
stools  soon  lose  their  usual  feculent  character  in  great  part  if  not  entirely.  They 
become  scanty,  so  that  not  more  than  about  half  an  ounce  is  evacuated  each 


DYSENTERY.  70. 

time.  For  the  most  part  they  usually  consist  of  a  sero-mucous  fluid,  in  which 
are  suspended  numerous  shreds  and  particles  of  varying  si/,«-.  These  are  blood- 
stained bits  of  mucus,  little  coagula  of  blood,  and  necrosed  pieces  of  mucous  mem 
brane.  One  or  another  of  these  constituent  parts  may  predominate,  so  that  there 
may  be  slimy,  purulent,  or  bloody  stools,  or  all  sorts  of  combinations  of  these 
varieties.  We  often  find,  besides,  a  few  small  masses  of  faeces,  usually  covered 
with  mucus.  We  sometimes  see  numerous  clumps  of  mucus,  resembling  sago  or 
frog's  spawn;  they  are  probably  mucous  casts  of  the  follicles.  Under  the  micro- 
scope the  greater  part  of  the  dysenteric  discharge  is  seen  to  consist  of  pus-corpus- 
cles and  blood.  There  are  also  cylinder  epithelium  and  an  enormous  amount  of 
detritus,  and  the  bacteria  of  putrefaction.  A  purely  dysenteric  stool  has  no  bad 
odoi',  except  that  in  the  worst  cases  of  gangrenous  dysentery  the  discharges  become 
blackish  and  extremely  offensive. 

The  rectal  teiiesmus  may  be  accompanied  by  a  cramp-like  pain  during  micturi- 
tion. There  are  often  violent  attacks  of  colic.  The  abdomen  is  usually  rather 
tense,  and  tender  on  pressure  along  the  line  of  the  colon,  but  without  tympanites. 
The  anus  may  be  red,  inflamed,  and  excoriated.  Gastric  symptoms  are  on  the 
whole  infrequent,  if  we  except  the  complete  anorexia  which  exists  in  all  severe 
cases.  Sometimes  there  is  repeated  vomiting.  Occasionally  hiccoughs  prove  dis- 
tressing.    The  tongue  usually  has  a  dry,  greasy  coating. 

The  symptoms  just  depicted  last  about  a  week  or  ten  days.  If  the  case  is  of 
much  intensity,  the  general  condition  is  also  greatly  affected.  The  patient  seems 
much  collapsed,  and  is'  very  languid  and  feeble,  with  a  small  and  rapid  pulse. 
The  skin  becomes  cool  and  rough,  the  voice  weak  and  hoarse.  There  is  pain  in 
the  muscles.  The  patient  wastes  away.  The  temperature  has  little  that  is  char- 
acteristic or  typical.  In  mairy  cases  there  is  no  fever  at  all,  and  the  temperature 
may  even  be  subnormal.  In  most  cases,  however,  there  is  an  irregular  fever, 
seldom  exceeding  104°  (40°  C),  and  having  remissions. 

In  the  worst  cases  the  general  weakness  may  increase  more  and  more,  and 
death  occur ;  but  with  us  a  favorable  termination  is  much  more  frequent.  The 
distress  gradually  diminishes,  the  stools  assume  more  and  more  of  a  feculent  char- 
acter, the  patient  becomes  stronger,  and  after  one  and  a  half  to  three  weeks  con- 
valescence is  established.  It  may  be  a  long  while,  however,  before  a  patient  com- 
pletely recovers  from  a  severe  attack.  A  third  possibility  is  the  transition  of  the 
acute  into  a  chronic  dysentery.  In  this  the  symptoms  of  a  chronic  colitis,  usually 
attendod  with  cachexia,  may  persist  for  months  and  years. 

Mild,  rudimentary  forms  of  dysentery  also  occur,  presenting  less  violent  intes- 
tinal symptoms,  and  recovering  at  the  end  of  a  few  days.  In  these  cases,  too 
great  sensitiveness  of  the  intestine  to  disturbing  influences  frequently  persists  for 
quite  a  long  time  after  the  illness.  There  may  be  exacerbations  of  the  disease,  and 
relapses. 

Complications  of  dysentery,  localized  in  other  organs,  are  rare,  at  least  in 
epidemics  here.  Abscess  of  the  liver  is  mentioned  oftenest  by  physicians  in  warm 
climates,  and  probably  is  best  explained  as  the  result  of  metastasis  by  way  of  the 
portal  system.  Articular  disturbances  also  occur,  and  inflammation  in  the  serous 
membranes.  A  few  cases  of  peritonitis  due  to  perforation  have  been  observed, 
and  a  combination  of  dysentery  and  a  "  general  scorbutic  diathesis  "  has  been  de- 
scribed. 

The  diagnosis  is  rarely  very  difficult.  It  is  based  exclusively  upon  the  intesti- 
nal symptoms  and  the  character  of  the  stools.  It  is  only  the  cases  of  secondary 
dysentery  which  occur  in  the  course  of  other  severe  diseases  that  can  easily  escape 
observation. 

The  prognosis  is  mainly  influenced  by  the  character  of  the  epidemic,  which,  as 


SO  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

we  have  said,  is  in  our  climate  usually  benign.  There  may  be  danger,  particu- 
larly to  elderly  people,  from  bodily  weakness  and  collapse. 

Treatment. — Prophylaxis  demands  that  the  isolation  of  the  patient  and  the  dis- 
infection of  the  stools  be  as  complete  as  possible.  The  healthy  must  be  very  care- 
ful during  an  epidemic  not  to  catch  cold,  and  to  avoid  errors  in  diet,  for  experi- 
ence shows  that  an  opposite  course  predisposes  to  the  disease. 

The  patient  must  be  kept  warm,  and  must  not  leave  his  bed,  even  if  the  attack 
be  mild.  The  diet  must  be  rigorous.  If  the  strength  is  fair,  thin  porridge,  milk, 
and  broths  suffice  for  some  days.  To  a  feebler  person  we  should  give  somewhat 
stronger  nourishment  from  the  start,  e.  g.,  eggs,  peptonized  meat,  and  wine.  Most 
patients  bear  liquids  that  are  lukewarm  better  than  those  which  are  cold. 

As  to  drugs,  the  habit  of  almost  all  experienced  physicians  is  to  give  at  first  a 
mild  laxative.  Although  opium  does  not  usually  control  the  diarrhoea  and  tenes- 
mus at  all,  it  is  the  rule  for  decided  improvement  to  follow  the  exhibition  of  the 
laxative.  During  the  first  days,  or,  if  need  be,  later,  we  give  two  to  four  table- 
spoonfuls  of  castor-oil  daily.  If  this  medicine  is  very  disagreeable  to  the  patient, 
we  can  replace  it  by  a  strong  infusion  of  rhubarb  (10-100).  In  southern  countries 
large  doses  of  calomel  (gr.  x  to  xv,  grm.  0"5-l)  are  customary,  and  are  highly 
praised  by  the  physicians  there.  Further  on  in  the  disease  we  may  content  our- 
selves with  giving  mistura  amygdalae ;  or  we  may  administer  bismuth  in  the  follow- 
ing mixture:  Bismuthi  subnit.,  parts  5;  mucilaginis  acacia?,  syrupi  simpl.,  ää  15; 
aquse  destil.,  120 — to  be  shaken  before  taking.  But  if  the  disease  should  get  worse 
again,  we  should  always  try  a  laxative. 

Emetics  at  the  beginning  of  the  disease  are  often  employed  in  the  tropics,  but 
seldom  with  us.  Ipecacuanha  {radix  antidysenterica),  given  in  large  doses  of  fif- 
teen to  thirty  grains  (1-2  grm.),  is  even  regarded  by  many  as  a  specific.  Numer- 
ous attempts  have  been  made  at  local  treatment  by  enemata.  Yet  no  brilliant 
results  can  be  claimed  for  any  of  these  methods  or  medicines.  A  decidedly  pallia- 
tive effect  can  be  obtained  from  the  injection  of  thin  starch  to  which  twenty  or 
thirty  drops  of  laudanum  have  been  added.  Suppositories  of  cocoa  butter  con- 
taining extract  of  opium  often  mitigate  the  tenesmus.  Other  injections  are  recom- 
mended, each  to  measure  §  ij  to  iijss.  (grm.  60-100),  and  to  contain  either  argenti 
nitrat.,  gr.  j  to  vj  (grm.  0-05-0-30),  or  plumbi  acetat.,  gr.  ij  to  viij  (grm.  0"l-0-5), 
or  potassii  chlorat.,  gr.  xv  to  xx  (grm.  1-1 -5).  Many  other  solutions  are  used. 
The  success  of  this  treatment  is,  however,  dubious.  In  all  cases  the  margins  of  the 
anus  must  be  protected  from  inflammation  by  frequently  washing  and  anointing 
the  skin. 

The  treatment  of  weakness  and  collapse  is  by  the  usual  stimulants — wine, 
ether,  camphor,  and  the  like.  In  chronic  dysentery  the  main  point  is  to  persevere 
in  a  strict  control  of  the  diet.  We  may  exhibit  astringents,  such  as  tannin  and 
columbo.  Subnitrate  of  bismuth  is  also  given,  and  nitrate  of  silver  and  acetate  of 
lead.  And  in  these  chronic  cases  a  long-continued  and  thorough  use  of  rectal 
irrigation  with  fluids  containing  some  mild  astringent  or  disinfectant  may  have  a 
good  effect. 

[Sporadic  dysentery  is  a  self-limited  disease,  and,  as  has  been  shown  by  Flint, 
runs  its  course  within  ten  days  without  medication.  Treatment,  however,  adds  to 
the  comfort  of  the  patient  and  shortens  the  course.  It  is  not  customary  with  us 
to  use  daily  laxatives.  If  there  is  any  doubt  as  to  whether  the  intestines  have  been 
emptied,  a  saline  should  be  given,  the  action  of  which  should  be  followed  by 
opium  in  sufficient  doses  to  allay  pain  and  tenesmus.  Subsequent  action  of  the 
bowels  is  best  obtained  by  simple  large  enemata.  In  weak  persons  castor-oil  is  to 
be  preferred  to  salines. 

In  epidemic  dysentery  active  treatment  is  much  more  important.     Laxatives 


CHOLERA.  81 

are  contra-indicated  by  sero-sangninolent  dejections  or  by  asthenia,  but  enemata 
can  be  freely  used.  Stimulation  is  often  required;  nutrition  must  be  carefully 
looked  after,  such  articles  being  chosen  as  are  digested  and  absorbed  by  the  upper 
portions  of  the  intestinal  tract,  leaving  as  little  residue  as  possible  to  pass  on  to 
the  inflamed  colon.  Opium  is  often  demanded  and  tolerated  in  large  doses,  and 
astringents,  such  as  the  acetate  of  lead,  gallic  acid,  and  the  pernitrate  of  iron,  are 
of  service. 

In  acute  dysentery  the  patient  should  be  instructed  not  to  yield  to  the  desire  to 
go  to  stool  if  he  can  help  it,  and  tenesmus  can  often  be  much  diminished  by 
simple  irrigation  of  the  lower  bowel  with  water,  which  may  be  warm  or  cold, 
whichever  the  patient  finds  more  agreeable. 

Chronic  dysentery  is  one  of  the  most  difficult  maladies  with  which  we  have  to 
deal.  In  its  treatment  a  sea  voyage,  or  removal  for  at  least  some  months  to  a 
climate  other  than  that  in  which  the  disease  originated,  is  of  far  more  value  than 
drugs. 

Amoebic  Dysentery. 

The  amoeba  coli,  first  found  by  Lösch  in  the  stools  of  a  dysenteric  patient,  has 
received  very  careful  study  at  the  Johns  Hopkins  Hospital,  and  forms  the  subject 
of  a  most  exhaustive  and  valuable  monograph  by  Councilman  and  Lafleur. 

The  living  organism  is  readily  seen,  and  recognized  especially  by  its  active 
amoeboid  movements  on  the  warm  stage  of  the  microscope.  If  the  faeces  contain 
small  gelatinous  masses,  these  will  be  found  to  provide  the  most  fruitful  field  for 
search.  The  numbers  of  the  organisms  vary  widely  in  different  cases,  and  even 
in  the  same  case,  from  day  to  day.  They  are  said  to  be  present  in  this  form  of 
dysentery  alone,  and  have  been  found  in  secondary  abscesses  of  the  liver  and  the 
lung,  alike  after  death  and  during  life.  They  should  be  sought  for  in  all  obstinate 
cases  with  dysenteric  symptoms. 

The  prognosis  is  uncertain,  and  the  cases  are  apt  to  drag  along  with  exacerba- 
tions and  remissions  of  the  symptoms.  But  recovery  does  take  place.  There  is 
notable  danger  of  the  formation  of  secondary  abscesses,  in  which  event  re- 
covery is  hardly  to  be  hoped  for.  The  only  treatment  which  seems  to  have  been 
of  much  service — beyond  a  general  hygienic  and  supportive  regimen — consists  in 
the  use  of  copious  injections  into  the  intestinal  canal  of  solutions  of  quinine, 
in  the  strength  of  one,  to  one  thousand  or  even  five  thousand.  Lösch  found  that 
contact  with  a  solution  of  the  latter  strength  for  one  minute  suffices  to  kill  the 
amoebae.] 


CHAPTER  XIII. 

CHOLERA. 

(Asiatic  Cholera.) 

Historical  Remarks.— The  home  of  genuine  Asiatic  cholera  is  India.  The  first 
epidemic  with  which  we  are  accurately  acquainted,  and  which  was  very  wide- 
spread, occurred  in  1817.  The  disease  was  probably  endemic  there  at  an  earlier 
period.  In  the  next  few  years  the  cholera  spread  in  all  directions,  and  reached 
Astrakhan  by  way  of  Persia.  Between  1830  and  1832  the  disease  made  its  first 
great  epidemic  progress  over  Europe.  Invading  all  European  Russia,  it  reached 
Germany  in  1831,  and  Prance  and  England  in  1832.  Then  came  many  smaller 
epidemics  up  to  1838,  when  there  was  a  complete  cessation  till  1816,  in  which  year 
the  disease,  again  starting  from  Asia,  overspread  Europe.  There  have  since  then 
6 


82  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

been  epidemics  in  many  places,  but  we  can  not  here  enter  into  the  particulars 
of  them.  The  last  time  that  cholei-a  occurred  to  any  extent  in  Germany  was 
in  1866,  during-  the  German-Austrian  war.  No  one  has  forgotten  the  somewhat 
violent  epidemic  which  prevailed  a  few  years  ago  (1883  and  1884)  in  France  and 
Italy. 

iEtiology. — Some  time  ago  it  had  become  evident  that  the  real  cause  of  cholera 
consists  in  the  infection  of  the  system  by  a  specific  micro-organism.  Koch  was, 
however,  the  first  to  succeed  in  the  search  for  the  poisonous  agent.  He  was  in 
charge  of  the  scientific  expedition  sent  out  by  the  German  Government  in  1883  to 
Egypt  and  India  for  the  purpose  of  investigating  the  disease.  Koch  found  in  the 
intestines  of  all  the  victims  of  cholera  whose  bodies  he  examined  a  certain  kind 
of  micro-organism  which  he  named  the  comma  bacillus.  It  is  shorter  than  the 
bacillus  of  tuberculosis,  but  somewhat  thicker,  and  it  is  usually  bent  in  the  shape 
of  a  comma,  or  even  like  a  semicircle  (see  Fig.  9).  In  the  culture-preparations, 
the  special  peculiarities  of  which  we  can  not  give  in  detail,  the  comma  bacilli 
grow  into  long  spiral  threads,  resembling  the  spirilli  of  recurrent  fever.  Exam- 
ined in  a  liquid,  the  individual  bacilli  are  seen  to  make  vigorous  movements. 
They  flourish  best  at  a  temperature  between  86°  and  104°  (30°  and  40°  C).  Below 
61°  (16°  C.)  they  cease  to  grow,  but  they  are  not  killed  even  by  a  greater  degree  of 
cold.  The  free  access  of  oxygen  is  absolutely  indispensable  to  their  growth.  They 
multiply  very  rapidly  in  liquids — e.  g.,  broth  or  milk — and  they  may,  under 
favorable  circumstances,  retain  their  vitality  for  many  weeks,  while  they  can  be 
readily  destroyed  by  desiccation.  In  this  again  they  resemble  the  genuine  spirilli, 
which  can  maintain  their  existence  only  in  fluids.  An  endogenous  formation  of 
spores,  as  we  shall  see  below  to  be  the  case  with  the  anthrax  bacilli,  does  not  take 
place,  but  Hueppe  has  established  by  actual  observation  that  frequently  two  small 
spherical  bodies  appear  on  some  indeterminate  spot  of  the  above-mentioned  spiral 
threads,  by  which  the  continuity  of  the  thread  is  interrupted.  This  process  goes 
on  until  finally  the  thread  is  replaced  by  a  considerable  number  of  very  minute 
round  cells,  which  are  apparently  united  to  one  another  by  a  kind  of  jelly  (forma- 
tion of  zoöglcea).  It  is  certain  that  the  round  cells  do  not  subdivide.  The  way 
in  which  they  are  formed  corresponds  with  quite  similar  processes  in  other  spiro- 
chaetae.  They  are  called  "  arthrospores,"  and  perhaps  represent  a  permanent  form 
of  the  comma  bacilli ;  for  they  resist  desiccation  and  other  injurious  influences 
much  better  than  do  the  comma  bacilli  themselves.  By  a  process  of  growth  the 
spherical  bodies  may,  under  favorable  circumstances,  give  rise  in  their  turn  to 
new  comma  bacilli. 

These  discoveries  of  Koch  have  since  been  confirmed  by  all  competent  investi- 
gators, while  the  various  alleged  refutations  of  Koch's  results  have  proved  errone- 
ous. It  has  been  shown  that  in  every  case  of  genuine  Asiatic  cholera  the  comma 
bacilli  are  present  in  the  intestine,  and  that  they  are  never  found  under  any  other 
circumstances.  Even  the  last  postulate  which  was  needed  to  show  their  patho- 
genic significance  has  been  fulfilled.  Rietsch  and  Nicati,  followed  by  Koch  him- 
self, have  succeeded  in  producing  cholera  in  a  guinea-pig  by  introducing  into  its 
duodenum  pure  comma  bacilli. 

Investigation  as  to  the  origin  of  cholera  must,  therefore,  now  meet  this  culmi- 
nating question:  Under  what  circumstances  and  through  what  channel  do  the 
comma  bacilli  penetrate  into  the  human  system,  and  in  what  manner  do  they 
there  excite  the  characteristic  processes  of  the  disease?  There  can  be  no  doubt 
that  among  us  Europeans,  and  probably  everywhere  except  in  India,  the  cholera 
is  invariably  imported.  It  is  equally  certain  that  the  dejections  of  cholera  patients, 
which  are  rich  in  comma  bacilli,  are  the  chief  if  not  the  only  agent  by  which  the 
disease  is  spread.     The  bacilli  which  escape  into  the  outer  world  with  the  stools 


I  > 


CHOLERA.  83 

find  abundant  means  to  prolong1  their  existence.  They  continue  their  growth 
upon  moistened  bed-clothes,  or  in  water  which  contains  a  sufficient  amount  of 
organic  substances,  or  in  food,  such  as  fruit  or  milk,  or  in  moist  earth  ;  and  the 
ways  by  which  they  can  in  turn  enter  the  system  of  a  healthy  human  being  are 
infinite  in  number.  It  is  easy  to  under- 
stand why  certain  persons — e.  g.,  laundress- 
es and  nurses — are  more  liable  to  infection 
than  others;  and  it  is  equally  intelligible 
that  the  spread  of  the  disease  should  often 
bear  a  relation  to  certain  outward  circum- 
stances. The  fact  has  long  been  a  familar 
one,  that  the  cholera  almost  always  pro- 
gresses along  the  world's  most  frequented 
highways,  and  that  it  never  travels  faster 
than  the  means  of  human  intercommunica-  „  1(1 ",'  %'\<fö,  j>  Y 
tion  render  possible.  This  is  important,  ~~7\Ti •^'^> n,  j ■ 
because  it  shows  plainly  that  the  germs  of  1/ ji'^'«'}' 
the  disease  are  not  disseminated  by  currents 
of  air.  It  is  easy  to  understand  that  the 
distribution  of  the  disease  should  sometimes 
correspond  with  that  of  water  destined  for 
personal  use.  Apparently  in  every  case  the  Fl%hVe£TjeÄVaMÄ^^ 
disease-producing  poison  enters  the  intesti-         days  on  a  wet  cloth.    The  .s-shaped  bacilli 

i  1  -it  i-  i  areata.    600  diameters. 

nal  canal,  for  the  comma  bacilli  are  found 

exclusively  in  the  intestine,  never  in  the  other  internal  viscera;  and  this  is  true 
not  only  in  the  early  but  also  in  the  later  stages  of  the  disease.  We  must 
therefore  suppose  that  the  bacilli  are  swallowed,  and,  if  not  destroyed  by  the 
gastric  juice,  develop  their  pathogenic  functions  in  the  intestine.  In  apparent 
agreement  with  this  is  the  frequently  observed  fact  that  gastric  catarrh,  however 
acquired,  existing  at  the  time  of  an  epidemic,  always  predisposes  to  the  disease. 

The  views  thus  far  expressed  are  opposed  by  Pettenkofer.  He  ascribes  to  the 
condition  of  the  soil,  varying  with  time  and  place,  the  chief  role  in  the  spread  of 
cholera.  He  doubts  whether  the  poison  as  contained  in  the  stools  is  as  yet  effi- 
cient. It  must,  he  thinks,  undergo  further  development  in  an  appropriate  soil 
before  it  can  acquire  fresh  pathogenic  potency.  His  main  argument  is  drawn 
from  the  fact  that  certain  places,  particularly  those  on  rocky  soil,  enjoy  immu- 
nity; the  rarity  of  attacks  upon  shipboard  is  analogous.  He  points  out  that  in 
cholera  as  well  as  in  typhoid  (q.  v.)  there  is  an  evident  harmony  between  the 
frequency  of  the  disease  and  the  varying  stand  of  the  water  which  underlies  the 
surface  of  the  ground.  Further  investigations,  which  will  now  for  the  first  time 
have  a  firm  foundation,  afforded  by  the  discovery  of  the  comma  bacillus,  must 
decide  how  much  influence  the  condition  of  the  soil  does  exert  upon  the  dissemi- 
nation of  the  pathogenic  poison.  As  it  is,  we  feel  certain  that  to  give  exclusive 
prominence  to  the  condition  of  the  soil,  and  to  deny  the  possibility  of  infection  in 
any  other  way,  is  to  put  a  violent  interpretation  upon  the  observed  facts ;  while 
the  correctness  of  the  above-stated  views  of  Koch  is  becoming  more  and  more 
probable.  With  regard  to  the  constant  presence  of  other  micro-organisms  than 
the  comma  bacilli  in  the  intestine  and  the  internal  viscera  of  the  victims  of  cholera, 
as  claimed  by  Emmerich  and  others,  we  must  regard  them  as  associated  appear- 
ances which  have  nothing  to  do  with  the  true  choleraic  process. 

Most  cholera  epidemics  happen  in  the  months  of  summer.  Liability  to  the  dis- 
ease is  very  wide-spread,  although  some  remarkable  exceptions  are  seen.  Sex  is 
unimportant.      Age  has  more  influence.      The  disease  occurs  in  sucklings,  but, 


81  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

as  a  rule,  is  more  rare  among  children  than  among  adults.  Elderly  people  are 
very  apt  to  take  the  disease,  while  of  typhoid  fever  the  opposite  is  true.  Most 
authors  lay  great  stress  upon  predisposing  causes.  Among  these,  taking  cold 
is  not  so  important  as  are  errors  in  diet  and  mild  attacks  of  gastro-intestinal 
catarrh,  which  are  shown  by  numerous  observations  to  predispose  strongly  to 
the  disease  {vide  sup?*a).  The  stage  of  incubation  seldom  lasts  over  one  to  three 
days. 

Clinical  History.— As  is  the  case  in  most  acute  infectious  diseases,  the  intensity 
of  the  illness  varies  between  the  extremes  of  mildness  and  severity,  so  that  usually 
a  correct  interpretation  of  the  mildest  cases  is  rendered  possible  only  by  the  fact 
that  an  epidemic  exists.  These  insignificant  cases  are  called  simple  choleraic 
diarrhoea.  The  symptoms  are  those  of  a  violent  acute  intestinal  catarrh;  the 
dejections  are  watery,  rather  large,  painless,  and  number  about  three  to  eight  in 
twenty-four  hours.  There  is  considerable  malaise,  complete  anorexia,  and  thirst, 
and  there  may  already  be  indications  of  severer  choleraic  symptoms — vomiting, 
slight  pains  in  the  calves  of  the  legs,  and  diminished  secretion  of  urine.  Many 
cases  recover  after  a  few  days  or  a  week,  but  in  others  the  first  mild  diarrhoea 
is  succeeded,  at  the  end  of  about  one  to  three  days,  or  rarely  later  still,  by  a 
severe  attack  of  cholera.  In  such  cases  we  speak  of  a  "  premonitory  diarrhoea  of 
cholera." 

The  mild  forai  is  succeeded  in  a  gradual  transition  by  the  cases  designated 
as  "cholerine."  Cholerine  exhibits  the  symptoms  of  a  violent,  rather  sudden 
cholera  morbus.  It  often  begins  at  night.  To  the  diarrhoea,  which  now  and  then 
displays  even  at  this  time  the  characteristics  of  pronounced  cholera,  vomiting  is 
soon  added.  The  accompanying  constitutional  symptoms  are  rather  severe.  There 
is  great  languor  and  depression.  The  voice  grows  weak,  the  extremities  are  cool, 
the  pulse  is  small  and  accelerated,  painful  cramps  occur  in  the  calves  of  the  legs, 
the  urine  grows  scanty  and  perhaps  albuminous.  The  whole  attack  lasts  about  a 
week  or  two,  till  recovery  is  complete.  The  course  of  the  disease  is  not  infre- 
quently varied  by  repeated  improvements  and  relapses. 

From  these  cases  of  medium  severity  there  is  again  a  continuous  line  of  transi- 
tion to  the  pronounced  severe  form  of  cholera  proper.  Statistics  as  to  the  fre- 
quency of  the  separate  forms  can  not  be  given,  since  many  of  the  milder  cases 
escape  observation. 

The  true  attack  of  cholera  may  begin  suddenly  with  the  severest  symptoms. 
As  a  rule,  however,  it  is  preceded,  as  already  stated,  by  a  first  stage  of  brief  pre- 
monitory diarrhoea.  This,  after  one  to  three  days,  is  replaced  with  equal  sudden- 
ness by  the  severe  symptoms  of  the  second  or  "  algid  stage,"  or  "  cholera  asphyxia." 
Its  first  symptoms  are  the  abrupt  appearance  of  great  bodily  weakness,  chilliness, 
and  vertigo.  The  characteristic  gastro-intestinal  symptoms  soon  declare  them- 
selves. 

The  diarrhoea  grows  very  violent.  At  short  intervals  there  are  copious  painless 
dejections,  which  at  first  retain  somewhat  "of  a  feculent  character,  but  very  soon 
present  a  characteristic  resemblance  to  "  rice-water"  or  "whey."  A  single  stool 
will  measure  a  little  less  than  half  a  pint  (grm.  200).  The  stools  have  no  color  and 
almost  no  odor.  They  are  watery,  and  usually  deposit  a  finely  granular,  grayish- 
white  sediment  upon  standing.  Their  reaction  is  neutral  or  alkaline.  Only  one 
or  two  per  cent,  is  solid  matter,  with  a  little  albumen  and  a  relatively  large  amount 
of  sodic  chloride.  In  many  severe  cases  the  dejections  contain  more  or  less  blood. 
The  microscope  reveals  epithelium,  triple  phosphate,  and  numerous  micro-organ- 
isms. Of  these  last  a  part  are  the  comma  bacilli,  and  a  part  are  bacteria  of  putrefac- 
tion, etc.  If  the  comma  bacilli  be  demonstrated,  of  course  the  diagnosis  is  absolute. 
To  accomplish  this  we  take  a  coagulum  of  mucus  from  the  stool,  and,  spreading  it 


CHOLERA.  85 

upon  a  cover-glass  in  as  thin  a  layer  as  possible,  carefully  warm  the  glass  by  pass- 
ing it  repeatedly  through  a  flame,  in  order  to  dry  the  mucus  and  fix  it  in  its  place. 
The  preparation  is  then  stained  with  an  aqueous  solution  of  methyl  blue.  If  the 
bacilli  be  very  abundant,  the  microscopic  examination  suffices  for  their  demon- 
stration, although  complete  certainty  about  their  identity  depends  upon  their 
behavior  in  pure  culture-preparations.  These  must  therefore  be  instituted  in  all 
doubtful  cases ;  but  it  would  lead  us  too  far  if  we  entered  upon  the  particulars 
relating  to  such  cultures. 

These  excessive  evacuations  are  but  very  rarely  absent  or  nearly  absent. 
They  are  more  apt  to  fail  if  death  occurs  at  the  end  of  a  few  hours — cholera  sicca. 

[In  cholera  sicca  the  intestines  after  death  contain  the  characteristic  rice-water 
material  which,  perhaps  owing  to  paralysis  of  the  muscular  coat,  was  not  expelled 
during  life.] 

The  appearance  of  the  diarrhoea  is  soon  followed  by  frequent  though  rarely 
distressing  vomiting.  The  vomitus  consists  in  part  of  ingested  liquids  and  in  part 
of  an  actual  transudation  through  the  mucous  membrane  of  the  stomach  and  intes- 
tine.    Hiccoughs  may  accompany  and  follow  the  emesis. 

In  addition  to  these  prominent  digestive  symptoms  of  vomiting  and  profuse 
diarrhoea  there  are  complete  anorexia  and  excessive  thirst.  The  tongue  has  a  thick, 
dry  coat.  The  abdomen  is  usually  flat  and  soft,  or  it  may  be  concave  and  hard. 
Sometimes  we  may  feel  fluctuation  in  the  intestines,  due  to  their  being  filled  with 
fluid.  There  is  not  much  real  abdominal  pain ;  what  there  is,  is  described  as  a 
"  feeling  of  heat  and  pressure  "  around  the  umbilicus. 

At  the  same  time  very  severe  symptoms  develop  in  other  organs.  The  circu- 
latory system  is  chiefly  affected. 

The  action  of  the  heart  may  be  stimulated  at  the  beginning  of  the  attack.  The 
patient  complains  of  palpitation  and  great  precordial  anxiety.  After  a  brief  time, 
however,  cardiac  weakness  appears,  and  continually  increases.  The  action  of  the 
heart  becomes  very  weak,  and  the  heart-sounds  feebler  and  feebler.  The  pulse  at 
the  wrist  grows  very  small,  and  is  usually  somewhat  accelerated.  In  a  severe  case 
the  pulse  vanishes  completely  after  a  few  hours. 

This  collapse  of  circulation  makes  itself  quickly  evident  in  the  appearance  of 
the  patient.  The  face  and  extremities  grow  cool,  and  then  ice-cold ;  the  complex- 
ion becomes  partly  livid  and  partly  a  bluish  gray;  the  lips  are  almost  black.  The 
surface  temperature  may  fall  below  95°  (35°  C),  while  in  the  rectum  febrile  tem- 
peratures may  often  be  observed,  reaching  102°  (39°  C.)  and  higher.  The  eye  and 
cheek  grow  very  hollow,  the  skin  becomes  wrinkled,  and  loses  all  its  elasticity. 
The  voice  grows  hoarse  and  feeble  (voice  of  cholera).  Respiration  is  laborious 
and  superficial.  The  mind  may  remain  unclouded  to  the  end,  but  usually  there  is 
great  apathy,  and  all  acuteness  of  perception  is  impaired.  But  few  patients  are 
restless  and  excited.     Reflex  action  is  much  impaired. 

One  characteristic  symptom  is  the  cramps  in  the  muscles.  These  are  usually 
very  painful,  and  consist  in  tonic  contractions  of  the  muscles,  particularly  those 
of  the  calf  of  the  leg,  but  also  those  of  the  toes,  thighs,  arms,  and  hands.  The 
cramps  occur  spontaneously  or  upon  the  least  provocation,  last  a  few  minutes,  and 
recur  at  short  intervals.  The  precise  reason  of  their  occurrence  is  not  yet  known. 
It  may  be  the  effect  of  poison  (vide  infra).  They  can  be  observed  in  other  severe 
acute  diseases,  although  most  marked  in  cholera.  They  sometimes  occur  in  cholera 
morbus. 

In  a  well-developed  attack  of  cholera  there  is  almost  invariably  oliguria  or 
anuria.  The  urine,  if  any  be  secreted,  is  concentrated,  with  abundant  sediment, 
and  very  often  contains  albumen.  In  many  cases  not  one  drop  of  urine  reaches 
the  bladder  for  days,  and  this  condition  persists  till  death  or  recovery. 


86  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

The  symptoms  thus  far  depicted,  if  taken  as  a  whole,  represent  the  algid  stage, 
which  seldom  lasts  more  than  one  or  two  days.  In  many  cases  death  occurs 
during  this  period.  It  is  ushered  in  by  the  tokens  of  extreme  general  prostration, 
and  may  take  place  after  a  few  hours,  or  more  frequently  in  the  second  half  of  the 
first  day.  But  in  other  cases  the  "  stage  of  reaction  "  succeeds.  This  may  he  a 
true  compensatory  period,  leading  directly  to  convalescence.  The  evacuations 
become  less  frequent  and  more  feculent,  and  the  vomiting  ceases.  The  pulse 
becomes  stronger,  the  cyanosis  and  coolness  of  the  extremities  diminish,  and  an 
abundant  perspiration  is  not  infrequent.  After  a  few  days  urine  is  again  excreted, 
which  is  almost  invariably  quite  albuminous,  and  usually  contains  casts  and  red 
blood-globules.  If  convalescence  be  uninterrupted,  however,  the  urine  very  soon 
becomes  perfectly  normal,  and  after  a  week  or  two  the  patient  is  to  be  regarded  as 
completely  recovered. 

Departures  from  this  favorable  course  of  the  stage  of  reaction  are  frequent. 
Recovery  may  be  interrupted  by  repeated  relapses  into  the  previous  condition,  and 
sometimes  with  a  fatal  result.  Or,  instead  of  convalescence,  there  is  developed  a 
severe  third  stage,  usually  with  fever.  This  stage  ordinarily  bears  the  generic 
name  of  cholera  typhoid,  although  it  is  subject  to  manifold  variations  in  its  clin- 
ical symptoms  as  well  as  its  exciting  causes. 

Cholera  typhoid  may  present  an  actually  typhoidal  general  condition  with 
severe  fever.  There  is  a  considerable  elevation  of  temperature,  headache,  and 
dullness.  The  pulse  is  full  and  rapid,  the  face  flushed.  The  skin,  particularly 
that  of  the  extremities,  sometimes  presents  the  so-called  choleraic  eruption,  in  the 
form  of  an  erythema,  roseola,  urticaria,  or  the  like.  This  variety  of  cholera 
typhoid  ends  after  a  few  days  in  recovery,  or  else  passes  into  one  of  the  following 
conditions. 

A  second  form  of  cholera  typhoid  is  distinguished  by  the  development  of  the 
most  diverse  local  inflammations.  Thus,  there  may  be  a  severe  dysenteric  or  diph- 
theritic inflammation  of  the  small  and  large  intestine,  attended  by  offensive  puru- 
lent and  bloody  stools.  Pneumonia  is  also  possible,  as  well  as  purulent  bronchitis, 
diphtheritic  inflammation  of  the  larynx,  pharynx,  bladder,  and  female  genitals, 
parotitis,  and  sometimes  erysipelas  and  pyaemia.  And  when  we  consider  that, 
besides  all  these  conditions,  the  usual  intestinal  symptoms,  or  those  of  choleraic 
nephritis,  may  exist  also,  it  is  evident  how  varied  the  clinical  picture  may  be. 
The  development  of  these  local  affections  frequently  lays  the  foundation  for 
numerous  sequelae. 

Choleraic  nephritis  gives  rise  to  the  third  or  uraemic  variety  of  cholera  typhoid. 
The  secretion  of  urine  is  almost  suspended.  The  little  that  is  still  passed  contains 
numerous  casts,  albumen,  and  frequently  renal  epithelium  and  white  and  red 
blood-globules.  Somewhere  toward  the  end  of  the  first  week,  or  possibly  earlier, 
there  are  grave  nervous  symptoms,  to  be  regarded  as  uraemic :  first  there  is  head- 
ache and  vomiting,  then  sopor  and  coma,  or  delirium  and  convulsions.  Most  of 
these  cases  are  fatal. 

Pathology. — We  are  now  acquainted  with  the  manifold  symptoms  and  varieties 
of  the  disease.  If  we  seek  for  the  pathological  changes  which  control  the  process, 
and  endeavor  to  find  some  correspondence  between  them  and  the  symptoms,  we 
shall  be  disappointed.  At  least,  in  its  early  stages,  cholera  is  merely  a  severe  local 
disease  of  the  intestine.  We  find  the  serous  layer  of  the  coils  of  the  small  intes- 
tine rose-red  from  congestion.  The  mucous  membrane  is  in  a  state  of  catarrhal 
inflammation:  it  is  swollen,  reddened,  and  at  first  covered  with  a  layer  of  tough, 
transparent  mucus ;  but  very  soon  an  abundant  transudation  flows  into  the  canal, 
so  that  the  intestinal  coils  are  filled  with  a  large  amount  of  clear  fluid,  looking 
like  "  rice-water  "  or  "  gruel,"  and  so  devoid  of  bile  as  to  indicate  the  suspension  of 


CHOLERA.  87 

its  secretion.  The  signs  of  inflammation  of  the  mucous  membrane  now  grow  more 
pronounced.  The  solitary  follicles  and  Peyer's  patches  become  swollen,  with 
edges  of  a  vivid  red,  and  frequently  there  are  many  small  ecchymoses  in  the 
mucous  membrane.  The  extensive  desquamation  of  the  epithelial  lining  of  the 
intestine  has  also  been  regarded  as  important,  because  it  was  regarded  as  in  part 
the  cause  of  the  copious  transudation.  Still  it  may  be  questioned  whether  the 
desquamation  is  not,  at  least  to  some  extent,  a  post-mortem  change.  In  yet  later 
stages  of  the  disease  the  intestinal  trouble  very  frequently  assumes  a  croupous- 
diphtheritic  character.  The  surface  is  necrosed  and  ulcerated  in  many  places,  and 
the  contents  of  the  intestine  are  no  longer  colorless,  but  sanious  and  bloody,  with  a 
foul  odor. 

Otherwise  most  of  the  post-mortem  lesions  correspond  to  what  was  obvious 
at  the  bedside.  The  muscles  exhibit  an  early  and  persistent  rigor  mortis,  and  fre- 
quently contract  in  such  a  way  as  to  throw  the  corpse  into  some  unusual  posture. 
All  the  internal  organs  are  remarkably  dry,  pale,  and  anaämic.  The  left  ventricle 
is  contracted.  The  blood  lies  mostly  in  the  large  veins,  the  right  side  of  the 
heart,  and  the  cerebral  sinuses.  It  is  thickened,  is  but  little  clotted,  and  is  said  to 
resemble  the  juice  of  bilberries  or  huckleberries.  The  spleen  is  not  enlarged— an 
exception  to  the  rule  in  infectious  diseases.  The  kidneys  present  marked  passive 
congestion,  most  pronounced  in  the  cortex.  The  microscope  reveals  a  greater  or 
less  degree  of  parenchymatous  nephritis,  with  great  destruction  of  the  epithelium. 
If  death  takes  place  at  a  rather  advanced  stage  of  the  disease,  the  tissues  have  lost 
their  characteristic  dryness,  and  the  most  diverse  local  lesions,  including  nephri- 
tis, may  be  found  to  have  occasioned  death. 

If  we  search  for  the  connection  between  the  pathological  changes  just  de- 
scribed and  the  cause  of  the  disease,  or  again  between  these  lesions  and  the  clini- 
cal symptoms,  the  first  point  to  guide  us  is  that  the  comma  bacilli  are  found 
only  in  the  lumen  of  the  intestine,  and  never  in  the  blood  or  in  other  parts  of 
the  body.  The  intestinal  symptoms  are  satisfactorily  explained  by  this  abnor- 
mal state  of  the  intestine,  but  for  all  the  other  grave  symptoms  we  have  to 
seek  some  special  cause.  The  desiccation  which  the  body  undergoes  as  a  result 
of  the  excessive  liquid  dejections  can  not  fail  to  affect  the  tissues,  but  can  not 
fully  explain  the  symptoms,  for  at  least  the  circulatory  disturbances  and  the 
cardiac  failure  may  develop  before  large  evacuations  have  occurred.  It  has  also 
been  settled  beyond  question  by  means  of  the  newer  investigations  that  precisely 
the  worst  symptoms  of  cholera,  namely,  the  muscular  cramps,  the  subnormal  tem- 
perature, and  the  changes  in  the  blood,  are  occasioned  by  the  chemical  results  of 
tissue  metamorphosis  in  the  comma  bacilli,  that  is,  by  the  so-called  toxines. 
Many  of  these  have  been  already  isolated  chemically  by  Brieger.  In  this  connec- 
tion the  fact  discovered  by  Hueppe  is  of  the  greatest  interest,  that  the  lack  of 
oxygen  which  the  bacilli  in  the  intestinal  canal  must  experience  favors  the 
abundant  production  of  toxines. 

As  to  the  complications  which  occur  in  the  later  stages  of  the  disease  and  which 
are  embraced  under  the  generic  name  of  cholera  typhoid,  we  regard  them  as 
mainly  secondary.  The  choleraic  process  itself  does  not  cause  them,  hut  is  merely 
the  occasion  for  their  appearance.  The  examination  of  the  intestine  in  such  cases 
shows  that  numerous  other  varieties  of  bacteria  follow  closely  upon  the  comma 
bacillus,  gaining  entrance  to  the  system  by  treading  in  its  footsteps. 

The  diagnosis  of  a  pronounced  case  of  cholera  has  no  difficulties  at  the  time  of 
an  epidemic.  We  must  always  he  somewhat  cautious  about  sporadic  cases,  for 
violent  intestinal  disturbance,  simulating  perfectly  the  milder  forms  of  cholera, 
may  he  excited  by  other  causes.  In  this  connection  we  should  mention  the 
cholera  morbus  common  among  us;  and  poisoning,  particularly  acute  arsenical 


88  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

poisoning,  may  give  rise  to  symptoms  wonderfully  like  cholera.  But  now  that 
Koch's  discovery  has  been  made,  the  diagnosis  of  all  such  doubtful  cases  becomes 
perfectly  certain  if  we  can  demonstrate  the  presence  of  comma  bacilli  in  the 
stools  {vide  supra).  We  have  no  doubt  that  this  demonstration  will  also  lead 
us  to  a  decisive  conclusion  as  to  the  ^etiological  importance  of  mild  choleraic 
attacks. 

The  prognosis  should  always  be  guarded  at  the  beginning,  even  if  the  symptoms 
be  mild,  for,  as  already  mentioned,  a  simple  diarrhoea  may  prove  to  be  "  premon- 
itory "  of  a  severe  attack  of  cholera.  During  the  real  attack  the  prognosis  grows 
graver  in  proportion  as  the  case  presents  the  characteristics  of  asphyxia  and 
cyanosis.  The  mortality  in  many  epidemics  is  frightful.  All  the  inhabitants  of  a 
bouse  or  street  may  in  a  brief  period  be  swept  away.  Minute  statistics  are  diffi- 
cult to  give.  If  we  count  the  typical  cases  alone,  the  mortality  is  not  infrequently 
fifty  to  seventy  per  cent.  In  about  two  thirds  of  the  fatal  cases  death  occurs  during 
the  first  days  of  the  stage  of  asphyxia,  and  in  about  one  third  during  the  second 
period,  known  as  "  cholera  typhoid."  The  influence  of  the  diet  and  the  hygienic 
surroundings  of  the  patient  before  his  illness  is  important.  A  greater  proportion 
of  children  and  old  people  perish  than  of  the  middle-aged. 

Treatment.— The  measures  to  be  taken  to  prevent  the  spread  of  the  disease, 
when  it  has  once  started  in  a  place,  we  can  not  here  discuss.  We  can  merely  say 
that  the  greatest  care  should  be  taken  to  have  the  ingesta  pure,  particularly  the 
milk  and  water,  that  the  further  extension  of  the  disease  may  be  hindered  simply 
by  isolating  the  localities  attacked  as  completely  as  possible,  or  at  least  regulating 
intercourse  with  them  very  strictly.  We  must  try  to  prevent  the  communication 
of  the  disease  by  isolating  individuals  attacked,  and  by  disinfecting  the  dejections 
with  five-per-cent.  carbolic  solution,  and  likewise  disinfecting  everything  that 
may  have  been  contaminated  by  the  excreta,  such  as  linen  and  bed-clothes,  for 
which  dry  heat  is  the  agent.  We  must  content  ourselves  with  a  brief  mention  of 
these  facts.  It  is  very  important  to  disinfect  the  stools  as  promptly  as  possible, 
since  Wood  has  discovered  the  remarkable  fact  that  the  cholera  bacilli  in  the 
intestine,  because  of  the  lack  of  oxygen  there,  become  much  more  sensitive  to  ex- 
ternal influences  although  they  produce  more  toxine,  as  stated  above.  Individual 
prophylaxis  is  of  the  greatest  importance.  It  has  been  proved  again  and  again 
that  a  mild  intestinal  catarrh  will  predispose  to  cholera,  and  will  aggravate  the 
attack  if  cholera  does  occur;  so  that  the  slightest  gastric  or  intestinal  disturbance 
at  the  time  of  an  epidemic  of  cholera  demands  the  greatest  attention  both  as  to 
diet  and  medicine.  We  may  well  quote  from  the  last  proclamation  of  the  Prus- 
sian Department  of  Public  Improvement  (Cultusministerium),  that,  "by  exercising 
and  promoting  cleanliness  and  moderation,  each  person  will  not  only  best  pro- 
tect himself,  but  also  most  efficiently  support  the  efforts  of  the  authorities  in 
behalf  of  the  common  weal." 

[The  vital  importance  of  the  serious  treatment  of  a  beginning  diarrhoea  during 
a  cholera  epidemic  can  not  be  too  strongly  insisted  on.  Rest,  simple  diet,  and  a 
little  medication  will,  in  the  vast  majority  of  instances,  entirely  prevent  serious 
consequences.  The  apparently  trifling  character  of  the  symptoms  is  apt  to  lead 
people  into  a  false  security.  Those  who  can  leave  an  infected  district  should  do 
so  without  delay. 

With  reference  to  the  prevention  of  an  epidemic,  a  pure  water  supply  and 
strict  cleanliness  in  its  broad  sense  possess  far  more  virtue  than  cordons  of  troops 
or  measures  of  quarantine.  It  is  more  practicable  to  destroy  the  soil  than  to  keep 
out  the  seed  in  these  days  of  constant  and  rapid  international  communication.  The 
systematic  disinfection  of  all  cholera  discharges  or  articles  soiled  by  them  should 
be  a  matter  of  course.] 


CHOLERA. 


89 


The  drug  chiefly  used  at  the  beginning  of  cholera  is  opium,  which  forms  the 
chief  constituent  of  the  various  "'cholera  drops."  The  best  form  is  the  tincture,  in 
doses  of  ten  to  twenty  drops,  or  gr.  \  to  j  (0'03-0'05  grm.)  of  powdered  opium, 
repeated  every  two  or  three  hours.  A  more  complicated  formula  is:  Tr.  opii,  1 
grm. ;  vin.  ipecac,  3;  tr.  valerian,  aeth.  [P.  G. :  valer.,  part  1  ;  sps.  setheris,  5],  10; 
ol.  menth.  pip.,  gtt.  v.  M.  S. ;  Twenty  to  thirty  drops.  Or  we  may  give  tinctura 
opii  benzoica  [an  elixir  of  which  two  hundred  parts  contain  one  part  of  opium 
four  of  benzoic  acid,  and  two  parts  each  of  camphor  and  oil  of  anise]. 

The  opium  treatment  approved  itself  in  the  last  epidemic,  although  a  few 
physicians  regard  it  as  irrational,  and  prefer  to  give  at  the  beginning  of  the  disease 
one  or  two  good-sized  doses  of  calomel  (gr.  v  to  viij,  grm.  0'3  to  0'5).  Cantani  and 
other  Italian  physicians  praise  highly  enemata  of  a  solution  of  tannin  (warm 
water,  previously  boiled,  two  quarts  (2,000  grammes);  tannin,  gr.  xlv-xc  (3'0-6'0); 
acaciae,  §  i j  (50-0);  tinct.  opii,  gtt.  30-50)  or  some  disinfectant.  Hueppe  advises 
large  doses  of  salol  internally. 

When  the  attack  is  fully  developed  we  usually  continue  the  use  of  opium. 
The  patient  is  wrapped  up  in  warm  blankets  and  subjected  to  friction ;  or  warm 
oil  may  be  rubbed  into  the  skin.  Hot  tea  may  be  given,  or  strong  coffee,  or  broth, 
or  mulled  w^ine.  Hot  baths,  to  which  mustard  may  be  added,  have  proved  bene- 
ficial in  repeated  instances.  Vomiting  is  to  be  controlled  by  morphine  or  ice. 
The  painful  cramps  in  the  calf  of  the  leg  require  subcutaneous  injections  of 
morphine.  The  feebler  the  action  of  the  heart  becomes,  the  more  energetic  must 
be  the  stimulants  employed.  We  may  give  champagne,  or  inject  camphor  or  ether. 
The  attempt  has  been  made  again  and  again  to  make  good  the  loss  of  fluid  by 
injecting  a  solution  of  common  salt  beneath  the  skin  or  into  the  veins.  Samuel 
recommends  for  this  purpose  a  solution  containing  six  parts  of  sodic  chloride  and 
one  part  of  sodic  carbonate  in  one  thousand  parts  of  water,  at  a  temperature  of 
about  100°  (38°  C).  Finally,  injections  have  been  made  into  the  peritoneal  cavity 
of  a  0-5  per  cent,  solution  of  sodic  chloride,  or  in  other  cases  of  a  0'3  per  cent, 
solution  of  sodic  carbonate,  and,  it  is  claimed,  with  benefit. 

Great  caution  must  be  exercised  about  the  diet,  not  merely  during  the  attack 
itself,  but  for  a  considerable  time  afterward.  At  first  we  can  allow  only  thin  por- 
ridge, milk  broths,  and  possibly  a  soda  biscuit.  It  is  advisable  to  administer  dilute 
hydrochloric  acid  with  the  food. 

The  treatment  of  cholera  typhoid  varies  greatly,  of  course,  according  to  the 
kind  of  attack.  The  separate  affections  should  receive  their  customary  treatment. 
[In  the  first  stage,  absolute  rest,  opium,  and  lumps  of  ice  by  the  mouth  ad  libi- 
tum are  the  chief  measures  on  which  reliance  is  to  be  placed.  It  should  be  remem- 
bered that  the  entire  function  of  the  intestinal  tract  is  reversed ;  thus,  instead  of 
an  absorbing,  it  has  become  an  excreting  surface. 

In  the  stage  of  collapse  the  nervous  system  is  more  or  less  paralyzed,  the  blood 
is  damaged  by  the  loss  of  its  watery  constituents,  and  the  circulation  of  that  fluid 
is  greatly  impeded.  The  subcutaneous  or  gastric  absorption  of  chugs  is  conse- 
quently delayed  or  suspended.  The  utility  of  any  active  internal  treatment  dur- 
ing this  stage  is  very  questionable.  Certainly  narcotism  by  opium  is  highly  un- 
desirable. Mild  external  stimulation  and  the  tentative  administration  of  ice  and 
small  quantities  of  champagne  or  food  are,  at  all  events,  not  likely  to  do  harm. 
Nature  sometimes  reasserts  herself  when  the  conditions  are  seemingly  desperate. 
and  the  third  stage,  or  that  of  reaction,  comes  on.  In  this  stage,  careful  nursing 
and  a  sensible  symptomatic  but  in  no  way  meddlesome  treatment  are  most  like- 
ly to  be  followed  by  good  results.] 


90  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

CHAPTER  XIV. 

MALARIAL   DISEASES. 

{Intermittent  Fever.     Fever  and  Ague.     Swamp  Fever.) 

iEtiology  and  Pathological  Anatomy.— Malarial  poisoning  is  the  best  example 
of  a  purely  "  miasmatic "  affection.  The  poison  which  produces  the  disease  is 
without  doubt  localized  in  certain  places,  in  which  every  human  being  is  liable  to 
become  its  victim.  But  if  an  infected  person  comes  to  a  place  free  from  malaria 
and  not  naturally  favorable  to  its  development,  there  is  no  danger  that  he  will 
cause  the  disease  in  others.  The  disease  is  never  caught  through  contact  with  the 
patient.  It  is  not  at  all  contagious ;  the  malarial  poison,  after  it  has  once  pene- 
trated into  the  body,  has  practically  no  opportunity  to  escape  again  in  an  efficient 
form  from  the  diseased  system  into  the  outer  world.  But  the  blood  of  a  patient 
injected  into  a  healthy  person  may  transfer  the  disease  (Gerhardt  and  others). 

If  we  except  the  polar  zones,  there  are  few  regions  where  malaria  is  not  endem- 
ic in  certain  parts,  at  least  from  time  to  time,  if  not  constantly.  There  is,  how- 
ever, great  variation  in  the  virulence  as  well  as  in  the  number  of  cases.  While  the 
common  forms  of  intermittent  fever  are  very  frequent  in  Germany,  in  numerous 
places,  yet  the  grave  forms  of  the  disease  are  very  rare.  Other  lands  are  notorious 
for  the  severe  malarial  diseases,  e.  g.,  Hungary,  the  lands  lying  on  the  lower 
Danube,  the  Roman  Campagna,  the  Pontine  marshes,  Sicily,  and  numerous  dis- 
tricts in  other  parts  of  the  world,  chiefly  tropical.  Numerous  observations  have 
only  served  to  confirm  the  statement  that  the  soil  is  the  true  home  and  cradle  of 
the  malarial  poison,  and  that  the  virus,  escaping  thence  into  the  lower  strata  of 
the  atmosphere,  may  be  taken  into  the  system,  probably  during  inspiration.  Per- 
manent dampness  of  the  soil  is  essential  to  the  development  of  the  malarial  poison. 
This  explains  why  marshy  districts  are  so  often  malarial.  The  ground  must  not 
be  covered  by  a  great  amount  of  water,  but  must  during  the  dry  season  lie  ex- 
posed to  the  atmospheric  air.  The  access  of  air  to  the  moist  soil  seems  to  be  a 
second  essential  condition  for  the  development  of  the  malarial  germs.  A  third 
influential  factor  is  the  temperature  of  the  air,  as  proven  by  the  great  prevalence 
of  the  disease  in  southern  countries  and  in  the  summer  season. 

With  regard  to  the  nature  of  the  malarial  poison,  the  work  of  late,  and  in 
especial  of  Italian,  investigators  (Marchiafava  and  Celli,  Golgi,  and  others),  has  led 
to  interesting  conclusions.  According  to  these  authorities,  the  generators  of 
malarial  disease,  the  malarial  "  plasmodia,"  belong  to  the  lowest  class  of  animal 
life,  the  protozoa,  and  to  that  subdivision  known  as  sporozoa.  The  Plasmodium 
enters  the  blood  and  penetrates  the  red  blood- corpuscles,  where  it  has  a  lively 
amoeboid  motion.  It  evidently  lives  upon  the  tissue  of  the  red  corpuscles.  The 
haemoglobin  of  the  latter  is  thus  changed  into  melanin,  a  substance  which  ap- 
parently contains  no  iron,  and  the  black  granules  of  which  are  usually  seen  in  the 
body  of  the  Plasmodium.  After  the  red  globule  occupied  by  the  Plasmodium  is 
completely  destroyed,  the  micro-organism  becomes  free  in  the  blood-current. 
Particles  of  pigment  collect  in  its  center,  while  on  its  periphery  new  generations 
are  formed  by  splitting  and  subdivision.  These  new  bodies  appear  to  be  mainly 
present  in  the  spleen,  liver,  and  marrow  during  the  afebrile  interval;  while  at 
the  time  of  the  paroxysms  of  fever  they  enter  the  blood  once  more  and  penetrate 
into  the  red  globules.  It  is  a  very  interesting  fact  that  the  different  forms  of  in- 
termittent fever,  and  in  especial  the  tertian  and  quartan  varieties,  probably  owe 
their  development  to  different  kinds  of  plasmodia,  in  which  the  developmental 
phases  occupy  different  lengths  of  time.  We  can  therefore  by  means  of  inocula- 
tion transfer  from  one  human  being  to  another  only  that  variety  of  intermittent 


MALARIAL  DISEASES.  91 

which  the  first  patient  exhihits,  whether  tertian  or  quartan.  The  quotidian  type 
is  probably  clue  to  the  development  of  two  cases  of  tertain  fever  in  the  same  in- 
dividual, side  by  side;  whereby  each  separate  tertian  owes  its  development  to  a 
special  generation  of  the  plasmodium.  It  is  Golgi's  view  that  the  severe  tertian 
forms  of  malaria  are  caused  by  a  special  variety  of  plasmodium,  which  is  distin- 
guished by  the  appearance  of  crescentic  forms  of  development. 

Although  no  one  has  yet  been  successful  in  establishing  this  view  of  the 
Plasmodia  by  means  of  pure  cultures  and  inoculation  of  the  same,  yet  the  relation 
of  the  plasmodium  to  malaria  seems  evident  from  the  fact  that  in  every  patient 
with  malaria  the  plasmodia  can  be  easily  demonstrated  in  the  blood  (even  without 
any  staining),  while  these  same  forms  are  never  detected  in  the  blood  except  in 
malaria.  The  way  in  which  the  plasmodia  enter  the  human  body  is  not  yet 
known.     It  may  be  by  inhalation  or  by  the  stings  of  insects. 

The  investigations  with  regard  to  the  plasmodium  of  malaria  have  also  ex- 
plained the  long-recognized  fact  that  in  chronic  malaria  large  amounts  of  pigment 
collect  in  the  internal  viscera.  These  deposits  are  most  abundant  in  the  spleen, 
which  in  the  chronic  varieties  of  the  disease  develops  into  a  firm,  hard  tumor;  but 
they  are  also  found  in  the  bone-marrow,  liver,  brain,  and  kidneys,  leading  finally 
in  the  liver  and  the  kidneys,  in  frequent  instances,  to  processes  of  chronic  degen- 
eration and  inflammation.  It  is  especially  noteworthy  that  in  those  patients  who 
present  the  most  marked  cerebral  disturbances  (pernicious  comatose  fever,  vide 
infra),  the  cerebral  capillaries  are  found  to  be  completely  occluded  with  pigmented 
plasmodia. 

[Periodical  fever  is  very  widely  distributed  in  the  United  States,  and  in  the 
southern  portions  occurs  in  severe  though  not  in  the  severest  forms.  Some  regions 
which  were  formerly  free  from  it  are  no  longer  so,  and,  vice  versa,  some  regions 
which  were  greatly  subject  to  it  are  now  exempt;  these  changes  are  closely  con- 
nected with  the  clearing  and  upturning  of  virgin  soil  largely  impregnated  with 
decaying  vegetable  matter,  and  with  the  subsequent  cultivation  of  the  same  for 
considerable  periods  of  time.  The  poison  does  not  extend  far  above  the  surface  of 
the  ground,  as  is  shown  by  the  relative  safety  of  sleeping  in  the  upper  as  compared 
with  the  lower  story  of  a  house;  during  the  night  the  poison  seems  to  exist  in 
greater  intensity  than  during  the  day.  Attacks  are  more  liable  to  occur  during 
the  spring  and  autumn  than  at  other  seasons. 

The  hopes  which  have  been  entertained  in  some  quarters  that  malarial  regions 
might  be  rendered  healthy  by  large  plantations  of  the  Australian  eucalyptus  globu- 
lus, a  rapidly  growing  tree  which  absorbs  immense  quantities  of  water,  do  not 
seem  likely  to  be  realized  in  the  light  of  French  experience  in  Africa,  and  in  that 
of  the  Trappist  monks  in  Italy.] 

Klebs  and  Tommasi-Crudeli  have  made  extensive  investigations  as  to  the  nature 
of  the  malarial  poison.  We  must  regard  it  as  organic.  The  authorities  just 
named  state  that  the  true  cause  of  malaria  is  a  specific  variety  of  bacillus.  They 
found  peculiar  bacilli  and  their  spores  both  in  the  earth  of  malarial  regions  and 
in  the  adjacent  strata  of  the  atmosphere;  and,  by  infecting  rabbits  with  these, 
they  were  able  to  induce  attacks  of  fever,  swelling  of  the  spleen,  and  the  charac- 
teristic formation  of  pigment  matter  (vide  infra).  Before  this,  bacilli  and  spores 
had  been  found  in  the  blood  and  spleen  of  patients  suffering  from  malaria.  It  can 
not  yet  be  said  just  how  much  significance  these  discoveries  have. 

[To  Laveran  really  belongs  the  credit  for  the  discovery  and  accurate  descrip- 
tion of  the  plasmodium.  His  work  in  Algiers  has  been  substantiated  by  observers 
in  widely  separated  malarial  regions,  and,  at  the  same  time,  no  very  important 
additions  have  been  made  to  it. 

It  is  difficult  to  overrate  the  diagnostic  and  therapeutic  importance  of  this  dis- 


92  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

covery.  The  ordinary  intermittents  are  usually  easy  of  diagnosis,  but  the  remit- 
tent forms  often  simulate  typhoid  fever,  while  the  pernicious  form  may  resemble 
uraemia  or  intracranial  disease.  Especially  in  pernicious  cases  life  may  be  saved 
by  prompt  and  appropriate  treatment,  which  must  be  based,  of  course,  on  accurate 
diagnosis.  The  following  details  may  be  of  use  to  those  who  are  not  familiar  with 
the  method  of  blood  examination.  The  finger  tips  should  first  be  scrubbed  with  a 
nail-brush,  and  soap  and  water,  and  then  washed  in  alcohol  or  ether,  to  obviate  the 
danger  of  mistaking  minute  particles  of  dirt  for  the  pigment-granules  derived  from 
the  destruction  of  red  blood-corpuscles.  A  portion  of  a  drop  of  blood  is  then  to  be 
received  on  a  scrupulously  clean  object-  or  cover-glass,  and  squeezed  out  between 
the  two,  so  that  a  thin  layer  of  blood  with  separation  of  the  individual  corpuscles 
is  secured.  The  amoeboid  forms  of  the  plasmodium  retain  their  movements  for  a 
number  of  minutes  in  a  warm  room,  much  longer,  of  course,  with  a  warm  stage. 
The  presence  of  pigment  granules  in  the  red  corpuscles  may  be  the  readiest  indi- 
cation of  the  presence  of  the  organism.  The  crescentic  forms  are  found  more 
especially  in  chronic  cases  which  have  been  under  treatment  by  quinine,  as  is 
stated  by  Osier.  Many  of  the  other  forms  can  be  found  in  the  blood  only  during 
a  paroxysm.  The  editor  has  seen  them  in  abundance  in  a  cachectic  malarial 
patient  from  Panama,  and  failed  to  find  them  again  after  a  single  large  dose  of 
quinine,  which  terminated  the  chills. 

In  dried  and  stained  specimens  it  is  easier  to  detect  the  organisms,  but  amoeboid 
movement  is,  of  course,  lost.] 

Liability  to  the  disease  is  very  wide-spread.  No  race,  no  age,  no  sex,  enjoys 
immunity.  It  is  a  noticeable  fact  that  those  who  have  had  the  disease  once  are 
all  the  more  apt  to  have  it  again.  Former  patients,  although  they  feel  perfectly 
well  in  a  non-malarious  region,  are  very  liable  to  fresh  attacks,  or  at  least  much 
discomfort,  as  soon  as  they  re-enter  an  infected  district.  The  time  of  incubation 
does  not  seem  to  be  constant.  It  is  put  at  from  six  to  twenty  days,  but  may  be 
shorter.  We  shall  consider  below  chiefly  the  common  forms  of  intermittent,  such 
as  appear  among  us  in  Germany,  contenting  ourselves  with  a  very  brief  description 
of  the  severer  forms. 

Varieties  of  Malarial  Disease. 

1.  Intermittent  Fever.— This  is  the  simplest  form,  and  has  for  its  especial  char- 
acteristic the  relative  brevity  of  the  febrile  attacks,  which  almost  always  exhibit  a 
remarkably  uniform  type.  A  febrile  attack  of  this  kind  is  frequently  the  very 
first  symptom  of  the  disease.  In  other  cases  the  paroxysm  of  fever  is  preceded  by 
a  prodromal  stage  lasting  several  days,  during  which  the  patient  feels  languid, 
has  no  real  appetite,  complains  of  headache  and  pain  in  the  back  of  the  neck  and 
in  the  limbs,  and  often  even  thus  early  presents  a  slightly  yellowish  complexion 
and  an  enlarged  spleen. 

In  the  typical  attack  of  intermittent  fever  there  are  three  stages.  The  attack 
begins  with  a  chill.  There  is  pronounced  malaise,  attended  by  intense  chilliness 
and  more  or  less  shivering.  The  skin  is  cool  and  pale,  the  face  may  be  somewhat 
livid.  The  temperature  of  the  interior  of  the  body  is  elevated,  and  rapidly  rises 
higher.  In  by  far  the  greater  number  of  cases  the  attack  occurs  in  the  morning, 
or  at  least  before  noon,  and  but  seldom  later  in  the  day.  This  cold  stage  varies 
greatly  in  length,  usually  lasting  an  hour  or  two. 

The  chilliness  is  followed  by  the  hot  stage.  The  skin  grows  burning  hot,  the  face 
flushes,  the  pulse,  which  was  before  small,  becomes  full,  and  the  action  of  the  heart 
is  excited.  At  first  the  temperature  continues  to  increase,  and  reaches  in  this  stage 
its  maximum  for  the  attack.    It  is  exceptional  for  it  to  remain  under  104°  (40°  C), 


MALARIAL  DISEASES. 


93 


and  by  no  means  rare  for  it  to  touch  106°,  or  even  107°  (41°-41'5°  C).  This  stage 
almost  always  lasts  longer  than  the  preceding, generally  about  three  to  five  hours. 
The  temperature  may  begin  to  fall  as  early  as  the  latter  part  of  the  hot  stage,  but 
may  persist  till  the  beginning  of  the  third  stage. 

In  this,  sweating,  stage  the  skin  grows  moist,  and  there  is  soon  a  profuse  gen- 
eral perspiration.  The  patient  begins  to  feel  much  better.  In  a  few  hours  the 
temperature  usually  becomes  normal,  and,  after  lasting  in  all  about  eight  to  twelve 
hours,  the  attack  is  over.  It  may  be  shorter  or  rarely  longer.  Usually,  however, 
the  temperature  keeps  on  sinking  slowly,  so  as  to  be  still  subnormal  even  on  the 
next  morning,  perhaps  not  above  97°  (36°  C). 

There  are  certain  peculiarities  in  the  temperature-curve  which  we  have  our- 
selves observed.  The  elevation  of  temperature  is  almost  invariably  more  rapid 
than  its  decline.  The  rise  is  most  rapid  during  the  first  hours  of  the  cold  stage, 
and  slower  during  the  first  portion  of  the  hot  stage.  The  ascent  is  but  very  sel- 
dom interrupted.  During  the  hot  »tage,  when  the  fever  is  highest,  in  the  neigh- 
borhood of  106°  F.  (41°  C),  there  are  not  infrequently  two  little  summits  to  the 
fever-curve,  if  the  temperature  be  taken  at  short  intervals.  But  the  temperature 
may  for  hours  remain  the  same.  The  temperature  generally  begins  to  fall  some 
little  time  before  the  perspiration  is  evident.  The  decline  is  slow.  It  may  be  per- 
fectly continuous,  or  it  may  be  interrupted  by  fresh  elevations,  which  are  some- 
times slight  and  sometimes  considerable.  In  many  cases  the  descent  is  by  steps, 
the  temperature  remaining  the  same  for  half  an  hour  or  an  hour,  and  then 
abruptly  falling  a  couple  of  degrees  and  remaining  for  a  time  at  this  new  level. 

The  chief  characteristic  is  not,  however,  the  nature  of  the  single  attacks,  but 
the  peculiar  manner  of  their  repetition.  If  the  case  is  not  under  treatment,  the 
single  attacks  keep  recurring  for  a  time,  either  daily,  as  in  the  quotidian  variety, 
or  every  second  day.  This  latter  type  of  tertian  intermittent  fever  (cf.  Figs.  10 
and  11)  is  probably  the  most  frequent.     There  may  exceptionally  be  still  longer 


41-0° 


40  0° 


390° 


38  0C 


3T'0C 


36-0° 


suss:  ■ 

■»■HI 

SÜSS      :   on 

EiälS!  8  !' 

E 

inn 
■■an 

BMIBSIH 
IHIBI1  . 
IMIHIHII 

IHIHI 

5!8B«i 


HfitSB 


■IIJH      ■■■ 
EHl'flKSHB 


Fig.  10.— Quotidian  intermit- 
tent fever. 


410° 


40-0° 


39  '0C 


38-0° 


360c 


■■■■I 

i  HIS  SB  SKI 

mil»     li'iafiii 

HIIBBII  EIGIlf 

mum     ■■■■■ 

SÜSSES! 


IB1II 

nil. 
_iiii__ 

■MHHHI 


i  If  IUI 

iiiiai 
iiikii 


IS! 


IB  HE     IIIIIMHH 


-IBJI 

niHlBE 
■■!■■■ 


ü»  HB  VW  IB 

rifiHHHVH!  ■«■  - 

::;jr/7  hmhhb;  HhftH  : 


Fig.  11. — Tertian  intermittent  fever. 
[Chinin  2'0  =  Quinine,  30  grains.] 


afebrile  intervals.  Thus  we  have  quartans,  quintans,  etc.  If  there  are  two  at- 
tacks in  one  day,  a  rare  event  among  us,  we  have  a  double  quotidian.  If  there  is 
a  violent  attack  every  second  day,  and  on  the  intervening  days  there  are  milder 


94  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

attacks,  it  is  a  case  of  double  tertian.  Very  often  the  attacks  do  not  recur  at  just 
the  same  time  of  day,  but  a  few  hours  earlier  each  time.  Less  frequently  they 
are  later.  This  peculiarity  is  expressed  by  the  term  "  anticipating "  or  "retard- 
ing," as  the  case  may  be — e.  g.,  a  retarding  tertian  ague.  In  cases  of  long  stand- 
ing, the  paroxysms  may  finally  lose  all  regularity,  so  that  the  fever  is  described  as 
"erratic." 

Next  to  the  febrile  attacks,  the  swelling  of  the  spleen  is  the  most  constant  and 
important  symptom.  It  is  usually  considerable  and  capable  of  demonstration  by 
percussion  and  palpation.  At  first  the  tumor  increases  with  every  fresh  attack, 
and  diminishes  but  little  during  the  intervals.  After  the  patient  is  freed  from  his 
attacks  of  fever  the  spleen  may  continue  enlarged  for  some  time.  It  is  tender  on 
pressure.  The  liver  may  likewise  be  swollen,  but  this  is  less  constant  and  also 
less  important. 

Certain  changes  in  the  skin  are  very  characteristic,  chief  among  which  is  a 
peculiar  yellowish-brown  discoloration.  This  is  due  to  an  abnormal  deposition  of 
pigment  in  the  skin.  Herpes  on  the  lips  or  nose  is  seen  very  frequently  during 
the  attacks.  We  have  seen  one  case  of  herpes  on  the  cornea.  Mention  has  also 
been  made  of  urticaria,  purpura,  and  other  eruptions. 

Other  internal  organs  than  those  already  spoken  of  are  rarely  much  disturbed. 
One  symptom  should  be  mentioned,  which  we  have  ourselves  seen  several  times,  viz., 
a  quite  marked  acute  dilatation  of  the  heart  during  the  attack.  There  were  no  bad 
results,  and  the  normal  condition  was  soon  re-established.  We  may  hear  during 
the  attack  functional  cardiac  murmurs  of  a  blowing  character.  Thoracic  exam- 
ination, particularly  if  made  during  the  attack,  may  afford  the  signs  of  a  dry 
bronchitis.  Sometimes  there  is  considerable  diarrhoea,  or  other  evidence  of  intes- 
tinal derangement.  Catarrhal  jaundice  is  confined  to  the  severer  cases.  Some- 
times the  urine  has  a  moderate  amount  of  albumen.  Genuine  nephritis  is  met 
with  only  in  the  graver  varieties  of  the  disease.  The  increased  excretion  of  urea 
on  the  days  of  the  fever  results,  as  in  any  fever,  from  the  increased  destruction  of 
albumen.  Severe  pain  in  the  cervical  and  upper  dorsal  vertebrae  is  regarded  as 
characteristic  of  intermittent. 

Besides  the  typical  attacks,  rudimentary  and  modified  ones  are  not  rare,  in 
which  the  separate  stages  are  ill  defined,  or  in  part  wanting.  We  are  most  apt  to 
see  this  in  cases  which  have  been  already  treated  with  quinine.  Children  do  not 
have  a  true  rigor.  They  merely  become  pale  or  livid.  They  may  present  marked 
nervous  symptoms. 

2.  Pernicious  Intermittent  Fever,— This  dangerous  form  occurs  only  in  the 
true  malarial  districts,  and  is  often  preceded  by  a  few  attacks  of  a  milder  charac- 
ter. Then  appear,  in  addition  to  the  more  or  less  perfectly  marked  stages  of  the 
febrile  attack,  other  graver  symptoms  which  not  infrequently  end  in  death.  Severe 
nervous  symptoms  are  most  frequent.  There  may  be  unconsciousness,  coma, 
delirium,  or  epileptiform  or  tetanic  convulsions.  None  of  these  symptoms  persist 
longer,  as  a  rule,  than  does  the  common  sort  of  an  attack,  and  in  a  favorable  case 
vanish  completely  wThen  the  sweating,  which  is  usually  profuse,  begins.  The 
great  danger  comes  from  the  recurrence  of  the  attacks.  A  second  form  of  perni- 
cious intermittent  fever  causes  violent  gastro-intestinal  symptoms,  which  may 
almost  exactly  imitate  the  algid  stage  of  cholera,  with  vomiting,  diarrhoea,  and  col 
lapse ;  or  there  may  be  severe  cardialgia,  dysentery,  and  the  like.  In  the  so-called 
pernicious  intermittent  with  jaundice,  intense  jaundice  appears  during  the  attack, 
with  vomiting  and  diarrhoea,  and  sometimes  the  gravest  nervous  symptoms. 
There  are  certain  very  peculiar  forms,  in  which  local  diseases,  such  as  pleurisy  or 
pneumonia,  can  be  demonstrated  during  every  attack,  but  vanish  wholly  or  in 
part  when  the  temperature  declines,  only  to  appear  again  during  the  next  attack. 


MALARIAL  DISEASES.  95 

[The  pernicious  form  occurs  in  isolated  cases  wherever  the  ordinary  variety  of 
the  disease  prevails,  but  is  much  more  common  in  the  Southern  and  Western 
States,  and  there  varies  in  frequency  in  different  years.  Periodicity  in  the  attack 
is  not  always  observed.  The  pernicious  character  is  not  always  manifested  in  the 
first  attack,  one  or  more  mild  paroxysms  being  often  precedent.  In  this  country 
the  algid  form  of  pernicious  periodic  fever  is  often  called  ''congestive  chills,"  and 
this  form  is  more  common  than  the  comatose  or  another  form  not  mentioned 
by  the  author— the  hsemorrhagic.  In  the  latter  the  blood  escapes  from  the  kidneys, 
and  less  constantly  from  the  mucous  membrane.  During  the  late  civil  war  the 
mortality  in  the  white  soldiers  of  the  United  States  army  from  pernicious  malarial 
fever  was  23 "91  per  cent.] 

3.  Remittent  and  Continuous  Forms  of  Malarial  Fever.— These  are  generally 
severe,  and  are  seen,  like  the  preceding,  only  in  the  worst  haunts  of  malaria.  The 
proof  that  they  have  the  same  aetiology  as  intermittent  fever  lies  in  the  fact  that 
they  are  sometimes  developed  out  of  the  milder  forms;  but  it  is  to  be  noticed  that 
many  types  of  disease  which  physicians  in  the  tropics  describe  as  malarial  affec- 
tions have  not  yet  been  proved  to  our  satisfaction  to  have  an  actual  identity  of 
origin  with  the  common  intermittent  fever.  The  symptoms  of  this  variety  are 
likewise  those  of  a  severe  constitutional  infection.  Gastro-intestinal  symptoms 
may  predominate ;  or  there  may  be  such  grave  nervous  symptoms  as  coma,  delir- 
ium, and  convulsions;  or  there  may  be  jaundice,  hagmaturia,  and  even  a  general 
haemorrhagic  diathesis ;  or  various  local  disorders  may  exist,  such  as  pneumonia, 
nephritis,  and  hepatic  and  splenic  abscesses.  The  fever  is  high,  but  without  any 
sort  of  regular  intermissions,  maintaining  for  one  or  two  weeks  a  remittent  or  a 
tolerably  continuous  type.  Milder  forms  may  end  in  recovery  after  eight  to  four- 
teen days,  but  often  death  ensues  at  this  time,  or  even  earlier. 

[The  remittent  form  apparently  shows  a  greater  intensity  of  the  poison  or  a 
greater  susceptibility  of  the  individual.  In  the  United  States  army,  from  1861  to 
1866,  its  mortality  was  twelve  times  as  gi'eat  as  that  from  the  intermittent  form.] 

4.  Chronic  Malarial  Cachexia.— This  occurs  in  the  true  malarial  regions,  and 
affects  not  only  people  who  have  had  frequent  attacks  of  pronounced  intermittent 
or  remittent  fever,  but  also  those  who  have  never  had  acute  attacks.  The  condi- 
tion is  chronic.  It  may  exhibit  a  genuine  intermittent  character.  The  patient 
usually  has  a  decidedly  yellowish,  malarial  complexion,  and  almost  always  the 
spleen  is  evidently  enlarged.  There  are  no  regular  febrile  attacks,  but  merely 
symptoms  of  general  debility,  anorexia,  tendency  to  diarrhoea,  or,  more  rarely, 
constipation,  vertigo,  wakefulness,  frequent  perspiration,  pains  in  the  muscles  and 
joints,  dyspnoea,  and  palpitation.  There  may  be  such  nervous  symptoms  as  trem- 
bling, paralysis,  and  mental  disturbance ;  or  we  may  see  intestinal  symptoms  and 
jaundice.  Dropsy  occurs ;  also  epistaxis,  cutaneous  ecchymoses,  and  other  signs 
of  a  scorbutic  condition.  The  spleen  and  liver  gradually  become  greatly  hyper- 
trophied  and  melanotic.  At  the  same  time  there  may  be  an  irregular  fever, 
approaching  either  an  intermittent  or  a  remittent  in  type.  Finally,  secondary 
diseases  are  possible — e.  g.,  tuberculosis,  amyloid,  or  dysentery — and  these  may 
prove  the  immediate  cause  of  death.  The  milder  forms  may  be  cured,  but  seldom 
unless  the  patient  abandons  for  ever  the  malarial  district. 

5.  Masked  Intermittent. — This  is  the  designation  of  cases  where,  although 
there  is  no  fever,  certain  other  disturbances  arise  in  regular  intermittent  attacks. 
Chief  among  these  is  neuralgia.  Its  favorite  seat  is  the  supra-orbital  branch  of 
the  trigeminus.  It  may  occur  in  the  other  branches  of  the  same  nerve,  or  in  the 
sciatic,  the  anterior  crural,  the  nerves  of  the  brachial  plexus,  and  elsewhere.  Car- 
dialgia  and  enteralgia  may  occur  in  the  same  way.  These  attacks  last  from  thirty 
minutes  to  several  hours,  and  are  frequently  associated  with  all  sorts  of  constitu- 


96  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

tional  symptoms,  but,  as  we  have  said,  are  afebrile.  There  may  be  a  splenic  tumor, 
which  aids  diagnosis;  but  this  sign  may  be  wanting. 

Numerous  other  intermittent  disorders  besides  neuralgia  have  been  described 
as  masked  intermittent.  The  list  includes  anaesthesia,  convulsions,  and  paralysis; 
also  intermittent  haemorrhage,  oedema,  cutaneous  affections,  and  intestinal  symp- 
toms. We  must  add,  however,  that  those  who  have  described  diseases  of  this  sort, 
some  of  which  seem  strange  enough,  have  not  always  been  as  critical  as  they 
ought,  and  have  omitted  to  prove  satisfactorily  that  such  cases  should  be  referred 
to  malarial  poisoning. 

Diagnosis. — It  is  often  very  difficult  to  diagnosticate  a  case  of  intermittent  fever 
at  the  first  visit,  particularly  in  a  place  where  malarial  poisoning  is  infrequent. 
The  history  of  the  case  is  by  no  means  always  enough  to  put  one  on  the  right 
track ;  and  a  single  examination  of  the  patient  may  prove  equally  negative  in  its 
practical  results,  whether  it  is  made  during  the  febrile  stage  or  in  the  interval. 
Continued  observation,  however,  will  almost  always  disclose  the  regularity  of  the 
febrile  attacks,  the  splenic  tumor,  the  characteristic  complexion,  and  the  herpes ; 
and  our  diagnosis  becomes  evident.  Still  it  is  not  very  exceptional  for  an  inter- 
mitting fever  to  be  takeu  at  first  for  an  intermittent  malarial  one,  while  event- 
ually some  quite  different  disease  is  found  to  produce  the  symptom.  Pyaemia 
may  give  rise  to  mistakes  of  this  kind ;  also  purulent  phlebitis,  acute  ulcerative 
endocarditis,  and  even  tuberculosis.  We  should  be  very  cautious  in  making  a 
hasty  diagnosis  of  "  irregular  intermittent  fever."  Our  own  experience  has  taught 
us  that  almost  in  variably  the  case  turns  out  to  be  something  else.  Where  there  is 
doubt  we  may,  in  addition  to  a  careful  consideration  of  all  the  symptoms  and  a 
thorough  physical  examination,  be  aided  by  the  therapeutic  action  of  quinine 
{vide  infra).  If  a  high  fever  of  intermitting  type  is  affected  by  large  doses  of 
quinine  but  temporarily  if  at  all,  then  a  diagnosis  of  malarial  intermittent  fever  is 
rendered  doubtful. 

Treatment. — Malarial  poisoning  is  one  of  the  few  diseases  upon  which  we  can 
make  a  direct  attack  with  assured  success.  In  quinine  we  possess  a  remedy  which 
probably  acts  upon  the  very  cause  of  the  disease,  and  the  therapeutic  efficiency  of 
which  is  undisputed.  Quinine  is  therefore  the  sovereign  remedy  in  all  forms  of 
malarial  poisoning,  and  is  often  the  only  drug  employed.  In  the  mild  cases, 
which  are  the  only  kind  that  occur  among  us,  we  do  not  usually  give  the  remedy 
upon  the  instant  that  the  patient  comes  under  treatment.  It  is  best  to  wait  for 
one  or  two  attacks,  partly  to  make  sure  of  our  diagnosis,  and  partly  to  learn  what 
the  type  of  the  fever  is,  whether  quotidion,  tertian,  anticipating,  or  recurring  at  the 
same  hour.  And  in  most  cases  this  delay  works  no  harm  to  the  patient.  Dur- 
ing the  attack  itself  there  is  seldom  any  use  in  special  treatment.  Of  course, 
the  patient  must  stay  in  bed  and  be  kept  warm  during  the  cold  stage,  and  have 
lighter  coverings  during  the  hot  stage.  During  the  afebrile  interval  the  patient 
may  be  up  if  he  feels  strong  enough  and  is  careful.  Quinine  is  given  about  five 
or  six  hours  before  the  next  attack  is  due.  It  is  best  to  administer  one  large 
dose  of  twenty  to  thirty  grains  (1*5-2  grm.),  either  in  solution  or  in  capsules  of 
seven  grains  (0'50  grm.)  each.  If  the  quinine  be  given  in  powder  or  capsules,  it 
is  a  good  way  to  follow  it  with  a  few  drops  of  muriatic  acid,  to  promote  its  solu- 
tion in  the  stomach.  Often  one  large  dose  prevents  the  next  attack.  In  other 
cases  it  does  occur,  but  with  less  subjective  disturbance,  no  chill,  and  more 
moderate  fever.  We  must  then  give  another  large  dose  before  the  second  at- 
tack is  expected.  If  the  attack  does  not  take  place,  then  we  may  give  for  several 
days  quinine  to  the  amount  of  eight  grains  (0-5  grm.)  per  diem.  After  all,  re- 
lapses are  possible,  even  at  the  end  of  several  weeks ;  but  they  yield  readily  to 
quinine. 


MALAEIAL  DISEASES.  97 

Judging  from  our  own  experience,  conchinine  is  the  only  one  of  the  other  prep- 
arations of  cinchona  which  is  as  efficient  as  quinine.  It  costs  only  half  as  much, 
and  is  prescribed  in  just  the  same  way.  A  disadvantage  is  that  it  is  more  apt  than 
quinine  to  excite  vomiting.  All  the  other  preparations  of  Peruvian  bark,  such  as 
chinoidine  and  cinchonine,  are  much  more  uncertain  in  their  action. 

In  the  treatment  of  pernicious  intermittent  fever,  of  the  masked  forms,  of  the 
remittent  and  continued  fevers,  and  of  malarial  cachexia,  the  chief  remedy  is  like- 
wise quinine,  given  in  sufficient  doses.  Baccelli  has  shown  that  sometimes  in 
pernicious  fever  the  direct  injection  of  quinine  into  a  vein  may  suve  life.  In  all 
cases  of  considerable  duration  it  is  also  of  the  greatest  importance  to  remove  the 
patient  from  the  malarial  region,  if  it  can  possibly  be  done.  This  often  proves  to 
be  the  only  way  to  avoid  relapses  and  attain  a  perfect  cure. 

In  cases  of  longer  standing,  quinine  sometimes  loses  its  power.  Then  we  resort 
to  arsenic.  It  is  frequently  employed  in  malarial  cachexia  and  in  intermittent 
neuralgia,  either  alone  or  combined  with  iron.  We  give  gtt.  v  to  viij  of  Fowler's 
solution  two  or  three  times  a  day  in  water.  It  is  still  better  to  give  pills  of  arseni- 
ous  acid  containing  gr.  sV-sV  (0*002-0  "003)  and  gradually  increasing  to  a  daily 
dose  of  gr.  £-£  (0*010-0  "012).  It  maybe  added  that  arsenic  is  also  said  to  have 
a  prophylactic  virtue :  a  long-continued  use  of  it  is  stated  to  render  a  person  proof 
against  malarial  poisoning.  It  may  also  be  mentioned  that  a  favorite  remedy  for 
chronic  malarial  cachexia  among  the  Italian  peasants  is  a  decoction  of  lemons.  It 
is  even  highly  praised  by  local  physicians.  A  finely  sliced  lemon  is  put  with  three 
glassfuls  of  water  and  boiled  down  to  one  glassful.  We  will  not  speak  of  the 
numerous  other  remedies  recommended,  such  as  eucalyptus,  pipeline,  pilocarpine, 
berberine,  and  many  others,  for  they  can  be  entirely  dispensed  with. 

The  management  of  the  severe  varieties  of  malarial  disease  involves  sympto- 
matic treatment  as  well  as  the  administration  of  quinine.  We  can  not  enter  into 
the  particulars.  In  combating  the  grave,  nervous,  intestinal,  pulmonary,  and  renal 
symptoms,  the  dropsy  and  the  anaemia,  the  physician  must  conform  to  the  general 
rules  of  treatment. 

[There  is  nothing  to  be  gained  by  allowing  a  patient  to  have  an  unnecessary 
chill.  If  there  is  a  reasonable  probability  that  his  paroxysms  are  due  to  malaria, 
a  prompt  effort  should  be  made  to  cut  them  short.  Four  hours  is  the  shortest 
time  that  it  is  safe  to  allow  for  quinine  by  the  stomach  with  probability  that  the 
expected  chill  will  be  prevented.  The  drug  acts  much  more  promptly  when 
given  hypodermically.  The  hydrobromate  is  preferred  by  some  to  the  sulphate 
for  subcutaneous  use  on  account  of  the  necessity  of  using  acid  to  dissolve  the 
latter,  and  the  consequent  risk  of  abscess.  Such  a  risk  should  have  no  weight  if 
the  physician  has  any  suspicion  that  he  has  to  deal  with  the  pernicious  form  of 
the  disease.  If  the  stomach  is  irritable,  the  remedy  can  be  given  by  enema. 
Quinine  can  also  be  given  by  suppository,  though  it  may  thus  produce  some  irri- 
tability of  the  rectum.  But  the  impossibility  of  disguising  the  bitter  taste  of  the 
remedy  or  of  making  children  swallow  capsules  renders  this  a  valuable  means  of 
treatment  sometimes  in  infants  and  young  children. 

Warburg's  tincture  is  an  antiperiodic  which  does  good  service  in  cases  which 
do  not  yield  to  the  ordinary  methods  of  treatment. 

The  hypodermic  injection  of  pilocarpine  is  reported  to  atort  an  impending 
chill. 

Some  prefer  divided  and  smaller  to  the  single  and  large  dose  of  quinine  or  one 
of  its  substitutes,  a  difference  of  view  which  is  of  minor  importance. 

In  the  remittent  forms  boldness  in  the  use  of  quinine  is  required.     Cinchonism 
should  be  induced  as  promptly  as  may  be,  and  maintained  to  a  mild  degree  for 
several  days;  the  quantity  of  the  drug  can  then  be  gradually  diminished. 
7 


98  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

The  treatment  of  the  pernicious  forms  of  periodic  fever  presents  itself  under 
three  main  heads : 

1.  The  prevention  of  pernicious  paroxysms. 

2.  The  treatment  of  the  paroxysm  when  present. 

3.  The  prevention  of  a  recurrence. 

1.  We  have  seen  that  very  frequently  the  pernicious  character  is  manifested 
after  the  occurrence  of  one  or  more  mild  attacks ;  consequently,  in  localities  and 
seasons  marked  hy  the  occurrence  of  grave  cases  it  is  an  imperative  duty  to  treat 
every  mild  case  promptly  and  energetically,  a  course  which  unquestionably  saves 
many  a  life. 

2.  The  management  of  the  paroxysm  differs  according  to  the  form  which  it 
assumes ;  in  other  words,  is  largely  symptomatic.  Bemiss  (Pepper's  "  System  of 
Medicine  ")  says :  "  The  cure  of  a  congestive  chill  is  one  of  the  most  difficult  prob- 
lems the  physician  can  possibly  encounter."  Heat  externally,  opium  and  chloro- 
form by  the  mouth,  and  morphine  and  atropine  subcutaneously,  nutrition  by  the 
stomach  or  rectum,  according  to  circumstances,  and  alcoholics  if  the  action  of  the 
heart  is  feeble,  are  the  measures  of  widest  application. 

Whatever  the  type  of  the  attack,  a  weak  heart  calls  for  alcoholic  stimulation. 
Cinchonism  is  always  to  be  induced  as  rapidly  as  possible. 

In  the  comatose  form  it  is  to  be  remembered  that  the  cerebral  and  other  nervous 
symptoms  are  not  due  to  congestion,  but  probably  to  a  combination  of  the  malarial 
and  secondary  blood-poisons.  To  quote  Bemiss  again:  "Efforts  to  nourish  the 
patient  must  never  be  relaxed.  One  must  see  many  of  these  cases  before  he  can 
realize  how  often  they  recover  from  conditions  apparently  hopeless  when  promptly 
treated  and  properly  nourished." 

The  haemorrhagic  form,  like  the  others,  demands  cinchonism  and  careful  nutri- 
tion, but  also  haemostatics.  Purgative  doses  of  calomel  are  indicated  in  some  cases 
of  each  form,  but  should  not  be  given  in  a  routine  manner. 

3.  Prompt  cinchonism  is  the  chief  means  of  attaining  the  third  aim  of  treat- 
ment. Removal  to  a  healthy  locality  should  be  secured  if  possible,  and  the  general 
condition  of  the  patient  requires  careful  attention. 

It  remains  to  add  that  those  going  to  a  malarial  region  can  often  avoid  con- 
tracting the  disease  by  taking  advice  of  a  local  physician  as  to  hygienic  precau- 
tions, and  by  moderate  divided  doses  of  quinine.] 


CHAPTER  XV. 
TYPHO-MALARIAL   FEVER. 

[This  is  not  a  distinct  disease,  but  expresses  a  combination  in  the  same  indi- 
vidual at  the  same  time  of  the  effects  of  the  special  poison  causative  of  each  affec- 
tion. Typhoid  being  a  continued  fever,  its  complication  with  malaria  results  in  a 
pyrexia  of  a  remittent  type.  Typho-malarial  fever  occurs  in  malarial  regions, 
especially  in  the  Southern  States,  and  may  be  seen  in  non-malarial  regions  in  the 
persons  of  those  in  whom  malaria,  contracted  elsewhere,  is  in  a  more  or  less 
active  state. 

The  characteristic  symptoms  of  the  two  diseases  are  intermingled,  those  of 
typhoid,  the  graver  disease,  usually  predominating.  The  history  of  the  case 
and  careful  observation  of  the  symptoms  will  generally  clear  up  any  doubts 
felt  as  to  the  diagnosis  in  the  early  stages.  It  would  naturally  be  supposed  that 
the  combined  affections  must  produce  an  illness  more  severe  in  character   and 


DENGUE.  99 

more  unfavorable  as  regards  prognosis  than  belongs  to  simple  typhoid.  Such 
does  not,  however,  seem  to  be  the  case.  Woodward's  statistics  show  that  the 
mortality  of  uncomplicated  typhoid  was  far  greater  among  the  white  and  col- 
ored troops  alike  during  our  late  civil  war  than  was  the  mortality  of  typho-inala- 
rial  fever. 

The  treatment  as  regards  the  typhoid  fever  differs  in  no  way  from  that  suitable 
for  cases  of  the  ordinary  affection ;  the  periodic  element  demands  the  manage- 
ment appropriate  to  simple  intermittent  or  remittent  fever.] 


CHAPTER  XVI. 
DENGUE. 

[This  affection  has  never  appeared  in  Germany,  and  hence,  doubtless,  was 
omitted  by  the  author.  The  name  "  dengue  "  is  supposed  to  be  a  Spanish  corrup- 
tion of  dandy,  the  term  dandy  fever  having  been  applied  to  the  disease  by  the 
West  India  negroes  on  account  of  the  stiff  carriage  of  those  affected  by  it.  An- 
other name  is  "break-bone  fever." 

The  disease  generally  appears  in  epidemics,  and  is  almost  exclusively  confined 
to  tropical  and  semi-tropical  countries.  In  1780  an  epidemic  supposed  to  be 
dengue  prevailed  in  Philadelphia,  and  outbreaks  have  occured  repeatedly  in  the 
Southern  States  during  this  century.  In  1880  Charleston,  Savannah,  New 
Orleans,  and  other  Southern  cities  were  visited  by  it.  There  are  those  who  main- 
tain that  dengue  and  epidemic  influenza  are  identical,  a  view  which  the  facts  do 
not  seem  to  the  editor  to  bear  out. 

iEtiology. — -As  to  the  causation  but  little  is  known.  Those  who  have  had 
opportunities  of  studying  the  disease  consider  it  both  contagious  and  infectious, 
and  the  inference  that  it  depends  on  a  specific  germ  is  readily  suggested.  It 
seems  to  prefer  low  lands  along  the  sea-shore,  and  to  be  influenced  by  meteoro- 
logical conditions  in  that  it  generally  prevails  during  the  summer  and  disappears 
as  cold  weather  comes  on.  Neither  age,  sex,  nor  condition  affords  any  protection 
from  the  disease ;  it  was  thought  by  Dickson  that  one  attack  generally  confers  im- 
munity for  life. 

Pathology. — The  disease  is  so  rarely  fatal  that  few  opportunities  have  been 
afforded  for  its  post-mortem  study.  So  far  as  is  known,  it  has  no  peculiar  lesions. 
The  prominence  and  the  character  of  the  muscle  and  joint  pains  have  led  some 
observers  to  think  the  affection  related  in  some  way  to  rheumatism. 

Symptoms  and  Course. — The  onset  is  usually  sudden,  but  a  pronounced  chill  is 
said  never  to  occur.  Prodromata  similar  to  those  of  other  infectious  diseases  are 
sometimes  observed,  but  the  first  symptom  is  very  often  pain  and  stiffness  in  the 
muscles  and  joints,  with  frequent  swelling  of  the  latter.  The  lai'ge  and  small 
joints  are  equally  affected,  and  the  pain  is  increased  by  motion.  With  the  pain 
there  is  a  rise  in  temperature  and  in  the  frequency  of  the  pulse.  The  pain  is  apt 
to  increase  during  the  first  two  or  three  days  and  disappear  on  the  fifth,  but  irregu- 
lar remissions  are  liable  to  occur.  As  the  thermometer  falls  the  pain  and  other 
symptoms  diminish,  but  reappear  in  full  force  with  any  subsequent  rise.  During 
the  later  days  of  the  disease  a  skin  eruption  appears  on  the  upper  part  of  the  body, 
and  in  severe  cases  becomes  general  in  about  two  days.  This  eruption  is  very 
variable  in  character ;  it  may  appear  simply  as  an  erythema,  or  simulate  the  erup- 
tions of  scarlet  fever,  rubeola,  lichen,  or  urticaria;  it  is  apt  to  be  associated  with 
well-marked  heat  and  itching  of  the  skin.     In  mild  cases  the  eruption  is  evanes- 


100  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

cent  or  absent.  Swelling  of  the  lymphatic  glands  is  not  uncommon ;  in  severe 
cases  the  mucous  membrane  of  the  mouth,  throat,  and  nose  is  reddened,  and  haem- 
orrhage from  the  outlets  of  the  body  has  been  observed.  Pregnant  woman  are 
apt  to  miscarry.  Delirium  is  rare  in  adults,  but  common  in  children ;  the  face  is 
generally  flushed,  and  the  eyes  are  injected;  the  tongue  becomes  increasingly 
coated  as  the  disease  progresses,  the  appetite  is  lost,  nausea  is  not  uncommon, 
vomiting  is  rare.  The  bowels  and  the  kidneys  present  no  constant  or  distinctive 
symptoms. 

In  mild  cases  recovery  is  sometimes  rapid;  sometimes,  and  especially  after 
severe  cases,  convalescence  is  very  tedious,  the  muscular  and  articular  pain  and 
stiffness  passing  off  gradually,  and  the  glandular  swelling  lasting  for  weeks. 
Copious  skin  eruptions  are  followed  by  desquamation. 

Diagnosis  and  Prognosis. — As  to  diagnosis  there  can  seldom  be  any  difficulty 
during  the  prevalence  of  an  epidemic.  The  first  cases  are  the  only  ones  which  are 
liable  to  be  mistaken,  and  even  their  nature  can  not  remain  long  in  doubt.  The 
prognosis  is  uniformly  good. 

Treatment. — We  are  acquainted  with  no  agent  capable  of  aborting  or  cutting 
short  the  disease ;  nor  is  there  any  known  measure  of  prophylaxis  except  for  an 
individual  to  keep  away  from  those  places  in  which  the  affection  is  known  to  pre- 
vail. 

The  treatment  of  the  attack  is  simply  symptomatic ;  notable  pain  calls  for 
opium  in  some  form.  Quinine  has  not  seemed  to  be  of  service.  Debility  follow- 
ing the  attack  demands  suitable  alimentation  and  tonics.] 


CHAPTER  XVII. 
YELLOW   FEVER. 

[This  disease  is  not  a  visitant  of  Germany,  but  its  consideration  can  not  be 
omitted  from  a  text-book  on  the  practice  of  medicine  for  use  in  America.  In  the 
following  description  the  aim  will  be  to  bring  out  the  more  important  features  of 
the  disease,  while  for  fuller  details  the  reader  is  referred  to  larger  works  and 
monographs. 

.ffitiology. — Yellow  fever  is  an  acute  infectious  disease,  confined  within  certain 
geographical  limits,  and  occurring  chiefly  in  epidemics  of  greater  or  less  extent. 
In  certain  localities,  notably  Havana  and  New  Orleans,  a  season  rarely  passes 
without  some  sporadic  cases.  The  influence  of  temperature  is  well  established ; 
the  disease  prevails,  namely,  during  the  summer  or  the  warm  season,  and  is 
abruptly  arrested  by  one  or  two  decided  frosts;  dampness  is  favorable  to  it.  That 
it  depends  ultimately  on  a  special  cause  and  does  not  originate  de  novo  are  undis- 
puted facts ;  but  we  still  remain  in  ignorance  as  to  the  precise  nature  of  this  special 
cause.  The  poison  appears  to  be  more  active  at  night  than  during  the  day,  prefers 
low-lying  districts,  and  in  them  hugs  the  ground  to  a  certain  extent.  Bad  sanitary 
conditions  are  most  important  accessory  causes  of  the  disease,  furnishing  the  soil 
for  the  multiplication  of  the  poison.  There  can  be  little  doubt  that,  under  the 
observance  of  strict  personal  and  public  cleanliness,  yellow  fever  visitations  might 
be  made  simply  a  matter  of  history.  The  transmission  of  the  poison  probably 
takes  place  solely  through  the  atmospheric  air,  thus  finding  its  way  to  the  blood 
through  the  lungs;  conclusive  evidence  is  lacking  that  it  gains  entrance  to  the 
system  through  the  alimentary  canal.  While  the  air  is  the  medium  of  transmis- 
sion, the  distance  to  which  the  poison  can  be  carried  by  the  air  alone  is  very  short; 


YELLOW   FEVER.  101 

it  can,  however,  be  transported  to  an  indefinite  distance  by  fomites,  especially  if  in- 
closed in  trunks,  packing-cases,  letters,  and  the  like.  Its  vitality  may  tbus  be  main- 
tained for  very  long  periods.  It  is  a  remarkable  fact  tbat  in  large  cities  the  infec- 
tion may  be  of  great  virulence,  but  confined  to  a  limited  district  or  districts,  by 
carefully  shunning  which  unprotected  persons  are  comparatively  safe.  An  in- 
fected area  is  apt  to  extend  itself,  but  the  progress  is  slow,  and  is  interrupted  by 
streams  of  water,  high  walls,  or  simply  streets. 

That  the  disease  is  not,  strictly  speaking,  contagious  is  the  nearly  unanimous 
opinion  of  those  competent  to  form  one.  In  other  words,  the  poison  is  not  thrown 
off  in  a  matured  state  from  the  body  of  an  individual  suffering  from  the  disease; 
but,  after  being  so  thrown  off,  remains  in  the  atmosphere  or  lodges  on  solid  bodies, 
and  then  undergoes  changes  which  render  it  active  for  evil.  One  attack  of  the 
disease  renders  the  system  of  that  person  insusceptible  forever  after ;  the  natives 
of  a  yellow-fever  district  are  far  less  liable  to  contract  the  disease  than  are  those 
who  move  into  the  district  from  elsewhere;  until  these  have  passed  through  an 
attack  they  can  not  consider  themselves  as  acclimated.  The  negro  race  is  sus- 
ceptible to  the  disease,  though  in  a  less  degree  than  the  whites,  and  in  the  colored 
the  affection  is  far  less  fatal.  Neither  age  nor  sex  has  any  special  bearing  on  sus- 
ceptibility. That  fear,  anxiety,  worry,  or  anything  which  tends  to  depress  the 
nervous  system  increases  the  individual  liability  is  highly  probable.  The  stage 
of  incubation  is  very  variable,  ranging  from  one  day  to  three  weeks  or  even 
more. 

Pathological  Anatomy. — The  disease  involves  no  constant  and  peculiar  lesions. 
In  rapidly  fatal  cases,  congestion  and  often  haemorrhage  are  found,  especially  in 
the  nervous  system,  liver,  kidneys,  and  digestive  tract.  In  fatal  cases  of  longer 
duration  more  or  less  parenchymatous  degeneration  is  found.  A  fatty  degenera- 
tion of  the  liver  is  quite  common,  and  imparts  a  yellow  coloration  to  the  organ, 
giving  rise  to  the  terms  cafe  an  lait,  or  box-wood  liver.  Jaundice  of  the  skin  and 
tissues  generally  is  also  observable  after  death,  and  depends  upon  causes  in  no  way 
connected  with  mechanical  obstruction  to  the  flow  of  bile  into  the  intestine  during 
life.     Splenic  enlargement  is  conspicuous  by  its  absence. 

Course  and  Symptoms. — The  onset  of  the  disease  is  generally  sudden,  but  may 
be  preceded  for  a  few  days  by  malaise  and  other  signs  of  general  constitutional 
disturbance ;  the  initial  chill  is  seldom  severe,  reaction  following  soon  and  the 
thermometer  rising  to  102°-105° ;  hyperpyrexia  is  rare.  The  pulse-rate  does  not 
increase  proportionately  with  the  fever.  The  face  becomes  flushed  and  the  eyes 
injected  and  watery ;  headache  and  pain  in  the  back  are  early  and  usually  very 
prominent  symptoms.  The  bowels  are  confined ;  the  tongue  is  apt  to  be  clean  if 
it  was  so  before  the  disease  came  on ;  the  stomach  is  iisually  somewhat  irritable, 
and  there  may  be  vomiting;  moderate  epigastric  tenderness  is  common;  the  mind 
remains  clear,  as  a  rule,  but  delirium  is  not  very  uncommon,  and  in  children  a 
convulsion  may  usher  in  the  attack  as  in  other  acute  infectious  diseases ;  the  con- 
dition of  the  urine  is  at  first  not  remarkable,  but  albumen  may  soon  appear.  This 
hot  or  febrile  stage  may  last  from  twelve  hours  to  several  days.  The  pulse  gen- 
ally  declines  in  frequency  before  the  disease  has  reached  its  maximum.  As  the 
fever  disappears  the  other  symptoms  vanish  also,  and  the  second,  or  "  stage  of 
calm,"  begins.  From  this  point  recovery  may  be  rapid  and  uninterrupted,  the 
whole  disease  consisting  of  but  a  single  febrile  paroxysm  of  greater  or  less  inten- 
sity and  of  short  duration. 

In  grave  cases,  and  gravity  is  often  foreshadowed  in  the  first  stage  by  marked 
capillary  congestion  of  the  surface  of  the  body  irrespective  of  the  intensity  of  the 
other  symptoms,  and  after  a  stage  of  calm  lasting  for  some  hours,  but  rarely  ex- 
ceeding twenty-four,  more  distinctive  symptoms  appear.     The  pulse  is  very  com- 


102  ACUTE  GENEEAL  INFECTIOUS  DISEASES. 

pressible,  the  surface  of  the  body  is  cool,  vomiting  occurs  or  becomes  more  promi- 
nent, and  haemorrhage  is  now  apt  to  take  place.  The  escape  of  blood  into  the 
stomach,  its  retention  and  the  changes  which  it  there  undergoes,  and  its  subse- 
quent expulsion,  explain  the  dreaded  and  characteristic  symptom  known  as  "black 
vomit."  Tai'ry  stools  sometimes  are  observed.  Haemorrhage  elsewhere  is  also 
common,  occurring  from  the  gums,  the  nose,  eyes,  uterus,  kidneys,  into  the  skin, 
etc.  Albuminuria  with  casts  is  very  common.  Jaundice,  sometimes  of  a  lemon- 
yellow  hue,  comes  on,  and  is  rarely  lacking  in  severe  cases.  From  this  symptom 
the  name  of  the  disease  is  derived. 

In  cases  marked  by  more  or  less  complete  suppression  of  urine,  coma  and  con- 
vulsions, probably  largely  uraemic,  come  on.  Some  severe  cases  are  of  the  u  walk- 
ing "  type,  the  patients  going  about  while  the  malady  is  far  advanced,  or  even  up 
to  the  time  of  death.     As  a  rule,  however,  muscular  prostration  is  marked. 

If  the  disease  does  not  prove  fatal  in  this  third  stage,  convalescence  comes  on 
more  or  less  gradually,  and  is  followed  by  complete  recovery;  relapses,  however, 
occasionally  occur. 

The  duration  of  the  affection  is  variable  but,  on  the  whole,  short,  usually  being 
less  than  a  week. 

Diagnosis. — In  mild  cases  the  symptoms  are  not  distinctive,  and  the  diagnosis 
at  the  commencement  of  an  epidemic  is  not  likely  to  be  reached  except  by  an 
experienced  observer,  and  even  by  him  more  or  less  conjecturally.  During  an 
epidemic  the  severe  lumbar  pain,  the  headache,  the  suffusion  of  the  eyes,  and  the 
moderate  gastric  irritability,  are  all-sufficient  for  diagnostic  purposes.  Severer 
cases  are  also  marked  by  capillary  congestion  of  the  surface  of  the  body,  and  the 
third  stage  with  the  black  vomit,  haemorrhage,  jaundice,  slow  pulse,  scanty  urine, 
and  prostration  is  characteristic.  Of  course,  all  the  above  symptoms  are  not  pres- 
ent in  every  case.  The  only  disease  which  can  well  give  rise  to  confusion  is  remit- 
tent fever  with  jaundice.  This  affection  has  a  different  temperature  curve,  is  not 
confined  to  the  yellow-fever  zone,  is  controlled  by  quinine,  and  is  not  accompanied 
by  black  vomit. 

Prognosis. — This  varies  in  any  given  locality  with  the  character  of  the  preva- 
lent epidemic.  The  death-rate  is  sometimes  very  high,  sometimes  moderate ;  it  is 
greater  in  hospital  than  in  private  practice. 

In  the  first  stage  of  the  disease  the  chief  element  in  the  formation  of  the  prog- 
nosis seems  to  be  the  presence  of  marked  and  general  capillary  congestion  of  the 
skin,  a  symptom  which  foretells  a  severe  attack.  The  absence  of  this  symptom  is 
rather  less  important  than  its  presence.  Cases  may  turn  out  to  be  severe  in  which 
it  is  lacking.  The  frequent  deceptiveness  of  the  stage  of  calm  is  to  be  remem- 
bered. 

Yellowness,  black  vomit,  and  suppression  of  urine  are  symptoms  denoting  the 
greatest  gravity,  but  do  not  justify  the  complete  abandonment  of  hope. 

Treatment. — There  are  no  means  in  our  power  of  aborting  the  disease.  Pre- 
vention is  to  be  attained  by  cleanliness  in  its  large  sense,  and  by  careful  quaran- 
tine against  things  rather  than  persons.  Individuals  from  infected  localities  may 
safely  be  admitted  into  non-infected  localities,  provided  that  they  and  their  cloth- 
ing and  effects  are  thoroughly  disinfected.  Merchandise,  the  mails,  and  the  like, 
must  be  excluded  or  disinfected.  So  also  vessels  and  all  other  means  of  commu- 
nication. 

The  earlier  proper  treatment  can  be  instituted,  the  better.  Absolute  rest  and 
good  ventilation  are  the  first  requisites.  Emetics  and  cathartics  are  not  indicated 
by  the  disease  itself;  the  condition  of  the  stomach  and  bowels  should  be  inquired 
into,  and  indigestible  food  or  an  accumulation  of  faeces  should  be  removed  if 
present.     A  hot  mustard  foot-bath  early  in  the  attack  is  useful.     For  the  lumbar 


EPIDEMIC  CEREBRO-SPINAL  MENINGITIS.  103 

pains,  opium  or  morphine  arc  indicated.  Sinapisms,  or  other  similar  external 
counter-irritants,  with  ice  internally,  and  hydrocyanic  acid  or  chloroform,  are 
serviceable  against  gastric  irritability.  High  fever  is  to  be  combated  by  cold 
spongings,  the  wet  pack,  and  the  cold  bath.  For  haemorrhage,  styptic  remedies 
may  be  used,  though  it  is  doubtful  whether,  when  given  internally,  they  are  really 
of  much  benefit.  Of  course,  no  medication  is  to  be  resorted  to  which  is  likely  to 
heighten  a  tendency  to  emesis. 

Suppression  of  urine  is  to  be  met  by  dry  cups  to  the  loins,  diuretic  remedies 
internally  if  the  condition  of  the  stomach  allows,  or  the  hot-air  bath.  The  results 
of  pilocarpine  are  disappointing  according  to  Bemiss,  who  states  that  he  has  seen 
good  effects  from  large  enemata  of  water,  preferably  cold,  if  there  be  notable  fever 
in  these  cases.  Prostration  is  an  indication  for  the  use  of  alcoholic  stimulants, 
among  which  iced  dry  champagne  ranks  high.  It  will  be  seen  that  the  treatment 
is  entirely  symptomatic.  The  disease  is  self-limited,  has  a  short  course,  and  the 
patient  will  recover  if  he  can  be  kept  alive  until  the  poison  is  exhausted.  During 
the  attack  and  until  convalescence  is  thoroughly  established  the  management  of 
the  diet  is  all-important.  Small  quantities  of  the  most  easily  assimilable  food 
may  be  given  at  short  intervals  if  they  are  tolerated  by  the  stomach ;  if  not,  ali- 
mentation must  be  by  the  rectum,  and  the  lower  bowel  in  this  disease  is  generally 
in  a  fair  condition  for  this  method  of  nutrition. 

Courage  and  hopefulness  on  the  part  of  the  physician  may  do  much  good,  and 
the  services  of  a  skillful  and  experienced  nurse  are  of  the  utmost  importance.  I 
am  told  that  in  New  Orleans,  and  perhaps  elsewhere,  it  is  customary,  for  those 
who  are  not  protected  and  can  afford  this  course,  to  secure  in  advance  a  nurse  as 
soon  as  an  epidemic  breaks  out.  They  then  take  to  their  beds  at  the  first  sign  of 
illness.] 


CHAPTER  XVIII. 

EPIDEMIC   CEREBRO-SPINAL   MENINGITIS. 

{Spotted  Fever.     Cerebrospinal  Fever.) 

iEtiology. — The  epidemic  form  of  cerebro-spinal  meningitis  has  been  known 
only  since  the  beginning  of  this  century.  The  first  epidemics  were  observed  in 
southern  France  and  in  Geneva.  Smaller  ones  occurred  in  Germany  in  1822  and 
1853 ;  but  it  was  not  till  1863  that  the  disease  became  at  all  frequent  among  us. 
Since  that  date  there  have  been  more  or  less  extensive  epidemics  almost  every 
year.  The  southern  and  central  portions  of  Germany  are  particularly  liable  to 
them.     Sporadic  cases  may  occur  at  any  time. 

Most  of  the  epidemics  appear  in  the  winter  and  spring.  We  do  not  know  any 
particular  factors  which  promote  the  disease.  It  often  seems  to  be  decidedly 
endemic.  Barracks,  work-houses,  and  the  like  have  been  marked  by  tolerably 
extensive  epidemics.  Whether  the  disease  can  be  carried  by  patients  to  places 
previously  free  from  it  is  still  uncertain.  It  is  not  directly  contagious.  Children 
and  young  adults  are  the  most  frequent  victims ;  but  now  and  then  elderly  persons 
are  attacked.     Sex  can  not  be  shown  to  have  much  influence. 

That  the  disease  is  infectious  is  clearly  shown  not  only  by  its  epidemic  and  en- 
demic character,  but  by  its  whole  course.  The  peculiar  pathogenic  organisms 
and  the  manner  of  infection  have  not  yet,  however,  been  ascertained.  It  is  an 
interesting  fact  that  Fränkel's  pneumonia  bacilli  have  been  recently  several 
times  detected  in  the  purulent  exudation  upon  the  meninges,  so  that  some  investi- 
gators have  suggested  that  croupous  pneumonia  and  epidemic  meningitis  may 


104  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

be  closely  related  from  an  aetiological  standpoint,  even  if  they  are  not  actually 
two  forms  of  a  single  disease.  The  author  can  not  as  yet  wholly  accept  this 
view.  It  is  indeed  certain  that  the  pneumonia  bacilli  may  sometimes  secondarily 
reach  the  meninges  and  here  excite  a  purulent  suppuration  ("  pneumatic  menin- 
gitis," that  is,  metastatic  meningitis  complicating  pneumonia) ;  nor  is  it  impos- 
sible that  the  pneumonia  bacilli  sometimes,  and  particularly  at  the  time  of  an  epi- 
demic of  pneumonia,  do  enter  directly  into  the  meninges  and  occasion  a  menin- 
gitis ;  but  for  the  genuine  epidemic  meningitis  we  must  seek  some  special  pathog- 
enic cause.  Otherwise  it  would  be  impossible  to  explain  why  the  same  germs 
should  sometimes  find  their  way  exclusively  into  the  lungs  and  at  other  times 
and  in  other  localities  invariably  into  the  cerebral  meninges. 

With  regard  to  the  gate  of  entrance  of  infection  in  primary  epidemic  menin- 
gitis, perhaps  the  specific  poison  may  enter  through  the  nostrils  and  the  cribriform 
plate  to  the  otherwise  so  well  protected  envelopes  of  the  central  nervous  system. 

[Sanitary  conditions  seem  to  play  a  less  important  role  in  this  than  in  many 
other  infectious  diseases.  During  the  epidemic  which  visited  New  England  in 
1873  the  writer  was  interne  at  the  Massachusetts  General  Hospital,  and  there  saw 
a  number  of  cases.  The  disease  was  also  prevalent  among  horses  at  the  same 
time,  and  it  is  curious  to  note  that  a  like  association  of  the  affection  in  men  and 
animals  was  observed  in  Vermont  in  1811,  and  in  New  York  city  in  1871.  During 
the  year  1873,  216  deaths  were  returned  as  due  to  this  malady  in  the  city  of 
Boston.] 

Pathological  Anatomy. — The  autopsy  discloses  an  acute  purulent  cerebro-spinal 
leptomeningitis.  It  is  only  in  rapidly  fatal  cases  that  slight  and  incipient  lesions 
have  been  met  with.  As  a  rule,  the  extent  and  intensity  of  the  objective  lesions 
correspond  to  the  severity  of  the  symptoms.  In  the  brain  the  purulent  inflamma- 
tion attacks  the  convexity  as  well  as  the  base.  It  is  usually  most  marked  along 
the  larger  blood-vessels  and  in  the  fissures  of  the  cortex.  Of  the  spinal  cord  the 
posterior  surface  suffers  most.  Frequently  the  lumbar  portion  is  more  affected 
than  the  parts  above.  It  is,  however,  exceptional  for  the  disease  to  be  limited  to 
the  meninges  ;  it  is  prone  to  extend  into  the  underlying  parenchyma.  The  micro- 
scope reveals  clumps  of  pus-corpuscles  about  the  blood-vessels,  where  they  pene- 
trate into  the  tissues,  and  not  infrequently  there  are  numerous  centers  of  genuine 
encephalitis.  These  latter  may  be  visible  to  the  naked  eye.  Exceptionally  there 
may  even  be  cerebral  abscesses  of  considerable  size.  The  vessels  are  distended 
with  blood,  clear  into  the  central  ganglia,  and  ecchymoses  are  frequent.  The 
cerebral  ventricles  are  usually  enlarged,  and  filled  with  a  cloudy  serum,  or  even 
witb  pus.  It  is  plain  that  these  lesions  of  the  cerebro-spinal  parenchyma  greatly 
modify  the  clinical  picture,  and  that  they  must  frequently  have  more  to  do  with 
the  severity  of  the  symptoms  than  has  the  leptomeningitis  itself. 

Clinical  History, — Prodromata  are  relatively  rare,  and  if  present  they  are  not 
severe,  being  confined  to  general  malaise,  with  slight  headache,  and  pain  in  the 
limbs.  Usually  the  disease  begins  rather  suddenly;  there  is  intense  headache, 
often  mainly  felt  in  the  back  of  the  head,  pain  and  stiffness  in  the  back  of  the 
neck,  and  great  general  discomfort.  It  is  not  rare  for  vomiting  to  occur  at  first. 
Very  often  there  are  among  the  early  symptoms  such  important  mental  disturb- 
ances as  stupor  or  delirium.  There  is  usually  fever  from  the  first.  An  initial 
rigor  may  occur,  but  it  is  not  the  rule. 

The  intensity  of  these  first  symptoms  is  uncertain.  Subsequently  to  them 
the  course  of  the  disease  may  vary  greatly.  First  there  are  very  acute,  vio- 
lent forms,  termed  "  explosive  "  {meningitis  cerebrospinalis  siderans,  meningite 
foudroyante),  where  the  cerebral  symptoms  are  very  severe,  and  the  patient 
survives  only  a  few  days  or  even  hours.     Again,  there  are  abortive  cases.     These 


EPIDEMIC  CEREBROSPINAL  MENINGITIS.  105 

begin  with  equally  threatening1  symptom^,  hut  after  a  few  days  completely 
recover  with  remarkable  rapidity.  The  majority  of  cases  last  about  two  to 
four  weeks.  In  severe  cases  death  may  come  as  early  as  the  first  week.  The 
disease  is  often  protracted  to  six  or  eight  weeks'  duration,  or  even  longer,  and 
may  end  in  death  after  all.  Cases  that  last  a  good  while  sometimes  exhibit 
a  remarkably  intermittent  character.  Finally,  the  number  of  mild  cases  is  not 
small  in  which  none  of  the  symptoms  are  very  pronounced,  and  recovery  is 
relatively  early. 

The  symptoms  of  the  disease  may  be  divided  into  (1)  the  severe  general  symp- 
toms, referable  to  the  brain  and  spinal  cord;  (2)  the  more  localized,  nervous  symp- 
toms; and  (3)  the  results  of  the  constitutional  infection,  including  fever  and  dis- 
eases localized  in  other  parts  of  the  body. 

1.  Among  the  less  definite  cerebral  symptoms  headache  is  important.  It  is 
usually  terribly  severe.  It  is  chiefly  occipital,  but  sometimes  is  frontal  or  tem- 
poral. Like  most  of  the  symptoms  of  meningitis,  the  headache  undergoes  very 
frequent  changes  in  intensity  during  the  course  of  the  disease.  For  a  time  it  may 
remit,  only  to  recur  with  fresh  severity.  Marked  vertigo  and  a  sense  of  fullness 
in  the  head  may  accompany  it. 

The  pain  in  the  head  is  re-enforced  by  intense  pain  in  the  nape  of  the  neck  and 
back,  due  to  the  spinal  meningitis.  There  is  almost  always  considerable  tender- 
ness along  the  whole  spinal  column.  The  erector  spinae  is  contracted,  making 
the  back  straight  and  rigid,  or  even  producing  opisthotonos;  and  the  head  is 
bent  backward  by  the  reflex  contraction  of  the  muscles  in  the  back  of  the  neck. 

In  most  of  the  severe  cases  intelligence  is  blunted ;  we  find  all  degrees  of  dis- 
turbance, from  slight  drowsiness  to  delirium  on  the  one  hand,  or  deep  coma  on  the 
other.  These  symptoms  likewise  may  undergo  frequent  variation  in  their  inten- 
sity.    General  convulsions  occur  in  very  sevei'e  cases  alone,  and  are  of  evil  omen. 

The  vomiting  is  also  to  be  regarded  as  of  cerebral  origin.  It  frequently  is  an 
early  symptom,  but  may  be  deferred. 

2.  Symptoms  referable  to  the  individual  cerebral  nerves  are  manifold  and 
variable.  The  most  frequent  disturbances  are  in  the  nerves  that  supply  the  mo- 
tores  oeuli.  They  include  strabismus ;  nystagmus,  or  slow  movements  independ- 
ent of  volition;  unilateral  or  bilateral  ptosis;  slow  reaction  of  the  pupils,  or 
inequality  of  them,  or  myosis  or  mydriasis.  In  the  area  of  distribution  of  the 
facial  there  is  often  a  noticeable  contraction  of  the  muscles,  giving  the  face  a 
peculiar,  painfully  distorted  look.  Trismus,  or  tetanus  of  the  masseters,  is  rare,  and 
usually  a  bad  sign. 

Disturbance  of  the  nerves  of  special  sense  is  frequent.  Deafness  may  be 
due  to  the  stupor,  but  is  often  the  result  of  an  extension  of  the  inflammation 
to  the  acoustic  nerve.  The  purulent  inflammation  may  be  propagated  as  far  as 
the  labyrinth,  or  even  into  the  middle  ear.  Tinnitus  aurium  is  also  frequent. 
Disturbances  of  vision  are  far  less  frequently  observed,  but  optic  neuritis  has 
been  repeatedly  found  by  the  ophthalmoscope.  Severe  purulent  irido-choroiditis 
has  been  also  observed.  It  is  probably  chie  to  extension  of  the  inflammation 
along  the  sheath  of  the  optic  nerve.  Conjunctivitis  and  keratitis  sometimes  occur ; 
but  they  are  probably  caused  by  external  injuries  rendered  possible  by  the  imper- 
fect closure  of  the  lids,  or  the  diminished  sensitiveness  of  the  parts.  We  have 
several  times  found  the  sense  of  smell  diminished. 

Disturbances  in  the  area  of  distribution  of  the  spinal  nerves  are,  on  the  whole, 
less  frequent.  The  only  one  of  value  in  diagnosis  is  the  cutaneous  hyperesthesia. 
It  is  apt  to  be  particularly  severe  in  the  extremities,  and  it  may  be  so  extreme  that 
the  light  touch  of  a  finger  or  a  needle  causes  great  pain.  Sometimes  there  is  a 
slight  twitching  in  the  muscles  of  the  extremities.     This  has,  however,  no  special 


106  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

significance.  There  is  often  rigidity  and  stiffness  of  the  muscles.  Kernig  has 
called  attention  to  the  frequent  appearance  of  flexure  contractions  in  the  legs, 
and  sometimes  also  in  the  arms,  if  the  patients  are  caused  to  sit  up  or  if  the 
thigh  is  passively  hent  upon  the  trunk.  As  might  he  expected,  there  is  no 
invariable  rule  about  the  reflexes.  The  cutaneous  reflexes  are  usually  well 
marked,  and  the  tendon  reflexes  may  be;  but  in  some  cases  we  have  found  the 
tendon  reflexes  markedly  diminished  or  even  abolished.  Such  a  condition  is 
probably  due  to  some  lesion  of  the  fibers  of  the  posterior  nerve-roots. 

All  of  the  nervous  symptoms  above  enumerated  result  from  one  of  two 
causes — either  the  roots  of  the  nerves  are  affected  by  the  purulent  exudation, 
or  the  inflammation  extends  inward  to  the  central  organs  themselves.  This 
extension  is  the  explanation  also  of  other  symptoms  sometimes  observed — viz., 
hemiplegia,  paraplegia,  partial  convulsions,  and  aphasia. 

3.  In  addition  to  all  these  nervous  disturbances,  we  see  also  symptoms  refer- 
able to  other  parts  of  the  body.  Of  this  class  there  is  one  cutaneous  affection  which 
is  a  very  valuable  aid  to  diagnosis.  Herpes  labialis  or  herpes  facialis  is  apt  to 
appear  soon  after  the  beginning  of  the  meningitis.  It  is  seen  in  more  than  half 
the  cases,  and  as  frequently  in  severe  as  in  mild  attacks.  Other  eruptions  occur 
now  and  then — e.  g.,  roseola,  urticaria,  or  petechiae.  Sometimes  they  are  so  sym- 
metrically distributed  upon  the  two  halves  of  the  body  as  to  suggest  the  idea  of  a 
nervous  origin. 

The  digestive  system  seldom  displays  severe  symptoms  beyond  the  vomiting 
already  mentioned.  Anorexia  and  constipation  are,  indeed,  usually  present,  as 
in  many  grave  diseases.  We  have  seen  mild  dysentery  a  few  times.  Now  and 
then  a  slight  jaundice  has  been  noticed.  The  spleen  is  often  somewhat  swollen, 
but  very  rarely  attains  great  size. 

Swelling  of  the  joints  has  been  observed  quite  often ;  it  is  much  moi'e  frequent 
in  some  epidemics  than  in  others.  The  enlargement  may  be  an  early  or  a  later 
symptom.     It  does  not  usually  prove  to  be  of  grave  omen. 

The  urinary  apparatus  is  seldom  affected.  The  urine  may  contain  some  albu- 
men and  a  few  casts.  Polyuria  is  an  interesting  symptom,  probably  of  nervous 
origin.  It  is  more  apt  to  occur  in  the  latter  part  of  the  disease.  In  a  number  of 
cases  sugar  has  been  found  in  the  urine.  Cystitis  is  a  secondary  disorder  which 
is  not  very  rare,  particularly  in  severe  cases  where  the  catheter  has  been  used. 

Pulmonary  and  bronchial  symptoms  are  likewise  secondary.  They  occur  very 
often  in  bad  cases.  It  is  evident  how  easily  the  stupor  of  the  patient  may  lead  to 
the  inhalation  of  solid  matter,  with  consequent  bronchitis  and  lobular  pneu- 
monia. 

Lesions  of  the  circulatory  system  are  rare.  Acute  endocarditis  has  been  ob- 
served only  a  few  times.  The  pulse  is  usually  somewhat  accelerated,  seldom  ren- 
dered slower.  Very  frequently  the  pulse-rate  is  remarkably  variable,  undoubt- 
edly because  of  variation  in  the  supply  of  nervous  force.  Slight  irregularities  in 
the  pulse  are  also  common. 

4.  The  fever  in  epidemic  meningitis  conforms  to  no  single  type.  It  does  not 
correspond  at  all  to  the  severity  of  the  other  symptoms ;  the  worst  cases  may  run 
their  course  with  little  or  no  fever.  In  most  cases  the  fever  has  irregular  remis- 
sions. It  seldom  exceeds  104°  (40°  C).  Sometimes  the  fever  exhibits  a  decidedly 
intermittent  character.  It  is  in  these  cases  particularly  that  we  find  the  variation 
in  the  intensity  of  all  the  symptoms  of  which  mention  has  been  made  repeatedly. 
The  variations  in  the  temperature  do  not,  however,  always  run  parallel  with  the 
changes  in  the  other  symptoms.  In  mild  cases  the  fever  is  usually  moderate  and 
brief.  The  abortive  attacks  may  present  high  temperatures  at  first,  but  these 
quickly  abate.     In  case  of  a  fatal  issue  there  is  sometimes  hyperpyrexia  before 


EPIDEMIC  CEREBRO-SPINAL  MENINGITIS.  107 

death,  reaching  108°  to  109°  (42°-43°  C).  In  the  severer  but  not  fatal  cases  the 
fever  declines  slowly  but  irregularly.  The  fever  may  be  over,  long  before  the 
other  symptoms  disappear. 

It  is  impossible  to  portray  all  the  forms,  symptoms,  and  courses  the  di< 
may  have.  The  chief  forms  have  been  already  mentioned;  but  in  reality  these 
are  only  types  which  run  into  one  another  without  sharply  defined  border-lin»  8. 
It  is  in  itself  a  characteristic  of  epidemic  meningitis  that  most  of  the  more  tedious 
cases  have  a  variable,  uncertain  course.  We  may  even  meet  with  a  complete 
intermission  of  all  the  symptoms,,  lasting  for  quite  a  while,  so  that  the  return  of 
the  trouble  may  fairly  be  called  a  relapse. 

Sequelae  are  not  rare  after  severe  cases.  Persistent  deafness  is  the  most  fre- 
quent. It  results  from  the  complications,  already  mentioned,  which  affect  the 
labyrinth  and  the  middle  ear.  Little  children  may  become  deaf  and  dumb. 
Again,  vision  may  be  deranged,  because  of  retinitis,  atrophy  of  the  optic  nerve, 
or  corneal  opacities,  etc.  It  is  not  very  rare  for  meningitis  to  leave  grave  nerv- 
ous disorders  behind  it.  These  are  frequently  the  symptoms  of  a  chronic  hydro- 
cephalus. We  may  observe  headache,  sudden  unconsciousness,  or  even  convul- 
sions, mental  impairment,  and  weakness  of  the  extremities.  Or  there  may  be 
localized  disturbances  due  to  permanent  injury  of  limited  portions  of  the  brain  or 
spinal  cord,  such  as  hemiplegia,  paraplegia,  and  aphasia.  From  many  of  these 
conditions  there  may  be  a  gradual  recovery,  but  others  prove  incurable. 

The  diagnosis  of  cerebro-spinal  meningitis  is  not  difficult  in  a  well-developed 
case,  particularly  if  the  prevalence  of  an  epidemic  puts  us  in  mind  of  the  disease. 
Diagnosis  is  more  difficult  in  sporadic  cases,  and  most  of  all  when  the  patient 
does  not  come  under  observation  till  he  is  very  ill  and  when  we  can  not  obtain  the 
previous  history.  Important  factors  are  the  abrupt  onset,  the  speedy  appearance 
of  grave  cerebral  symptoms,  the  characteristic  headache  and  pain  in  the  back,  the 
stiffness  of  the  neck,  and  the  herpes  labialis. 

If  we  find  evident  symptoms  of  meningitis,  we  have  still  to  decide  whether  the 
case  is  one  of  primary  epidemic  disease,  or  secondary,  perhaps  due  to  extension 
from  some  other  jiart.  Bearing  this  last  possibility  in  mind,  we  should  examine 
the  ears  carefully;  for,  as  is  well  known,  chronic  otitis  media  may  set  up  a  puru- 
lent meningitis.  Again,  it  may  be  very  difficult  to  exclude  a  tubercular  menin- 
gitis. Here  we  should  consider  other  conditions  that  might  render  tuberculosis 
probable,  such  as  the  general  condition  of  the  patient,  heredity,  previous  pleurisy, 
the  results  of  thoracic  examination,  or  scrofulous  disease  of  the  bones  or  joints. 
The  existence  of  herpes  points  toward  epidemic  meningitis,  for  it  is  exceptional 
in  the  other  forms  of  the  disease.  It  is  sometimes  difficult  to  distinguish  between 
meningitis  and  severe  cases  of  other  acute  infectious  diseases — e.  g.,  typhoid 
fever  and  septic  diseases.     Here  we  must  weigh  all  the  circumstances  carefully. 

This  is  a  good  opportunity  to  mention  the  secondary  meningitis  which  is 
said  to  occur  with  relative  frequency  just  at  the  time  of  an  epidemic.  The  com- 
bination of  croupous  pneumonia  (q.  v.)  with  purulent  meningitis  has  been 
repeatedly  observed.  Still,  it  is  not  easy  to  determine  whether  the  cause  of  this  sec- 
ondary meningitis  is  actually  identical  with  that  of  the  epidemic  form  (vide 
supra).  In  other  acute  diseases,  like  typhoid  and  articular  rheumatism,  when 
they  occur  at  the  time  of  an  epidemic,  the  ''  tendency  to  meningitis  "  is  potent 
enough  to  make  meningeal  symptoms  more  frequent  than  usual.  It  has  not  been 
clearly  demonstrated,  however,  that  this  fact  is  actually  due  to  the  epidemic  men- 
ingitis. 

The  prognosis  depends  chiefly  upon  the  severity  of  the  cerebral  symptoms. 
Yet  we  should  be  guarded  in  our  utterances,  even  when  the  case  seems  mild,  or 
has  apparently  made  the  first  steps  toward  convalescence.     The  disease  sometimes 


108  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

changes  for  the  worse  at  a  late  period.  In  general  the  mortality  is  ahout  thirty  to 
forty  per  cent.  Probably  this  estimate  does  not  take  into  account  many  very 
mild  cases. 

Treatment  is  purely  symptomatic.  There  is  no  specific  for  meningitis.  A 
valuable  remedy  is  cold  applications.  Ice-bags  are  placed  upon  the  head,  and,  if 
possible,  along  the  spine.  There  are  long  and  narrow  rubber  ones  for  the  latter 
purpose.  These  applications  are  borne  well  by  most  patients  and  afford  decided 
relief.  The  local  abstraction  of  blood  has  also  an  undeniably  beneficial  influence, 
however  difficult  this  may  be  to  explain.  Leeches  are  put  behind  the  ears,  and 
cupping-glasses  on  the  back  of  the  neck  and  along  the  spine.  Mercurial  ointment 
is  often  rubbed  in,  not  only  locally  but  also  in  the  same  way  as  in  treating  syphi- 
lis. Its  use  is  doubtful.  The  narcotics  are  of  great  value.  The  best  is  morphine 
given  subcutaneously.  It  lessens  the  pain,  and  often  affords  the  uneasy  and  deliri- 
ous patient  rest  and  sleep.  Chloral  and  bromide  of  potash  may  also  be  employed. 
Iodide  of  potash  is  often  given  internally,  to  the  amount  of  twenty  to  thirty  grains 
(grm.  l-5-2)  in  a  day.  It  is  said  to  act  as  an  ''absorbent,"  particularly  in  tedious 
cases. 

The  fever  hardly  ever  requires  special  treatment.  If  the  fever  intermits,  still 
quinine  exerts  no  permanent  influence.  Antipyrine  is  better  borne,  and  it  also 
sometimes  relieves  the  nervous  symptoms.  Bathing  involves  manipulations  which 
most  patients  find  unpleasant  and  painful,  so  that  baths  can  seldom  be  employed, 
at  least  in  the  more  acute  stages  of  the  disease.  Later,  warm  baths  are  often 
beneficial.  Local  complications — e.  g.,  affecting  the  eye  or  the  ear — require  special 
treatment.  The  swelling  of  the  joints  which  sometimes  occurs  we  have  thought 
to  be  somewhat  relieved  by  salicylic  acid. 


CHAPTER  XIX. 

SEPTIC  AND  PYEMIC  DISEASES. 

{Spontaneous  Septticopycemia.) 

The  septic  and  pyasrnic  processes  which  follow  serious  injuries  or  operations 
belong  to  surgery ;  but  analogous  diseases  occur  in  persons  who  are  apparently  in 
perfect  condition.  They  take  the  form  of  an  extremely  severe  acute  infectious 
disease,  usually  fatal.  There  is  often  the  greatest  difficulty  in  diagnosticating 
these  cases  during  life.  Probably  the  most  intelligible  way  in  which  to  present 
these  interesting  and  clinically  important  diseases  will  be  to  start  with  their 
pathology,  and  subsequently  to  speak  of  their  aetiology  and  clinical  history. 

Pathological  Anatomy  and  iEtiology . — The  most  striking  features  at  the  autopsy 
of  such  cases  is  that  there  is  never  found  a  lesion  of  one  organ  exclusively.  Several, 
or  it  may  be  almost  all  of  the  organs,  exhibit  numerous  limited  foci  of  disease.  The 
lesions  sometimes  consist  for  the  most  part  of  multiple  abscesses,  sometimes  of 
numerous  ecchymoses,  and  sometimes  of  combinations  of  the  two.  The  abscesses 
are  found  chiefly  in  the  lungs,  kidneys,  liver,  spleen,  muscles,  heart,  brain,  and 
thyroid  gland.  Quite  extensive  purulent  inflammation  is  also  found.  This  attacks 
the  joints  by  preference,  but  also  the  pleura  and  meninges  and  the  eye,  where 
it  causes  purulent  choroiditis,  panophthalmitis,  and  purulent  degeneration  of  the 
vitreous.  The  ecchymoses  are  most  frequent  upon  the  surface  of  the  body,  the 
serous  membranes  (e.  g.,  the  pericardium  and  the  pleura),  the  retina,  and  conjunc- 
tiva; and  also  in  the  brain  and  the  pelvis  of  the  kidney.  Besides  these  multiple 
abscesses  and  ecchymoses,  there  is  frequently  another  disorder,  which  seems  to  be 


SEPTIC  AND  PYEMIC  DISEASES.  109 

the  very  focus  of  the  disease,  viz.,  acute  ulcerative  endocarditis  (cf.  the  appro- 
priate chapter).  This  usually  attacks  the  mitral  valve,  more  rarely  the  valves 
of  the  aorta,  and  quite  exceptionally  the  valves  of  the  right  side  of  the  heart. 
Finally  come  a  number  of  changes  common  to  all  severe  constitutional  infectious 
diseases — acute  splenic  tumor,  "cloiidy  swelling"  of  the  liver  and  kidneys,  a  dry- 
ness and  dark-red  color  of  the  muscles,  etc. 

A  glance  over  this  pathological  picture  makes  us  feel  certain  that  some  per- 
nicious agency  pervades  the  whole  system.  And  this  factor  we  can,  in  all  cases, 
demonstrate  beyond  a  doubt  to  be  bacteria.  In  this  way  is  established  the  etio- 
logical unity  of  many  forms  of  disease  which  were  once  regarded  as  quite  distinct 
because  of  their  different  localizations,  for  instance,  endocarditis,  osteomyelitis,  and 
phlegmon.  These  micro-organisms  are  found  not  only  in  the  exudations  due  to  the 
endocarditis,  but  also  in  the  midst  of  numerous  small  foci  of  inflammation  situated 
in  the  internal  organs,  where  they  usually  completely  fill  some  little  blood-vessel 
with  what  is  called  an  embolus  of  micrococci.  The  large  foci  of  inflammation  visi- 
ble to  the  naked  eye  are  mostly  purulent — i.  e.,  are  abscesses.  Most  of  the  internal 
viscera  also  contain  very  minute  foci,  devoid  of  nuclei,  and  in  a  state  of  "  coagula- 
tion-necrosis." These  are  visible  through  the  microscope  alone.  They  may  be 
combined  with  ecchymoses,  and  usually  they  are  when  seen  already  surrounded 
by  a  zone  of  secondary  inflammation.  This  necrosis  of  tissue  seems  to  be  the  first 
thing  which  the  bacteria  accomplish.  The  cixtaneous,  retinal,  and  other  ecchy- 
moses are  frequently  attended  by  the  presence  of  bacteria;  but  this  relation  is  not 
always  observed.  The  relations  here  are  perplexed,  because  we  have  to  consider 
not  merely  the  especial  peculiarities  of  the  different  forms  of  bacteria  (vide  infra), 
but  also  the  direct  effect  of  the  micro-organisms  themselves  in  distinction  from  the 
chemical  poisons  ("  toxines  ")  generated  by  the  same.  The  formation  of  pus  itself 
seems  to  be  invariably  dependent  upon  the  presence  of  bacteria,  while  on  the  other 
hand  the  haemorrhages  may  apparently  follow  purely  chemical  intoxication.  The 
prevailing  custom  is  to  term  the  cases  of  multiple  abscess  pyaeniic,  and  those  where 
there  are  merely  ecchymoses  and  foci  of  inflammation,  without  actual  suppura- 
tion, septic  in  the  narrower  sense  of  the  term.  But  as  the  two  forms  are  often 
combined,  we  also  speak  of  a  "  septicopyemia."  From  a  strictly  etiological  stand- 
point it  is  not  probable  that  all  the  septicopyemic  diseases  are  to  be  regarded  as 
identical.  It  is  certain  that  in  most  cases  of  pyaemia  the  Streptococcus  pyogenes 
may  be  regarded  as  the  special  cause  of  the  disease.  In  less  frequent  instances  it 
is  the  Staphylococcus  pyogenes  aureus  which  enters  into  the  general  circulation 
and  produces  pyaemic  conditions,  and  it  is  probable  that  still  other  varieties  of 
bacteria  are  sometimes  concerned.  Whether  in  human  beings  specific  septicemic 
bacteria  are  ever  present  is  still  unsettled.  The  general  opinion  is,  as  already 
mentioned,  that  septicemia  in  the  narrower  acceptation  of  the  word  corresponds 
more  to  an  intoxication  of  the  body,  whether  due  to  the  toxines  of  putrefaction  or 
to  those  generated  by  the  pyogenic  bacteria.  Brieger's  admirable  investigations 
have  shown  that  the  Streptococcus  pyogenes  produces  large  amounts  of  trimethyl- 
amin  and  the  staphylococcus  large  amounts  of  ammonia. 

Of  course  the  bacteria,  which  are  the  real  cause  of  the  disease,  must  have  pene- 
trated into  the  body  from  the  external  world.  In  fact,  careful  search  will  reveal, 
in  the  great  majority  of  cases,  the  place  of  infection.  It  follows  that  the  idea  of 
an  actual  "spontaneous"  pyemia,  arising  within  the  system,  must  be  entirely 
abandoned. 

The  factors  which  most  frequently  excite  septic  or  pyemic  infection  are  as  fol- 
low: 1.  The  condition  subsequent  to  labor  or  abortion,  particularly  the  latter. 
The  raw  surface  of  the  uterus  furnishes  ingress  to  the  septic  poison.  Nor  is  it  by 
any  means  the  invariable  rule  that  the  uterus  and  its  appendages  should  exhibit 


HO  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

any  considerable  pathological  change  as  a  result  of  this  absorption.  We  do  find, 
often  enough,  diphtheritic  and  gangrenous  inflammation  at  the  place  where  the 
placenta  was  inserted,  or  purulent  thrombi  in  the  veins  of  the  uterus  and  of  the 
pelvis;  but  in  other  cases  the  uterus  is  merely  a  gate  of  entrance  for  the  poison, 
remaining  itself  unharmed.  2.  The  septic  poison  may  also  be  absorbed  through 
slight  abrasions  of  the  skin,  etc. ;  and  these  may  be  almost  completely  healed  by 
the  time  the  severe  symptoms  of  disease  are  developed.  Bed-sores  belong  in  this 
category.  3.  Ulcers,  of  the  mucous  membranes  may  give  rise  to  infection.  This 
is  the  explanation  of  those  cases  of  sepsis  which  complicate  typhoid  fever,  dysen- 
tery, or  diphtheria.  4.  Lastly,  we  sometimes  find  no  other  source  for  the  pyaemia 
than  a  suppurating  disease  of  the  bones,  joints,  or  other  parts,  previously  existing. 
The  above  enumeration  by  no  means  exhausts  all  the  possibilities.  Still,  it  will  be 
found  to  explain  most  cases.  The  more  minutely  we  search  for  a  possible  place 
of  entrance  for  the  septic  virus,  the  less  often  we  fail  to  find  one.  [The  editor  has 
seen  two  clear  cases,  one  confirmed  by  autopsy,  of  general  septic  infection  and 
malignant  endocarditis  as  a  sequel  of  gonorrhoea.] 

When  the  poison  has  once  made  its  way  into  the  system,  it  can  be  disseminated 
through  various  channels.  It  may  be  carried  by  the  lymphatics  into  the  general 
circulation.  A  purulent  phlebitis  may  be  excited  at  the  point  of  infection ;  and 
this  in  turn  may  excite,  cbiefly  through  embolism,  secondary  abscesses.  These 
abscesses  occur  first  in  the  lungs  and  then  in  other  organs.  It  seems  to  be  possi- 
ble for  a  purulent  phlebitis  to  arise  in  a  vein  remote  from  the  place  of  infection. 
The  valves  of  the  heart  often  greatly  promote  the  dissemination  of  the  septic  mat- 
ter. The  virus  is  prone  to  fasten  upon  them,  probably  purely  from  mechanical 
causes.  This  results  in  acute  endocarditis.  In  such  a  case  we  must  regard  the 
endocarditis  merely  as  one  of  the  symptoms  of  the  universal  septic  infection.  But 
the  valves  are  a  fertile  soil  for  the  propagation  of  the  poison,  and  emboli  carry 
away  from  them  a  great  deal  of  infectious  matter  to  the  various  organs ;  and  so 
the  acute  endocarditis  becomes  in  many  instances  the  central  factor  in  the  whole 
process.     Yet  in  other  cases  there  is  little  or  no  endocarditis. 

Clinical  History. — It  is  our  intention  to  discuss  below  those  cases  chiefly  which 
are  of  interest  to  the  physician  rather  than  the  surgeon — i.  e.,  where  the  septico- 
pyseniia  is  an  apparently  primary,  acute,  and  grave  disease.  Many  of  the  essential 
traits  of  this  type  of  disease  are  identical  with  those  of  the  pyaemia  which  compli- 
cates the  effects  of  serious  wounds  or  the  inflammation  subsequent  to  childbirth ; 
but  it  is  precisely  because  no  cause  at  all  presents  itself  that  many  cases  of  the 
disease  seem  so  obscure,  and  are  so  often  wrongly  diagnosticated.  Besides,  the 
patient  may  be  very  ill  indeed  before  the  physician  sees  him ;  and  this  adds  greatly 
to  the  difficulties  of  a  correct  diagnosis. 

The  beginning  of  the  disease  is  usually  rather  abimpt.  An  apparently 
healthy  person  is  attacked  with  febrile  symptoms,  headache,  and  "  rheumatic  " 
pains  in  the  muscles,  joints,  and  loins.  There  may  also  be  gastro-intestinal  symp- 
toms of  considerable  severity,  including  vomiting  and  diarrhoea.  Usually  the 
patient  feels  ill  enough  to  take  speedily  to  his  bed.  The  symptoms  now  increase 
rapidly,  and  develop  into  a  severe  illness  which  may  resemble  either  a  bad  case  of 
typhoid  fever  or  miliary  tuberculosis.  Or  the  cerebral  symptoms,  such  as  head- 
ache, stupor,  and  delirium,  may  become  so  prominent  that  the  attack  seems  like 
meningitis.  If  the  trouble  in  the  joints  {vide  infra)  predominates  and  there  are 
signs  of  endocarditis,  the  disease  may  at  first  be  taken  for  a  violent  attack  of  acute 
articular  rheumatism. 

Taking  up  the  separate  symptoms,  we  shall  first  name  those  which  belong  to 
every  severe  acute  infectious  disease  and  have  nothing  characteristic  about  them. 
In  this  list  belong  the  general  prostration,  the  anorexia,  the  mental  disturbance, 


SEPTIC  AND  PYiEMIC  DISEASES.  Ill 

the  stupor  and  delirium,  the  headache,  the  subjective  symptoms  of  fever,  the  dry- 
ness of  the  tongue,  and  finally  the  acute  splenic  tumor  which  can  often  be  made 
out.  There  are,  however,  other  and  more  characteristic  symptoms;  and  it  is 
chiefly  upon  these  that  the  diagnosis  rests,  provided  we  can  make  one  at  all. 
These  are : 

1.  The  Course  of  the  Fever. — In  many  cases  it  must  be  confessed  that  this  is 
not  at  all  characteristic.  It  may  even  he  so  like  that  of  typhoid  fever  as  to  lead  to 
a  wrong  diagnosis.  But  in  other  cases  the  temperature-curve  does  aid  us  greatly, 
viz.,  when  it  represents  an  intermitting  fever  with  marked  elevations,  reaching 
106°  (41°  C.)  and  higher,  and  often  accompanied  by  a  chill,  and  with  subsequent 
deep  depressions.  The  curve  may  thus  come  to  resemble  closely  that  of  a  quotid- 
ian or  even  tertian  intermittent  fever.  Sometimes,  again,  the  course  of  the  fever 
is  made  up  of  similar  paroxysmal  elevations,  separated  by  periods  of  ordinary  re- 
mitting fever. 

2.  Cutaneous  Symptoms. — These  are  very  frequent,  and  a  great  aid  to  diag- 
nosis. The  haemorrhages  into  the  skin  are  of  chief  importance.  They  may  he 
either  punctiform  petechiae  or  more  extensive  ecchymoses.  If  petechia?,  it  may 
be  very  hard  to  distinguish  between  sepsis  and  the  purpura  of  small-pox  (q.  v.). 
Of  other  cutaneous  appearances,  the  first  in  relative  frequency  is  an  erythema 
resembling  scarlatina.  It  is  not  improbable,  as  we  have  already  said,  that  many 
cases  which  have  been  described  as  severe  scarlet  fever  occurring  during  child- 
bed were  in  reality  septic  disease.  Eoseola,  wheals,  pustulous  eruptions,  herpes, 
and  phlegmonous  inflammations  have  also  been  observed. 

3.  Ocular  Disturbances. — The  purulent  inflammations  of  the  eye,  which  are 
probably  of  embolic  origin  and  which  may  develop  into  diffuse  septic  panoph- 
thalmitis, have  been  known  for  some  time.  Lately,  Litten  and  others  have  called 
attention  to  more  minute  changes  in  the  fundus  of  the  eye.  These  are  revealed 
through  the  ophthalmoscope,  and  have  great  diagnostic  value.  Chief  among 
them  is  retinal  haemorrhage,  which  is  sometimes  accompanied  by  a  white  spot  in 
the  center,  corresponding  to  a  necrosis  of  the  retina  in  that  place ;  but  there  may 
be  similar  white  spots  without  haemorrhage. 

4.  Circulatory  Disturbances.— An  ability  to  recognize  the  cardiac  lesions 
would  be  very  desirable ;  but  often  this  is  imrjossible  before  death.  The  pulse  is 
indeed  frequently  much  accelerated  and  irregular ;  but  such  signs  alone  lead  to 
no  definite  conclusion.  Endocardial  murmurs  are  often  wanting,  even  in  cases 
where  the  autopsy  discloses  abundant  exudation  and  ulcers  upon  the  valves. 
Still,  in  some  cases  of  this  sort  we  have  found  the  heart-sounds  noticeably  deficient 
in  clearness.  Sometimes  we  hear  blowing  sounds,  which  might,  however,  quite 
naturally  be  regarded  as  functional.  There  are  no  noticeable  changes  in  the 
blood.  Bacteria  have  not  yet  been  demonstrated  in  the  blood  of  the  patient  during 
life.  Sometimes  a  distinct,  though  moderate,  increase  in  the  number  of  white 
blood-corpuscles  is  observed. 

5.  The  grave  cerebral  symptoms  are  for  the  most  part  quite  analogous  to  those 
in  other  severe  acute  infectious  diseases.  They  may  be  present,  and  yet  no  marked 
objective  lesions  may  be  found  after  death.  In  other  cases  they  have  an  anatomi- 
cal basis — in  purulent  meningitis,  haemorrhagic  pachymeningitis,  cerebral  haemor- 
rhage, or  abscess.  These  conditions,  just  enumerated,  may  excite  localized  cerebral 
symptoms,  e.  g.,  hemiplegia. 

6.  Affections  of  the  joints  are  comparatively  frequent,  and  of  great  value  in 
diagnosis.  We  may  find  purulent  inflammation,  or  even  periarticular  abscesses. 
If  they  appear  early  in  the  attack,  they  may,  as  we  have  said,  lead  to  an  erroneous 
diagnosis  of  acute  articular  rheumatism.  Suppurative  processes  affecting  the 
periosteum  and  the  marrow  of  the  bones  not  infrequently  accompany  the  joint 


112  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

affections.  If  there  is  decided  suppuration  in  the  bones  we  speak  of  an  acute 
osteomyelitis,  especially  in  the  lower  extremities.  This  condition  is  almost 
always  occasioned  by  the  staphylococcus  aureus.  In  earlier  times  such  cases 
were  termed  bone-typhoid.     Finally,  abscesses  in  the  muscles  are  not  uncommon. 

7.  Renal  changes  are  frequent,  but  seldom  produce  striking  clinical  symptoms, 
or  prove  of  value  iu  diagnosis.  The  urine  often  contains  a  moderate  amount  of 
blood  and  albumen;  but  yet  it  may  not  be  essentially  altered  in  cases  where  the 
autopsy  discloses  extensive  renal  abscesses  or  ecchymoses,  or  hgemorrhages  into 
the  mucous  membrane  of  the  pelvis.  In  other  cases,  however,  an  acute  septic 
nephritis  is  conjoined  with  the  infarctions  and  abscesses,  and  then  the  urine 
exhibits  all  the  characteristics  of  acute  Bright's  disease,  having  a  large  amount  of 
albumen,  red  and  white  blood-corpuscles,  epithelium,  and  casts. 

8.  The  pulmonary  symptoms  are  in  part  secondary.  Bronchitis  and  lobular 
pneumonia  develop  as  in  all  other  severe  constitutional  diseases.  The  pulmonary 
abscesses  of  themselves  give  rise  usually  to  no  objective  symptoms— or,  at  most,  to 
a  marked  dyspnoea,  out  of  all  proportion  to  the  scanty  physical  signs.  Empyema 
is  a  not  infrequent  result  of  infection  of  the  pleura,  due  to  the  foci  of  disease 
which  are  situated  upon  the  outer  surface  of  the  lungs.  If  the  aspiratin g-needle 
shows  the  actual  existence  of  empyema,  this  fact  may  make  the  diagnosis  of  the 
constitutional  disease  much  easier. 

9.  Of  the  abdominal  symptoms  we  have  already  mentioned  the  acute  splenic 
tumor.  It  is  almost  impossible  to  diagnosticate  infarctions  and  abscesses  in  the 
spleen.  If  the  spleen  is  enlarged  and  noticeably  painful,  we  may  suspect  their 
existence.  There  are  sometimes  quite  severe  intestinal  symptoms,  such  as  a  pro- 
fuse ''  septic  diarrhoea,"  in  cases  where  the  autopsy  does  not  show  any  particularly 
grave  lesions.  Still  intestinal  ecchymoses  and  intestinal  diphtheria  have  some- 
times been  observed.  We  should  mention  that  often  the  skin  has  a  faint 
jaundiced  hue.  This  is  sometimes  the  result  of  duodenal  catarrh,  but  perhaps  it  is 
at  other  times  hsematogenous. 

Course  of  the  Disease  and  Prognosis. — The  entire  course  of  a  septic  case  may 
be  comprised  within  a  few  days,  for  a  severe  attack  is  always  thus  quickly  termi- 
nated by  death.  Protracted  cases  are  also  seen,  where  the  sufferings  last  one  to 
two  weeks,  or  even  longer;  but  in  these,  again,  the  end  is  almost  invariably 
unfavorable.  It  is  not  impossible  that  there  are  milder  and  curable  forms. 
Our  acquaintance  with  these  last  is,  however,  so  slight  that  we  can  not  state  any 
particulars  about  them. 

Diagnosis. — It  is  self-evident  that  a  disease  which  combines  symptoms  so 
manifold  and  so  ambiguous  must  be  very  difficult  to  recognize.  We  will 
recapitulate  the  chief  diseases  to  be  excluded.  A  case  may  greatly  resemble 
typhoid  fever  when  there  is  persistent  prostration,  diarrhoea,  an  eruption  like 
roseola,  and  an  enlarged  spleen.  In  discriminating,  we  should  consider  with  great 
care  the  possible  aetiology — e.  g.,  external  injuries;  and  we  should  look  for  septic 
retinitis,  swelling  of  the  joints,  cutaneous  ecchymoses,  and  an  intermitting  form 
of  fever.  It  is  all  the  more  possible  for  the  disease  to  resemble  meningitis,  because, 
as  we  have  said,  meningeal  disturbance  may  be  one  of  the  symptoms  of  the  sepsis 
and  color  the  whole  picture.  Here  the  symptoms  of  septic  poisoning  already  men- 
tioned would  be  of  some  value  in  diagnosis,  and  the  physical  signs  of  endocarditis 
or  of  a  greatly  enlarged  spleen  would  be  worth  still  more.  There  may  be  equal 
difficulty  in  the  differential  diagnosis  between  acute  sepsis  and  acute  miliary  tuber- 
culosis. Here  we  should  consider  carefully  each  separate  symptom,  and,  above 
all,  the  aetiology,  searching  for  something  that  would  explain  the  occurrence  of 
sepsis  on  the  one  hand,  or  of  acute  miliary  tuberculosis  (q.  v.)  on  the  other. 
If  we  found  miliary  tubercles  in  the  choroid  by  means  of  the  ophthalmoscope, 


HYDROPHOBIA.  1  1 3 

or  tubercle  bacilli  in  the  blood,  all  doubt  would  vanish.  At  the  beginning-  of  a 
septic  attack  the  rigors  may  arouse  suspicions  of  intermittent  fever.  Usually  tbe 
early  appearance  of  other  symptoms  corrects  this  idea;  but,  if  not,  the  power!  css- 
ness  of  quinine  will.  If  a  severe  acute  nephritis  has  developed  itself  in  a  septic 
case,  all  the  symptoms  may  be  erroneously  referred  to  uraemia.  But  persistent 
observation  will  usually  lead  us  to  the  right  conclusion.  As  to  the  conditions  of 
great  prostration  resembling  acute  sepsis,  which  occur  in  acute  (primary)  ulcer- 
ative endocarditis  and  in  severe  articular  rheumatism,  see  the  appropriate 
chapters. 

The  treatment  can  be  merely  symptomatic.  Of  course  we  try  again  and  again 
to  cut  short  the  attacks  of  fever  by  large  doses  of  quinine  or  antipyrine,  but 
never  with  any  but  temporary  success.  Baths,  stimulants,  and,  if  necessary, 
narcotics  are  the  other  chief  remedies  employed. 


CHAPTER  XX. 

HYDROPHOBIA. 

{Babies  canina.) 

^Etiology.  Rabies  in  Dogs. — A  peculiar  infectious  disease  sometimes  occurs  in 
dogs,  and  more  rarely  in  some  other  animals — viz.,  the  wolf,  fox,  cat,  cow,  and 
horse.  Men  who  are  bitten  by  the  animal  may  catch  the  disease,  and  thus  become 
the  victims  of  terrible  symptoms  originating  in  the  central  nervous  system. 

Two  forms  of  madness  are  distinguished  in  dogs — the  raving  madness  and  the 
quiet  madness.  Bollinger  describes  the  raving  form  as  beginning  with  prodro- 
mata,  the  melancholy  stage,  lasting  one  to  three  days.  The  animal  is  low-spirited, 
timorous,  and  without  appetite.  Then  comes  the  stage  of  irritation  or  of  mania, 
in  which  the  animal  is  attacked  with  an  impulse  to  bite.  It  seems  determined  to 
run  away  and  rove  about,  and  it  utters  a  peculiar  howl.  The  dog  will  not  touch 
his  ordinary  food,  but  often  swallows  straw,  hair,  earth,  bits  of  wood,  etc.  In  the 
third  or  paralytic  stage  paralysis  appears.  The  dog  looks  lean  and  wretched,  and 
always  dies  on  the  tenth  day  at  the  latest.  In  what  is  called  the  quiet  madness 
there  is  no  maniacal  stage.  The  symptoms  of  paralysis,  affecting  chiefly  the  hind 
limbs  and  the  lower  jaw,  occur  earlier  and  are  sooner  fatal.  Marked  pathological 
changes  are  not  found.  There  are  pulmonary  and  intestinal  catarrh  and  passive 
congestion  of  the  viscera,  and  the  stomach  often  contains  foreign  bodies  in  place 
of  the  usual  partially  digested  food. 

[On  the  Western  plains  hydrophobia  is  said  not  infrequently  to  follow  skunk 
bites.  The  bite  is  inflicted  during  sleep  on  persons  passing  the  night  in  the  open 
air  or  in  tents  to  which  the  animal  can  gain  access.] 

Rabies  is  transferred  to  the  human  being  almost  invariably  by  the  bite  of  some 
raving  animal,  and  this  animal  is  almost  always  a  dog.  The  poison,  which  is 
not  yet  known  m  its  pure  form,  is  evidently  contained  in  the  saliva  or  slaver  and 
in  the  blood  of  mad  animals,  and  can,  by  means  of  these  substances,  be  success- 
fully inoculated  upon  other  animals.  Pasteur  has  discovered  another  way  to  pro- 
duce the  disease  experimentally.  He  takes  minute  portions  of  the  brain,  medulla 
oblongata,  or  some  other  internal  viscus  of  a  mad  dog,  and  either  injects  them 
into  the  veins  of  a  healthy  animal,  or  trephines,  and  then  inserts  them  beneath 
the  meninges.  The  virulence  of  the  rabic  poison  when  thus  manipulated  undergoes, 
under  special  conditions,  very  peculiar  alterations,  which  will  be  detailed  at  the 
close  of  this  chapter. 


114  ACUTE  GENEEAL  INFECTIOUS  DISEASES. 

The  liability  to  rabies  does  not  seem  to  be  universal  among  human  beings. 
About  one  half  of  those  who  are  bitten  by  mad  animals  exhibit  no  subsequent 
symptoms.  Still  this  can  be  only  in  part  due  to  inherent  immunity  from  the  dis- 
ease, and  must  in  part  result  from  imperfect  infection.  The  duration  of  incu- 
bation till  rabies  finally  breaks  out  seems  to  vary  greatly.  As  a  rule  it  is  about 
three  to  six  months,  but  observers  have  reported  instances  both  of  shorter  and  of 
much  longer,  duration. 

Clinical  History. — The  disease  begins  with  a  general  feeling  of  indisposition, 
anorexia,  headache,  and  uneasiness.  This  last  is  partially  explained,  to  be  sure, 
by  a  dread  of  what  is  impending.  If  the  bite  was  in  the  face,  frequent  convulsive 
sneezing  may  occur.  Even  now,  in  this  prodromal  stage,  a  marked  aversion  to 
liquids  is  a  usual  and  early  symptom.  The  attempt  to  swallow  excites  slight  con- 
vulsive disturbances.  Painful  sensations  may  arise  Once  more  in  the  bitten  place, 
although  this  has  usually  been  cicatrized  long  before,  and  the  neighboring  lymph- 
glands  are  often  found  to  be  swollen. 

Only  a  day  or  two  later  the  second,  hydrophobic  stage  begins.  The  especial 
characteristic  of  this  consists  in  the  peculiar  attacks  of  tonic  convulsions.  The 
pharynx  suffers  most,  but  convulsions  also  seize  the  muscles  of  respiration  and  those 
of  the  trunk  and  extremities.  A  terrible  feeling  of  anxiety  and  oppression  accom- 
panies these  attacks,  so  that  one  who  has  once  witnessed  the  sight  can  never  forget 
it.  The  convulsions  always  seem  to  be  reflex,  and  are  produced  by  the  slightest 
causes,  particularly  by  any  attempt  to  swallow,  or  sometimes  by  the  very  sight  of 
water.  They  recur  at  gradually  diminishing  intervals,  and  last  from  a  few  min- 
utes to  half  an  hour.  The  excitement  of  the  patient  may  reach  the  pitch  of  delir- 
ium or  mania.  The  pulse  is  full  and  rapid.  The  temperature  is  usually  only 
slightly  elevated,  but  it  may  be  high.  There  is  great  thirst,  accompanied  by  burn- 
ing pain  in  the  throat.     Often  there  is  marked  salivation. 

This  condition  lasts  one  to  three  days.  Then  death  occurs,  ushered  in  by  vio- 
lent convulsions.  Or  death  may  be  preceded  by  a  brief  third  stage  of  paralysis, 
during  which  there  are  no  convulsive  attacks.  Cases  of  recovery  in  man,  if  they 
ever  happen,  are  extremely  rare. 

The  result  of  the  autopsy  is  practically  negative.  The  disease  is  an  infectious 
one  and  therefore  we  should  hardly  think  it  a  priori  certain  that  such  object- 
ive cerebral  lesions  would  be  found  as  might  of  themselves  account  for  the  grave 
clinical  symptoms.  The  microscope  has  repeatedly  detected  very  minute  haem- 
orrhages, clusters  of  lymph-cells  around  the  blood-vessels,  etc.  The  throat  may 
present  the  signs  of  catarrh.  The  lungs  are  congested,  and  often  cedematous. 
The  blood  is  dark,  with  few  clots.  The  heart,  liver,  and  spleen  are  apparently 
normal. 

The  diagnosis  is  usually  easy,  particularly  if  we  know  of  the  possibility  of 
infection.  We  are  guided  by  the  convulsions  following  attempts  to  swallow,  as 
well  as  by  the  whole  group  of  symptoms.  Hydrophobia  is  distinguished  from 
traumatic  tetanus  by  the  absence  of  trismus  and  of  the  characteristic  tension  of 
the  muscles  of  the  back  and  abdomen,  by  the  convulsions  coming  in  separate 
attacks,  and  by  the  usually  greater  length  of  incubation.  There  is  only  one 
form  of  tetanus  which  bears  very  great  resemblance  to  rabies,  viz.,  the  so-called 
hydrophobic  tetanus  {vide  infra).  It  should  be  mentioned  that  the  mere  dread 
of  hydrophobia  may  cause  an  easily  excited  person  to  have  the  nervous  symp- 
toms of  the  disease,  but  of  course  without  disastrous  results.  Hysteria,  also, 
may  give  rise  to  convulsions  on  swallowing  somewhat  resembling  those  of  hydro- 
phobia. 

However  hopeless  treatment  seems,  we  must  at  least  try  to  mitigate  the  pa- 
tient's suffering.     Narcotics  accomplish  this  best; — e.  g.,  opium  or  chloral,  or,  most 


HYDROPHOBIA.  115 

useful  of  all,  the  inhalation  of  chloroform.  Curare  has  been  administered  repeat- 
edly, and  does  seem  to  lessen  the  violence  of  the  attacks. 

Prophylaxis  is  extremely  important.  We  can  not  consider  in  detail  the  regu- 
lations (muzzling)  which  the  government  should  make  in  order  to  pi'event  the 
spread  of  the  disease.  As  to  individual  prophylaxis,  every  suspicious  bite  should 
be  very  thoroughly  disinfected,  and  then  cauterized  either  with  nitrate  of  silver, 
caustic  potash,  or  the  red-hot  iron.  It  has  also  been  recommended  that  the  entire 
wound  or  scar  should  be  excised,  along  with  any  swollen  lymphatic  glands  which 
may  be  found  in  the  neighborhood.  Internal  remedies  to  prevent  the  outbreak 
of  the  disease  are  probably  quite  useless.  Cantharides,  belladonna,  calomel,  and 
arsenic  have  been  given  for  this  purpose,  but  without  success.  On  the  other  hand, 
Pasteur  has  recently  made  a  series  of  extremely  remarkable  observations  which 
have  led  to  a  special  method  of  prophylactic  inoculation  against  rabies  in  human 
beings.  If  a  bit  of  the  spinal  marrow  taken  from  a  mad  dog  is  introduced  beneath 
the  dura  mater  of  a  rabbit  by  means  of  trephining,  the  animal  exhibits  the  symp- 
toms of  rabies  after  fourteen  days'  incubation.  If  in  the  same  way  a  second  rab- 
bit is  inoculated  from  the  first,  and  so  on,  the  virulence  of  the  inoculated  material 
increases  gradually  with  every  inoculation,  while  the  period  of  incubation  grows 
shorter  and  shorter,  till  it  lasts  but  seven  days.  Beyond  this  point  the  period  of 
incubation  does  not  seem  to  diminish.  If,  on  the  other  hand,  the  same  series  of 
inoculations  are  made  on  apes,  the  virulence  of  the  poisonous  matter  does  not  in- 
crease, but  diminishes.  And  if  dogs  are  inoculated  with  material  artificially 
attenuated  in  this  manner,  the  animals  remain  in  good  health,  and  furthermore 
attain  an  immunity  against  more  virulent  inoculations,  so  that  they  may  be  bitten 
by  mad  dogs  without  becoming  infected. 

Pasteur  has  also  announced  a  still  more  simple  and  valuable  method  of  artifi- 
cial attenuation  of  the  virus.  He  removes  small  portions  of  the  spinal  marrow  of 
rabbits  which  are  suffering  from  rabies  in  its  most  violent  form  produced  by  the 
above  detailed  method,  and  these  bits  of  marrow  he  exposes  to  air  which  has 
been  wholly  deprived  of  moisture.  In  this  way  the  poison  contained  in  the  spinal 
marrow  gradually  and  progressively  loses  its  virulence,  until  it  finally  becomes 
inert.  A  portion  of  spinal  marrow  which  by  long  drying  has  completely  lost 
its  original  virulence  is  then  rubbed  up  in  sterilized  bouillon  and  injected  into 
some  animal — for  instance,  a  dog — and  then  in  regular  succession  pieces  of 
marrow  which  have  been  dried  for  shorter  and  shorter  periods  and  so  contain 
more  and  more  of  the  poison,  until  finally  the  point  is  reached  when  it  is  pos- 
sible to  use  for  the  injection  pieces  which  are  perfectly  fresh  and  extremely  poi- 
sonous, without  affecting  the  animal's  health.  That  is,  the  animal  has  attained 
immunity  from  the  disease.  This  second  method  has  now  been  employed  by 
Pasteur  on  several  thousands  of  human  beings  who  were  said  to  have  been  bitten 
by  mad  dogs;  and  he  claims  that  only  a  comparatively  small  number  of  the  indi- 
viduals inoculated  by  him  have  eventually  suffered  from  rabies. 

It  is  true  that  many  doubts  are  still  expressed  with  regard  to  the  practical  value 
of  Pasteur's  investigations.  The  above  detailed  experimental  observations  must 
however,  have  some  foundation  in  fact,  although  they  should  be  tested  carefully 
and  repeatedly.  If  we  compare  Pasteur's  statements  with  the  facts  known  about 
prophylactic  inoculation  with  anthrax  (see  the  appropriate  chapter)  and  about 
vaccination,  we  certainly  can  not  restrain  the  thought  that  we  are  here  upon  the 
threshold  of  discoveries  the  future  significance  of  which  is  immeasurable. 


116  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

CHAPTER  XXI. 

GLANDERS. 

(Farcy.) 

iEtiology. — Glanders  is  a  disease  of  the  horse  and  some  animals  allied  to  it — 
viz.  the  ass  and  mule.  It  can,  however,  be  transferred  to  man.  It  is  characterized 
by  peculiar  new  growths,  either  like  nodes  ("  farcy-buds  "),  or  more  rarely  diffuse. 
These  ai'e  very  prone  to  suppurate  and  break  down.  Such  nodes,  and  the  ulcers 
which  they  leave  behind  them,  occur  most  frequently  in  the  mucous  membraue 
of  the  nose.  In  horses  the  purulent  nasal  discharge  is  one  of  the  earliest  and  most 
important  symptoms  of  the  disease.  Similar  nodes  are  found  in  the  larynx, 
lungs,  liver,  spleen,  and  kidneys,  and  often  also  in  the  skin.  The  cutaneous  swell- 
ings and  deep,  crater-like  ulcers  belong  to  that  form  of  the  disease  which  is  called 
"farcy."  The  corresponding  lymphatic  vessels  and  glands  are  usually  much 
swollen.  The  animal  has  fever,  grows  weaker  and  weaker,  and  almost  invariably 
dies  at  the  end  of  one  to  three  weeks. 

Glanders  in  man  is  always  referable  to  infection  from  a  diseased  animal, 
although  in  certain  instances  it  is  impossible  to  demonstrate  the  source.  The 
disease  is  therefore  commonest  among  persons  who  have  much  to  do  with  horses 
— e.  g.,  hostlers,  coachmen,  farmers,  and  cavalrymen.  The  virus  is  usually  con- 
veyed by  the  pus  and  nasal  secretions  of  the  diseased  animals.  A  little  of  this 
falls  upon  some  excoriation  on  the  hand  or  some  crack  in  the  skin,  and  is  absorbed. 
Man  does  not  seem  very  liable  to  the  disease ;  it  is  of  rare  occurrence. 

Löffler  and  Schutz  have  discovered  the  specific  disease-producing  agent.  These 
investigators  were  able  to  demonstrate  in  all  the  products  of  glanders  delicate 
bacilli  about  the  size  of  the  bacilli  of  tuberculosis.  These  bacilli  could  be  reared 
artificially,  and,  if  inoculated  upon  horses  and  other  animals,  gave  rise  to  a  typical 
attack  of  glanders  in  every  instance.  The  bacilli  of  glanders  can  scarcely  ever  be 
detected  in  the  blood.  It  is  also  very  interesting  that  they  rapidly  lose  their  viru- 
lence in  purified  cultures  outside  of  the  living  body.  This  is  one  more  proof  of 
the  fact,  which  is  lately  coming  more  and  more  into  prominence,  that  the  external 
influences  surrounding  the  life  of  bacteria  modify  greatly  their  biological  pecul- 
iarities. 

Clinical  History. — The  period  of  incubation  lasts  about  three  to  five  days,  and 
sometimes  longer.  The  first  symptoms  are  local,  if  the  infection  has  resulted  from 
a  visible  injury.  There  is  considerable  swelling  and  pain  in  this  spot,  and  usually 
considerable  lymphangitis  in  its  neighborhood.  In  other  cases,  however,  the  dis- 
ease begins  with  indefinite  constitutional  symptoms,  such  as  fever,  headache,  and 
pain  in  the  limbs,  so  that  there  may  be  some  resemblance  to  a  beginning  typhoid 
fever.  The  local  and  general  disturbances  increase,  and  the  disease  soon  attacks 
other  parts  of  the  body.  There  are  usually  pustules,  or  larger  abscesses  in  the 
skin.  These  burst  and  discharge  offensive  pus,  leaving  behind  them  irregular, 
deep  ulcers.  Not  infrequently  the  joints  are  swollen.  The  mucous  membranes 
are  also  attacked ;  chief  among  these  troubles  are  ulcers  in  the  nose.  The  nose 
swells  as  if  with  erysipelas,  and  there  is  a  purulent,  foul-smelling  discharge.  The 
nose  rarely  escapes.  The  conjunctivae,  throat,  mucous  membrane  of  the  mouth, 
and  the  larynx  also  undergo  inflammation  and  ulceration.  A  violent,  diffuse 
bronchitis  develops.  Sometimes  there  is  considerable  disturbance  of  the  stomach 
and  intestine,  giving  rise  to  vomiting  arid  diarrhoea.  At  the  same  time  the  con- 
stitutional symptoms  become  more  and  more  severe.  The  patient  grows  stupid  or 
delirious.  In  some  few  cases  the  severe  cerebral  symptoms  are  due  to  a  purulent 
meningitis,  perhaps  through  extension  of  the  inflammation  by  contiguity  from 


GLANDERS.  1  1 7 

the  nose.  The  fever  is  high.  Sometimes  it  is  quite  continuous.  More  rarely 
there  are  chills  and  great  elevations,  as  in  the  fever  of  pyaemia.  The  pulse  is  rapid 
and  small.  The  spleen  is  seldom  much  enlarged.  The  urine  may  contain  a  trace 
of  albumen. 

In  these  severe  acute  cases  the  termination  is  almost  always  fatal.  Death 
occurs  at  the  end  of  about  two  to  four  weeks.  There  are  cases  with  a  more  chronic 
course,  with  tedious  persistence  of  the  troubles  in  the  skin  and  mucous  membranes, 
and  milder  febrile  and  constitutional  symptoms.  Such  attacks  appear  at  first  tol- 
erably favorable,  but  may  later  assume  the  acute  form,  or  they  may  run  on  for 
months,  and  at  last  end  in  complete  recovery. 

The  autopsy  reveals  a  condition  greatly  resembling  that  in  pyaemia.  We  find 
abscesses  in  many  parts,  particularly  the  muscles  and  the  lungs,  and,  next  in  fre- 
quency to  them,  the  spleen,  brain,  and  other  viscera.  In  the  mucous  membrane  of 
the  nasal  cavities,  the  pharynx,  and  the  larynx,  are  found  nodes  and  ulcers,  such 
as  occur  in  the  horse.  As  in  septicaemia,  there  are  often  numerous  haemorrhages 
into  the  serous  and  mucous  membranes.  It  has  already  been  mentioned  that  the 
specific  bacilli  of  glanders  are  present  in  the  abnormal  secretions. 

Diagnosis. — Without  the  aid  of  setiological  factors  the  diagnosis  of  glanders 
is  often  very  difficult.  Indeed,  until  recently  there  have  been  instances  where 
even  the  autopsy  did  not  suffice  to  exclude  pyaemia.  But  now  that  the  specific 
bacilli  have  been  discovered  we  can  clear  up  all  doubts.  We  can  not,  however, 
enter  into  a  particular  description  of  the  distinguishing  characteristics  of  these 
bacilli.  Their  demonstration  requires  pure  cultures.  At  the  bedside  also  aeti- 
ology is  all-important  in  diagnosis — e.  g.,  exposure  to  infection,  or  occupation. 
Experience  with  a  limited  number  of  cases  renders  it  probable  that  in  the  future 
we  .shall  be  able  to  demonstrate  the  bacilli,  during  the  life  of  the  patient,  in  the 
nasal  secretions  or  the  contents  of  the  abscesses.  The  most  characteristic  symp- 
toms are  the  nasal  and  cutaneous.  In  a  case  that  takes  a  chronic  course  there  is  a 
possibility  of  mistaking  the  cutaneous  ulcers  for  syphilitic  sores. 

We  have  already  implied  that  the  treatment  of  acute  cases  is  almost  hopeless. 
We  must  do  all  we  can  in  the  way  of  cleanliness  and  disinfection  to  improve  the 
local  condition  of  the  skin,  the  nose,  and  the  throat.  Appropriate  agents  are  car- 
bolic and  salicylic  acids  and  chlorine-water.  Further  treatment,  by  means  of 
baths,  quinine,  and  stimulants,  should  be  in  accordance  with  the  general  rules  for 
the  care  of  severe  acute  infectious  diseases.  Potassic  iodide  has  been  recom- 
mended as  an  internal  remedy. 


CHAPTER  XXII. 

MALIGNANT  PUSTULE. 

(Anthrax.     Charbon.    Splenic  Fever.    Mycosis  intestinalis.     Carbunculus  contagiosus.) 

iEtiology. — The  cause  of  malignant  pustule  is  the  infection  of  the  body  with  a 
specific  kind  of  bacilli,  the  bacillus  anthracis.  This  organism  was  discovered  by 
Pollender  in  1849,  and  a  few  years  later,  independently,  by  Brauell. 

These  bacilli  are  very  minute  cylinders,  about  seven  to  twelve  micromilli- 
metres  in  diameter.  They  are  found  in  enormous  numbers  in  the  blood  and 
organs  of  animals  which  die  of  anthrax.  Aniline-staining  makes  them  more 
easily  visible.  By  means  of  blood  containing  the  bacilli,  Davaine  (1S63)  and 
others  have  inoculated  many  animals  with  the  disease,  including  mice,  rats, 
guinea-pigs,  cows,  sheep,  goats,  and  birds.     The  bacilli  can  also  be  isolated  and 


118 


ACUTE  GENERAL  INFECTIOUS  DISEASES. 


cultivated,  and  then  produce  infection.  This  is  proof  positive  that  they  are  the 
actual  carriers  of  contagion.  The  rapid  increase  of  the  anthrax  bacilli  in  the 
blood  goes  on  by  subdivision.  In  the  artificial  cultivations,  however,  the  bacilli 
grow,  as  Koch  has  shown,  into  quite  long  threads,  in  which  shortly  appear  minute, 
brilliant  egg-shaped  bodies  (cf.  Figs.  12  A  and  12  B).  The  threads  become  disinte- 
grated, setting  free  the  little  shining  ovoids,  the  spores  of  anthrax,  to  grow  into 

bacilli.  The  bacilli  can  live 
only  a  relatively  brief  time ; 
but  the  spores  have  un- 
usual tenacity  of  existence. 
They  may  remain  dried  up 
for  years,  and  then  be 
brought  to  further  develop- 
ment if  placed  in  favorable 
conditions  of  heat  and 
moisture.  If  the  spores  are 
transferred  to  animals,  they 
develop  into  bacilli,  and 
there  is  scarcely  room  to 
doubt  that  men  and  animals 
are  quite  as  often  infected 
by  spores  as  by  full-grown  bacilli.  There  are  facts  which  render  it  not  impi'ob- 
able  that  the  anthrax  bacilli  exist  in  other  places  than  the  bodies  of  men  or  ani- 


A  B 

Fig.  12a.— Anthrax  bacilli.  (From  Koch.)  650  diameters.  A,  from 
the  blood  of  a  guinea-pig.  B,  from  the  spleen  of  a  mouse  after 
three  hours'  culture  in  the  aqueous  humor. 


^ 


9      &      m 

B 


Fig.  12  b.— Anthrax  bacilli  ;  spore  formation  and  spore  germination.  (From  Koch.)  A,  from  the  spleen 
of  a  mouse  after  twenty-four  hours'  culture  in  the  aqueous  humor,  spores  arranged  like  strings  of 
beads  in  the  filaments.  650  diameters.  B,  germination  of  the  spores.  650  diameters.  C,  the  same, 
with  a  higher  power.    1650  diameters. 

mals,  and  may  there  complete  their  circle  of  development.  Such  places  are 
marshes,  the  banks  of  streams,  and  the  like.  If  it  is  possible  for  them  to  be 
carried  by  high  water  to  the  pasture  lands,  we  have  an  explanation  of  those 
sudden  endemic  appearances  of  anthrax  which  sometimes  occiir  in  places  pre- 
viously free  from  the  disease. 

Anthrax  in  animals  is  of  great  practical  importance,  because  its  favorite 
victims  are  the  herbivorous  domestic  animals — viz.,  the  cow,  sheep,  and  horse. 
Among  these  it  is  terribly  destructive.  It  is  remarkable  that  the  Carnivora  enjoy 
almost  complete  immunity.  The  disease  usually  runs  a  very  acute  course  in  ani- 
mals. Indeed,  it  often  seems  like  apoplexy ;  the  apparently  healthy  animal  sud- 
denly falls,  suffers  for  a  few  minutes  from  convulsions  and  dyspnoea,  and  dies. 
Other  cases  have  a  somewhat  longer  and  more  intermittent  course,  but  in  these 
also  recovery  is  very  rare. 


MALIGNANT  PUSTULE.  1  1 9 

Probably  human  beings  are  infected  in  most  cases  by  direct  inoculation.  Shep 
herds,  farmers,  butchers,  and  others  who  come  in  contact  with  animals  suffering 
from  anthrax,  are  liable  to  infection  through  any  little  wound  or  scratch  upon  the 
hands.  Very  often  the  disease  is  caught  from  hides,  hair,  or  other  parts  of  dead 
animals.  In  workshops  and  factories  where  wool  and  hides  have  been  used  which 
came  from  diseased  animals,  anthrax  lias  repeatedly  occurred.  Curriers,  rope- 
makers,  paper-makers,  and  those  who  handle  horse-hair  and  wool,  are  all  exposed. 
Anthrax  has  also  earned  the  name  of  "  rag-pickers'  disease."  Another  way  of  infec- 
tion, supposed  to  happen  among  animals  as  well  as  men,  is  through  the  sting  of 
insects — e.  g.,  flies — bringing  the  poison  from  diseased  animals.  It  is  not  likely 
that  the  virus  can  be  absorbed  through  the  unbroken  skin,  or  by  the  lungs.  It  is 
certain,  howevei-,  that  the  intestine  may  afford  ingress  to  the  infectious  matter. 
Koch  has  proved  this  by  putting  spores  in  the  food  of.  sheep.  Intestinal  mycosis 
in  man  (vide  infra)  may  very  possibly  be  due  to  a  similar  mode  of  infection. 
Many  cases  of  poisoning  from  eating  meat  have  been  referred  to  the  ingestion  of 
the  flesh  of  animals  who  died  from  anthrax. 

Clinical  History. — Anthrax  in  man  has  two  distinct  forms.  These  may  appear 
in  combination.  The  first  begins  with  a  local  disorder  of  the  skin  at  the  point  of 
infection — viz.,  the  malignant  pustule,  or  anthrax  carbuncle.  The  second  and 
rarer  form  presents  the  symptoms  of  a  severe  acute  constitutional  infection.  An 
accompanying  cutaneous  disorder  is  sometimes  observed. 

1.  The  malignant  pustule  usually  comes  on  the  hand,  the  arm,  or  the  throat, 
and  appears  from  three  to  seven  days  after  infection.  A  vesicle  forms  at  the 
infected  spot,  grows  rapidly,  becomes  excoriated,  and  usually  takes  on  a  charac- 
teristic appearance,  being  of  a  dark-bluish  or  black  color.  The  surrounding 
parts  become  diffusely  swollen  and  red.  Secondary  vesicles  may  surround  the 
original  one.  The  swelling  becomes  more  and  more  extensive.  Inflamed  lymph- 
vessels  or  veins  radiate  in  red  lines  from  the  pustule,  and  the  neighboring  glands 
are  also  affected.  These  appearances  are  accompanied  by  fever,  and  more  or  less 
prostration.  In  a  favorable  case  the  swelling  subsides,  the  scab  falls  off,  and 
thei'e  is  at  last  complete  recovery.  But  in  other  cases  the  constitutional  infection 
becomes  more  and  more  prominent,  and  eclipses  the  local  disorder.  The  fever  and 
prostration  increase.  Severe  intestinal  symptoms  appear,  or  else  stupor,  delirium, 
and  other  nervous  disturbances;  and  death  may  ensue  after  a  few  days'  illness. 

2.  Intestinal  Mycosis. — A  better  name  would  be  intestinal  anthrax.  A  quite 
different  picture  is  presented  by  this  second  form,  which  gets  its  name  from  the 
marked  intestinal  lesions.  In  this  the  cutaneous  disorder,  if  it  exists  at  all,  is 
insignificant,  compared  with  the  severe  constitutional  disturbance.  It  is  only 
within  a  few  years  that  the  labors  of  Buhl,  Waldeyer,  E.  Wagner,  Leube,  and 
others  have  shown  that  attacks  of  this  kind  have  any  connection  with  anthrax. 
So  few  cases  have  thus  far  been  observed  that  it  is  impossible  at  present  to  give  a 
definite  and  complete  description  of  the  disease. 

In  cases  of  this  sort  the  attack  is  usually  rather  sudden,  beginning  with  chilli- 
ness, vomiting,  headache,  and  languor.  The  diagnosis  is  usually  very  obscure  at 
first,  unless  the  calling  of  the  patient  suggests  the  possibility  of  anthrax.  On 
careful  exammation,  we  may  find  some  places  where  the  skin  is  broken,  or  pos- 
sibly a  small  characteristic  pustule.  In  a  case  which  came  under  our  own  obser- 
vation a  pustule  had  existed  on  the  back  of  the  right  hand  for  some  weeks  before 
severe  symptoms  appeared,  but  had  not  attracted  the  attention  of  the  patient  at  all. 
In  this  case,  therefore,  the  constitutional  infection  seems  to  have  come  from  the 
local  disease.  But  in  other  cases  cutaneous  troubles,  in  the  form  of  small  car- 
buncles may  occur  secondarily  in  the  course  of  the  disease.  Haemorrhages  into 
the  skin  and  mucous  membranes  also  occur. 


120  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

Of  other  Symptoms,  the  gastro-in  testin  al  deserve  to  be  mentioned  first.  Vomit- 
ing occurs  frequently,  and  also  a  moderate,  painless,  and  sometimes  bloody  diar- 
rhoea. There  is  usually  severe  dyspnoea,  and  a  marked  sense  of  oppression  in  the 
thorax,  but  without  objective  pulmonary  signs.  Very  soon  there  is  collapse ;  the 
nose  and  extremities  grow  cool ;  the  pulse  is  rapid,  but  small;  and  there  is  livid- 
ity.  In  a  few  instances  tetanic  or  epileptiform  convulsions  have  been  observed. 
The  temperature  is  seldom  much  elevated.  It  may  be  subnormal.  In  a  few  days 
the  prostration  becomes  complete,  and  death  ensues. 

Milder  forms  apparently  occur,  but  here  the  diagnosis  may  not  be  absolutely 
certain.  We  have  seen  a  few  such  cases  originating  in  a  rope-walk  where  Russian 
hair  was  used.  The  constitutional  symptoms  were  only  moderately  severe,  the 
fever  was  mild,  and  recovery  occurred  after  about  two  or  three  weeks. 

Pathology. — In  the  fatal  cases  of  anthrax  the  intestinal  lesions  are  the  most 
characteristic.  Besides  the  signs  of  catarrhal  inflammation,  we  find  peculiar 
lesions  in  the  mucous  membrane  of  the  small  intestine,  and  sometimes  in  the  upper 
portion  of  the  colon.  These  consist  of  dark,  infiltrated  spots,  with  haemorrhages, 
the  spots  being  somewhat  larger  than  a  silver  dime.  The  microscope  reveals 
numerous  collections  of  anthrax  bacilli,  situated  chiefly  in  the  lumen  of  the 
blood-vessels.  The  spleen  is  usually  only  moderately  enlarged,  but  dark  and  con- 
gested. There  may  be  ecchymoses  in  the  kidneys,  the  brain,  and  the  serous  mem- 
branes. Often  there  is  swelling  of  the  lymph-glands.  In  one  case  which  we 
saw,  with  slight  intestinal  lesions,  the  mesenteric  glands  were  considerably  en- 
larged, and  the  bronchial  lymph-glands  were  perfectly  enormous.  The  bacilli 
are  found  in  all  the  organs  mentioned. 

The  diagnosis  of  a  malignant  pustule  is  seldom  difficult,  particularly  if  atten- 
tion be  directed  to  the  aetiology.  All  doubt  is  over  if  we  find  the  bacilli.  The 
cases  of  intestinal  mycosis  may  be  more  obscure.  Here,  too,  the  demonstration  of 
bacilli  in  the  blood  is,  of  course,  of  the  greatest  importance,  but  reports  have  thus 
far  been  scanty  of  endeavors  to  find  them  during  life  in  man. 

Treatment. — 1.  Prophylactic  inoculation.  Toussaint  and  Pasteur  were  the  first 
to  show  that  the  virulence  of  anthrax  bacteria  can  be  artificially  diminished  by 
certain  external  influences.  If  the  bacilli  are  kept  under  cultivation  for  several 
weeks  at  an  unchanging  temperature  of  106°  to  107'5°  (42°-43°  C),  they  pre- 
serve their  external  appearance  completely,  as  well  as  their  ability  to  grow,  but 
gradually  lose  their  power  of  infection.  Inoculations  made  with  this  "vaccine 
virus  "  produce  at  most  an  insignificant  disturbance.  But  what  is  especially  re- 
markable is  that  the  animals  thus  vaccinated  are  said  to  enjoy  immunity  thereafter 
from  infection  with  actual  anthrax.  Pasteur  was  the  first  to  make  this  assertion; 
and  he  proposed  that  the  prophylactic  inoculation  of  sheep  and  other  animals 
liable  to  anthrax  should  be  undertaken  on  a  large  scale,  promising  the  farmers 
that  very  great  benefit  would  result.  This  promise  has  not  yet  been  completely 
fulfilled,  although  there  can  be  no  doubt  that  in  general  Pasteur  was  correct.  Ex- 
periments instituted  by  Koch  and  others  have  shown  that,  although  Pasteur's  vac- 
cination protects  against  the  artificial  inoculation  of  anthrax,  it  does  not,  at  least 
as  now  performed,  afford  immunity  from  the  natural  anthrax,  which  usually 
results  from  infection  within  the  intestine.  French  investigators  have  lately 
made  known  new  methods  of  producing  an  artificial  diminution  of  the  growth 
and  virulence  of  anthrax  bacilli,  and  in  part  also  of  other  varieties  of  bacteria. 
Chauveau  has  found  that  cultures  of  anthrax  bacilli  exposed  for  several  days  to 
an  atmospheric  pressure  of  three  to  twelve  atmospheres,  or  to  compressed  oxygen, 
lose  a  portion  of  their  virulence ;  and  that  animals  inoculated  with  bacilli  thus  at- 
tenuated gain  an  immunity  to  inoculations  with  the  original  anthrax  poison.  The 
statements  of  Arloing  are  very  remarkable.     He  says  that  the  direct  play  of  sun- 


TRICHINOSIS.  121 

light,  or  even  of  a  concentrated  artificial  light,  upon  the  cultures  exercises  a  re- 
straining influence  upon  the  growth  and  poisonous  properties  of  the  hacilli,  and 
that  inoculation  material  weakened  in  this  way  may  be  employed  for  the  protec- 
tion of  animals. 

2.  The  treatment  of  malignant  pustule  is  surgical.  Cauterization  is  often  tried 
with  such  materials  as  caustic  potash,  nitric  acid,  or  carbolic  acid;  but  it  should 
always  be  borne  in  mind  that  such  manipulations  may  easily  contribute  to  a  local 
extension  of  the  anthrax  poison.  For  the  same  reason  one  should  hesitate  to 
incise  or  to  excise  the  pustules.  We  are  therefore  usually  obliged  to  confine  our- 
selves to  the  prescription  of  a  suitable  position  for  the  affected  member,  and  the 
application  of  an  ice-bag  over  the  diseased  spot.  The  treatment  of  intestinal  my- 
cosis must  be  purely  symptomatic.  We  may  try  the  effect  of  calomel,  salicylic 
acid,  stimulants,  and  baths. 


CHAPTER  XXIII. 

TRICHINOSIS. 

(TricMnatous  disease.) 

The  Natural  History  of  Trichinse—  The  trichina  spiralis,  one  of  the  class  of 
round  worms  or  nematoda,  has  long  been  known  to  occur  occasionally  in  the^mus- 
cles  of  men  and  certain  animals ;  but  it  was  not  until  1860  that  Zenker  showed 
that  trichinae  are  capable  of  exciting  in  man  a  dangerous  and  sometimes  fatal  dis- 
ease. Since  then  numerous  individual  cases  and  quite  extensive  epidemics  have 
been  reported;  and  the  labors  of  Virchow,  Leuckart,  and  others  have  taught  us  the 
anatomy  and  mode  of  development  of  this  peculiar  parasite. 

The  trichina  appears  in  two  shapes — as  intestinal  trichina  and  as  muscular  tri- 
china. The  intestinal  form  is  a  small  white  worm,  visible  to  the  naked  eye.  The 
female  is  3-4  mm.  long,  the  male  only  1-1  "5  mm.  They  have  well-developed 
digestive  and  sexual  organs.  The  male  is  distinguished  by  two  little  processes  at 
the  tail.  The  muscular  trichina  {vide  Fig.  13)  is  a  small  worm  0-7-l  mm.  long. 
It  is  found  coiled  up  among  the  muscular  fibers,  inside  a  connective-tissue  capsule, 
which  is  often  calcified. 

The  events  in  the  life  of  the  trichina  are  remarkable.  If  living  muscular  tri- 
chinae reach  the  human  stomach,  viz.,  through  the  eating  of  trichina tous  pork,  the 
capsules  are  dissolved,  and  the  trichinae,  thus  set  free,  grow  in  two  or  three  days 
into  sexually  perfect  intestinal  trichinae.  In  the  uterus  of  the  impregnated  female 
the  eggs  develop  into  embryos,  which  are  born  already  hatched.  The  birth  of  em- 
bryos begins  seven  days  after  the  ingestion  of  the  muscular  trichinae,  and  seems  to 
continue  for  some  time.  A  single  female  is  said  to  produce  more  than  one  thou- 
sand embryos.  These  latter  begin  their  travels  soon  after  birth,  and  reach  the  vol- 
untary muscles.  As  to  the  routes  they  choose  we  are  still  somewhat  in  doubt. 
Some  authorities  state  that  the  trichinae  penetrate  through  the  walls  of  the  intes- 
tine and  the  abdominal  cavity  into  the  connective  tissue.  Others  affirm  that  they 
enter  -the  lymphatic  vessels,  or  exceptionally  the  blood-vessels.  They  penetrate 
into  the  primitive  fibers  ot  the  muscles,  and  cause  them  to  disintegrate.  Finally, 
they  coil  themselves  up,  attain  the  size  of  muscular  trichinae  in  about  fourteen 
days,  and  become  encapsulated.  Each  capsule  usually  contains  but  one,  although 
it  may  inclose  as  many  as  four.  The  capsule  is  formed  partly  by  an  excretion 
from  the  trichina,  and  partly  from  the  reflex  hyperplasia  of  the  surrounding  con- 
nective tissue.  The  process  of  development  is  now  complete.  The  muscular  tri- 
chinae seem,  unlike  the  intestinal  form,  to  have  a  very  long  lease  of  life,  and  usually 


122 


ACUTE   GENERAL  INFECTIOUS  DISEASES. 


endure  till  the  death  of  their  host.  They  are  often  found  accidentally  at  autopsies. 
They  are  most  abundant  in  the  diaphragm,  the  intercostal  muscles,  the  muscles 
of  the  laiynx  and  throat,  and  in  the  biceps. 

./Etiology  of  Trichinosis. — The  only  cause  yet  known  for  trichinatous  disease  in 
man  is  the  ingestion  of  trichinatous  raw  or  underdone  pork — e.  g.,  smoked  ham. 
Swine  are  pre-eminently  subject  to  trichinae.  They 
probably  become  infected  in  various  ways,  e.  g.,  from 
the  faeces  of  human  beings  and  swine  suffering  from 
trichinosis,  or  through  the  ingestion  of  the  trichinatous 
flesh  of  other  swine.  The  waste  of  slaughter-houses  is 
often  fed  out  to  swine,  and  the  disease  thus  disseminated. 
Many  affirm  that  swine  are  also  infected  by  eating  rats 
infested  with  trichinae. 

Clinical  History. — The  symptoms  in  man  correspond 
in  general  to  the  developmental  and  vital  processes  of 
the  trichinae,  as  above  depicted.  In  individual  cases, 
however,  the  separate  stages  are  quite  often  obscured, 
probably  because  all  the  parasites  do  not  develop  simul- 
taneously, or  because  there  are  relapses.  The  first 
symptoms  are  gastro-intestinal.  At  the  commencement 
there  is  a  feeling  of  pressure  in  the  epigastrium,  with 
nausea  and  vomiting.  Later,  diarrhoea  is  prominent, 
becoming  in  some  cases  so  violent  as  to  remind  one  of 
cholera.  It  is  not  impossible,  although  rare,  to  find  in- 
testinal trichinae  in  the  stools.  Sometimes  there  is  con- 
stipation instead  of  diarrhoea.  In  some  cases  the  initial 
gastro-intestinal  symptoms  are  but  slight.  Frequently, 
even  in  the  beginning  of  the  disease,  there  is  complaint 
of  pain  and  stiffness  in  the  muscles,  too  early  for  it  to 
be  due  to  the  migrations  of  the  trichinae. 

The  genuine  severe  muscular  symptoms,  due  to  the 
myositis  produced  by  the  trichinae  in  the  muscles,  do 
not  begin  till  the  second  week,  or  even  later.  In  many 
cases,  where  the  invading  parasites  seem  to  be  relatively 
few  in  number,  the  muscular  symptoms  are  slight,  or 
wholly  absent.  In  the  more  severe  cases,  however,  they 
may  be  extremely  violent  and  distressing.  The  muscles 
become  swollen,  firm  and  hard,  very  tender  on  pressure, 
and  very  painful.  The  patient  avoids  all  movements 
and  contraction  of  the  muscles  as  much  as  possible,  lying, 
with  flexed  arms  and  with  legs  either  extended  or  like- 
wise flexed,  motionless  in  bed.  The  patellar  reflex  almost  always  disappears,  and 
on  testing  the  electrical  reactions  there  is  found  a  considerable  diminution  of  mus- 
cular excitability  to  both  the  galvanic  and  faradic  currents,  sometimes  associated 
with  delayed  contractions,  and  abnormally  long  duration  of  the  same  after  the 
stimulus  ceases  (Eisenlohr).  The  masseters  and  the  pharyngeal  and  laryngeal 
muscles  are  attacked,  so  that  there  is  difficulty  in  mastication  and  deglutition,  and 
hoarseness.  The  participation  of  the  motores  oculi  causes  pain  in  the  eyes.  The 
condition  of  the  diaphragm,  intercostals,  and  abdominal  muscles  causes  serious 
difficulty  in  respiration.  There  is  distressing  dyspnoea,  and  expectoration  is  so 
hampered  that  secretions  accumulate  in  the  air-passages.  Some  of  the  fatal  cases 
of  trichinosis  are  principally  due  to  this  impairment  of  respiration.  The  condi- 
tion may  be  aggravated  by  diffuse  bronchitis  or  lobular  pneumonia. 


I'}" 


An 


Fig.  13.— (From  Heller.) 

isolated  primitive  bundle 
with  two  free  trichinae  in 
the  sheath  of  the  sarco- 
lemma.    Much  enlarged. 


TRICHINOSIS.  122 

Third  in  the  list  of  important  symptoms  comes  oedema.  It  appears,  toward  the 
end  of  the  first  week,  in  the  eyelids.  Somewhat  later  it  involves  the  upper  and 
lower  extremities.  What  produces  it  is  not  quite  clear.  It  has  heen  regarded  as 
in  part  inflammatory  and  in  part  the  result  of  occlusion  and  thrombosis  of  the 
smaller  lymphatics.  Cutaneous  eruptions  also  develop — e.  g.,  vesicles,  wheals, 
petechias,  and  pustules.  Frequently  there  is  profuse  perspiration,  consequent 
upon  which  abundant  crops  of  miliaria  or  sudaminamay  appear. 

In  well-marked  cases  there  may  be  quite  high  fever  and  other  severe  constitu- 
tional symptoms  in  addition  to  the  local  disturbances  already  discussed.  The 
temperature  may  for  a  time  reach  104°  to  106°  (40°-41°  C);  hut  the  fever  is 
seldom  continuous  for  any  length  of  time,  being  usually  interrupted  hy  fre- 
quent and  considerable  intermissions.  There  are  also  a  rapid  pulse,  headache, 
stupor,  and  other  symptoms  suggesting  typhus  or  typhoid  fever.  In  fact,  the  first 
case  in  which  trichinosis  was  recognized  at  the  autopsy  (hy  Zenker  of  Dresden) 
had  been  regarded  before  death  as  typhoid.  The  urine  may  be  albuminous;  and, 
in  rare  instances,  nephritis  is  seen. 

The  duration  of  the  disease  varies  widely.  There  are  mild  cases  often  unrec- 
ognized, which  get  well  after  slight  symptoms  have  lasted  two  or  three  weeks. 
More  pronounced  cases  occupy  six  to  eight  weeks,  or  even  a  much  longer  time.  Of 
the  more  severe  cases  about  one  third  prove  fatal,  usually  from  the  fourth  to  the 
sixth  week.  Sometimes  death  is  caused  by  the  severity  of  the  constitutional  dis- 
turbance, but  usually  from  disabled  respiration.  Even  if  the  case  ends  favorably, 
recovery  is  often  very  tedious. 

Pathology. — The  autopsy  reveals  little  that  is  characteristic  excepting  the 
changes  in  the  muscles.  There  are  sometimes  the  signs  of  haernorrhagic  catarrhal 
inflammation  of  the  small  intestine.  The  spleen  is  not  enlarged.  Very  often 
the  liver  is  decidedly  fatty.  What  should  cause  this  in  trichinosis  has  not  yet 
been  determined.  The  lungs  often  present  islets  of  lobular  pneumonia,  or  even 
sometimes  of  gangrene.  The  trichinae  are  found  in  the  muscles,  beginning  with 
the  fifth  week.  They  can  be  recognized  by  the  naked  eye  as  little  whitish  lines. 
We  have  already  named  the  muscles  chiefly  infested.  Under  the  microscope 
we  see  the  fibers  in  which  the  trichinae  lie  transformed  into  a  fine  granular 
mass.  The  nuclei  of  the  muscular  fibriliae  are  greatly  increased  in  number  in  the 
neighborhood  of  the  coiled-up  parasite.  Finally,  the  sarcolemma  collapses,  and 
becomes  greatly  thickened  upon  its  external  surface  by  a  hyperplasia  of  connect- 
ive tissue.  The  muscles  also  present  many  other  degenerative  changes,  such  as  a 
flaky  disintegration,  waxy  degeneration,  and  the  formation  of  vacuoles.  There 
is  furthermore  a  marked  increase  of  nuclei  in  the  interstitial  tissue  of  the  muscles. 
Within  the  intestines  are  sometimes  to  be  found,  even  after  several  weeks'  illness, 
numerous  living  intestinal  trichinae — a  fact  of  importance  from  a  therapeutic 
point  of  view. 

Treatment. — The  trichinae  may  still  be  alive  in  pork  that  has  been  smoked 
or  salted  or  half-cooked — e.  g.,  many  sausages  are  unsafe.  The  only  possible 
prophylaxis,  as  far  as  the  individual  is  concerned,  is  therefore  to  avoid  all 
such  food.  A  real  protection  for  the  public  against  the  disease  is  also  afforded 
by  governmental  microscopic  inspection  of  meat,  as  already  established  in  many 
places. 

When  an  individual  has  become  infected  with  trichinae,  if  it  is  possible 
that  intestinal  trichinae  still  are  present,  the  treatment  must  always  begin  with 
the  exhibition  of  purgatives,  such  as  compound  infusion  of  senna,  calomel,  or 
castor-oil.  Of  the  remedies  which  are  calculated  to  destroy  the  intestinal  ü-ichinae, 
glycerine,  which  was  first  recommended  by  Fiedler,  seems  to  be  the  most  efficient. 
It  must  be  given  in  rather  large  doses,  say  a  tablespoonful  every  hour.     Other 


124  ACUTE  GENERAL  INFECTIOUS  DISEASES. 

drugs  are  much  less  reliable,  but  we  will  name  among  them  benzine  in  the  dose 
of  one  to  two  drachms  (grm.  4  to  8)  in  capsules,  and  picric  acid  in  pills — the  daily 
dose  being  5  to  8  grains  (grm.  0*3-0  "5). 

Later  on,  when  the  invasion  of  the  muscles  has  already  begun,  we  are  unfortu- 
nately almost  without  resource.  The  muscular  pains  can  be  alleviated  by  nar- 
cotics, particularly  morphine  subcutaneously,  poultices,  and  chloroform-oil  as  an 
embrocation.*  Protracted  warm  baths  are  excellent.  Antipyrine  and  salicylic 
acid  are  also  said  to  dp  good  in  many  cases. 

*  Generally  one  part  of  chloroform  to  ten  of  olive-oil.  It  is  not  officinal  in  Germany,  but  is  weaker 
than  the  linimentum  chloroformi  (U.  S.  P.). — Teans. 


DISEASES   OF   THE   RESPIRATORY   ORGANS. 


SECTION  I. 
Diseases   of  the  Nose* 

CHAPTER  I. 
OORYZA. 

{Snuffles.     Rhinitis.) 

JEtiology. — The  well-known  symptoms  of  coryza  depend  upon  a  catarrhal 
inflammation  of  the  nasal  mucous  membrane.  Although  this  catarrh  may  often 
be  due  to  infectious  influences,  still  we  can  not  deny  that  it  is  one  of  those  dis- 
eases which  may  be  caused  by  taking  cold.  Daily  experience  teaches  us  how  often 
coryza  follows  an  evident  exposure  to  cold,  like  wetting  the  feet.  We  may  men- 
tion its  contagiousness  as  an  argument  in  favor  of  its  infectious  character,  and 
this  may  be  illustrated  by  the  fact  that  it  may  be  conveyed  by  handkerchiefs, 
kissing,  etc.,  but  an  experimental  transmission  of  common  coryza  has  not  yet  been 
successful. 

Coryza  may  also  arise  from  the  action  of  chemical  irritants  or  mechanical  irri- 
tants, like  dust,  on  the  nasal  mucous  membrane.  The  iodine  coryza,  which  occurs 
from  the  internal  use  of  iodine,  is  especially  noteworthy.  In  this  form  iodine 
can  easily  be  detected  in  the  nasal  secretion.  The  idiosyncrasy  of  many  people  to 
ipecacuanha  is  also  well  known,  the  very  smell  of  it  setting  up  a  coryza.  A 
severe  coryza  is  the  chief  symptom,  too,  in  hay  fever,t  which  is  probably  due  to 
the  action  of  the  pollen  of  certain  grasses  on  the  respiratory  mucous  membrane. 

*  Special  treatises  on  the  pathology  and  therapeutics  of  nasal  diseases  are  to  he  found  in  the  follow- 
ing works:  Michel,  "Krankheiten  der  Nasenhöhle."  Fraenkel,  "Diseases  of  the  Nose,"  in  "Ziems- 
sen's  Cyclopedia."  Störk,  "  Klinik  der  Krankheiten  des  Kehlkopfes,  der  Nase.,  und  des  Kachens." 
Schech,  "  Krankheiten  der  Mundhöhle,  des  Kachens,  und  der  Nase."  Moldenhauer,  "  Krankheiten  der 
Nasenhöhlen,"  etc. 

t  The  disease  called  hay  fever  {catarrhus  cestivus)  is  of  frequent  occurrence  in  England  and  North 
America,  although  rare  with  us  in  Germany.  It  usually  affects  men  in  middle  life,  less  often  women. 
Some  individuals  are  peculiarly  liahle  to  the  disease.  For  them  an  attack  may  he  produced  merely 
by  walking  across  a  meadow  or  near  a  grain-field  at  that  season  when  the  grasses  are  in  bloom,  i.e., 
about  May  to  July.  As  already  intimated,  it  is  supposed  that  the  grains  of  pollen  excite  the  disease, 
being  diffused  in  the  air  and  thus  drawn  into  the  nostrils.  At  any  rate,  they  have  repeatedly  been 
found  in  the  nasal  secretion  and  also  in  the  tears  of  affected  persons.  The  symptoms  consist  in  a  very 
severe  coryza,  with  burning  of  the  nose  and  violent  sneezing.  The  erectile  tissue  of  the  nose  is  probably 
acutely  swollen.  Usually  these  symptoms  are  accompanied  by  a  well-marked  conjunctivitis  with 
oedema  of  the  eyelids.  In  severer  cases  there  is  furthermore  a  catarrh  of  the  larynx  and  bronchi. 
There  is  frequently  a  tendency  to  violent  attacks  of  asthma  ("hay-asthma"),  especially  at  night 
(see  the  chapter  on  bronchial  asthma).  The  treatment  consists  first  in  avoiding  the  cause  by  change 
of  residence,  as  by  going  to  the  sea-shore.  For  the  nasal  catarrh  douches  are  chiefly  recommended, 
such  as  a  solution  of  1  part  of  quinine  to  500-1,000  parts  of  water,  or  a  solution  of  carbolic  acid.  The 
administration  of  iodide  of  potassium  might  be  tried,  particularly  where  there  is  asthma. 

(125) 


126  DISEASES  OF  THE  RESPIRATORY   ORGANS. 

Finally,  we  must  bear  in  mind  that  coryza  may  often  be  only  a  symptom  of  an- 
other disease  like  measles,  syphilis,  or  glanders,  and  that  severe  purulent  inflam- 
mation of  the  nasal  mucous  membrane  may  be  excited  by  the  presence  of  the 
secretion  from  a  gonorrhoeal  or  blennorrhceal  conjunctivitis. 

The  symptoms  of  coryza  are  in  most  of  the  milder  cases  of  a  local  nature  only. 
The  secretion  is  troublesome ;  at  first  it  is  scanty  and  mucous,  but  later  it  becomes 
more  abundant,  and  watery ;  and  sometimes  it  is  purulent.  The  nasal  passages  are 
not  infrequently  closed  from  the  swelling  of  the  mucous  membrane.  The  patient 
necessarily  has  to  breathe  through  the  mouth,  which  explains  the  well-known 
nasal  speech.  This  closure  of  the  nares  may  give  rise  to  dangerous  attacks  of 
dyspnoea  in  children,  especially  in  infants,  who  have  to  breathe  through  the  nose 
when  sucking  at  the  breast.  The  sense  of  smell  is  always  diminished.  The  local 
sensations  of  pain  and  burning  are  due  chiefly  to  a  mild  inflammation  of  the  skin 
of  the  nostrils  and  upper  lip  set  up  by  the  irritation  of  the  secretion.  The  irri- 
tated condition  of  the  inflamed  mucous  membrane  occasions  a  feeling  of  tick- 
ling and  itching  in  the  nose,  and  frequently  by  a  reflex  action  violent  sneezing. 
The  symptoms  are  more  severe  if  the  cavities  adjacent  to  the  nose  are  attacked  by 
catarrh,  and  if  in  them  accumulations  of  secretion  occur.  Marked  pain  in  the 
forehead  occurs  in  catarrh  of  the  frontal  sinuses.  The  sinuses  of  the  ethmoid  and 
sphenoid  bones,  and  the  antrum  of  Highmore,  may  also  be  implicated.  Much 
more  frequently  a  severe  coryza  sets  up  an  inflammation  in  adjacent  mucous 
membranes.  Thus  we  find  following  a  coryza  a  conjunctivitis,  an  affection  of 
the  ear,  a  sore  throat,  or  a  laryngitis.  In  persistent  coryza  an  eczema  is  not 
infrequently  excited  on  the  skin  of  the  upper  lip,  and  mention  has  already  been 
made  of  the  fact  that  coryza  may  sometimes  act  as  the  exciting  cause  of  an  ery- 
sipelas. 

In  severe  coryza  we  may  sometimes  have  quite  a  marked  general  disturbance, 
and  often  slight  elevations  of  temperature.  The  "  coryza  fever  "  in  children,  for 
instance,  is  well  known. 

Treatment. — Special  treatment  is  usually  unnecessary,  for  most  cases  recover 
of  themselves  in  a  few  days.  With  abundant  secretion,  especially  in  fresh  cases, 
Hager 's  "  coryza  remedy  "  [as  an  inhalation]  is  worthy  of  trial ;  this  consists  of 
ten  parts  each  of  alcohol  and  carbolic  acid,  and  five  parts  of  ammonia-water.  A 
snuff  of  calomel  is  also  greatly  praised.  When  the  secretion  forms  abundant  dry 
scabs,  an  attempt  should  be  made  to  wash  them  out  by  injections  of  warm  fluids, 
like  warm  milk.  The  upper  lip  and  the  nostrils  should  be  smeared  with  vaseline 
or  simple  ointment  to  protect  the  skin  from  the  action  of  the  secretion.  Only  in 
the  rare  cases  of  a  severe  purulent  catarrh  can  an  energetic  local  treatment  of  the 
nasal  mucous  membrane  be  necessary.  Here  we  may  use  douches,  sprays,  or 
inhalations  of  astringents  like  tannin  or  alum,  or  we  may  apply  caustics  like 
nitrate  of  silver. 


CHAPTER  II. 

CHRONIC    RHINITIS. 

{Rhinitis  chronica  hypertrophic«!  and  atrophica.     Osama.) 

1.  Chronic  Rhinitis. — It  is  in  many  cases  impossible  to  determine  the  causes  of 
hypertrophic  rhinitis.  Sometimes  the  condition  seems  to  develop  as  a  sequel  to 
frequently  repeated  nasal  catarrh,  although  in  this  case  the  relation  is  often 
reversed — it  being  the  chronic  rhinitis  which  occasions  a  predisposition  to  the 
frequent  acute  exacerbations  of  the  catarrh.     Certain  diatheses  (anasinia,  scrofula) 


CHRONIC  RHINITIS.  127 

appear  to  influence  the  development  of  the  disease.      This  is  also  true  of  occupa 
lions  which  expose  the  individual  to  dust  or  smoke,  and  sometimes  of  malforma 
tion  of  the  nose  (for  instance,  deviation  of  the  septum)  and  perhaps  also  of  heredi- 
tary predisposition. 

The  anatomical  changes  consist  in  a  slow  but  progressive  swelling  and  hyper- 
trophy of  the  mucous  membrane.  This  seems  spongy,  and  of  a  red  or  reddish- 
gray  color.  The  greatest  change  is  almost  always  found  over  the  inferior  turbi- 
nated bone,  and  next  to  that  over  the  middle.  In  advanced  cases  the  mucous 
membrane  presents  rough,  uneven  swellings,  and  even  polypi.  These  changes 
are  often  visible  upon  inspection  of  the  nostrils  anteriorly,  but  they  may  escape 
discovery  until  a  rhinoscopic  examination  of  the  posterior  choanu;  is  made. 

The  disturbance  occasioned  by  chronic  hypertrophic  rhinitis  may  be  very  con- 
siderable. Nasal  respiration  is  obstructed,  the  voice  nasal,  the  senses  of  smell 
and  taste  impaired.  The  nasal  secretion  is  for  the  most  part  increased,  but  it  may 
be  diminished.  Often  there  is  a  tendency  to  nose-bleed.  Many  patients  complain 
also  of  headache. 

The  frequent  involvement  of  neighboring  organs  is  important.  This  applies 
particularly  to  the  ear.  Deafness  is  caused  both  by  the  obstruction  of  the  open- 
ings of  the  Eustachian  tubes,  and  not  infrequently  also  by  extension  of  the  catarrh 
to  the  lining  membrane  of  the  tubes  and  the  middle  ear.  Very  frequently  the 
disease  is  associated  with  chronic  naso-pharyngitis  or  pharyngitis.  The  visible 
portion  of  the  nose  is  not  infrequently  affected,  as  shown  by  redness  and  swelling 
of  its  tip. 

A  fact  of  especial  interest  is  that  such  a  diseased  state  of  the  nasal  mucoiis 
membrane  may  give  rise  to  reflex  neuroses  (Voltolini,  Hack,  and  others).  Al- 
though, in  our  opinion,  many  of  the  specialists  on  the  nose  go  too  far  in  this  direc- 
tion, there  is  no  room  for  doubt  that  attacks  of  migraine,  vertigo,  certain  varieties 
of  headache,  and,  above  all,  many  forms  of  bronchial  asthma,  may  bear  a  close 
relation  to  diseases  of  the  nose.  We  shall  revert  to  this  point  later  on.  (See 
especially  the  chapter  on  bronchial  asthma.) 

The  treatment  of  chronic  hypertrophic  rhinitis,  in  order  to  be  successful,  de- 
mands complete  destruction  and  removal  of  the  hypertrophic  portions  by  means 
of  the  galvano-cautery.  For  particulars,  we  must  refer  to  the  directions  of  spe- 
cialists. In  milder  cases,  however,  benefit  may  follow  the  insufflation  of  a  powder 
composed  of  one  part  of  nitrate  of  silver  to  ten  or  twenty  of  common  starch,  or 
applications  of  lunar  caustic  may  be  made. 

2.  Chronic  Atrophic  or  Fetid  Bhinitis.  Ozeena  Simplex.— This  frequent  and 
peculiar  form  of  chronic  rhinitis  is  the  cause  of  that  well-known  condition  which  is 
characterized  by  a  peculiar  and  extremely  disagreeable  odor  from  the  nose,  which 
is  therefore  usually  termed  ozaena,  from  the  Greek  word  ofav,  to  stink.  The  disease 
consists  in  a  slow,  progressive  atrophy  not  only  of  the  mucous  membrane  with  its 
vessels  and  glands,  but  finally  also  of  the  bones,  and  this  atrophy  is  not  preceded 
by  hypertrophy.  Thus  the  nasal  cavities  become  abnormally  large.  The  tur- 
binated bones  grow  smaller  and  smaller,  so  that  finally  they  are  represented 
merely  by  narrow  ridges.  Furthermore,  the  scanty  purulent  secretion  has  a  tend- 
ency to  dry  up  and  form  adherent  greenish-yellow  scabs  and  crusts,  which 
undergo  a  peculiar  putrefactive  decomposition  and  give  rise  to  the  unbearable 
stench.  It  is  possible,  but  not  yet  demonstrated,  that  a  specific  kind  of  bacterium 
plays  a  part  in  the  process. 

The  ozaana  generally  develops  in  childhood.  It  usually  begins  insidiously,  but 
in  other  cases  apparently  is  a  sequel  of  some  acute  disease,  such  as  measles. 
Anaemia  and  scrofula  deservedly  rank  as  important  predisposing  causes. 

The  subjective  symptoms  are  often  not  marked.     This  is  partly  explained  by 


128  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

the  fact  that  the  patient  has  usually  completely  lost  his  sense  of  smell,  but  for 
that  very  reason  the  discomfort  of  his  friends  may  be  the  greater.  The  feeling' 
of  dryness  in  the  nose  may  prove  annoying,  and  there  are  often  complaints  of 
headache  and  of  pressure  in  the  eyes.  Inasmuch  as  the  naso-pharynx  and  the 
posterior  pharyngeal  wall  are  almost  always  implicated  in  the  process,  the  patient 
often  suffers  from  hacking  and  a  tendency  to  cough  and  vomit.  Such  portions 
of  the  secretion  as  are  swallowed  sometimes  give  rise  to  a  considerable  chronic 
disturbance  of  the  stomach.  Upon  physical  examination  we  are  first  struck  by 
the  unusual  breadth  of  the  nostrils.  With  the  rhinoscope  the  extent  of  the 
atrophy  is  still  better  seen.  The  mucous  membrane  is  pale  or  slightly  red,  and 
covered  with  dry  scabs.  Sometimes  superficial  ulcers  are  formed.  Usually,  as  we 
have  said,  the  superior  portion  of  the  pharyngeal  mucous  membrane  shares  in  the 
disease.  The  posterior  wall  of  the  pharynx  is  seen  to  be  atrophied,  smooth  as  if  it 
were  varnished,  and  often  covered  with  crusts.  The  process  may  involve  the  soft 
palate,  and  even  the  larynx,  and  not  infrequently  the  disease  is  associated  with 
inflammation  of  the  middle  ear. 

It  should  be  added  that  the  true  Ozaena  must  not  be  confounded  with  other 
processes  which  likewise  give  rise  to  a  foul  smell  from  the  nose.  Tuberculous 
disease  of  the  nasal  mucous  membrane  and  nasal  bones  is  not  rare,  particularly  in 
"  scrofulous  "  children  (Demme) ;  nor  should  we  forget  the  syphilitic  affections  of 
the  nose,  tertiary  and  hereditary  syphilis. 

Treatment. — The  treatment  of  ozaana  can  be  made  effective  only  by  the  aid  of 
local  applications  as  prescribed  by  specialists.  Even  then  the  treatment  is  a 
prolonged  one,  and  demands  much  patience  on  the  part  of  both  patient  and  physi- 
cian. Besides  local  applications,  we  must  also  bear  in  mind  the  necessity  of  consti- 
tutional treatment,  especially  in  syphilis  and  tuberculosis. 

The  object  of  local  treatment  is  to  remove  the  secretion  in  order  to  get  rid  of 
the  bad  odor.  Nasal  douches,  with  disinfectant  solutions  like  permanganate  of 
potassium  (1-3,000)  or  carbolic  or  corrosive  sublimate,  are  here  most  useful.  The 
solution  is  carefully  injected  into  the  nose,  or  the  fluid  is  allowed  to  run  gently 
into  one  nostril  from  an  irrigator  while  the  patient  keeps  his  head  bent  forward; 
it  then  runs  through  the  naso-pharynx  and  out  through  the  other  nostril.  The 
patient  soon  learns  to  retain  the  fluid  in  the  pharynx  and  eject  it  from  the  mouth. 
All  nasal  douches  must  at  first  be  used  with  care  and  under  the  eye  of  the  physi- 
cian. The  fluid  should  be  injected  at  the  lowest  pressure  possible,  so  that  none  of 
it  may  enter  the  adjacent  cavities  or  the  Eustachian  tube.  Furthermore,  all 
solutions  used  as  a  douche  must  be  luke-warm — 90°  to  95°  (25°-28°  R.).  Besides 
the  regular  use  of  douches,  painting  and  the  insufflation  of  powders,  like  boracic 
acid,  aceto-tartrate  of  aluminum,  etc.,  are  sometimes  employed.  The  insertion  of 
tampons  of  dry  absorbent  cotton  is  to  be  recommended;  under  their  use  the 
secretion  dries  less  easily  and  the  odor  is  diminished.  These  tampons  should  be 
changed  daily.  It  is  advantageous  to  medicate  the  tampons  with  a  one-per-cent. 
solution  of  creolin  or  with  Peruvian  balsam  or  some  similar  drug.  Tincture  of 
iodine  is  also  recommended.  Of  late  many  attempts  have  been  made  to  treat 
chronic  nasal  catarrh  by  the  galvano-cautery.  With  regard  to  the  details  of  this 
as  well  as  of  other  methods,  we  must  refer  to  special  treatises  on  the  subject. 


NOSE-BLEED.  \  29 


CHAPTER  III. 

NOSE-BLEED. 

( Epietaxie.) 

Although  in  many  cases  nose-bleed  is  only  a  symptom  of  some  other  disease, 
still  we  are  justified  in  a  short  description  of  it,  partly  because  frequently  repeated 
nose-bleeds  often  first  call  our  attention  to  some  other  existing  disease,  and  partly 
because  the  treatment  is  of  practical  importance. 

Many  persons  are  subject  to  habitual  nose-bleed,  which  comes  on  either  from 
slight  causes,  from  violently  blowing  the  nose,  from  physical  exertion,  from  over- 
heating, or  even  without  any  special  cause.  This  habitual  nose-bleed  is  sometimes, 
but  by  no  means  always,  the  sign  of  a  general  hsemorrhagic  diathesis,  which  is 
hereditary  in  many  families.  (See  the  chapter  on  Haemophilia.)  In  other  cases 
the  nose-bleed  is  the  result  of  some  chronic  disease.  It  occurs  especially  in  leu- 
kaemia, in  disease  of  the  heart,  in  contracted  kidney,  and  as  a  symptom  of  the  so- 
called  haemorrhagic  diseases,  like  scurvy,  purpura  haemorrhagica,  etc.  It  is 
also  not  uncommon  in  acute  febrile  diseases,  like  typhoid  and  scarlet  fever. 
Finally,  diseases  of  the  nose  itself  may  give  rise  to  haemorrhage.  The  occurrence 
of  nose-bleed  as  a  form  of  so-called  "  vicarious  menstruation  "  has  often  been 
described,  but  we  must  always  be  very  guarded  in  admitting  it  as  a  fact. 

In  many  cases  nose-bleed  is  a  very  transitory  symptom,  wholly  without  danger, 
and  in  one  sense  it  may  even  be  advantageous.  When  there  is  headache,  or  a 
feeling  of  fullness  in  the  head,  there  is  often  relief  after  an  epistaxis.  Nose- 
bleed is  dangerous,  however,  when  it  takes  place  in  those  who  are  already  weak 
and  anaemic,  or  when  it  is  so  persistent  and  abundant  as  to  cause  a  marked  general 
anaemia.  The  latter  is  recognized  by  the  pallor  of  the  face,  by  the  appearance  of 
general  weakness,  by  vertigo,  tinnitus,  and  a  weakened  pulse.  In  such  cases  the 
physician's  interference  is  always  necessary.  In  every  case  of  nose-bleed  it  is 
important  to  examine  the  posterior  wall  of  the  pharynx  in  order  to  see  whether 
the  blood  is  not  flowing  backward  from  the  posterior  nares.  The  haemorrhage  is 
often  thought  to  stop  when  no  more  blood  comes  from  the  nostrils,  and  yet  the 
blood  keeps  flowing  posteriorly. 

In  every  severe  nose-bleed  rest  is  the  chief  thing  to  be  enjoined,  and  the  patient 
must  be  told  to  avoid  unnecessarily  blowing,  wiping,  or  drying  the  nose.  By 
quietly  and  persistently  closing  the  nostrils  with  a  handkerchief  a  thrombus  is 
often  formed  without  any  further  medication,  and  the  bleeding  stops.  The  appli- 
cation of  cold  water  (iced  water),  in  which  a  little  vinegar  may  be  put,  is  a  good 
thing.  If  the  bleeding  does  not  stop,  we  may  next  try  a  tampon  of  common 
absorbent  cotton  or  styptic  cotton  in  the  nostril  from  which  the  blood  comes.  If 
this  does  not  succeed,  the  posterior  nares  must  be  plugged  by  means  of  a  uBel- 
locq's  canula."  In  case  of  emergency  we  may  use  an  elastic  catheter,  which  is 
passed  through  the  inferior  meatus  into  the  pharynx  and  out  by  the  mouth.  The 
tampon  is  fastened  to  the  catheter  and  brought  up  into  the  posterior  nares  by 
drawing  the  catheter  back  through  the  nose.  Internal  remedies  to  check  the 
blood  are  very  uncertain  in  their  action.  Ergotine,  in  one-grain  pills  (grm.  0"03), 
every  three  or  four  hours,  is  the  first  one  to  employ,  if  we  wish  to  try  to  check  the 
bleeding  by  this  means. 


130  DISEASES  OF  THE  RESPIRATORY   ORGANS. 

SECTION  II. 
Diseases  of  the  Larynx. 

CHAPTER  I. 

ACUTE  LARYNGEAL  CATARRH. 

{Acute  Laryngitis.) 

iEtiology. — Taking  cold  plays  a  prominent  part  in  the  aetiology  or  acute  laryn- 
geal catarrh,  as  every  one  knows.  Its  influence  can  not  properly  be  wholly 
denied,  since  the  more  intimate  relation  between  taking  cold  and  the  origin  of 
a  catarrh  is  still  unknown.  The  disposition  to  laryngitis  differs  very  much  in 
different  people,  so  that  some  take  a  catarrh  much  more  easily  and  more  fre- 
quently than  others.  Besides  cold,  direct  irritants  which  attack  the  laryngeal 
mucous  membrane  often  set  up  a  laryngitis;  among  these  are  in  particular  the 
inhalation  of  smoke  and  of  injurious  gases  and  vapors.  Many  laryngeal  catarrhs, 
too,  arise  from  excessive  speaking,  shouting,  or  singing,  particularly  if  other  injuri- 
ous influences  act  on  the  larynx  at  the  same  time.  Finally,  laryngitis  may  appear 
as  a  complication  or  as  a  secondary  affection,  in  other  diseases,  especially  in  measles, 
less  frequently  in  typhoid,  scarlet  fever,  and  erysipelas.  Catarrh  of  the  larynx  is 
very  often  combined  with  catarrh  of  the  nose,  the  pharynx,  and  the  larger  bronchi. 

Symptomatology. — Although  the  symptoms  of  laryngitis  usually  make  the 
diagnosis  easy  and  certain,  yet  an  accurate  understanding  of  the  extent  and 
intensity  of  the  catarrh  can  be  obtained  only  by  a  laryngoscopy  examination,* 
which  therefore  should  be  employed  in  every  severe  case.  The  laryngeal  mirror 
shows  a  decided  reddening  and  swelling  of  the  mucous  membrane,  varying  with 
the  intensity  of  the  catarrh,  and  most  marked  on  the  true  and  false  vocal  cords 
and  between  the  arytenoid  cartilages.  We  often  see  small  collections  of  mucus 
here  and  there  on  the  membrane.  In  individual  cases  different  parts  of  the 
larynx  are  especially  affected.  In  intense  inflammations  superficial  erosions  are 
often  met  with,  especially  on  the  vocal  cords.  In  other  cases  the  mucous  mem- 
brane shows  a  grayish-white  coloring  in  some  places,  due  to  a  thickening  of  the 
epithelium.  Small  haemorrhages  in  the  mucous  membrane  are  also  occasionally 
seen.  Very  often  we  see  on  phonation  an  incomplete  closure  of  the  glottis,  so  that 
a  little  oval  space  is  left  between  the  vocal  cords.  This  slight  "  catarrhal  paresis 
of  the  vocal  cords  "  is  probably  of  muscular  origin,  and  depends  chiefly  upon  an 
affection  of  the  thyro-arytaenoid  muscles. 

Of  the  other  symptoms  of  laryngeal  catarrh,  hoarseness  is  particularly  to  be 
mentioned,  for  in  many  cases  the  diagnosis  of  laryngitis  may  be  made  from  this 
alone.  It  is  either  due  directly  to  the  anatomical  changes  of  the  cords,  or  to  the 
paresis  just  mentioned.  The  degree  of  hoarseness  is  of  course  very  different  in 
different  cases,  and  varies  from  a  simple  "  roughening  "  or  "  deadening "  of  the 
voice  to  a  complete  loss  of  voice  (aphonia). 

*  More  extensive  observations  on  laryngoscopy  and  on  many  details  of  the  pathology  of  laryngeal 
diseases,  which  have  been  carefully  investigated  by  specialists  and  which  can  not  be  mentioned  here, 
are  to  be  found  in  the  following  works :  Türck,  "  Klinik  der  Krankheiten  des  Kehlkopfes,"  1866. 
Semeleder,  "  Laryngoskopie,"  1863.  Tobold,  "  Laryngoskopie,"  1874.  Störk,  "  Klinik  der  Krank- 
heiten des  Kehlkopfes,  der  Nase,  u.  des  Rachens,"  1880.  Mackenzie,  "  Diseases  of  the  Throat  and 
Nose,"  1880.  B.  Fraenkel  and  v.  Ziemssen,  "  Diseases  of  the  Larynx,"  in  Ziemssen's  "Cyclopaedia." 
Gottstein, "  Krankheiten  des  Kehlkopfes,"  third  edition,  1890.  Schnitter, "  Vorlesungen  über  die  Krank- 
heiten des  Kehlkopfes." 


ACUTE  LARYNGEAL  CATARRH.  131 

The  cough  in  laryngitis  may  he  very  severe,  and  is  often  recognizable  hy  its 
harsh,  hoarse  ring  as  a  "  laryngeal  cough."  It  is  at  first  usually  dry,  and  later  on 
it  is  associated  with  a  scanty  muco-purulent  expectoration,  which  is  sometimes 
tinged  with  blood. 

Paha  in  the  larynx  is  generally  only  moderate.  The  subjective  symptoms  con- 
sist chiefly  of  a  disagreeable  feeling  of  itching,  burning,  and  dryness  in  the  throat. 
After  prolonged  speaking,  however,  the  pain  in  the  larynx  may  sometimes  be  quite 
severe.  External  pressure  on  the  larynx  is  often  somewhat  painful.  Difficulty 
in  swallowing,  when  it  occurs,  is  usually  due  to  an  accompanying  pharyngitis, 
but  it  may  also  be  dependent  upon  an  affection  of  the  epiglottis  and  the  arytenoid 
cartilages. 

The  general  health  is  affected  in  very  different  degrees.  Many  patients  feel 
quite  well  except  for  the  hoarseness,  while  others  are  affected  with  considerable 
debility,  mild  headache,  and  even  at  times  slight  febrile  disturbances. 

Dyspnoea  is  not  present  in  the  common  laryngitis  of  adults,  even  if  there  is 
decided  swelling  of  the  false  vocal  cords  or  of  the  ary-epiglottic  folds.  There  is, 
however,  a  severe  form  of  acute  laryngitis,  the  so-called  laryngitis  hypoglottica 
acuta  gravis  (chorditis  vocalis  inferior),  affecting  not  only  children,  but  adults, 
in  which  well-marked  symptoms  of  suffocation  may  be  present.  In  this  form 
there  is  an  acute,  very  well  marked  swelling  of  the  mucous  membrane  in  the  in- 
ferior, "  sub-chordal,"  laryngeal  space,  which  leads  to  a  stenosis. 

In  children,  however,  on  account  of  the  greater  narrowness  of  the  child's 
larynx,  symptoms  of  stenosis  are  not  rare  even  in  the  milder  forms  of  laryngitis, 
and  therefore  they  have  led  to  the  establishment  of  a  special  disease,  the  so-called 
false  croup. 

The  false  croup  {laryngitis  stridula)  of  children  usually  follows  a  slight 
coryza.  A  harsh,  hollow,  ringing  cough  comes  on,  almost  always  suddenly  and 
usually  at  night,  by  which  the  child  is  awakened  out  of  sleep.  The  paroxysms  of 
coughing  are  broken  by  long-drawn,  noisy  inspirations.  The  child  is  anxious  and 
restless,  the  respiration  is  labored,  the  pulse  is  rapid.  Such  attacks  recur  several 
times  during  the  night.  The  next  day  the  child  is  quite  lively,  plays  about,  and 
has  at  most  a  slight  cough.  The  next  night,  rarely  sooner,  the  same  severe  attacks 
are  repeated.  After  that  there  remains,  as  a  rule,  nothing  but  a  slight  catarrh, 
which  completely  disappears  in  a  week  or  two.  These  sudden  attacks  have  their 
origin  partly  in  a  marked  swelling  of  the  mucous  membrane,  occurring  during 
sleep,  partly  in  a  neglected  accumulation  of  secretion,  and  probably  often  also  in 
a  reflex  spasm  of  the  glottis.  No  other  anatomical  cause  than  a  simple  catarrh  of 
the  larynx  is  apparent,  and  on  examining  the  pharynx,  and,  if  possible,  the  larynx 
also,  we  find  no  trace  of  that  diphtheritic  process  which  is  usually  present  in  true 
laryngeal  croup.  It  is  remarkable  that  many  children,  and  sometimes  several 
children  of  the  same  family,  have  a  specially  marked  predisposition  to  false 
croup.  The  statement,  therefore,  that  a  child  has  had  the  croup  several  times 
almost  always  means  that  it  has  had  this  form  of  false  croup  just  described. 

Acute  laryngitis  lasts  only  a  few  days  in  mild  cases,  and  a  week  or  more  in 
severe  cases.  With  improper  care  and  unreasonable  conduct  on  the  patient's  part 
an  acute  catarrh  may  run  into  the  chronic  form.  We  hardly  ever  see  a  fatal 
result  in  adults,  even  in  the  severe  form,  or  in  the  false  croup  of  children. 

The  treatment  of  acute  laryngitis  requires  that  especial  attention  be  paid  to  the 
removal  of  all  injurious  influences.  In  every  severe  laryngitis  the  patient  should 
stay  in  his  room,  and  children  are  better  off  in  bed.  The  patient  should  talk  as 
little  as  possible.  In  all  severe  cases  smoking,  too,  is  to  be  forbidden.  It  is  a  good 
plan  to  furnish  plenty  of  warm  drink.  Hot  milk,  mixed  with  Seltzer  or  Ems 
water,  is  readily  taken  by  most  patients.    If  there  is  an  inhaler  at  our  disposal,  we 


132  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

may  let  the  patient  inhale  simple  steam,  or  a  one-  or  two-per-cent.  solution  of 
common  salt  Inhalations  of  astringents  are  usually  unnecessary.  The  patient 
may  also  hreathe  steam  without  any  special  apparatus.  When  there  is  marked 
irritation  from  coughing-  we  may  give  a  little  morphine.  With  more  marked 
local  symptoms,  especially  if  there  is  much  pain  on  swallowing  from  swell- 
ing of  the  epiglottis  and  the  mucous  membrane  over  the  arytenoid  cartilages,  the 
patient  may  suck  pieces  of  ice  slowly.  In  severe  cases  of  acute  laryngitis,  with 
evident  symptoms  of  stenosis,  ice  must  he  energetically  used  as  an  internal  and  an 
external  application.  Sometimes,  too,  a  few  leeches  applied  in  the  region  of  the 
larynx  afford  distinct  relief.  Among  external  applications  a  mustard  plaster  over 
the  front  of  the  neck  is  to  be  recommended  when  there  are  marked  local  symp- 
toms.    Cold,  wet  compresses  about  the  neck  are  also  of  advantage  in  all  cases. 

In  the  false  croup  of  children  we  should  use,  as  a  rule,  the  same  treatment  as 
has  just  been  described.  The  child  should  take  warm  drink,  and  a  mustard 
paste  or  hot  poultices  should  be  applied  to  the  neck.  We  should  be  rather  cau- 
tious with  regard  to  the  favorite  treatment  with  emetics,  such  as  ipecac  and  sul- 
phate of  copper,  although  it  can  not  be  denied  that  they  sometimes  work  very 
well. 

These  means  are  entirely  sufficient  for  the  treatment  of  acute  laryngitis.  It  is 
only  exceptionally  that  we  find  ourselves  led  to  employ  in  acute  laryngeal  cataiTh 
an  energetic  local  treatment  of  the  laryngeal  mucous  membrane,  like  painting 
with  a  1-15  solution  of  nitrate  of  silver. 

We  must  bear  in  mind  that  a  rational  hardening  process  is  of  distinct  prophy- 
lactic value  in  persons,  especially  in  children,  with  a  recognized  tendency  to 
laryngitis,  sore  throat,  etc.  The  best  method  is  to  bathe  the  neck  and  chest  with 
cold  water  regularly  morning  and  night. 

[A  mild  emetic  can  do  no  possible  harm  in  false  croup,  and  very  often  cuts  the 
attack  short.  The  application  of  a  sponge,  moistened  with  water  as  hot  as  the 
child  will  bear,  to  the  region  of  the  larynx  deserves  mention.] 


CHAPTER  II. 

CHRONIC   LARYNGITIS. 

{Chronic  Laryngeal  Catarrh.') 

iEtiology. — Chronic  laryngitis  develops  from  an  acute  catarrh,  or  comes  on 
gradually  from  the  action  of  injurious  influences  on  the  larynx  (see  the  preceding 
chapter).  Chronic  laryngitis,  therefore,  is  in  many  cases  a  disease  arising  from 
the  occupation,  and  is  seen  especially  in  singers,  public  speakers,  criers,  inn-keep- 
ers, etc.  It  is  very  frequent  in  drunkards,  and  in  such  cases  it  is  almost  always 
associated  with  a  chronic  pharyngitis.  It  is  frequently  stated  that  too  long  a 
uvula  sets  up  a  chronic  laryngitis  by  constant  irritation  of  the  entrance  to  the 
larynx,  and  that  if  the  uvula  is  amputated  the  disease  is  cured. 

Symptomatology. — A  laryngoscopic  examination  is  very  desirable  in  acute 
laryngeal  catarrh,  but  it  is  the  physician's  absolute  duty  to  make  one  in  every 
chronic  laryngitis,  for  only  too  frequently  a  persistent  hoarseness  is  referred 
simply  to  catarrh  when  the  laryngoscope  gives  quite  another  cause  for  it,  such  as 
paralysis  of  the  vocal  cords  or  new  growths.  Furthermore,  we  must  always  re- 
member that  a  chronic  laryngitis  may  be  a  complication  of  tuberculosis,  syphilis, 
or  chronic  nephritis.     On  the  other  hand,  those  physicians  who  make  a  specialty 


CHRONIC  LARYNGITIS.  133 

of  laryngology  often  neglect  a  careful  and  satisfactory  examination  of  the  rest  of 
the  body  when  there  are  laryngeal  troubles. 

The  laryngoscopic  appearance  in  chronic  catarrh  may  be  so  like  that  in  an 
acute  catarrh  that  we  can  not  distinguish  between  them  without  the  history 
obtained  from  the  patient.  The  redness  of  the  mucous  membrane,  however,  is 
usually  less  intense,  and  the  vocal  cords  have  more  of  a  dirty  grayish-red  appear- 
ance. Quite  frequently  in  persistent  catarrhs  a  thickening  of  particular  parts  of 
the  mucous  membrane  is  developed,  especially  of  the  folds  between  the  arytenoid 
cartilages.  This  swelling  is  of  practical  importance,  because  it  furnishes  a  me- 
chanical hindrance  to  the  closure  of  the  arytenoid  cartilages,  and  in  that  way 
contributes  to  the  development  of  the  hoarseness.  We  also  find  limited  and 
marked  thickening  of  the  epiglottis,  the  false  vocal  cords  (especially  in  public 
speakers  and  preachers),  and  the  true  vocal  cords.  Türck  has  described  a  peculiar 
form  of  chronic  laryngitis,  in  which  rough  prominences  are  formed  in  the  middle 
of  the  true  vocal  cords,  under  the  name  of  chorditis  tuberosa.  We  not  infre- 
quently find  in  chronic  catarrh  superficial  erosions,  especially  on  the  true  vocal 
cords.  Superficial  but  very  painful  fissures  occur  upon  the  posterior  wall  of  the 
larynx  between  the  arytenoid  cartilages.  We  also  very  often  see  a  disturbance  of 
motion  of  one  or  both  vocal  cords,  due  sometimes  to  muscular  paresis  and  some- 
times to  mechanical  conditions. 

The  other  symptoms  of  chronic  laryngitis  are  hoarseness,  cough,  and  abnormal 
sensations  in  the  larynx.  The  hoarseness  is  of  every  degree,  from  mere  rough- 
ness, frequent  "  cracking  "  of  the  voice,  to  almost  complete  aphonia.  The  cough 
is  ringing,  hoarse,  deep,  and  rough.  The  expectoration  is  scanty,  usually  simply 
mucous,  but  sometimes  a  little  bloody.  The  subjective  sensations  in  the  larynx 
are  a  feeling  of  burning  and  itching,  and  of  dryness  and  tickling.  They  usually 
increase  after  any  protracted  use  of  the  voice. 

We  must  also  mention  as  a  very  rare  but  practically  important  and  peculiar 
form  of  chronic  laryngitis  the  chorditis  vocalis  inferior  hypertrophica  (Gerhardt), 
or  laryngitis  hypoglottica  chronica  hypertrophica  (Ziemssen).  In  this  form  there 
is  a  very  gradual  hypertrophy,  and  finally  a  contraction  of  the  mucous  and  espe- 
cially the  submucous  connective  tissue  in  the  inferior  laryngeal  space.  More 
rarely  the  same  changes  are  seen  in  the  upper  part  of  the  larynx.  The  special 
symptom  of  the  disease,  besides  a  chronic  hoarseness,  is  the  appearance  of  a  gradu- 
ally increasing  stenosis  of  the  larynx.  The  respiration  is  always  labored,  the 
inspiration  noisy  and  protracted.  In  many  cases  there  are  at  times  such  attacks 
of  suffocation  that  life  can  be  prolonged  only  by  tracheotomy.  The  diagnosis 
can  be  made  only  by  the  aid  of  the  laryngoscope.  We  see  beneath  the  glottis 
a  little  fissure  surrounded  by  the  thick  and  swollen  mucous  membrane  of  the 
laryngeal  walls. 

The  precise  aetiology  of  this  disease  is  as  yet  unknown.  It  appears  to  have 
nothing  to  do  with  syphilis,  contrary  to  the  former  belief. 

The  treatment  of  chronic  laryngeal  catarrh  is  always  a  tedious  and  laborious 
task,  the  success  of  which  depends  in  great  measure  upon  the  good  will  and 
energy  of  the  patient.  In  the  first  place,  then,  we  should  endeavor  to  remove  as 
far  as  possible  those  injurious  influences  which  have  excited  and  kept  up  the 
catarrh.  It  is  often  easier  to  give  good  advice  here  than  to  follow  it.  Neverthe- 
less, it  is  the  task  of  the  physician  to  impress  upon  the  patient  the  urgent  neces- 
sity of  taking  care  of  the  larynx,  and  to  forbid  as  far  as  possible  all  protracted 
speaking,  singing,  staying  in  smoke  or  dust,  smoking,  and  drinking  alcoholic 
liquors. 

Local  treatment  takes  the  second  place.  Among  the  most  useful  means  to 
employ  are  inhalations  of  astringent  solutions,  like  a  one-per-cent.  solution  of 


134  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

either  tannin  or  alum.  When  there  is  great  sensitiveness  of  the  larynx,  the 
patient  may  also  inhale  narcotics,  a  mixture  of  fifty  parts  of  cherry-laurel  water 
with  a  thousand  parts  of  water,  or  a  four-per-cent.  solution  of  bromide  of  potas- 
sium. The  inhalations  should  be  used  two  or  three  times  a  day,  and  last  about 
five  minutes  each  time.  Direct  applications  to  the  larynx  are  much  more  effective 
than  inhalations,  but  these  can  be  employed  only  by  the  aid  of  a  laryngeal  mirror. 
Of  these  we  use,  first  of  all,  nitrate  of  silver,  at  first  in  a  weak  solution  (one  to 
thirty) ;  later  in  a  more  concentrated  form  (one  to  ten,  or  even  one  to  five).  These 
applications  are  made  every  two  or  three  days.  Besides  nitrate  of  silver,  the  larynx 
may  also  be  painted  with  pure  tincture  of  iodine,  or  with  iodine  and  glycerine,  or 
with  concentrated  solutions  of  alum  or  tannin.  Where  the  secretion  of  mucus 
is  considerable  ,benefit  will  be  obtained  from  inhalations  of  turpentine,  or  of  oleum 
pint  or  oleum pini pumilionis  (P.  Gr.). 

Water-cures  are  also  often  prescribed  in  chronic  catarrh  of  the  larynx.  These 
are  so  far  of  advantage  that,  from  the  greater  care  which  the  patient  takes,  and 
from  the  good  air,  the  catarrh  improves.  Empirically,  we  prescribe,  especially 
for  "  full-blooded  "  patients,  the  cold  sulphur  springs,  like  Nenndorf,  Eilsen,  or 
Weilbach,  or  the  sulphate  of  sodium  waters,  like  Carlsbad  and  Marienbad,  while 
we  send  those  of  delicate  constitutions  to  Ems,  Salzbrunn,  Salzungen,  Reichenhall, 
or  Ischl. 

The  treatment  of  laryngitis  hypertrophica,  when  it  leads  to  stenosis,  must  be 
mechanical.  Schrötter,  in  particular,  has  devised  several  methods  in  order  to 
dilate  the  stenosis  gradually  by  the  introduction  of  bougies  and  harder  dilators. 
The  details  of  this  treatment  are  to  be  found  in  the  later  special  works  referred  to 
above. 


CHAPTER  III. 
LARYNGEAL  PERICHONDRITIS. 

iEtiology  and  Pathological  Anatomy. — The  inflammation  of  the  perichon- 
drium of  the  laryngeal  cartilages  is  in  very  rare  cases  apparently  a  primary 
disease.  It  is  much  more  frequently  secondary  to  other  laryngeal  affections, 
especially  tuberculosis  and  syphilis  of  the  larynx.  Furthermore,  it  develops 
secondarily  in  severe  acute  diseases,  most  frequently  in  typhoid  fever,  more 
rarely  in  small-pox,  diphtheria,  etc.  Superficial  ulcerative  processes  in  the  mu- 
cous membrane  often  precede  the  perichondritis  in  these  cases,  and  the  participa- 
tion of  the  perichondrium  in  the  inflammation  arises  from  their  gradual  deep- 
ening. Anatomically,  we  have  to  do  as  a  rule  with  a  purulent  inflammation, 
which  usually  leads  to  the  formation  of  circumscribed  abscesses.  Most  laryn- 
geal abscesses  have  their  origin  in  the  perichondrium.*  The  perichondrium  is 
m  part  destroyed  by  the  abscess  and  in  part  elevated  from  the  cartilage.  The 
cartilage  then  becomes  necrotic,  breaks  in  pieces,  and  is  expelled  in  small  particles 
or  in  masses. 

Perichondritis  occurs  most  frequently  in  the  cricoid  and  arytaenoid  cartilages, 
much  more  rarely  on  the  internal  or  external  surface  of  the  thyroid  cartilage. 
Hence  we  distinguish  an  internal  and  an  external  perichondritis.  A  perichon- 
dritis of  the  epiglottis  has  also  been  repeatedly  observed. 

Symptomatology. — In  the  rare  cases  of  primary  perichondritis,  marked  laryn- 
geal symptoms  are  speedily  developed  in  a  person  previously  healthy.     These 

*  Pure  submucous  abscesses,  the  so-called  phlegmonous  laryngitis,  occur  only  in  very  rare  cases. 


(EDEMA   OF  THE  GLOTTIS.  135 

symptoms  are  pain  and  tenderness  on  pressure  over  the  larynx,  hoarseness,  and 
cough;  and  to  them  are  usually  soon  added  the  signs  of  a  dangerous  stenosis  of 
the  larynx.  In  secondary  cases,  which  occur  almost  always  in  patients  who  are 
already  seriously  ill,  the  symptoms  of  stenosis  are  often  the  first  to  point  to  a  severe 
disease  of  the  larynx.  On  laryngoscopic  examination,  hesides  the  general  redness 
and  swelling  in  particular  places,  we  can  sometimes  recognize  a  circumscribed 
protrusion  of  the  mucous  membrane  caused  by  the  abscess.  We  often  find, 
besides,  a  considerable  collateral  oedema  of  the  surrounding  mucous  membrane, 
which  oedema  frequently  has  a  greater  share  in  the  production  of  stenosis  than  has 
the  primary  affection  itself.  The  dreaded  oedema  of  the  glottis  (oedema  of  the 
ary-epiglottic  ligament)  in  typhoid,  tuberculosis  of  the  larynx,  etc.,  is  usually  due 
to  perichondritis  of  the  cricoid  or  arytamoid  cartilages.  Finally,  we  can  see 
with  the  laryngoscope,  especially  in  perichondritis  arytamoidea,  a  considerable 
disturbance  of  motion  of  the  affected  arytaenoid  cartilage,  and  also  of  the  vocal 
cords.  In  the  later  stages,  if  the  abscess  has  been  opened,  or  if  it  breaks  of  its  own 
accord,  and  the  whole  cartilage  or  a  part  of  it  is  expelled,  we  can  make  out  the 
extent  of  the  destruction  that  results  more  accurately  by  the  laryngoscope. 

Laryngeal  perichondritis  terminates  fatally  in  a  great  number  of  cases  from 
the  development  of  stenosis.  In  other  cases  the  most  threatening  symptoms  may  be 
averted  for  a  time,  but  the  primary  disease,  such  as  tuberculosis,  finally  comes  to 
an  unfavorable  termination.  In  the  rare  cases  in  which  recovery  occurs  after 
primary  perichondritis  or  after  the  termination  of  the  primary  disease,  such  as 
typhoid,  this  recovery  is  often  incomplete,  since  a  chronic  stenosis  of  the  larynx 
remains  from  the  ensuing  cicatricial  contractions. 

The  diagnosis  is  usually  obscure  during  the  first  period  of  severe  symptoms  of 
stenosis,  since  it  is  difficult  to  make  a  laryngoscopic  examination,  and  it  is  also 
not  always  easy  to  determine  the  condition.  We  are  usually  justified,  however, 
in  making  the  diagnosis,  if  in  those  diseases  which  we  have  mentioned,  in  which 
we  know  by  experience  that  a  perichondritis  quite  frequently  occurs,  the  danger 
of  suffocation  arises  in  addition  to  the  other  laryngeal  symptoms.  It  is  of  prac- 
tical importance  to  recognize  stenosis  of  the  larynx  with  certainty,  for  it  demands 
a  speedy  therapeutic  interference. 

Treatment. — In  the  beginning  of  the  affection  we  may  try  to  reduce  the  inflam- 
mation by  the  internal  and  external  application  of  ice  or  by  leeches ;  but  if  ste- 
nosis of  the  larynx  occurs,  surgical  interference  is  usually  necessary,  for  only  in 
very  rare  cases  do  we  see  the  abscess  open  of  itself  and  a  subsidence  of  the 
dangerous  symptoms  follow.  In  the  majority  of  cases  the  patient  can  be  saved 
from  suffocation  only  by  tlie  timely  performance  of  tracheotomy.  The  laryngeal 
abscess  has  been  repeatedly  opened  internally  by  laryngologists  with  favorable 
results.  If  a  chronic  stenosis  of  the  larynx  remains  after  a  favorable  termina- 
tion of  the  disease,  either  the  patient  must  wear  a  tracheal  canula  all  his  life,  or 
the  attempt  may  be  made  to  dilate  the  stenosis  gradually  by  the  methods  referred 
to  in  the  preceding  chapter. 


CHAPTER  IV. 

(EDEMA   OF   THE   GLOTTIS. 

The  practical  importance  of  the  subject  demands  a  brief  special  description  of 
oedema  of  the  glottis,  by  which  name  we  mean  oedema  of  the  entrance  of  the  lar- 
ynx, especially  of  the  ary-epiglottic  ligaments.  We  have  already  learned  to 
recognize  laryngeal  perichondritis  as  one  of  its  most  frequent  causes.     In  less 


136  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

deeply  seated  inflammations  in  the  larynx  and  its  neighborhood,  however,  oedema 
of  the  glottis  may  sometimes  develop  as  a  dangerous  complication,  especially  in 
cases  of  laryngitis  occurring  in  the  course  of  severe  acute  diseases,  like  typhoid, 
small-pox,  or  erysipelas,  or  in  inflammations  of  the  larynx  arising  from  severe 
mechanical  or  chemical  irritation,  like  hot  steam  or  corrosive  substances,  or  from 
wounds  of  the  larynx,  or,  finally,  from  foreign  bodies  in  the  larynx.  The  col- 
lateral oedema  in  angina  Ludovici,  in  intense  inflammations  of  the  parotid  gland, 
or  the  tonsils,  etc.)  may  in  rare  cases  extend  to  the  ary-epiglottic  ligaments. 
Finally,  oedema  of  the  glottis  occurs  in  rare  cases  as  a  complication  of  general 
oedema  of  the  body,  as  a  result  of  Bright's  disease,  disease  of  the  heart,  emphysema 
of  the  lungs,  etc.  OEdema  of  the  glottis  has  been  repeatedly  observed  to  come 
on  quite  suddenly,  especially  in  Bright's  disease. 

The  chief  symptom  of  oedema  of  the  glottis  is  dyspnoea,  which  comes  on  as 
a  result  of  the  stenosis  of  the  entrance  of  the  larynx,  and  is  sometimes  extreme. 
At  first  this  is  chiefly  on  inspiration,  but  it  soon  comes  on  with  expiration  also. 
Respiration,  especially  inspiration,  is  accompanied  by  a  loud  laryngeal  stridor. 
As  a  result  of  the  incomplete  entrance  of  the  air,  the  efforts  at  inspiration  in- 
volve the  neck,  the  epigastrium,  and  the  sides  of  the  thorax.  We  see  with  the 
laryngoscope,  if  the  examination  be'  successful,  an  cedematous  swelling  of  the  ary- 
epiglottic  ligaments,  and  often  a  swelling  of  the  epiglottis  and  the  false  vocal 
cords.     Sometimes  we  succeed  in  feeling  the  swollen  parts  with  the  finger. 

If  the  dyspnoea  reaches  a  degree  which  threatens  life,  an  operation  is  the  only 
thing  which  can  afford  relief.  Laryngologists  attempt  to  reduce  the  swelling 
by  long  incisions  in  the  cedematous  parts.  If  this  does  not  succeed,  tracheotomy 
must  be  performed.  If  the  immediate  danger  to  life  is  thus  averted,  further 
treatment  should  be  directed  to  the  disease  which  has  given  rise  to  the  oedema. 


CHAPTER  V. 

TUBERCULOSIS   OF   THE   LARYNX. 

{Laryngeal  Phthisis.     Consumption  of  the  Larynx.) 

.ZEtiology. — Since  tuberculosis  of  the  larynx  is  in  most  cases  combined  with 
tuberculosis  of  other  organs,  especially  of  the  lungs,  we  must  refer  to  the  descrip- 
tion of  tuberculosis  of  the  lungs  for  the  general  aetiology  and  pathology  of  the 
disease.  A  particular  description  of  the  special  appearances  in  laryngeal  tuber- 
culosis, is,  however,  justifiable,  because  tuberculosis  may  at  times  begin  in  the  larynx 
and  may  remain  isolated  there,  at  least  for  a  time;  and,  furthermore,  in  many 
cases  of  laryngeal  tuberculosis,  which  are  evidently  combined  with  pulmonary 
tuberculosis,  the  laryngeal  symptoms  are  predominant  in  the  clinical  picture  of 
the  disease.  Many  physicians  have,  wrongly  as  we  think,  disputed  the  fact  that 
tuberculosis  can  begin  in  the  larynx.  Clinical  experience  not  infrequently  teaches 
us  that  men,  who  up  to  that  time  were  apparently  in  good  health,  are  attacked 
with  hoarseness,  the  disease  being  at  first  thought  to  be  a  common  laryngitis, 
but  at  last,  by  its  later  course,  proving  to  be  a  tuberculosis.  In  spite  of  the  most 
careful  examination,  there  are  not  to  be  found  at  first  the  slightest  physical 
signs  of  disease  in  the  lungs,  and  not  till  later  do  the  manifest  signs  of  a  pul- 
monary tuberculosis  succeed  the  symptoms  of  a  laryngeal  affection.  In  such  cases 
it  seems  to  us  an  affectation  to  claim  that  there  is  a  primary  pulmonary  tubercu- 
losis which  could  not  be  made  out  at  first.  Everything  is  much  more  in  favor  of 
the  opinion  that  the  tubercular  poison,  the  tubercle  bacilli,  may  sometimes  first 


TUBERCULOSIS  OF  THE  LARYNX.  i;;7 

fix  upon  the  larynx,  excite  the  first  symptoms  of  tuberculosis  there,  and  only  later 
attack  the  lungs. 

In  the  majority  of  cases  of  laryngeal  tuberculosis  the  symptoms  are  devel- 
oped, of  course,  secondarily  in  the  course  of  chronic  pulmonary  phthisis.  We 
shall  see  that  in  these  cases  the  disease  of  the  larynx  is  to  be  considered  as  the 
result  of  an  infection  of  the  mucous  membrane  of  the  larynx  by  the  tuberculous 
sputum  which  passes  over  it.  In  about  one  fourth  of  all  cases  of  pulmonary 
tuberculosis  this  complication  occurs,  if  we  include  all  the  mild  diseases  of 
the  larynx.  Marked  and  extensive  tuberculosis  of  the  larynx  is  much  rarer, 
however. 

Pathological  Anatomy.— In  its  anatomical  appearances  the  laryngeal  affection 
which  complicates  pulmonary  phthisis  or  occurs  primarily  is  at  first  usually  a 
simple  catarrh  of  the  mucous  membrane,  which  does  not  differ  in  any  remarkable 
way  from  any  other  laryngeal  catarrh.  Shallow  erosions,  too,  on  the  vocal 
cords  or  between  the  arytaenoid  cartilages  have  nothing  characteristic  in  them- 
selves. In  fact,  it  is  even  hard  to  decide  whether  the  simple  laryngeal  catarrh  and 
superficial  ulcers  in  the  larynx,  which  often  occur  in  phthisical  patients,  are  really 
in  every  case  specific  tubercular  affections.  Perhaps  they  are  often  only  the 
result  of  the  mechanical  irritation  from  the  frequent  cough  or  of  the  chemical 
irritation  from  the  sputum.  This  question  is  to  be  decided  finally  only  by  the 
discovery  of  the  special  tubercle  bacilli  in  the  laryngeal  affections  of  phthisical 
patients. 

The  more  marked  changes  in  the  larynx  in  phthisical  patients,  however,  are 
without  doubt  always  of  tubercular  origin.  In  these  we  find  a  characteristic 
tubercular  infiltration,  with  the  formation  of  miliary  tubercles  in  the  mucous  and 
submucous  tissues.  When  the  infiltrated  parts  break  down,  extensive  ulcers  are 
formed  which  always  extend  farther,  and  whose  favorite  seat  is  on  the  arytaenoid 
cai'tilages,  the  vocal  cords,  and  the  epiglottis.  From  the  latter  the  ulcers  not 
infrequently  extend  to  the  back  of  the  tongue.  In  severe  cases  we  often  find  a 
marked  collateral  oedema  in  the  neighboring  parts  accompanying  the  inflam- 
mation, and  sometimes  the  tubei'cular  perichondritis  which  has  already  been  de- 
scribed. 

Clinical  Symptoms. — In  the  beginning  of  tuberculosis  of  the  larynx  the  laryn- 
goscope usually  shows  nothing  but  the  appearances  of  a  simple  catarrh.  In  the 
later  stages,  however,  most  of  the  special  signs  of  the  destructive  tubercular  pro- 
cess, like  ulcers,  infiltration,  etc.,  can  be  very  satisfactorily  made  out.  In  fact, 
we  often  get  in  this  way  a  better  picture  of  the  disease  than  we  do  at  the  au- 
topsy, for  the  hyperaemia  and  swelling  of  the  parts  are  much  diminished  in  the 
cadaver. 

The  other  clinical  symptoms  of  tuberculosis  of  the  larynx  vary  very  much  with 
the  extent  and  intensity  of  the  process.  Sometimes  they  consist  merely  in  mod- 
erate roughness  and  hoarseness  of  the  voice,  but  in  other  cases  they  increase  to  the 
most  painful  condition  which  is  ever  seen  in  any  variety  of  tuberculosis.  This 
is  especially  apt  to  be  the  case  if  the  ulceration  involves  the  epiglottis  and  the 
arytaenoid  cartilages.  Swallowing  is  then  extremely  painful,  so  that  the  nutrition 
is  very  often  impaired,  and  painful  attacks  of  coughing  frequently  occur.  If 
severe  ulcerations  attack  the  vocal  cords,  and  their  free  mobility  is  affected  to  a 
marked  degree,  the  hoarseness  increases,  and  finally  reaches  a  complete  aphonia. 
Death  finally  occurs  from  general  inanition,  or,  exceptionally,  from  oedema  of  the 
glottis. 

The  diagnosis  of  tuberculosis  of  the  larynx  is  not  difficult  if  pulmonary 
phthisis  is  already  known  to  be  present.  When  attention  has  been  called  to  it 
from  the  onset  of  hoarseness  or  from  some  disturbance  in  swallowing,  we  recognize 


138  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

the  character  and  seat  of  the  changes  by  the  aid  of  the  laryngoscope.  The  diag- 
nosis, however,  may  present  much  difficulty  in  cases  where  we  are  not  sure  that 
an  affection  of  the  lungs  co-exists.  As  has  been  said,  the  symptoms  at  first  are  not 
unlike  those  of  a  simple  catarrh,  and  the  suspicion  of  the  existence  of  tuberculosis 
is  first  aroused  from  the  stubbornness  of  the  disease,  the  condition  of  the  patient, 
some  inherited  taint,  the  onset  of  fever,  and  the  remarkable  emaciation.  With 
the  changes  in  the  larynx  which  have  been  described  the  distinction  between 
tuberculosis  and  syphilis  may  be  very  difficult.  In  syphilis  of  the  larynx,  how- 
ever, we  find  that  co-existing  changes  in  the  pharynx  are  much  commoner 
than  in  tuberculosis,  and  the  cicatricial  formation  which  is  usually  visible  fur- 
nishes, besides,  a  very  characteristic  evidence  of  syphilis.  The  diagnosis  of  tuber- 
culosis of  the  larynx,  however,  is  made  perfectly  certain  in  all  doubtful  cases 
by  the  discovery  of  tubercle  bacilli  in  the  patient's  expectoration  or  in  the 
secretion  from  the  ulcer,  which  often  can  be  easily  obtained  by  the  aid  of  a  fine 
laryngeal  brush.  In  regard  to  the  laryngoscopic  appearances,  we  may  also  say 
that  a  thick  infiltration  of  the  epiglottis  with  a  partial  ulceration  of  the  same  is 
an  appearance  which  is  almost  exclusively  confined  to  tuberculosis.  The  same  is 
true  with  regard  to  a  marked  projecting  infiltration  of  the  inter-arytaenoid  re- 
gion. 

For  the  general  treatment  of  tuberculosis  the  reader  is  referred  to  the  con- 
sideration of  pulmonary  tuberculosis.  We  shall  here  discuss  merely  the  local 
treatment.  This  is  in  the  milder  forms  the  same  as  for  simple  laryngeal  catarrh. 
There  is  no  doubt  that  even  genuine  tuberculous  ulceration  of  the  larynx  may  be 
healed.  Nevertheless  permanent  cures  of  this  sort  are  exceptional.  Of  course 
very  much  depends  upon  the  general  condition  of  the  patient,  and  upon  the  co- 
existing state  of  the  lungs.  For  local  treatment  insufflations  of  iodoform  and 
iodol  were  for  a  time  strongly  recommended,  but  they  are  now  for  the  most  part 
abandoned.  Of  late  the  best  results,  comparatively  speaking,  have  been  reported 
from  the  local  employment  of  lactic  acid,  in  a  solution  of  thirty  per  cent,  to 
eighty  per  cent,  and  preceded  by  cocaine,  and  of  menthol  in  a  twenty-per-cent. 
solution  in  oil.  But  all  these  methods  of  treatment  demand  considerable 
dexterity.  Inhalations  are  for  the  most  part  merely  palliative.  We  have  always 
obtained  the  best  satisfaction  in  this  regard  from  inhalations  of  Peruvian  balsam. 
It  is  our  conviction  that  for  any  true  advance  in  the  treatment  of  laryngeal 
tuberculosis  we  must  look  to  sui'gery,  and  not  to  endo-laryngeal  manipulations, 
which  are  always  unsatisfactory  even  in  the  best  hands,  but  to  a  complete  excision 
of  the  diseased  tissue  by  means  of  laryngotomy.  In  advanced  cases  it  will  usually 
be  found  advisable  to  employ  merely  palliative  treatment. 

The  constant  use  of  cracked  ice,  and  especially  a  lavish  employment  of 
narcotics,  form  the  best  means  of  lessening  the  pain  and  the  difficulty  in  swallow- 
ing. Subcutaneous  injections  of  morphine  a  quarter  of  an  hour  before  each  meal 
often  afford  great  relief.  Besides  this,  we  can  paint  the  larynx  with  strong  solu- 
tions of  morphine,  blow  in  powdered  morphine,  or  let  the  patient  inhale  solutions 
of  morphine  or  bromide  of  potassium.  Cocaine,  which  is  an  excellent  local 
anaesthetic,  excels  all  these,  however,  in  potency  (von  Anrep).  If  we  paint  the 
ulcerated  mucous  membrane  at  the  entrance  of  the  larynx  with  a  ten-  or  twenty- 
per-cent.  solution  of  cocaine,  in  a  few  minutes  such  an  anaesthesia  of  the  affected 
parts  ensues  that  swallowing  may  take  place  without  any  pain.  The  following 
formula  may  be  used: 

3  Cocaini  muriatis gr.  xv-xxx  (l'O-2'O) ; 

Alcohol 3  ss  (2-0) ; 

Aquae  destillatae 3  ij  (8-0).         M. 


PARALYSES  OF  THE  LARYNGEAL  MUSCLES.  139 

Unfortunately,  the  action  of  cocaine  is  extremely  transitory,  so  that  the  paint- 
ing must  he  repeated  over  and  over  again. 


CHAPTER  VI. 
PARALYSES   OF   THE   LARYNGEAL   MUSCLES. 

1.  Paralyses  in  the  Distribution  of  the  Superior  Laryngeal  Nerve.— The  supe- 
rior laryngeal  nerve,  arising  from  the  vagus,  is  the  sensory  nerve  for  the  mucous 
membrane  of  the  upper  portion  of  the  larynx  down  to  the  glottis,  and  also  for 
the  mucous  membrane  of  the  epiglottis  and  its  neighborhood.  Besides  this,  it  also 
supplies  motor  fibers  to  the  crico-thyroid  muscle.  Clinical  experience  renders  it 
probable  that  the  superior  laryngeal  nerve  also  supplies  the  depressors  of  the 
epiglottis,  the  thyro-epiglottideus,  and  the  arytaeno-epiglottidei  muscles,  and  per- 
haps also  the  arytaenoideus  muscle.  The  last  three  muscles  mentioned,  however, 
perhaps  derive  some  motor  fibers  from  the  recurrent  nerve  also  (the  inferior 
laryngeal  nerve). 

Paralysis  of  the  crico-thyroid  muscles  and  of  the  depressors  of  the  epiglottis 
is  seen  most  frequently  after  recovery  from  diphtheria.  It  is  usually  a  part  of  a 
more  extensive  paralysis,  and,  in  addition,  is  frequently  associated  with  anaesthe- 
sia of  those  parts  of  the  mucous  membrane  which,  as  we  have  seen,  derive  their 
sensory  fibers  from  the  superior  laryngeal  nerve  (von  Ziemssen) . 

Paralysis  of  the  thyro-epiglottideus  and  the  arytaeno-epiglottidei  muscles  is 
recognized  by  the  immobility  and  the  erect  position  of  the  epiglottis,  which  is 
directed  toward  the  back  of  the  tongue. 

Paralysis  of  the  crico-thyroid  muscles  makes  the  voice  rough,  and  especially 
renders  the  production  of  high  tones  impossible,  since  for  this  purpose  we  need 
the  action  of  this  muscle  as  a  tensor  of  the  vocal  cords.  The  detection  of  this 
paralysis  by  the  laryngoscope  is  extremely  difficult.  Its  chief  signs  are  a  con- 
cavity of  the  edges  of  the  vocal  cords,  a  lack  of  visible  vibration  in  them,  and 
perhaps,  in  unilateral  paralysis,  a  higher  position  of  the  vocal  cord  on  the  sound 
side. 

For  paralysis  of  the  arytaenoideus  muscle,  vide  infra. 

2.  Paralyses  in  the  Distribution  of  the  Inferior  Laryngeal  or  Recurrent  Nerve. 
— The  recurrent  nerve  supplies  with  sensory  fibers  the  mucous  membrane  of  the 
inferior  cavity  of  the  larynx  below  the  glottis,  and  it  is  the  motor  nerve  for  all  the 
laryngeal  muscles  except  the  crico-thyroid,  and  except  possibly  the  depressors  of 
the  epiglottis  (vide  supra).  The  muscles  innervated  by  it  are  arranged  according 
to  their  function  in  the  three  following  groups : 

a.  The  openers  of  the  glottis — the  posterior  crico-arytaenoid  muscles  alone. 

b.  The  closers  of  the  glottis — the  lateral  crico-arytaenoids  and  the  arytaenoideus 
(transverse  and  oblique). 

c.  The  tensors  of  the  vocal  cords — the  thyro-arytaenoids,  which  act  usually 
as  closers  of  the  glottis,  but  which  very  often  produce  the  fine  differences  in 
tension  in  the  vocal  cords  which  are  necessary  in  singing  and  in  modulations  of 
speech.  They  accordingly  have  the  same  task  as  the  coarser- working  crico- 
thyroid muscles,  which  are  innervated  by  the  superior  laryngeal  nerve. 

The  motor  fibers  for  all  these  muscles  have  then  special  origin  in  the  accessory 
nerve,  from  which  they  pass  into  the  trunk  of  the  vagus,  and  from  this  into  the 
laryngeal  nerves. 

Most  of  the  paralyses  of  the  recurrent  nerve  are  of  peripheral  origin.     Except 


140  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

in  the  pure  muscular  pareses  (vide  supra),  which  arise  not  infrequently  in  the 
course  of  other  laryngeal  affections,  peripheral  paralyses  of  the  vocal  cords  occur 
with  the  greatest  relative  frequency  from  an  abnormal  pressure  on  the  trunk  of 
the  recurrent  nerve,  especially  in  aneurism  of  the  arch  of  the  aorta,  which  may 
cause  a  left-sided  paralysis.  Tumors  of  the  bronchial  glands,  cancer  of  the 
oesophagus,  thyroid  or  mediastinal  tumors,  and,  in  rare  cases,  even  large  pericar- 
dial effusions,,  may  also  cause  a  paralysis  of  the  recurrent  On  one  side.  Paralyses 
on  the  right  side  are  seen  quite  frequently  in  contractions  at  the  apex  of  the  right 
lung  and  in  the  rare  cases  of  aneurism  of  the  subclavian  artery.  The  paralyses 
of  the  laryngeal  muscles,  which  are  sometimes  met  with  after  recovery  from  diph- 
theria (q.  v.),  also  belong  to  the  peripheral  paralyses  of  the  recurrent  nerve, 
and  their  cause  is  to  be  found  in  a  degeneration  of  the  branches  of  the  affected 
nerves.  In  other  cases  the  paralysis  of  the  recurrent  nerve  is  due  to  an  affection 
of  its  fibers  in  the  vagus  or  even  in  the  accessorius.  Excluding  certain  injuries 
from  operations,  these  affections  are  usually  due  to  new  growths  which  cause  a 
paralysis  of  conduction.  Paralyses  of  the  recurrent  nerve  also  arise  from  affec- 
tions of  the  nucleus  of  the  accessory  nerve  in  diseases  of  the  medulla,  in  the 
different  forms  of  acute  bulbar  paralysis,  in  chronic  bulbar  paralysis,  in  multiple 
sclerosis,  etc.  The  frequent  hysterical  paralyses  in  the  distribution  of  the  re- 
current nerve  are  to  be  regarded  as  cerebral.  Finally,  paralyses  of  the  laryngeal 
muscles  are  sometimes  observed  for  which  we  are  not  in  a  position  to  find  any 
cause. 

1.  Complete  Paralysis  of  the  Becurrent  Nerve. — Paralysis  of  all  the  laryngeal 
muscles  supplied  by  the  recurrent  nerve  occurs  quite  frequently  in  the  pressure 

paralysis  of  the  trunk  of  the  recurrent,  or  of  its 
fibers  in  the  vagus.  With  the  laryngoscope  (see 
Fig.  14)  we  find  the  vocal  cord  on  the  paralyzed 
side  in  a  middle  position,  often  falsely  called  a 
"  cadaveric  position,"  and  completely  motionless 
on  respiration,  and  also  on  phonation.  On  pho- 
nating  as  strongly  as  possible,  the  vocal  cord  on 
the  sound  side  passes  beyond  the  median  line, 
_       '.     _,        „  n   t,    •<-•        the  arvtaenoicl  cartilage  also  crosses  the  line,  and 

Fig.  14.— (From  Ziemssen)    Position  •>  .        .     .  .  ln.  '. 

on  inspiration  in  paralysis  of  the    consequently  the  glottis  is  put  m  an  oblique  posi- 
conduction'in'ihe  recurrentnerve.     tion.     The  other  symptoms  are  sometimes  so  slight 

that  without  a  laryngoscopic  examination  we  do 
not  even  think  of  a  paralysis.  The  speech,  however,  is  usually  not  pure;  it 
often  breaks  into  a  falsetto,  and  the  patient  is  easily  tired  by  speaking.  With 
bilateral  paralysis  of  the  recurrent  nerve,  which  is  very  rare,  we  find  both  vocal 
cords  motionless  in  a  middle  position.  Complete  aphonia  exists,  and  it  is  impossi- 
ble to  cough,  since  in  coughing  we  have  to  make  at  first  a  complete  closure  of  the 
glottis.     There  is  no  dyspnoea,  however,  if  the  patient  keeps  quiet. 

2.  Paralysis  of  the  Dilators  of  the  Glottis,  tlie  Posterior  Crico-arytsenoid 
Muscles. — Bilateral  paralysis  of  these  muscles  is  a  very  rare  phenomenon,  but 
clinically  it  is  of  the  utmost  importance,  since  it  results  in  a  condition  of  most 
marked  inspiratory  dyspnoea.  This  condition  develops  gradually,  and  usually 
without  any  cause  that  has  been  satisfactorily  determined.  There  is  probably 
some  affection  of  the  nerves  themselves  which  finally  leads  to  the  paralysis.*  In 
most  cases  the  disease  lasts  for  years.  The  dyspnoea  may  increase,  especially  from 
external  causes,  to  severe  attacks  of  suffocation,  and  tracheotomy  is  frequently 

*  It  is  remarkable,  however,  that  a  purely  mechanical  hindrance  to  the  dilatation  of  the  glottis  may 
occur  from  the  formation  of  anchylosis  in  the  crico-aryttenoid  articulation. 


PARALYSES  OF  THE  LARYNGEAL  MUSCLES. 


141 


necessary.  In  paralysis  of  the  dilators  of  the  glottis  the  respiration  r;  so  changed 
that  inspiration  only  is  difficult,  protracted,  and  noisy,  while  expiration  is  free 
and  unhindered.  This  depends  on  a  valve-like  ac- 
tion of  the  vocal  cords.  They  are  drawn  together 
by  the  dilatation  of  the  thorax  on  inspiration,  while 
the  current  of  air  in  expiration  easily  pushes  them 
aside.  Phonation  is  usually  entirely  undisturbed. 
With  the  laryngoscope  (see  Fig.  15)  we  find  the 
glottis  changed  to  a  small  slit,  which  grows  nar- 
rower instead  of  wider  on  inspiration. 

The  prognosis  is  usually  unfavorable.     Only  in 

the  hysterical  can  these  apparently  severe  condi-   Fig  15. -(From  Ziemssen.)- Complete 
^  rr     .      .  .  bilateral  para'ysis  oi  the  posticus 

tions  appear  and  disappear  again  m  a  short  time.  at  the  moment  of  inspiration. 

3.  Paralysis  of  the  Thyro-arytsenoid  Muscles.— 

The  paralysis  or  paresis  of  these  muscles,  which  run  into  the  vocal  cords,  and 
which  are  their  chief  tensors,  is  one  of  the  most  frequent  of  the  paralyses  of  the 
laryngeal  muscles.  It  occurs  especially  in  acute  and  chronic  catarrh  of  the  laryn- 
geal mucous  membrane,  and  is  often  the  chief  cause  of  the  accompanying  hoarse- 
ness. It  also  frequently  develops  as  the  result  of  an  habitual  over-exertion  of 
the  voice  in  singers  and  public  speakers,  and  it  is  one  of  the  commonest  causes  of 
hysterical  aphonia. 

Paralysis  of  the  thyro-ary  taenoid  muscles  may  be  bilateral  or  unilateral.  It  is  fre- 
quently associated  with  a  paresis  of  the  other  closers  of  the  glottis,  the  arytaenoidei 
and  the  crico-thyroid  muscles.  With  the  laryngoscope  (see  Fig.  16),  in  the  ordina- 
ry bilateral  paresis  of  the  thyro-arytaenoid  muscles,  we  see  that  on  phonation  the 
glottis  does  not  close  completely,  but  that  an  oval  space  is  left  between  the  vocal  cords. 

In  unilateral  paralysis  the  affected  cord  shows  a  concavity  of  its  edge.  The 
voice  is  always  more  or  less  hoarse  and  low  and  the  speech  is  strained. 

In  many  cases,  after  a  cure  of  the  original  catarrh,  a  complete  recovery  from 
the  paralysis  may  follow  by  taking  good  care  of  the  voice.  Hysterical  paralyses 
are  diagnosticated  by  their  sudden  disappearance  and  reappearance,  usually  after 
some  psychical  disturbance.  They  are  quite  common  in  children  of  the  age  of  ten 
to  fourteen  years,  especially  in  girls.     (See  the  chapter  on  hysteria.) 

4.  Paralysis  of  the  arytsenoideus  muscle  is  rarely  an  isolated  phenomenon.  It 
is  sometimes  seen  in  laryngeal  catarrh  or  in  hysterical  aphonia.     The  voice  is 

quite  hoarse,  and  with  the  laryngoscope  (see  Fig.  17) 
we  find  on  phonation  that  the  whole  anterior  part  of 
the  vocal  cords  closes  well,  but  that  the  cartilaginous 
glottis  remains  open  as  a  triangular  gap  on  account  of 
the  imperfect  motion  of  the  arytsenoid  cartilages  to- 
ward each  other.  When  the  thyro-arytaenoids  are 
paralyzed  with  the  arytaenoideus,  the  glottis  shows  on 
phonation  a  narrow  hour-glass  opening  (see  Fig.  18). 
Both  the  anterior  and  the  posterior  portions  of  the 
glottis  fail  to  close,  while  the  vocal  processes  take  their 
usual  median  position  on  phonation  from  the  normal 

turning  of  the  arytaenoid  cartilages  inward  by  the  action  of  the  lateral  crico-ary- 

taenoid  muscles. 

5.  Paralysis  of  the  lateral  crico-arytaenoid  muscles,  as  an  uncomplicated  con- 
dition, has  never  been  observed  with  certainty.  Some  cases  of  a  complete  and 
simultaneous  paralysis  of  all  the  closers  of  the  glottis  have  been  described,  how- 
ever, in  which  the  vocal  cords  are  immovable  laterally  and  the  glottis  remains 
abnormally  wide  open. 


Fig.  16.— (From  Ziemssen.)— Pa- 
ralysis of  both  internal  thyro- 
arytsenoid  muscles  in  the 
course  of  an  acute  laryngitis. 


142 


DISEASES  OF  THE  RESPIRATORY  ORGANS. 


We  may  expect  success  from  the  treatment  of  paralysis  of  the  vocal  cords  only 
when  the  primary  disease  is  capable  of  cure.     If  catarrhal  or  other  diseases  of  the 


Fig.  17.— (From  Ziemssen.)  Paraly- 
sis of  the  arytaenoideus  in  acute 
laryngitis. 


Fig.  18.— (From  Ziemssen.)  Bilateral 
paralysis  of  the  thyro-arytaenoids 
combined  with  paresis  of  the  aryt- 
tsenoideus. 


larynx  co-exist,  we  must  first  treat  these  by  the  methods  already  mentioned. 
Paralysis  from  the  compression  of  tumors,  etc.,  may  be  relieved  in  rare  cases  by 
extirpation,  or  by  partial  resolution  of  the  tumors  when  of  strumous  origin.  In 
catarrhal,  diphtheritic,  and  the  so-called  "  rheumatic  "  pareses  —  that  is,  those 
which  occur  without  any  assignable  cause — and  also  in  all  hysterical  aphonias, 
electricity  often  works  very  well.  A  very  rapid  recovery  sometimes  occurs  in 
hysterical  paralyses,  but  it  is  not  always  permanent.  We  commonly  employ  ex- 
ternal faradization  of  the  neck  or  galvanization  through  the  larynx,  combined 
with  frequent  changes  of  the  current.  Ziemssen  has  made  electrodes  for  the  endo- 
laryngeal  irritation  of  single  muscles.  Internally  we  may  prescribe  preparations 
of  iron  and  small  doses  of  quinine,  especially  in  anaemic  patients.  Subcutaneous 
injections  of  strychnine  are  also  of  advantage,  in  doses  of  gr.  ^  to  gr.  ^  daily 
(grm.  0  003  to  0*01).  Methodical  efforts  at  speaking  and  breathing  are  of  great 
service  in  hysterical  aphonia. 


CHAPTER  VII. 

SPASM   OF   THE    GLOTTIS. 

(Millav''s  Asthma.     Tltymia  Asthma.) 

JEtiology. — Spasm  of  the  glottis  is  a  disease  which  occurs  almost  exclusively  in 
children  under  three  years  of  age,  and  which  consists  of  attacks  of  spasmodic 
closure  of  the  glottis,  and  consequently  of  most  severe  dyspnoea.  Boys  are  more 
frequently  attacked  by  this  disease  than  girls,  but  the  cause  of  this  is  wholly 
unknown.  The  old  name  of  thymic  asthma  arose  from  the  idea  that  the  at- 
tacks were  due  to  an  increase  in  the  size  of  the  thymus  gland,  but  this  opinion 
is  wholly  unfounded.  The  relation  between  spasm  of  the  glottis  and  rachitis  is 
remarkable,  but  it  is  unexplained.  Nearly  two  thirds  of  all  the  children  who 
suffer  from  spasm  of  the  glottis  are  rachitic,  but  the  opinion  which  was  once  held 
that  spasm  of  the  glottis  has  a  special  relation  to  the  rachitic  craniotabes  is  not 
clearly  proved.  The  fact  that  it  is  often  combined  with  eclampsia,  in  that  the 
attacks  of  spasm  of  the  glottis  are  aggravated  by  eclamptic  attacks,  and  that  the 
two  alternate  with  each  other,  is  an  argument  in  favor  of  a  central  origin  for 
the  disease.  In  the  cases  which  come  on,  as  they  often  do,  at  the  time  of  denti- 
tion, we  think  it  possible  to  assume  a  reflex  origin  for  the  spasm,  just  as  we  may 
in  those  cases  which  seem  to  follow  a  laryngitis  due  to  taking  cold. 

Symptomatology. — The  single  attacks  usually  come  on  suddenly  by  day  or  by 


DISTURBANCES  OF  SENSIBILITY   IN  THE  LARYNX.  143 

night,  either  without  any  cause  or  from  some  external  influence,  like  crying, 
swallowing  fluid,  or  some  psychical  disturbance.  They  usually  begin  with  a  deep 
inspiration,  followed  by  complete  cessation  of  respiration.  The  child  becomes 
pale,  cyanotic,  looks  anxiously  about,  rolls  his  eyes,  and  makes  strained  and 
labored  efforts  at  respiration.  In  severe  cases  there  is  a  temporary  loss  of  con- 
sciousness, and  tonic  and  clonic  spasms  in  the  muscles  of  the  extremities  and 
the  trunk,  as  has  been  mentioned.  The  attack  lasts  from  some  seconds  up  to  two 
minutes.  In  very  severe  cases  the  attack  may  be  immediately  fatal.  As  a  rule, 
however,  the  spasm  passes  off,  deep,  noisy  inspirations  follow,  and  in  a  short  time 
the  child  is  completely  well.  The  severity  of  the  attacks  varies,  moreover,  in 
different  cases,  and  it  varies  very  markedly,  too,  in  the  same  child.  Sometimes 
we  have  only  one  attack  or  a  small  number  of  them,  while  in  other  cases  they 
may  come  on  ten  or  twenty  times  a  day,  and  even  offener,  and  may  last  with 
varying  intensity  for  months.  If  the  child  reaches  his  third  year  the  disease 
almost  always  disappears,  but  quite  a  large  number  of  the  children  who  suffer 
from  spasm  of  the  glottis  die  before  that  age,  either  in  the  attack  itself  or  from 
other  affections. 

Pure  spasm  of  the  glottis  hardly  ever  occurs  in  adults,  but  similar  attacks  are 
sometimes  observed  in  hysteria. 

The  treatment/ must  be  especially  directed  to  the  child's  general  condition. 
The  child  is  usually  pale  and  emaciated,  aud  if  we  succeed  in  improving  its  nutri- 
tion with  iron  and  cod-liver  oil,  the  attacks  become  less  frequent,  milder,  and 
finally  may  wholly  disappear.  The  child  should  also  be  kept  in  moderately  warm 
air  and  guarded  from  any  exposure  to  cold.  Internal  remedies  to  prevent  the 
recurrence  of  the  attacks  are  very  uncertain  in  their  action.  We  may  employ 
bromide  of  potassium,  ten  to  thirty  grains  daily  (grm.  0-5-2'0);  musk,  ten  drops  of 
the  tincture  every  hour  or  two ;  oxide  of  zinc,  etc. 

In  the  attack  itself  the  child  must  be  raised  up.  The  face  should  be  sprinkled 
with  water,  or,  if  the  attack  be  of  long  duration,  a  cool  shower-bath  should  be 
given.  Friction  should  be  applied  to  the  skin,  aided  by  mustard,  or  a  mustard 
plaster  to  the  chest  and  calves.  If  the  attacks  are  very  frequent  and  intense, 
we  must  use  narcotics,  either  inhalations  of  chloroform  or  subcutaneous  injec- 
tions of  morphine,  with  care,  in  doses  for  a  child  of  -fa  to  ^  of  a  grain  (grm.  0-001 
to  0-005). 


CHAPTER  VIII. 
DISTURBANCES   OF   SENSIBILITY  IN  THE   LARYNX. 

Disturbances  of  sensibility  in  the  laryngeal  mucous  membrane  have  been 
observed  especially  in  the  distribution  of  the  superior  laryngeal  nerve,  in  the  epi- 
glottis, and  in  the  superior  cavity  of  the  larynx  above  the  glottis ;  hut  in  rare  cases 
they  are  also  observed  in  the  lower  portion  of  the  larynx,  which  is  supplied  with 
sensory  fibers  by  the  recurrent  nerve.  They  are  most  frequently  associated  with 
motor  disturbances,  particularly  with  hysterical  paralyses,  but  they  are  also  quite 
often  found  in  paralyses  of  diphtheritic  origin.  Anaesthesia  of  the  larynx  is  rec- 
ognized by  the  lack  of  sensation  which  the  patient  shows  when  we  touch  special 
parts  of  the  larynx  with  the  point  of  a  sound.  The  choking  and  coughing  reflexes 
are  almost  always  absent,  so  that  we  can  touch  the  whole  entrance  of  the  larynx 
with  the  finger  without  causing  discomfort. 

The  absence  of  the  reflexes  may  sometimes  be  dangerous,  especially  in  severe 
diphtheritic  and  bulbar  paralyses,  for,  as  a  result  of  it,  small  portions  of  saliva  may 


144 


DISEASES  OF  THE  RESPIRATORY   ORGANS. 


reach  the  larynx  in  swallowing,  and  fail  to  he  coughed  up,  but  may  be  drawn 
down  into  the  lungs,  where  they  set  up  a  bronchitis  and  a  lobular  pneumonia. 
This  danger  is  especially  great  if  at  the  same  time  the  patient  can  not  cough 
forcibly,  as  is  frequently  the  case  in  imperfect  closure  of  the  glottis.  Hysterical 
anaesthesia  is  the  only  form  where  there  is  no  fear  of  the  development  of  inhala- 
tion diseases  in  the  lungs. 

An  effective  prophylaxis  against  the  dangerous  condition  just  described  is 
possible  only  by  feeding  patients,  who  have  much  weakness  in  swallowing  and 
coughing,  by  means  of  the  oesophageal  tube. 


CHAPTER  IX. 

NEW   GROWTHS  IN   THE   LARYNX. 

Since  new  growths  in  the  larynx  are  of  interest  rather  to  specialists  and  sur- 
geons, we  will  here  only  glance  briefly  at  them.  We  must  remember  especially, 
however,  that  they  can  be  recognized  only  by  the  aid  of  the  laryngoscope.  It 
unfortunately  often  happens  that  a  patient  is  treated  for  a  long  time  without 
success  for  a  u  chronic  laryngeal  catarrh,"  until  the  laryngoscope  finally  shows 
that  a  new  growth  is  the  cause  of  the  hoarseness.  It  is  of  especial  importance, 
however,  to  make  a  diagnosis  as  early  as  possible,  particularly  in  carcinoma, 
since  the  earlier  the  operation  is  done  the  better  is  the  chance  for  success  (vide 
infra). 

A.    Benignant  New  Growths  in  the  Larynx. 

1.  Papilloma  is  one  of  the  commonest  new  growths  in  the  larynx.  It  forms 
glandular,  cauliflower-like  excrescences,  which  are  usually  situated  on  the  ante- 
rior part  of  the  vocal  cords,  rarely  on  the  false  cords.  The  base  of  the  swelling  is 
broad  or  pediculated.  We  do  not  know  the  special  cause  of  their  origin.  They 
sometimes  develop  upon  an  existing  chronic  catarrh. 

2.  Fibroma  in  the  larynx  is  comparatively  common.  The  tumors  known  as 
'l laryngeal  polypi"  are  usually  fibromata.     They  are  generally  situated  on  the 


Figs.  19  and  20.— (From  Ziemssen.)    Pediculated  fibromata. 

vocal  cords  and  form  whitish  or  reddish-brown  swellings,  from  the  size  of  a  pea  to 
that  of  a  cherry,  and  are  usually  pediculated  (see  Figs.  19  and  20).  People  who 
use  their  voices  very  much  are  especially  liable  to  the  formation  of  fibromata. 

3.  Cysts  and  "  mucous  polypi  "  rarely  occur.  They  are  probably  due  to  the 
retention  of  the  secretion  in  a  mucous  gland  from  the  stoppage  of  its  orifice. 
We  find  them  in  the  ventricles  of  Morgagni,  on  the  epiglottis,  etc. 

The  symptoms  which  are  excited  by  benignant  tumors  in  the  larynx  depend 
partly  upon  the  situation  and  partly  upon  the  size  of  the  new  growth.  Small 
polypi  may  exist  wholly  without  symptoms,  and  are  found  only  by  chance  on 


NEW  GROWTHS  IN  THE  LARYNX.  145 

laryngoscopic  investigation.  Usually,  however,  the  presence  of  hoarseness,  press- 
ure, and  itching  in  the  larynx,  or  respiratory  disturbances,  when  the  tumor  is  a 
large  one,  are  the  symptoms  which  give  occasion  for  an  examination. 

B.    Malignant  New  Growths.    Carcinoma  of  the  Larynx. 

Carcinomata  develop  usually  in  old  people,  either  primarily  in  the  larynx  or 
secondarily  from  affection  of  the  neighboring  organs.  In  the  first  case  the  vocal 
cords  or  the  ventricles  of  Morgagni  are  the  points  most  frequently  attacked.  An 
extension  of  the  disease  to  the  larynx  is  seen  especially  in  cancer  of  the  tongue  or 
pharynx,  rarely  in  cancer  of  the  oesophagus. 

The  symptoms  of  cancer  of  the  larynx  develop  slowly.  Hoarseness,  disturb- 
ance in  swallowing,  pains  in  the  larynx  often  shooting  up  into  one  ear,  the 
appearance  of  respiratory  symptoms,  and  finally  the  signs  of  general  weakness 
and  emaciation  which  are  seen  in  almost  all  forms  of  carcinoma,  form  the  picture 
of  the  disease.  The  diagnosis  is  possible  only  by  the  aid  of  the  laryngoscope. 
Besides  this,  a  digital  examination  may  at  times  be  of  diagnostic  value  by  the  detec- 
tion of  the  characteristic  hardness  about  the  entrance  or  in  the  neighborhood  of  the 
larynx.  A  general  description  of  the  laryngoscopic  appearances  can  not  be  given 
on  account  of  the  diverse  character  of  the  cases.  We  see  the  uneven,  injected  new 
growth,  covered  with  mucus  and  often  ulcerated,  and  hesides  this  at  times  the  sec- 
ondary appearances  of  catarirh,  a  developing  perichondritis,  etc.  With  a  little  care 
the  diagnosis  is  usually  tolerably  easy.  It  may  be  difficult,  however,  at  times,  to 
distinguish  it  from  tuherculosis  or  from  syphilis.  We  may  be  aided  in  such  cases 
by  the  discovery  of  the  tubercle  bacilli  or  by  the  results  of  anti-syphilitic  treatment. 
All  the  other  organs  of  the  patient  therefore  must  always  be  carefully  examined. 

Surgical  treatment  is  the  only  one  for  all  laryngeal  new  growths.  We  must 
refer  to  the  special  works  for  all  the  details.  Laryngologists  have  devised  numer- 
ous instruments  for  the  removal  of  benignant  polypi,  by  which,  under  the  guid- 
ance of  the  laryngoscope,  the  new  growth  is  cut,  snared,  squeezed,  or  torn  off. 
The  performance  of  the  operation  is  made  much  easier  by  the  advantage  of  the 
local  anesthesia  of  the  laryngeal  mucous  membrane  due  to  painting  with  cocaine 
(see  p.  138).  Nevertheless  we  firmly  believe,  about  these  growths  as  well  as  about 
tuberculosis  of  the  larynx,  that  the  "  endolaryngeal "  operations  should  be  more 
and  more  superseded  by  laryngotomy. — Carcinoma  of  the  larynx  can  be  cured 
only  through  removal  of  the  tumor  by  splitting  the  larynx  or  by  its  total  extirpa- 
tion. The  former  operation  is  comparatively  free  from  danger,  while  total  extir- 
pation has  met  with  success  as  yet  in  but  few  instances.  If  surgical  interference 
is  no  longer  practicable,  we  can  only  endeavor  to  mitigate  the  suffering  of  the 
patient  by  means  of  morphine,  cocaine,  and  other  narcotics. 


10 


140  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

SECTION  III. 

Diseases  of  the  Trachea  and  the  Bronchi. 

CHAPTER  I. 

ACUTE  CATARRH  OF  THE  TRACHEA  AND  THE  BRONCHI. 

{Tracheitis  and  Acute    Catarrhal  Bronchitis.) 

JEtiology. —Acute  catarrh  of  the  larger  air-passages,  of  the  trachea,  and  larger 
bronchi,  is  a  frequent  disease,  and  it  may  ofteu  arise  from  taking  cold.  It  is  con- 
ceivable that  the  inhalation  of  cold,  damp  air  sometimes  directly  affects  the  mucous 
membrane  of  the  upper  air-passages.  Bronchial  catarrh  is  very  often  associated 
with  a  coincident  catarrh  of  the  larynx,  and  more  rarely  of  the  pharynx.  In  the 
ordinary  mild  forms  the  catarrh  is  usually  confined  to  the  trachea  and  the  first 
large  branches  of  the  bronchi,  while  the  finer  bronchi  remain  healthy. 

More  intense  inflammation  of  the  bronchial  mucous  membrane  is  the  result 
of  active  mechanical  or  chemical  irritation.  A  severe  bronchitis  develops  after 
the  inhalation  of  noxious  gases,  nitrous  and  sulphurous  oxides,  chlorine,  bromine, 
etc.,  as  is  often  observed  in  operatives.  The  inhalation  of  smoke  and  dust, 
especially  vegetable  dust,  works  in  the  same  injurious  fashion,  and  the  followers 
of  many  trades  and  employments,  like  millers,  colliers,  etc.,  are  especially  subject 
to  disease  from  this  cause.  In  this  form  of  bronchitis  the  catarrh  often  extends  to 
the  finer  bronchi. 

The  bronchitis  which  develops  in  the  course  of  other  acute  and  chronic  diseases 
is  still  commoner  than  the  primary  forms  already  mentioned.  It  is  often  due  to 
infectious  causes,  like  certain  infectious  diseases,  especially  measles,  whooping- 
cough,  and  influenza.  In  these  diseases  bronchitis  is  one  of  the  most  constant 
local  affections,  and  is  probably  immediately  dependent  upon  the  primary  infec- 
tion. Bronchitis,  however,  develops  secondarily  in  most  of  the  other  acute  in- 
fectious diseases,  and  is  largely  due  to  the  inhalation  of  noxious  substances  from 
the  upper  part  of  the  air-passages.  This  is  the  explanation  of  the  bronchitis  in 
diphtheritic  processes  in  the  pharynx  and  larynx,  in  so  far  as  it  does  not  depend 
upon  a  direct  extension  of  the  disease,  and  also  of  the  bronchitis  in  small-pox,  etc. 
Bronchitis  may  also  be  met  with  in  all  other  forms  of  severe  disease,  because  re- 
tention of  secretion,  inflammation,  thrush,  etc.,  arise  in  the  cavity  of  the  mouth 
and  pharynx,  and  from  them  chemical  or  organic  irritants  may  easily  be  inhaled 
into  the  bronchi.  The  imperfect  expectoration  in  all  severe  diseases  is  a  still 
more  harmful  factor  than  this  inhalation.  The  secretion  remains  in  the  bronchi, 
processes  of  decomposition  arise  in  the  stagnating  mucus,  bacteria  collect  and  lead 
to  a  bronchitis,  and  finally  to  a  lobular  pneumonia  which  is  so  often  found  {vide 
infra).  The  swallowing  and  inhalation  of  portions  of  saliva,  which  easily  decom- 
pose, is  also  a  frequent  cause  of  secondary  bronchitis. 

We  do  not  know  how  far  we  may  claim  that  infectious  agents  act  as  a  cause  of 
primary  bronchitis,  yet  it  is  not  improbable  that  many  cases  have  such  an  aetiology. 
It  is  especially  likely  that  many  cases  of  bronchitis  due  to  "  catching  cold  "  really 
have  something  infectious  about  them,  and  that  the  preceding  exposure  to  cold 
has  merely  lowered  the  natural  powers  of  resistance,  and  thus  permitted,  or  at  any 
rate  promoted,  infection. 

Finally,  we  must  mention  that  an  acute  bronchitis  is  sometimes  merely  an  ex- 
acerbation of  a  previous  chronic  bronchitis. 

The  predisposition  to  acute  bronchitis  varies  in  different  persons.     "We  do  not 


ACUTE  CATARRH  OF  THE  TRACHEA  AND  THE  BRONCHI.  147 

know  definitely  on  what  ground  such  an  increased  predisposition  to  bronchial  dis- 
ease rests,  nor  why  we  meet  with  it  sometimes  in  the  weak  and  anamiic,  and  at 
other  times  in  the  so-called  "full-blooded"  persons.  Bronchitis  is  more  frequent 
in  children  and  old  people  than  in  those  in  middle  life.  Most  of  the  cases  occur 
in  the  spring  and  autumn. 

Symptoms. — Pain  in  the  chest  may  be  present  in  some  cases  of  simple  catarrhal 
bronchitis,  but  usually  only  in  a  moderate  degree.  In  severe  tracheitis  patients 
often  have  a  painful  feeling  of  soreness  in  the  neck  and  behind  the  upper  part  of 
the  sternum,  and  this  is  increased  on  cougbing.  The  mucous  membrane  of  the 
bronchi,  apparently,  has  no  nerve-fibers  which  are  sensitive  to  pain,  and  the  pains 
in  the  chest  which  are  often  present  in  bronchitis  are,  as  a  rule,  muscular  pains  in 
the  intercostal  muscles,  due  to  the  severe  paroxysms  of  cougbing. 

Cough  is  one  of  the  most  constant  symptoms  of  bronchitis,  and  by  it  usually 
the  attention  of  the  patient  or  of  the  physician  is  first  called  to  the  existing 
thoracic  affection.  The  cough  may  of  course  be  due  to  a  laryngitis,  if  that  is  also 
present.  There  is  no  doubt,  however,  but  that  a  cough  may  be  excited  in  a  reflex 
manner  from  the  mucous  membrane  of  the  tracbea  and  of  the  larger  as  well  as  of 
the  finer  bronchi.  Experiments  have  shown  that  the  point  of  bifurcation  of  the 
trachea  is  especially  irritable,  and  many  severe  paroxysms  of  coughing  may  be 
due  to  an  irritation  of  this  very  spot  from  the  accumulation  of  secretion.  The 
intensity  of  the  cough,  moreover,  is  very  different  in  individual  cases,  which  is 
due  in  part  to  the  degree  and  extent  of  the  bronchitis  and  in  part  to  the  reflex  irri- 
tability of  the  person  affected. 

The  expectoration  consists  of  the  secretion  from  the  inflamed  mucous  mem- 
brane. Its  abundance .  and  consistency  vary  very  much  in  the  different  cases. 
We  distinguish  a  catarrh  with  an  abundant  secretion,  and  the  so-called  "dry 
catarrh."  In  the  latter  only  a  little  viscid  sputum  is  expectorated,  but  in  the 
former  the  expectoration  is  more  abundant  and  muco-purulent.  Very  often  in 
the  beginning  of  the  disease  the  expectoration  is  scanty  and  viscid — the  sputum 
crudum  of  the  old  physicians ;  and  later  it  becomes  more  abundant,  more  fluid,  and 
more  purulent — the  sputum  coctum.  In  catarrh  of  the  finer  bronchi  the  expecto- 
ration may  contain  little  mucous  or  muco-purulent  casts  of  the  bronchi.  A  simple 
catarrhal  expectoration  shows  nothing  peculiar  under  the  microscope.  The  pus- 
corpuscles  are  often  swollen,  and  show  more  or  less  marked  fatty  degeneration.  A 
slight  admixture  of  blood  may  occasionally  be  present  in  severe  bronchitis,  hut  it 
usually  has  no  special  significance,  being  at  times  merely  the  result  of  severe 
fits  of  coughing.  A  more  marked  and  persistent  admixture  of  blood  is  seen  in 
the  catarrhal  sputum  in  some  cases  of  intense  bronchitis  in  drunkards,  so  that  we 
may  even  speak  of  a  "  hsemorrhagic  bronchitis. " 

Dyspnoea  is  usually  entirely  absent  in  simple  bronchitis,  but  marked  shortness 
of  breath  may  be  noticed  in  extensive  catarrh  of  the  finer  bronchi. 

Physical  Examination. — We  may  obtain  direct  evidence  of  the  condition  of 
the  tracheal  mucous  membrane,  with  due  practice,  by  the  laryngoscope.  We 
see  a  reddening  of  the  membrane,  and  sometimes  an  abnormal  abundance  of 
secretion  on  it,  if  there  is  a  tracheitis.  Other  methods  of  physical  examination 
are  at  our  service  for  judging  of  the  changes  in  the  bronchi. 

Inspection  of  the  thorax  shows  nothing  abnormal  in  the  milder  forms  of  bron- 
chitis. The  respiration  is  somewhat  accelerated  and  the  expiration  prolonged  in 
severe  bronchitis,  especially  if  the  finer  bronchi  are  affected.  Percussion  in 
uncomplicated  bronchitis  shows  nothing  abnormal  in  the  pulmonary  resonance. 
Auscultation,  too,  shows  nothing  unusual  in  many  cases  of  mild  catarrh  limited 
to  the  trachea  and  large  bronchi,  but  in  the  cases  where  the  smaller  bronchi  are 
the  seat  of  the  catarrh  and  there  is  a  marked  accumulation  of  secretion  in  them, 


148  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

we  hear,  besides  the  vesicular  respiration,  the  so-called  rhonchi  which  almost 
wholly  hide  it.  In  dry  bronchitis  we  speak  of  humming  or  buzzing  sounds, 
sonorous  rhonchi,  or  shrill,  whistling  sounds,  sibilant  rhonchi,  according  to  their 
pitch.  These  sounds  are  probably  due  to  stenosis,  and  are  caused  by  the  passage 
of  the  air  through  narrow  portions  of  the  bronchi.  The  narrowing  occurs  in  part 
from  the  swelling  of  the  mucous  membrane,  in  part  from  the  accumulation  of 
secretion.  The  masses  of  secretion  themselves,  if  they  are  set  in  vibration  at  the 
same  time,  may  possibly  take  part  in  the  production  of  the  humming  noises.  If 
the  amount  of  secretion  collected  in  the  bronchi  is  more  abundant  and  of  a  more 
fluid  consistency,  it  gives  rise  to  "  moist  rales  "  on  the  passage  of  the  air.  These 
are  distinguished  as  "  medium  "  or  "  small  moist  rales,"  according  as  they  occur  in 
the  larger  or  smaller  bronchi. 

Other  symptoms  of  disease  are  often  present  besides  those  already  mentioned 
as  being  directly  due  to  the  bronchitis.  The  general  health  is  usually  disturbed 
in  a  severe  bronchial  catarrh.  The  patient  does  not  feel  well,  and  has  less  appe- 
tite than  usual.  A  moderate  amount  of  fever  is  often  present,  especially  toward 
evening.  An  increase  of  temperature  above  102°  or  103°  (39°  C.)  is  rarely  seen 
except  in  children.  The  patient  sometimes  complains  of  headache,  which  is  in- 
creased by  severe  coughing. 

The  separate  forms  of  bronchitis  are  distinguished  chiefly  by  the  degree  of 
extension  of  the  catarrh. 

1.  The  Milder  Forms  of  Acute  Bronchitis. — In  most  cases  of  simple  primary 
bronchitis,  as  well  as  in  many  milder  attacks  of  secondary  bronchitis,  the  catarrh 
is  limited  to  the  mucous  membrane  of  the  larger  bronchi.  Exposure  to  cold  and 
other  injurious  influences  are  frequent  causes  of  the  primary  form.  The  symp- 
toms are  moderate.  The  cough,  however,  maybe  quite  troubJesome.  Often  fever 
is  absent  or  but  slight.  Upon  auscultation,  particularly  over  the  lower  lobes,  but 
sometimes  over  the  entire  lungs,  and  usually  with  some  symmetry  of  distribution, 
are  heard  numerous  rather  coarse  wheezing  or  rattling  sounds ;  but  in  many  cases, 
as  we  have  said,  there  may  be  nothing  abnormal  heard,  so  that  the  diagnosis  will 
have  to  rest  merely  upon  the  subjective  discomfort  in  the  chest,  the  cough,  and 
the  expectoration.  With  proper  care,  simple  primary  bronchitis  runs  its  course  in 
a  few  days,  or  at  the  most  in  a  few  weeks,  and  ends  in  complete  recovery.  If  the 
patient  exposes  himself  recklessly,  or  the  ^etiological  factors  continue  to  be  active, 
the  disease  may  however  prove  to  be  very  tedious,  and  finally  develop  into  chronic 
bronchitis. 

2.  The  Severer  Febrile  Forms  of  Acute  Bronchitis.— Sometimes  acute  bron- 
chitis assumes  a  severer  form,  whether  because  the  influences  which  give  rise  to 
it  are  unusually  violent,  or  because  it  is  due  to  some  special  and  as  yet  little  known 
cause  (perhaps  infectious).  In  such  cases  the  symptoms  are  more  marked,  the 
bronchial  rales  more  abundant,  the  general  condition  of  the  patient  worse.  Not 
infrequently  there  is  fever  for  several  days,  or  even  for  one  or  two  weeks,  the  type 
being  irregularly  remittent,  but  the  temperature  seldom  exceeds  102°  or  103°  (39° 
to  39*5°  C).  The  author  has  not  infrequently  noticed  that  there  is  more  liability 
in  the  severer  forms  of  acute  bronchitis  to  have  the  disease  mainly  limited  to  one 
lobe,  or  at  least  to  one  lung,  but  the  disease  may  be  diffuse.  This  form  of  the  dis- 
ease also  has  a  favorable  prognosis  except  in  feeble  or  elderly  persons. 

3.  Catarrh  of  the  Finer  Bronchi— Capillary  Bronchitis.— A  simple  primary 
bronchial  catarrh  rarely  extends  to  the  finer  bronchi  in  adults.  The  secondary 
bronchitis,  however,  which  develops  in  other  severe  diseases  (vide  supra),  often 
extends  into  the  ultimate  divisions  of  the  bronchi,  and  finally  leads  to  the  forma- 
tion of  nodules  of  lobular  pneumonia — "  catarrhal  pneumonia"  (vide  infra).  We 
recognize  the  implication  of  the  finer  bronchi  by  hearing  the  high,  shrill,  whist- 


ACUTE  CATARRH  OF  THE  TRACHEA  AND  THE  BRONCHI.  149 

ling  rhonclii  [sibilant  rhonclii],  or  the  abundant  small,  moist  rales.  Respiratory- 
symptoms  may  be  quite  marked  in  extensive  catarrh  of  the  finer  bronchi.  Res- 
piration is  evidently  accelerated,  and  expiration  is  usually  prolonged.  There  is 
often  quite  a  severe  cough.  The  expectoration  is  muco-purulent  and  usually  not 
very  abundant. 

Capillary  bronchitis  in  children  is  of  great  practical  importance.  Every  bron- 
chitis in  young  children  has,  as  experience  tells  us,  a  tendency  to  attack  the 
smaller  bronchi.  Extensive  bronchitis  is  seen  especially  in  weak  children  who 
are  rachitic  or  predisposed  to  tuberculosis.  Children  have  an  especial  predisposi- 
tion to  be  attacked  with  bronchitis  at  the  time  of  the  first  dentition,  but  it  is  also 
seen  at  an  even  earlier  age. 

The  parents'  attention  is  usually  called  to  the  disease  by  the  appearance  of  a 
cough,  which  is  excited  especially  by  the  child's  crying.  Small  children  never 
expectorate,  for  they  swallow  the  secretion  which  is  coughed  up  into  the  pharynx. 
The  rapidity  of  respiration  is  very  striking,  it  being  increased  to  sixty  or  eighty, 
or  even  more,  in  a  minute.  The  respiration  is  also  labored,  but  it  is  usually  super- 
ficial, and  in  severe  cases  irregular.  There  is  generally  a  distinct  respiratory  play 
of  the  alas  nasi.  We  often  see  a  retraction  of  the  lower  lateral  portions  of  the 
thorax  on  inspiration  as  a  result  of  the  imperfect  entrance  of  air  into  the 
smaller  bronchi.  The  expiration  is  frequently  noisy  and  groaning  in  children. 
We  hear  extensive  small,  moist  rales  over  the  lungs.  In  severe  cases  the  child 
becomes  restless,  anxious,  perhaps  markedly  pale  and  cyanotic,  and  finally  apa- 
thetic and  stupid.  In  such  cases,  however,  we  have  no  longer  to  deal  with  simple 
bronchitis,  but  catarrhal  pneumonia  has  already  developed.  The  disease  almost 
always  runs  its  course  with  fever,  the  temperature  rising  to  104°  (40°  C.)  and 
over.  The  pulse  is  increased  to  120  or  140  or  more  per  minute.  The  duration  of 
the  disease  is  seldom  less  than  two  or  three  weeks,  and  it  may  last  much  longer. 
Death  may  ensue,  especially  in  ill-nourished  children,  partly  as  a  result  of  general 
weakness,  and  also  directly  from  the  imperfect  respiration.  In  such  cases  we  find 
at  the  autopsy  not  only  diffuse  bronchitis,  but  also  almost  always  lobular  pneu- 
monia. In  many  cases  a  gradual  recovery  finally  takes  place  in  spite  of  the  most 
severe  symptoms. 

The  secondary  bronchitis  in  children  complicating  measles,  whooping-cough, 
diphtheria,  etc.,  has  the  same  tendency  to  involve  the  finer  bronchi  and  to  lead  to 
lobular  pneumonia. 

In  conclusion,  we  must  mention  that  acute  bronchitis  in  old  people  also  readily 
attacks  the  finer  bronchi,  and  may  be  dangerous  partly  from  the  general  exhaus- 
tion, partly  from  the  occurrence  of  respiratory  symptoms,  as  in  lobular  pneumonia. 

Diagnosis. — The  diagnosis  of  bronchitis  presents  no  special  difficulty.  It  is 
obtained  directly  by  the  discovery  of  rhonchi  on  auscultation.  If  these  fail,  we 
conclude  that  there  is  a  mild  catarrh  of  the  larger  bronchi  from  the  presence  of 
cough  and  expectoration,  if  no  cause  for  the  cough  is  to  be  found  in  an  affection 
of  the  larynx.  The  question  is  more  difficult,  but  it  must  always  be  considered, 
whether  a  given  bronchitis  is  a  common  primary  catarrh  or  secondary  to  some 
other  affection.  This  question  naturally  can  be  decided  only  by  a  very  careful 
examination  of  the  body.  We  must  always  remember,  furthermore,  that  severe 
pulmonary  affections  may  be  at  first  quite  latent  and  show  objectively  merely  the 
signs  of  simple  bronchitis,  while  later  pneumonia,  a  tubercular  affection,  or  some- 
thing similar,  develops.  A  bronchitis  which  is  unilateral,  or  in  which  the  signs 
are  to  be  found  in  circumscribed  localities,  must  therefore  be  regarded  as  suspi- 
cious. It  has  long  been  known  that  bronchitis  in  the  apices  of  the  lungs,  the  "  apex- 
catarrh,"  is  often  the  first  objective  change  to  be  met  wTith  in  pulmonary  phthisis. 
We  can  only  conjecture,  and  not  pronounce  with  certainty  on  objective  evidence, 


150  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

whether  nodules  of  lobular  pneumonia  are  present  or  not  in  diffuse  bronchitis 
affecting-  the  finer  bronchi. 

From  what  has  been  said,  it  is  clear  that  we  should  be  cautious  in  our  prog- 
nosis regarding  every  severe  bronchitis,  especially  in  children  and  old  people. 
Tbe  prognosis  in  the  milder  forms  of  bronchitis  is  of  course  always  very  favor- 
able. 

Treatment. — The  prophylaxis  of  primary  bronchial  catarrh  consists  in  the 
removal  of  all  theinjurious  influences  mentioned  which,  as  experience  shows,  may 
give  rise  to  a  bronchitis.  A  careful  hardening  of  the  skin  to  the  effects  of  a  change 
in  temperature  is  of  service  in  persons,  particularly  children,  who  have  a  special 
tendency  to  bronchitis,  as  we  have  already  said  in  regard  to  the  prophylaxis  of 
laryngitis.  It  is  very  important  to  remember,  in  this  connection,  that  we  can  also 
be  successful  in  our  prophylactic  measures  against  secondary  bronchitis.  Keep- 
ing the  mouth  and  pharynx  clean,  urging  deep  inspirations,  and  aiding  expectora- 
tion by  the  timely  use  of  tepid  baths  and  shower-baths,  may  often  prevent  a  bron- 
chitis or  keep  it  within  bounds,  while  it  would  surely  develop  if  the  patient  were 
neglected. 

Simple  hygienic  measures  suffice  in  the  treatment  of  mild  cases  of  acute  bron- 
chitis. The  patient  should  be  kept  warm,  should  remain  in  his  room,  or,  if  there 
be  any  fever,  in  bed.  Diaphoretic  remedies  have  long  been  praised  as  especially 
potent  in  the  treatment  of  acute  bronchial  catarrh.  The  patient,  therefore,  should 
drink  hot  tea,  pectoral  tea*  (Brustthee),  or  elder  tea,  etc.,  or  hot  milk  mixed  with 
Seltzer,  a  remedy  whose  efficacy  is  frequently  praised  by  the  patient.  Local 
treatment  of  the  mucous  membrane  by  inhalations  is  usually  illusory,  for  only 
the  smallest  part  of  the  inhaled  fluid  reaches  the  bronchi.  We  may,  however, 
always  prescribe  inhalations  of  warm  steam,  or  a  one-  or  two-per-cent.  solution 
of  common  salt,  especially  with  a  dry  cough  and  a  secretion  which  is  hard  to 
loosen. 

Otherwise  we  must  employ  symptomatic  treatment.  A  mustard  plaster  or  a 
cold,  wet  compress  about  the  chest  does  good  service  Avith  severe  subjective  thoracic 
symptoms.  In  bad  cases  a  few  dry  cups  may  be  very  useful  in  adults,  but  local 
abstractions  of  blood  are  never  necessary  in  simple  bronchitis.  If  there  is  trouble- 
some irritation  on  coughing,  so  as  to  disturb  the  rest,  we  may  prescribe  small 
doses  of  morphine,  five  to  ten  grains  of  Dover's  powder  (grm.  O^-O^ö),  fifteen  to 
twenty  drops  of  cherry-laurel  water,  codeine,  etc.  When  expectoration  is  difficult, 
we  may  use  the  so-called  expectorants — ipecac,  chloride  of  ammonium,  apomor- 
phine,  etc. 

We  have  already  repeatedly  mentioned  the  use  of  tepid  baths  and  shower- 
baths,  indicated  in  severe  diffuse  bronchitis  developing  secondarily  in  the  course 
of  other  acute  diseases. 

Tepid  baths  with  shower-baths,  two  or  three  times  a  day,  are  also  to  be  used  as 
a  most  powerful  remedy  in  severe  cases  of  capillary  bronchitis  in  children.  The 
baths  assist  expectoration  and  guard  against  the  possibility  of  the  development  of 
lobular  pneumonia.  Wet  packs  applied  to  the  thorax  or  over  the  whole  body  are 
serviceable.  Children  are  wrapped  to  the  neck  in  a  sheet  which  has  been  pre- 
viously dipped  in  water  at  a  temperature  varying  with  the  degree  of  the  fever 
from  68°  to  77°  (16°  to  20°  R.)  and  well  wrung  out.  It  is  well  to  leave  the  arms 
free.  A  dry  woolen  blanket  may  be  wrapped  around  the  moist  sheet.  This  pro- 
cedure must  be  repeated  three  or  four  times  a  day.     As  to  other  remedies,  we  use 

*  A  favorite  German  household  remedy,  consisting  of  an  infusion  of  eight  parts  of  althaea,  three 
parts  of  licorice,  one  part  of  orris-root,  four  parts  of  colt's-foot,  and  two  parts  each  of  mullein  and  anise- 
seed. — Tkans. 


CHRONIC  BRONCHITIS.  151 

the  same  as  in  adults.  With  weak  children  our  care  must  be  to  keep  up  the 
strength  by  furnishing  the  most  nourishing  food  possible  and  giving  small 
amounts  of  wine.  An  emetic  is  sometimes  indicated  in  cases  with  an  abundant 
accumulation  of  mucous  in  the  bronchi,  and  is  of  good  service.  As  experience 
has  shown,  we  should  use  opiates  for  small  children  only  with  the  greatest  care. 
Senega  and  benzoin  may  be  used  as  expectorants. 

In  the  bronchitis  of  old  people  our  chief  aim  should  be  to  keep  up  and  improve 
the  patient's  strength.  We  prescribe  liquor  ammonii  anisatus,  infusion  of  senega, 
etc.,  to  aid  expectoration,  which  is  usually  difficult,  since  the  cough  is  feeble. 
Tepid  baths  may  be  of  advantage,  but  they  must  be  used  with  care. 


CHAPTER  II. 

CHRONIC   BRONCHITIS. 

{Chronic  Bronchial  Catarrh.) 

JEtiology. — Chronic  bronchial  catarrh  may  develop  gradually  from  external 
causes,  or  in  rare  cases  it  may  follow  an  acute  bronchitis.  The  same  noxious 
influences  which  excite  an  acute  bronchitis  may,  by  the  frequent  repetition  of 
their  action,  result  in  a  chronic  bronchitis. 

In  a  large  number  of  cases  severe  chronic  bronchial  catarrh  is  not  an  independ- 
ent disease,  but  occurs  as  a  complication  or  a  result  of  other  diseased  conditions. 
The  combination  of  chronic  bronchitis  with  emphysema  of  the  lungs  {vide  infra) 
is  the  most  common.  A  large  number  of  cases  also  are  the  result  of  some  form 
of  heart  disease,  like  valvular  disease  or  myocarditis,  or  of  disease  of  the  vessels, 
leading  to  stasis  in  the  pulmonary  circulation,  and  finally  to  a  chronic  catarrh  of 
the  bronchi.  Chronic  bronchial  catarrh  in  renal  diseases  also  depends,  in  part 
at  least,  upon  circulatory  disturbances.  Finally,  we  find  a  more  or  less  extensive 
chronic  catarrh  of  the  bronchi  in  other  chronic  affections  of  the  lungs  and  pleura, 
as  in  tuberculosis  or  pleurisy. 

Chronic  bronchitis  is  seen  especially  in  adults  and  old  people,  and  more  fre- 
quently in  men  than  in  women. 

Pathological  Anatomy. — Chronic  bronchitis  is  characterized  anatomically  by  a 
marked  venous  hyperaemia  of  the  bronchial  mucous  membrane.  The  whole  tissue 
itself  is  often  thickened,  and  the  surface  of  the  membrane  is  swollen.  In  old 
cases,  however,  we  finally  meet  with  an  atrophy  of  all  the  layers  of  the  mucous 
membrane.  One  of  the  most  frequent  results  of  a  chronic  bronchitis  is  a  cylin- 
drical dilatation  of  the  middle  and  lesser  bronchi — bronchiectasis.  This  arises 
gradually  from  the  loss  of  elasticity  of  the  diseased  bronchial  walls,  increasing 
their  tendency  to  give  way,  as  well  as  from  the  pressure  of  the  stagnating  secre- 
tions. 

Symptoms  and  Course  of  the  Disease.— The  symptoms  which  are  due  to  chronic 
bronchitis  are  disturbances  of  respiration,  cough,  and  expectoration.  To  these 
should  be  added  the  results  of  a  physical  examination. 

The  cough  is  of  very  different  severity  in  different  cases.  Usually  it  is  worse 
eaidy  in  the  morning,  in  the  evening,  and  at  night,  than  in  the  daytime.  The 
amount  of  expectoration  is  also  subject  to  great  variations.  In  many  cases  there 
is  a  dry  cough  (catarrhe  sec,  vide  infra),  in  which  only  small  amounts  of  tough, 
viscid  sputum  are  expectorated.  In  other  cases  the  expectoration  is  more  abun- 
dant and  muco-purulent,  and  sometimes  excessive  and  quite  thin.  Microscopic- 
ally, it  has  no  special  characteristic  appearances,  but  it  contains  only  the  usual 


152  DISEASES  OP  THE  RESPIRATORY  ORGANS. 

elements  of  sputum — pus-coi*puscles  mixed  with  pavement  epithelium,  often  many- 
bacteria,  sometimes  needles  of  fat  acids,  and  rarely  a  few  pointed  octahedral  crys- 
tals, the  so-called  asthma  crystals  (vide  infra).  Small  amounts  of  blood  may  be 
seen  in  severe  chronic  bronchitis,  but  they  do  not  have  any  bad  significance. 

Dyspnoea  of  moderate  degree  may  also  be  present  in  uncomplicated  and  exten- 
sive bronchitis.  In  the  cases  in  which  it  is  severe,  however,  it  is  usually  due  to 
other  conditions  affecting  the  heart  or  lungs. 

Physical  Examination. — The  percussion  in  bronchitis  shows  no  special 
change.  At  most  the  resonance  may  be  somewhat  tympanitic  from  the  relaxa- 
tion of  the  lung-tissue,  especially  in  the  lower  and  posterior  portions  of  the  lungs, 
or,  with  an  abundant  retention  of  secretion  in  the  bronchi,  it  may  be  a  little 
diminished.  Auscultation  may  give  either  rhonchi,  whistling,  hissing,  humming, 
etc.,  or  moist  rales,  according  to  the  extent  of  the  catarrh  and  the  amount  and 
consistency  of  the  secretion.  The  sounds  are  usually  to  be  heard  over  the  whole 
lung,  or  especially  over  the  lower  lobes,  because  here  the  catarrh  is  usually  most 
marked,  and  retention  of  secretion  is  most  apt  to  occur.  The  respiratory  murmur 
in  some  places  may  be  quite  obscured  by  the  rales.  Otherwise  it  is  vesicular, 
sometimes  exaggerated,  sometimes  rough  and  indefinite.  Expiration  is  usually 
prolonged.  The  respiratory  murmur  may  be  much  diminished,  or  even  entirely 
suppressed  in  places  where  the  bronchi  are  stopped  by  secretion,  which  happens 
most  frequently  in  the  lower  lobes. 

Except  in  mild  cases,  we  usually  distinguish  several  different  forms  of  chronic 
bronchial  catarrh,  which  may  run  into  one  another. 

1.  The  dry  chronic  catarrh  (catarrhe  sec  of  Laennec)  is  the  form  in  which  the 
mucous  membrane  has  only  a  very  slight  secretion.  The  cough  is  usually  very 
troublesome  and  labored,  but  the  patient  raises  merely  a  little  tough  sputum,  or 
none  at  all.  On  auscultation  we  hear  sibilant  rhonchi,  but  no  moist  rales.  This 
form  of  catarrh  is  usually  associated  with  pulmonary  emphysema,  and  asthmatic 
attacks  are  also  frequent.     The  disease  is  stubborn,  and  usually  lasts  for  years. 

2.  The  so-called  bronchial  blennorrhcea  is  that  form  of  chronic  bronchitis  in 
which  we  find  a  very  copious  secretion  from  the  mucous  membrane.  (  The  cough 
is  therefore  associated  with  a  very  abundant  and  quite  thin  expectoration,  the 
amount  of  which  in  the  twenty-four  hours  may  exceed  a  pint  (half  a  litre).  The 
expectoration  runs  together  in  the  sputa-cup  and  usually  separates  on  standing,  the 
more  purulent  portion  sinking  to  the  bottom,  and  the  sero-mucous  portion,  which 
is  usually  frothy  on  the  surface,  remaining  at  the  top.  Numerous  moist  rales  are 
heard  in  the  lungs,  especially  in  the  lower  portions.  These  diminish  if  large 
amounts  of  sputum  are  coughed  up.  Anatomically,  the  bronchi  are  almost  al- 
ways found  dilated  in  this  form  of  chronic  bronchitis. 

3.  The  so  called  serous  bronchorrhcea  ("  catarrhe  pituiteux "  of  Laennec)  is 
quite  rare  but  very  interesting.  It  is  characterized  by  the  expectoration  of  a  very 
lai'ge  amount  of  frothy,  purely  serous,  thin  sputum.  The  cough  usually  comes  on 
in  very  violent  paroxysms  which  last  from  half  an  hour  to  an  hour  or  more.  The 
respiratory  symptoms  are  quite  severe,  especially  during  these  attacks,  and  have 
given  rise  to  the  old  and  useful  term  "  asthma  humidum.^  The  expectoration 
collected  in  twenty-four  hours  may  amount  to  one  or  two  quarts  (litres).  Ex- 
amination of  the  lungs  usually  gives  very  abundant  and  extensive  moist  rales. 
The  resonance  on  percussion  is  normal  or  a  little  diminished,  from  the  accumula- 
tion of  secretion. 

The  special  cause  of  this  peculiar  disease  is  quite  obscure.  It  is  either  an 
independent,  very  chronic  trouble,  which  may  last  for  years  with  a  varying  course, 
or  it  may  occur  secondarily  in  other  affections,  especially  in  chronic  contraction  of 
the  kidney.     We  once  saw  a  very  severe  case  of  the  indspendent  and  apparently 


CHRONIC  BRONCHITIS.  153 

quite  uncomplicated  form  in  a  young  woman  who  had  high  fever  at  times,  and 
who  became  much  broken  down  physically. 

Course  of  the  Disease. — The  course  of  most  chronic  bronchial  catarrhs  is  very 
protracted.  The  disease  usually  has  frequent  remissions  and  fresh  exacerbations. 
The  patient  is  tolerably  well  in  the  pleasanter  time  of  the  year  if  he  takes  good 
care  of  himself,  but  in  autumn  and  winter,  or  after  exposure  to  various  noxious 
influences,  the  catarrh  grows  worse  and  the  patient's  symptoms  increase.  If  the 
disease  has  lasted  for  years,  we  usually  find  symptoms  in  the  lungs,  like  emphy- 
sema or  chronic  tuberculosis,  or  in  the  heart,  like  secondary  dilatation  and  hyper- 
trophy of  the  right  ventricle,  which  symptoms  gradually  become  more  severe. 
The  details  of  these  conditions  are  to  be  found  in  the  appropriate  sections. 

Diagnosis. — The  diagnosis  of  chronic  bronchitis  is  not  difficult  in  itself,  and 
may  easily  be  made  by  considering  the  patient's  symptoms  and  by  judging  of  the 
result  of  the  physical  examination.  We  must  always  consider,  however,  whether 
the  bronchitis  is  not  a  result  or  a  complication  of  some  other  chronic  disease. 
Therefore  in  every  case  of  chronic  bronchitis  the  heart  and  the  urine  must  be 
carefully  examined,  as  well  as  the  lungs. 

Prognosis. — Chronic  bronchitis  is  in  most  cases  a  very  stubborn  affection,  which 
frequently  shows  improvement,  but  from  which  complete  recovery  is  rare.  The 
prognosis  also  depends  greatly  upon  the  patient's  circumstances,  and  upon  the 
possibility  of  his  taking  care  of  himself  and  avoiding  all  harmful  exposure.  In 
secondary  bronchitis  the  question  whether  the  bronchitis  is  capable  of  material 
improvement  or  not  of  course  depends  mainly  upon  the  prognosis  of  the  primary 
disease. 

The  danger  in  primary  chronic  bronchitis  comes  from  the  final  development 
of  its  sequelae,  especially  from  the  gradual  appearance  of  pulmonary  emphysema, 
dilatation  of  the  heart,  etc. 

Treatment. — The  only  hope  of  success  in  severe  cases  in  any  method  of  treat- 
ing chronic  bronchitis  is  in  removing  the  patient  completely,  at  least  for  a  time, 
from  the  action  of  injurious  influences.  The  favorable  result  of  the  baths  and 
health  resorts  that  are  employed  depends  largely  upon  this,  that  patients  enjoy  in 
them  complete  bodily  rest,  and  are  far  better  protected  from  dust  and  the  changes 
in  the  weather  than  at  home.  We  must  make  the  patient  comprehend  the  neces- 
sity of  this  condition  as  the  basis  of  any  treatment.  If  he  can  not  go  to  a 
suitable  climate  during  the  cold  season,  he  must  keep  his  room  in  all  unpleasant 
weather,  but  at  other  times  he  may  be  permitted  to  stay  in  the  open  air.  Further- 
more, the  patient  must  be  warned  to  avoid  as  completely  as  possible  those  harm- 
ful influences  which  his  calling  and  manner  of  life  entail,  and  among  which 
especially  is  the  bad  air  in  our  inns  and  restaurants.  Food  should  be  easily 
digestible,  and,  in  people  inclined  to  corpulence,  sparingly  taken.  Alcohol  is  to 
be  permitted  only  in  a  moderate  degree.  We  combat  the  tendency  to  constipa- 
tion, which  is  often  present,  by  dietetic  remedies,  by  taking  fruit,  especially  grapes, 
prunes,  etc. ,  honey,  Graham  bread,  or  by  mild  laxatives,  like  the  bitter  waters, 
Friedrichshall,  Ofner,  etc. 

If  the  circumstances  of  the  patient  permit  and  his  condition  requires  it,  we 
should  send  him  south  in  the  autumn  in  order  to  avoid  the  evils  of  a  northern 
winter.  The  rule  is  to  send  patients  with  a  bronchial  catarrh  when  there  is  much 
secretion  to  health-resorts  with  a  dry  climate— for  example,  to  the  western  Riviera, 
San  Remo,  Bordighera,  Mentone,  Cannes,  etc.  The  somewhat  dry  yet  cooler 
climate  of  Meran,  Gries,  or  Arco  is  suitable  for  patients  with  a  stronger  constitu- 
tion. Patients  with  dry  bronchitis  usually  find  themselves  at  their  best  in  a 
warm  but  not  too  dry  climate.  If  we  wish  to  be  sure  of  avoiding  the  winter's 
cold,  we  must  choose  Sicily,  Egypt,  or  Madeira  for  a  residence.      Of  the  more 


154  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

northern  -winter  resorts  we  may  mention  here  places  on  the  eastern  Riviera, 
Nervii,  Spezzia,  etc.,  except  Venice,  Pisa,  or  Rome. 

We  must  recommend  especially,  in  bronchitis,  a  suitable  summer  residence 
outside  of  large  and  dusty  cities.  Any  private  country  residence  in  a  well-wooded 
and  protected  place  is  of  advantage.  If  we  wish  to  send  patients  to  a  bath, 
Marienbad,  Kissingen,  or  Homburg  are  proper  places  for  corpulent  people  who 
also  suffer  from  digestive  disturbances,  while  we  may  send  weaker  patients  to 
Ems,  Soden,  Badenweiler,  Ischl,  or  Reichen  hall.  Milk  cures,  whey  cures,  and 
grape  cures  are  also  prescribed  in  many  cases  of  chronic  bronchitis,  the  milk  cure 
in  particular  for  weak  and  anaemic  individuals.  A  summer  residence  on  the  sea, 
best  on  the  Baltic,  is  very  serviceable  for  many  patients  with  bronchitis. 

The  inhalation  treatment  is  much  employed  in  chronic  bronchitis,  but  we 
should  not  cherish  too  high  hopes  about  its  use.  The  best  inhalations  in  dry 
catarrhs  are  simple  steam,  a  two-per-cent.  solution  of  common  salt  or  bicarbonate 
of  sodium,  Ems  water,  etc.  In  cases  with  marked  secretion,  inhalations  of  oil  of 
turpentine  are  most  to  be  praised.  The  simplest  way  is  to  pour  a  teaspoonful  of 
oil  of  turpentine  into  hot  water  and  inhale  the  vapor  as  it  arises.  The  so-called 
turpentine-pipe,  however,  is  more  convenient  and  more  efficacious.  This  consists 
of  a  flask,  which  is  filled  to  the  height  of  several  inches  with  water  and  then  with 
a  layer  of  oil  of  turpentine  or  of  oleum  pint  pumilionis  (P.  G.),  some  two  centi- 
metres thick.  "Two  glass  tubes,  open  at  both  ends,  are  passed  through  the  cork. 
One,  straight,  tube  extends  down  into  the  layer  of  water ;  the  lower  end  of  the  other 
is  free  in  the  upper  part  of  the  flask.  The  outer  portion  of  this  last  tube  is  long 
enough  to  be  bent  at  an  angle  and  forms  the  mouth-piece  of  the  pipe  which  the 
patient  sucks.  He  thus  breathes  the  air  which  is  filled  with  turpentine  vapor. 
We  have  treated  many  patients  in  this  way,  who,  for  a  number  of  hours  a  day, 
"  smoked  "  their  turpentine-pipes. 

In  treating  chronic  bronchitis  the  pneumatic  method  *  was  considerably  em- 
ployed for  a  time ;  that  is,  the  patient  was  made  to  breathe  artificially  compressed 
air,  or  to  expire  into  air  of  a  less  than  atmospheric  tension,  by  means  of  a  movable 
pneumatic  apparatus,  as  proposed  by  Waldenburg  and  others.  Of  late,  however, 
this  method  of  treatment  has  l'eceived  less  favor,  inasmuch  as  actual  results  have 
fallen  decidedly  short  of  the  benefit  promised.  In  Ems,  Reichenhall,  and  other 
places  special  pneumatic  cabinets  have  been  arranged,  filled  with  compressed  air, 
in  which  patients  remain  for  varying  lengths  of  time. 

The  different  alkaline  mineral  waters — Seltzer,  Ems,  "Victoria,  etc. — are  next  to 
be  mentioned  among  internal  remedies,  which  may  also  be  used  efficaciously  at 
home.  The  numerous  expectorants,  like  ipecac  and  apomorphine,  are  especially 
valuable  in  dry  bronchitis.  In  bronchial  blennorrhcea  we  know  empirically 
that  the  internal  use  of  balsams  causes  a  distinct  diminution  of  the  secretion. 
Oil  of  turpentine  is  the  most  active,  and  may  be  given  internally  in  gelatine  cap- 
sules, two  or  three  capsules  a  day,  or  mixed  with  milk,  in  doses  of  ten  or  fifteen 
drops  two  or  three  times  a  day.  Lepine,  G.  See,  and  other  French  physicians 
recommend  terpine  as  still  more  effectual.  This  is  a  derivative  of  turpentine,  and 
is  best  employed  in  pills  containing  one  and  a  half  grains  (0-l),  of  which  two 
or  even  more  are  to  be  taken  three  times  a  day.     It  may  also  be  given  in  solution 

*  Details  of  the  pneumatic  treatment  may  be  found  in  the  following  works :  R.  v.  Vivenot,  Jr., 
"Zur  Kenntniss  der  physiologischen  Wirkungen  und  der  therapeutischen  Anwendung  der  ver- 
dichteten Luft,"  Erlangen,  18G8.  Waidenburg,  "  Die  pneumatische  Behandlung  der  Eespirations-  und 
Circulationskrankheiten,"  Berlin,  1880.  Knauthe,  "  Handbuch  der  pneumatischen  Therapie,"  Leip- 
zig, Wigand,  1876.  Schnitzler,  "  Die.  pneumatische  Behandlung  d.  Lungen-  u.  Herzkrankheiten," 
Wien,  1877  (40  Seiten).  Oertel,  "Handbuch  d.  respiratorischen  Therapie"  (v.  Ziemssen's  "Allg. 
Therapie,"  ii,  4),  Leipzig,  Vogel,  1881. 


FOETID  BRONCHITIS.  1 :, :, 

as  follows  :  Terpine,  2\  drachms  (grm.  10);  alcohol,  q.  s.  ad  sol.  faciundam;  aq. 
dest.,  6  ounces,  6  drachms  (200  grm).  Misce.  Sig:  Two  or  three  tablespoon  fuls 
daily.  Balsam  of  copaiba  and  balsam  of  Peru  are  also  used  internally.  We 
should  be  very  sparing-  of  narcotics  at  first,  but  in  severe  cases  we  can  not  wholly 
dispense  with  them. 

[The  iodide  of  potassium  in  closes  of  five  to  ten  grains  thrice  daily  is  sometimes 
distinctly  curative.  An  out-door  life,  free  diet,  moderate  alcoholic  stimulus, 
tonics,  and  woolen  clothing  do  much  to  promote  recovery.] 

Local  applications  to  the  chest  in  the  form  of  embrocations,  mustard  plasters, 
dry  cups,  or  cold  wet  compresses  are  to  be  used,  especially  with  severe  dyspnoea, 
or  with  pain  and  a  feeling  of  oppression  in  the  chest.  Regular  cold  sponging  of 
the  chest  serves  to  harden  and  strengthen  the  patient. 

Warm  baths  are  very  well  borne  by  many  patients  with  chronic  bronchitis. 
Sometimes,  too,  vapor  baths,  if  taken  with  caution,  may  be  of  service,  especially  in 
strong  and  corpulent  patients. 

In  all  secondary  chronic  catarrhs  our  chief  attention,  beyond  the  symptomatic 
treatment  of  the  bronchitis,  must  be  directed  to  the  treatment  of  the  underlying 
disease.  If  we  succeed  in  once  more  regulating  the  heart's  action  where  there  is 
uncompensated  heart  disease,  or  in  establishing  diuresis  where  there  is  renal  dis- 
ease, we  may  also  in  that  way  cause  improvement  in  the  existing  bronchial 
catarrh. 


CHAPTER  III. 

FCETID   BRONCHITIS. 

{Putrid  Bronchitis.) 

^Etiology. — By  putrid  or  foetid  bronchitis  we  mean  that  form  of  bronchitis  in 
which  the  secretion  of  the  mucous  membrane  undergoes  a  putrid  decomposition, 
and  in  which,  consequently,  the  expectoration  takes  on  a  peculiar  and  extremely 
foul  odor.  The  cause  of  foetid  bronchitis  is  usually  the  entrance  of  the  bacteria 
of  putrefaction  into  the  bronchi  by  means  of  the  inspired  air.  Only  in  rare  cases 
does  it  arise  from  a  pulmonary  gangrene  of  embolic  origin  {vide  infra). 

The  opportunity  for  the  agents  of  putrefaction  to  enter  the  bronchi  with  the 
inspired  air  is  of  course  often  given,  but  a  foetid  bronchitis  naturally  is  excited 
only  when  they  can  remain  there  and  increase.  Their  retention  and  their  further 
development  is  chiefly  favored,  as  we  know,  by  diseased  conditions  which  already 
exist  in  the  bronchi.  A  great  number  of  cases  of  foetid  bronchial  catarrh  there- 
fore develop  secondarily  upon  other  pulmonary  affections  of  longer  standing. 
Thus  the  expectoration  may  quite  suddenly  change  and  take  on  a  foetid  character 
in  the  course  of  a  chronic  or  rarely  of  an  acute  bronchitis  or  of  phthisis.  Bron- 
chiectasis {vide  infra)  greatly  favors  the  development  of  this  putrid  change,  for 
in  it  the  retention  and  stagnation  of  large  amounts  of  secretion  furnish  the  aid 
and  occasion  for  it.  If  a  putrid  decomposition  of  the  secretion  begins  in  one  part 
of  the  bronchial  system,  the  further  extension  of  the  process  follows  from  direct 
infection. 

In  rare  cases  putrid  bronchitis  also  develops  in  lungs  which  were  previously 
apparently  sound — primary  foetid  bronchitis. 

Symptoms  and  Course;  Anatomical  Changes.— If  a  foetid  bronchitis  arises  in 
the  course  of  some  other  chronic  pulmonary  disease,  its  appearance  may  be  marked 
by  a  sudden  impairment  of  the  general  condition,  by  high  fever,  often  associated 
with  numerous  chills,  and  by  an  increase  of  the  thoracic  symptoms,  like  pain  and 


156  DISEASES  OF  THE  EESPIEATORY  ORGANS. 

cough.  The  change  in  the  expectoration,  the  peculiarity  of  which  was  first 
accurately  described  by  Traube,  is  characteristic.  There  is  a  repulsive,  sweetish, 
putrid  smell.  The  expectoration  is  usually  quite  abundant;  the  consistency  is 
rather  thin.  On  standing,  the  sputum  shows  a  very  marked  division  into  three 
layers.  Tbe  upper  layer  consists  of  a  very  frothy,  muco-purulent  stratum,  con- 
sisting in  part  of  individual  masses,  from  which  a  number  of  coarser  or  finer  fibers 
float  down  into  the  middle  layer.  This  middle  layer  consists  of  a  dirty-green 
muco-serous  fluid.  At  the  bottom  of  the  vessel  is  found  the  third  layer,  which  is 
often  the  thickest,  and  is  composed  entirely  of  pus.  It  consists  of  pus-corpuscles 
which  have  sunk  to  the  bottom,  and  is  of  a  rather  thin,  greasy  consistency.  With 
the  naked  eye  we  generally  recognize  a  number  of  little  whitish-gray  plugs  and 
particles  in  it.     These  so-called  "  Dittrich's  plugs,"  which  are  easily  crushed  under 

a  cover-glass,  are  quite  characteristic.  Microscop- 
ically, they  consist  of  decomposed  pus-corpuscles, 
detritus,  and  bacteria,  and  usually  contain  very 
many  needles  of  fat  acids  arranged  in  bundles 
(see  Fig.  21). 

We  often  find  also  in  the  sputum  large  masses 
of  fungi,  especially  great  bunches  of  twisted  lep- 
tothrix  fibers,  which,  by  an  unpracticed  eye,  may 
readily  be  mistaken  for  elastic  fibers.  The  latter 
are,  of  course,  never  found  in  the  expectoration  of 
a  simple  foetid  bronchitis,  but  only  in  the  deep- 
Fig.  21— Crystals  of  fat  acids.  seated,  destructive  processes  in  the  lung,  like  gan- 

grene. On  chemical  examination  of  the  sputum, 
the  ordinary  products  of  putrefaction  may  be  found — volatile  fat  acids,  especially 
butyric  and  valerianic  acids,  also  sulphuretted  hydrogen,  leucine,  tyrosine,  etc. 

The  breath  of  the  patient,  as  well  as  the  sputum,  is  very  often  foul-smelling, 
and  so  offensive  that  he  becomes  a  burden  to  his  associates. 

The  signs  which  foetid  bronchitis  gives  on  physical  examination  are  those  of 
an  ordinary  bronchitis.  In  a  great  number  of  cases  we  also  find  signs  of  con- 
solidation and  contraction  of  the  lung,  of  pleurisy,  etc.,  which  do  not  belong  to 
foetid  bronchitis  as  stich,  but  are  due  to  complications  or  sequelae. 

The  most  frequent  of  these  sequelae  is  the  development  of  a  "  reactive  "  lobular 
inflammation,  a  pure  pneumonia,  which  follows  a  catarrh  which  has  attacked  the 
finer  bronchi.  These  pneumonias  frequently  run  into  gangrene,  so  that  we  very 
often  find  a  number  of  larger  or  smaller  nodules  of  pure  gangrene  besides  the  ex- 
tensive foetid  bronchitis  in  the  lungs.  In  many  of  these  cases  the  foetid  bronchitis 
is  certainly  the  primary  process,  and  the  development  of  the  nodules  of  gangrene 
is  secondary ;  yet  we  shall  see  later  that  the  reverse  may  also  be  true.  Foetid  bron- 
chitis and  gangrene  of  the  lungs  run  into  each  other  so  often,  both  clinically  and 
anatomically,  that  there  is  no  sharp  line  to  be  drawn  between  them.  If  the 
nodules  are  superficial,  and  reach  the  pleura,  the  infection  attacks  this,  and  we 
have  a  purulent  or  even  an  ichorous  pleurisy. 

The  smaller  and  medium-sized  bronchi  are  almost  always  found  in  a  condition 
of  cylindrical  dilatation  in  old  foetid  bronchitis.  Their  mucous  membrane  is  in- 
tensely inflamed,  and  often  ulcerated  superficially.  On  its  surface  we  see  in  the 
cadaver  the  greasy  purulent  masses  and  the  plugs  which  we  find  in  the  expectora- 
tion during  life. 

Whatever  may  be  the  case  with  the  general  course  of  foetid  bronchitis,  its 
beginning  is  often  quite  sudden  and  acute,  both  in  the  primary  and  in  the  second- 
ary forms,  as  we  have  said.  The  patient  is  attacked  with  fever,  which  may  often 
be  quite  high,  and  with  a  stitch  in  the  side,  and  cough,  and  expectoration.     Later, 


FCETID  BRONCHITIS.  157 

the  characteristic  peculiarities  described  above  appear.  The  further  course  of  the 
disease  is  almost  always  chronic,  lasting  for  years,  but  subject  to  many  variations. 
Very  often  manifest  improvement,  and  even  apparent  recovery,  takes  place,  until 
suddenly  there  is  a  new  attack  of  fever  and  thoracic  symptoms.  The  general 
condition  and  nourishment  of  the  patient  may  be  quite  good  for  a  long  time, 
except  during  the  periods  of  marked  exacerbation  of  tbe  disease.  Patients  with 
chronic  foetid  bronchitis  often  appear  somewhat  bloated,  but  also  pale  and  slightly 
cyanotic.  Peculiar  clubbed  thickenings  of  tbe  terminal  phalanges  of  tbe  fingers 
gradually  develop,  as  in  many  cases  of ' bronchiectasis.  Slight  oedema  of  tbe 
lower  extremities  is  also  sometimes  present. 

Symptoms  referable  to  other  organs  may  be  wholly  absent.  We  see  most 
frequently  disturbances  of  the  stomach,  loss  of  appetite,  and  nausea,  which  proba- 
bly comes  from  swallowing  the  foetid  sputum.  Patients  also  complain  of  occa- 
sional rheumatic  pains  in  the  muscles  and  joints,  which  may  perhaps  be  due  to  an 
absorption  of  septic  matter.  In  conclusion  it  must  be  mentioned  that  in  fortunately 
rare  cases  of  foetid  pulmonary  disease  pyogenic  germs  reach  the  brain  by  metas- 
tasis, and  here  give  rise  to  purulent  meningitis  or  cerebral  abscess. 

The  danger  of  the  disease,  apart  from  the  exceptional  occurrence  just  mentioned, 
lies  in  the  possible  extension  of  the  process  to  the  lungs  and  the  development  of 
pulmonary  gangrene  and  its  sequela?.  We  hardly  ever  find  a  simple  foetid  bron- 
chitis in  the  cadaver,  but  we  almost  always  see  other  processes  besides,  which  have 
been  mentioned  above — reactive  pneumonia,  pulmonary  gangrene,  etc.  These 
processes  develop  very  readily,  and  make  rapid  progress  in  old,  decrepit  persons, 
who  live  under  bad  external  conditions,  in  whom  putrid  processes  in  the  lungs 
are  frequent. 

The  diagnosis  of  foetid  bronchitis  is  not  difficult  in  itself,  for  the  diagnosis  of  a 
putrid  process  in  the  lung  may  be  made  from  the  stinking  sputum  alone.  It  may 
be  difficult  to  decide  whether  we  have  to  do  merely  with  a  foetid  bronchitis,  or 
with  a  pulmonary  gangrene  also.  Decisive  indications  of  gangrene  are  derived 
from  physical  examination — dullness,  bronchial  respiration,  and  large,  moist  rales 
— and  also  the  discovery  of  elastic  fibers  and  fragments  of  parenchyma  in  the 
expectoration. 

The  prognosis  must  be  made  with  care  in  every  case  of  foetid  bronchitis.  If 
the  external  circumstances  of  the  patient  are  favorable,  he  may  remain  in  toler- 
able health  for  years.  We  must  always  be  prepared  for  the  appearance  of  new 
exacerbations  of  the  disease  and  of  affections  of  the  lung  itself. 

Treatment. — The  chief  aim  of  treatment  must  be  to  bring  the  putrid  processes 
in  the  bronchi  to  a  stand-still  by  the  death  of  the  agents  of  putrefaction.  The 
difficulty  of  fulfilling  this  task  lies  in  the  impossibility  of  getting  the  disinfecting 
material  to  act  on  the  bronchial  mucous  membrane  in  the  necessary  amount  and 
concentration.  Nevertheless,  we  can,  without  doubt,  at  least  relieve  a  foetid  bron- 
chitis and  keep  it  in  check  by  the  judicious  use  of  inhalations.  Inhalations  of  a 
two-per-cent.  solution  of  carbolic  acid  are  most  useful,  given  for  five  or  ten  min- 
utes several  times  a  day.  These,  however,  are  sometimes  not  well  borne  if  long 
continued,  and  they  may  excite  mild  symptoms  of  carbolic  poisoning — like  head- 
ache, malaise,  and  dark  carbolic  urine.  We  have  often  used  with  good  results 
the  "  carbolic  mask  "  recommended  by  Curschmann,  a  kind  of  respirator  fastened 
in  front  of  the  nose  and  mouth,  containing  cotton  in  a  special  receptacle  impreg- 
nated with  carbolic  acid,  equal  parts  of  carbolic  acid  and  alcohol,  or  other  remedies 
like  turpentine  or  creasote.  Many  patients  can  wear  these  masks,  with  occasional 
interruptions,  for  many  hours  a  day.  Turpentine  is  most  used  next  to  carbolic 
acid.  Turpentine  can  be  used  by  inhalation  and  also  internally.  Likewise  ter- 
pine  and  myrtol  are  often  of  decided  benefit.     We  have  very  recently,  in  the 


158  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

clinique  at  Erlangen,  had  good  results  frorn  inhalations  of  oleum  pini  pumilionis 
(employed  as  described  on  p.  154  for  the  inhalation  of  turpentine).  Both  inhala- 
tions and  the  internal  exhibition  of  turpentine  are  of  distinct  value.  We  may 
also  try  acetate  of  lead  internally,  one  or  two  grains  (grm.  0 '05-0  10)  in  powder 
every  two  hours. 

In  other  respects  all  tbe  general  hygienic  and  symptomatic  methods  of  treat- 
ment recommended  for  common  chronic  bronchitis  are  also  useful  in  foetid  bron- 
chitis. The  sputum . should  be  disinfected  by  putting  strong  carbolic  acid,  etc., 
into  the  sputa -cup  to  lessen  the  bad  odor.  It  is  a  very  good  plan  to  keep  the  car- 
bolic spray  at  work  in  the  patient's  room  as  often  and  as  long  as  possible,  or  the 
air  may  be  impregnated  with  oleum  pini  pumilionis. 


CHAPTER  IV. 

CROUPOUS  BRONCHITIS. 

{Fibrinous  or  Pseudo-membranous  Bronchitis) 

Croupous  bronchitis  is  a  peculiar  form  of  disease  of  the  bronchial  mucous 
membrane,  of  very  rare  occurrence,  in  which  there  is  a  formation  of  extensive 
fibrinous  patches  in  the  bronchi.  Only  that  form  of  croupous  bronchitis  which 
occurs  primarily  in  the  bronchi  is  to  be  considered  here,  and  not  the  secondary 
form,  which  on  the  one  side  is  associated  with  diphtheria  in  the  pharynx  and 
larynx,  and  on  the  other  with  croupous  pneumonia. 

The  aetiology  of  the  disease  is  as  yet  wholly  unknown.  From  analogy  with 
other  well-known  croupous  inflammations  of  mucous  membranes,  we  must  look 
here  for  some  noxious  influence  which  destroys  the  epithelium,  but  up  to  this  time 
we  are  entirely  ignorant  of  its  character.  Individuals  in  youth  and  middle  age, 
somewhere  between  ten  and  thirty  years  old,  are  the  chief  victims.  Men  are 
attacked  somewhat  more  frequently  than  women.  The  disease  comes  on  either  in 
persons  who  were  previously  healthy — the  essential  croupous  bronchitis — or  in 
those  who  have  already  suffered  from  some  other  disease,  especially  some  chronic 
pulmonary  affection — the  symptomatic,  secondary  croupous  bronchitis.  It  is  not 
certain  whether  the  last-named  cases  can  have  the  same  serological  relation  as  the 
cases  of  pure  primary  fibrinous  bronchitis.  Fibrinous  bronchitis  has  been  ob- 
served in  the  course  of  typhoid  fever. 

Symptoms  and  Course. — Primary  fibrinous  bronchitis  occurs  in  two  forms, 
acute  and  chronic.  The  acute  form  begins  quite  suddenly,  with  fever,  coiigh,  pain 
in  the  chest,  and  severe  dyspnoea  which  speedily  develops.  The  fibrinous  coagula, 
which  alone  render  the  diagnosis  possible,  appear  in  the  expectoration  either  at 
once,  or  after  the  existence  for  some  days  of  what  is  apparently  simple  catarrhal 
bronchitis. 

These  coagula  form  complete  casts  of  the  bronchi,  and  are  more  or  less  branch- 
ing. They  are  of  a  whitish  color  and  of  quite  a  dense,  elastic  consistency.  The 
main  stem  may  be  a  centimetre  thick,  and  from  it  the  further  ramifications  branch, 
dividing  dichotomously.  The  largest  casts  are  ten  or  fifteen  centimetres  long. 
On  section,  we  usually  find  a  free  lumen  within,  and  generally  recognize  a  definite 
laminated  structure  in  the  membrane.  In  many  places  they  are  enlarged  and 
swollen.  Microscopically,  we  find  white  blood-corpuscles  in  and  upon  the  hyaline 
ground-substance  of  the  casts,  and  also  red  blood-corpuscles,  sometimes  epithelial 
cells,  and  quite  often  the  peculiar  pointed  octahedral  crystals  which  are  also  found 
in  the  expectoration  in  bronchial  asthma  (vide  infra).     The  so-called  "  spirals  " 


CROUPOUS  BRONCHITIS.  150 

{vide  infra)  have  also  been  found  in  the  expectoration  of  fibrinous  bronchitis. 
Chemically  the  casts  consist  of  coagulated  albumen.  Tbeir  solubility  in  alkalies, 
especially  in  lime-water,  is  of  therapeutic  importance. 

On  coughing-,  the  patient  usually  raises  a  simple  mucous  or  muco-purulent  ex- 
pectoration beside  the  casts,  and  in  this  sputum  the  casts  are  imbedded.  They  are 
often  first  discovered  by  pouring  the  whole  amount  of  sputum  into  water,  when 
they  unfold  and  spread  out.  The  expectoration  also  contains  not  infrequently  a 
slight  admixture  of  blood. 

The  subjective  symptoms  of  the  patient  may  be  very  violent.  The  dyspnoea 
sometimes  attains  a  high  and  alarming  degree.  It  ceases  when  a  large  cast  is  ex- 
pectorated after  a  severe  paroxysm  of  coughing.  Such  attacks  may  recur  every  day 
or  two.     In  other  cases,  however,  the  subjective  symptoms  are  comparati  vely  si ight. 

Physical  examination  of  the  lungs  gives  little  that  is  characteristic.  In  uncom- 
plicated cases  percussion  gives  nothing  abnormal,  or  at  most  the  signs  of  an 
acute  emphysema.  Auscultation  gives  the  ordinary  signs  of  bronchitis,  not  char- 
acteristic in  themselves,  such  as  rhonchi,  or  moist  rales.  If  a  large  bronchus  is 
plugged,  the  respiratory  excursions  and  the  respiratory  murmur  are  almost  en- 
tirely absent  in  the  corresponding  portion  of  the  lung,  but  after  the  expectoration 
of  a  cast  the  murmur  once  more  becomes  audible. 

The  duration  of  acute  cases  is  sometimes  only  a  few  days,  at  most  a  few  weeks. 
In  favorable  cases  the  fever,  which  at  times  is  quite  high,  soon  disappears,  the 
respiratory  symptoms  grow  milder,  the  expectoration  of  the  casts  ceases,  and  there 
is  a  complete  and  permanent  recovery.  In  severe  cases,  however,  death  often 
ensues  with  all  the  symptoms  of  suffocation.  The  acute  form  sometimes  becomes 
chronic,  but  this  is  rare. 

The  chronic  form  of  fibrinous  bronchitis  may  last  for  years.  Usually  the  con- 
dition grows  worse  periodically,  at  varying  intervals  of  time,  and  at  each  exacer- 
bation casts  are  expectorated,  while  in  the  interval  there  is  apparently  merely  a 
simple  bronchial  catarrh.  Some  observations  are  also  recorded  in  medical  litera- 
ture of  people  who  have  expectorated  these  casts  at  intervals  for  years  without  any 
special  disturbance  of  their  health  or  their  nutrition.  In  some  cases  other  chronic 
pulmonary  affections,  like  tuberculosis,  finally  develop. 

The  pathological  anatomy  of  fibrinous  bronchitis  is  not  yet  satisfactorily 
known  on  account  of  the  rarity  of  the  affection.  The  changes  in  the  lungs 
found  at  the  autopsy  of  fatal  cases  have  usually  been  complications,  like  pneu- 
monia, pleurisy,  or  tuberculosis,  which  stood  in  no  direct  relation  to  the  fibrinous 
bronchitis.  A  loss  of  epithelium  has  been  discovered  in  some  cases  in  the  parts 
of  the  bronchial  mucous  membrane  that  were  attacked. 

Prognosis. — In  all  acute  cases  the  prognosis  should  be  guarded,  for  we  know 
that  about  one  fourth  of  the  cases  terminate  fatally.  The  chronic  cases,  as  has 
been  said,  are  usually  very  protracted  and  are  subject  to  frequent  recurrences, 
but  they  differ  from  the  acute  cases  in  being  much  less  dangerous. 

Treatment. — We  make  special  use  for  inhalations  of  those  remedies  which,  as 
we  have  said,  are  able  to  dissolve  the  casts.  We  usually  employ  a  two-  to-five- 
per-cent.  solution  of  carbonate  or  bicarbonate  of  sodium,  and  above  all  lime- 
water,  either  pure  or  diluted  with  an  equal  volume  of  water.  The  internal 
administration  of  iodide  of  potassium,  in  doses  of  twenty  to  forty-five  grains 
(grm.  l-5-3-0)  a  day,  proves  of  advantage  in  many  cases.  Energetic  inunction 
with  mercurial  ointment  is  sometimes  of  service.  Expectoration  of  the  casts  may 
be  aided  in  many  cases  by  such  expectorants  as  senega  and  benzoic  acid,  or  by 
the  timely  use  of  emetics.  We  do  not  know  any  remedies  which  are  able  to  pre- 
vent a  return  of  the  attacks  in  the  chronic  form.  The  treatment,  except  at  the 
time  of  the  attacks,  is  the  same  as  in  ordinary  chronic  bronchial  catarrh. 


160  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

CHAPTER  V. 

WHOOPING-COUGH. 

(Pertussis.     Tussis  convulsiva.) 

iEtiology. — By  the  name  "  whooping-cough  "  we  mean  a  specific  disease  of  the 
mucous  membrane  of  the  air-passages,  which  is  chiefly  seen  in  children,  and  is 
characterized  by  a  peculiar  violent  and  paroxysmal  cough.  Sporadic  cases  are  of 
almost  constant  occurrence  in  large  cities,  but  the  disease  often  appears  in  epi- 
demic outbreaks.  Epidemics  of  whooping-cough  follow  epidemics  of  measles 
with  remarkable  frequency. 

Whooping-cough  is  without  doubt  contagious,  and  therefore  often  attacks  one 
child  after  another  in  the  same  family.  Kindergartens,  orphan  asylums,  and 
nurseries  aid  very  much  in  extending  the  disease.  The  contagious  element  seems 
to  be  connected  with  the  air  expired  by  the  patient,  particularly  with  the  secretion 
from  the  mucous  membrane  expectorated  after  coughing.  Children  are  most  sub- 
ject to  an  attack  up  to  the  age  of  six  years ;  from  that  age  the  disposition  to  the  dis- 
ease decreases  rapidly  with  increasing  years.  Whooping-cough  is  seen,  indeed,  in 
adults,  but  it  is  quite  rare,  and  almost  always  comparatively  mild  and  rudimentary. 

The  epidemic  onset,  the  contagiousness,  and  the  whole  course  of  the  disease 
favor  the  theory  of  its  infectious  nature.  The  presence  of  the  organisms  which 
are  supposed  to  be  the  poison  of  the  disease  has  not  yet  been  certainly  demon- 
strated, although  many  have  claimed  to  discover  characteristic  organisms  in  the 
sputa  of  patients.  These  statements,  however,  all  conflict,  and  lack  well-attested 
and  methodical  proof.  If  a  patient  has  once  had  the  disease,  he  is  almost  inva- 
riably secure  against  a  new  attack. 

Symptoms  and  Course  of  the  Disease. — Whooping-cough  begins  with  the  symp- 
toms of  a  catarrh  of  the  trachea  and  bronchi,  which  develops  more  or  less  rapidly, 
and  which  at  first  often  shows  nothing  characteristic.  We  can  at  this  period 
make  a  tolerably  probable  diagnosis  only  at  a  time  when  an  epidemic  is  prevailing, 
or  in  case  the  child's  associates  have  already  been  attacked  with  the  disease.  The 
cough  is  often  quite  severe  at  the  beginning,  but  it  does  not  yet  come  on  in  dis- 
tinct paroxysms.  Examination  of  the  chest  shows  nothing  peculiar  except  a  few 
rhonchi.  There  is  often  a  coryza,  with  frequent  sneezing,  and  there  is  sometimes 
a  mild  conjunctivitis.  The  child  is  restless  and  feverish,  especially  toward  night. 
The  temperature  may  repeatedly  reach  103°  or  104°  (39°-40°  C.)  in  this  initial 
fever.  The  duration  of  this  first  so-called  catarrhal  stage  varies,  but  it  usually 
lasts  a  week  or  ten  days. 

The  catarrhal  stage  gradually  passes  into  the  second,  convulsive  stage,  without 
any  sharp  boundary.  The  cough  becomes  more  violent,  and  comes  on  in  the 
separate  paroxysms  of  whooping-cough  which  are  characteristic  of  the  disease. 
We  do  not  know  the  particular  reason  why  the  cough  has  this  paroxysmal  char- 
acter, but  a  nervous  factor  probably  plays  the  chief  part  in  it. 

The  peculiarity  of  the  attack  consists  in  the  violent,  paroxysmal  fits  of  cough- 
ing, which  are  from  time  to  time  interrupted  by  deep,  long-drawn,  loud,  and 
shrill  inspirations,  due  to  the  occurrence  of  a  spasmodic  contraction  of  the  glottis. 
Exceptionally  there  are  cases  without  this  loud  whistling  inspiration.  The  child 
becomes  markedly  cyanotic  during  the  attack,  the  veins  in  the  neck  swell,  and 
tears  come  into  the  eyes.  Haemorrhage  into  the  conjunctiva,  nose-bleed,  and  in 
some  cases  haemorrhages  into  other  organs,  like  the  ear,  the  skin,  and  the  brain,* 

*  In  one  instance  we  observed  the  very  rare  occurrence  of  a  hemiplegia  during  a  paroxysm  of 
whooping-cough. 


WHOOPING-COUGH.  161 

often  come  on  as  a  result  of  this  stasis.  Vomiting'  very  often  occurs  either  during 
a  paroxysm  or  at  its  close.  Involuntary  evacuations  of  urine  and  faeces  may  also 
follow  from  the  violent  contraction  of  the  abdominal  muscles.  Exceptionally  vv<; 
observe  still  more  severe  symptoms  with  a  paroxysm:  a  complete  spasmodic  cessa- 
tion of  respiration  with  imminent  danger  of  suffocation,  or  sometimes  general 
convulsions. 

The  paroxysms  vary  with  the  severity  of  the  disease,  frequently  appearing 
ten  or  fifteen  times  in  twenty -four  hours;  sometimes  with  greater  frequency — 
fifty  times  or  more.  They  also  occur  at  night  as  often  or  even  oftener  than  in 
the  daytime.  They  come  on  either  spontaneously  or  from  some  special  predis- 
posing cause.  We  may,  for  example,  excite  a  paroxysm  artificially  by  pressing 
on  the  larynx  or  by  making  the  child  cry.  If  there  are  several  children  with 
whooping-cough  in  the  same  room  and  a  paroxysm  attacks  one  of  them,  the 
others,  as  a  rule,  soon  begin  to  cough  too.  Some  prodromal  symptoms  often  pre- 
cede the  peculiar  paroxysm,  such  as  general  uneasiness,  rapid  respiration,  or 
vomiting.  At  the  end  of  a  paroxysm  many  children  remain  very  feeble  and 
exhausted,  but  others  recover  very  rapidly,  and  are  playing  again  quite  briskly  a 
few  minutes  after. 

In  general  the  child  feels  quite  well  in  the  interval  between  the  paroxysms, 
but  the  effects  of  the  violent  attacks  of  coughing  may  of  course  often  be  seen. 
Besides  the  occasional  hemorrhages  into  the  conjunctiva,  we  find  the  eyelids 
somewhat  swollen,  their  veins  dilated  and  blue,  and  showing  through  the  skin. 
A  small  ulcer  is  quite  frequently  formed  on  the  fraenum  of  the  tongue,  the  origin 
of  which  is  to  be  referred  to  mechanical  causes.  The  tongue  is  violently  pro- 
truded in  the  severe  paroxysms  of  coughing,  and  the  fraenum  is  thus  pulled  or 
torn,  or  injured  by  the  sharp  lower  incisors. 

Physical  examination  of  the  lungs  shows  nothing  abnormal  in  uncomplicated 
cases  except  a  few  moist  rales  or  rhonchi.  Sometimes  the  rhoncbi  are  wanting,  or 
are  present  in  small  numbers  only  a  short  time  before  a  paroxysm,  but  in  other 
cases  an  intense  diffuse  bronchitis  is  developed,  which  often  leads  to  the  develop- 
ment of  a  lobular  pneumonia  {vide  infra).  Sometimes,  but  not  always,  there  is 
an  acute  catarrhal  inflammation  of  the  bronchi,  and  especially  of  the  posterior 
wall  of  the  larynx. 

The  fever,  which  is  usually  present  in  the  first  or  catarrhal  stage,  is  absent  in 
the  convulsive  stage.  The  child  is  free  from  fever  for  the  most  part.  We  often 
find  a  slight  rise  of  temperature  up  to  100°  or  101°  (38°-38-5°  C),  but  only  toward 
night.  Higher  and  more  persistent  fever  points  to  the  development  of  complica- 
tions, especially  on  the  part  of  the  lungs. 

The  convulsive  stage  seldom  lasts  less  than  three  or  four  weeks,  and  often 
much  longer,  up  to  three  or  four  months.  The  paroxysms  gradually  become  less 
frequent  and  less  violent  {stadium  decrementi),  until  they  finally  disappear 
entirely ;  but  relapses  and  fresh  exacerbations  also  occur  in  this  stage.  Finally, 
however,  the  disease,  in  uncomplicated  cases,  goes  on  to  a  permanent  and  com- 
plete recovery. 

Complications  and  Sequelae. — The  severe  results  which  sometimes  follow  whoop- 
ing-cough are  probably  partly  due  to  the  direct  action  of  the  specific  causes 
of  the  disease,  and  partly  to  complications  of  a  secondary  nature  whose  origin 
is  merely  favored  by  the  whooping-cough.  The  most  important  are  complications 
in  the  lungs.  A  lobular,  catarrhal  pneumonia  often  develops  after  a  severe 
bronchitis  which  involves  the  finer  bronchi.  In  such  cases  the  respiration  be- 
comes hurried  and  superficial,  the  fever  higher,  and  the  general  condition  bad 
even  in  the  times  between  the  paroxysms.  On  examination  of  the  lungs,  we  hear 
numerous  moist  rales,  especially  over  the  lower  lobes,  and  we  can  sometimes 
11 


162  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

make  out  dullness  on  one  or  both  sides  if  there  is  extensive  pneumonic  infiltration. 
Such  cases  are  always  very  protracted,  and  many  children  succumb,  partly  from 
the  disturbance  of  respiration  and  partly  from  general  weakness  and  inanition. 

Complications  in  other  organs  are  much  rarer.  Among  the  most  frequent  are 
attacks  of  diarrhoea  which  exhaust  the  cbild's  nutrition.  Many  observers  have 
also  mentioned  the  quite  frequent  occurrence  of  a  croupous  or  diphtheritic 
inflammation  in  the  pharynx  and  larynx  in  the  course  of  whooping-cough. 
Finally,  a  case  under  our  own  observation  may  here  be  mentioned,  in  which 
death  occurred  with  severe  nervous  symptoms,  convulsions,  and  coma.  At  the 
autopsy  very  numerous  capillary  haemorrhages  were  found  in  the  brain. 

.  Pulmonary  emphysema  is  the  first  thing  to  be  mentioned  among  the  sequelae 
of  whooping-cough.  From  the  marked  pressure  which  the  severe  and  frequent 
outbursts  of  coughing  exert  from  within  upon  the  alveoli  of  the  lungs,  they  gradu- 
ally become  dilated.  An  acute  lobular  emphysema  ("acute  pulmonary  infla- 
tion ")  is  set  up  which  sometimes  passes  into  a  typical  chronic  pulmonary  emphy- 
sema {vide  infra).  Chronic  bronchial  catarrh  may  also  remain  for  a  long  time 
after  an  attack  of  whooping-cough. 

A  third  important  sequel  of  whooping-cough  is  pulmonary  tuberculosis.  The 
bronchitis  and  lobular  pneumonia  which  occur  during  a  whooj)ing-cough.  some- 
times do  not  improve,  especially  in  weak  children  with  a  tubercular  tendency. 
The  fever  continues  high,  the  child  grows  thin,  and  constantly  becomes  more  and 
more  miserable.  At  the  autopsy  we  find  cheesy  nodules  in  the  lungs,  cheesy  bron- 
chial glands,  and  at  times  tuberculosis  of  other  organs.  These  cases  signify  that 
when  a  tubercular  infection  is  present,  but  is  still  latent,  the  whooping-cough  acts 
as  an  exciting  cause  for  the  outbreak  of  the  disease,  or  that  a  greater  receptivity 
to  infection  with  tubercular  poison  is  created  by  the  whooping-cough.  Möbius 
has  lately  reported  the  occurrence  in  a  few  cases  of  paralysis  as  a  sequel  of 
whooping-cough.  This  usually  begins  in  the  lower  and  extends  to  the  upper 
extremities,  and  is  apparently  due  to  neuritis. 

The  diagnosis  of  whooping-cough  can  not  be  made  with  certainty,  as  we  have 
said,  until  the  second  or  convulsive  stage.  It  is  easy  then,  however,  since  the 
characteristic  attacks  occur  in  no  other  affection  of  the  lungs  in  like  manner 
and  with  like  frequency  and  duration.  If  we  have  no  opportunity  to  observe  the 
attack  itself,  and  have  to  depend  upon  the  description  of  the  friends,  the  diagnosis 
is  sometimes  more  uncertain.  In  such  cases,  however,  certain  signs  are  often 
present :  the  child  has  a  bloated  aspect,  or  we  may  find  slight  haemorrhages  into 
the  conjunctiva,  or  ulcers  on  the  fraenum  of  the  tongue,  which  make  the  diag- 
nosis highly  jjrobable.  Under  some  circumstances  we  may  also  make  the  attempt 
to  bring  on  the  paroxysm  artificially  {vide  supra). 

The  prognosis  is  favorable  with  the  majority  of  children  if  they  are  previously 
strong  and  healthy.  Very  young  children  are  in  more  danger  than  older  ones. 
There  is  danger  if  secondary  pneumonia  develops,  and  if  the  general  nutrition  and 
strength  of  the  child  suffer.  As  soon  as  the  diagnosis  is  certain  we  must  call  the 
attention  of  the  parents  to  the  probable  long  duration  of  the  disease.  Regard 
must  also  be  paid  to  the  possibility  of  the  development  of  sequelae,  especially  in 
weak  children  suspected  of  tuberculosis. 

Treatment. — Since  the  disease  is  protracted  and  is  not  devoid  of  danger,  it  is  our 
duty,  when  an  epidemic  of  whooping-cough  prevails,  to  guard  children  from  it  as 
far  as  possible.  If  one  child  in  a  family  is  taken  ill,  the  other  children  must  be 
rigorously  kept  away  from  him.  If  circumstances  permit,  we  should  prefer  to 
send  them  away  to  another  place  free  from  whooping-cough. 

With  regard  to  the  treatment  of  the  disease,  we  must  first  endeavor  to  fulfill 
general  dietetic  and  hygienic  indications.     The  child  should  breathe  good,  pure 


WHOOPING-COUGH.  \  63 

air,  and  for  this  reason  it  is  often  advisable  to  transfer  the  patient  to  a  larger  room, 
with  as  much  air  and  sunlight  as  possible.  The  atmosphere  should  not  be  too  dry, 
and  it  is  advisable  to  employ  a  spray  of  carbolizcd  water  occasionally,  or  to  hang 
up  sheets  moistened  with  the  same  in  the  room.  In  good  weather  the  child  should 
be  out  of  doors  a  large  part  of  the  time,  provided  fever  has  ceased.  City  children 
are  to  be  sent,  if  possible,  into  the  country.  The  food  should  be  good  and  nour- 
ishing, but  dry  and  crumbly  articles  should  be  avoided,  being  apt  to  excite  cough. 
Warm  or  lukewarm  baths  frequently  prove  very  beneficial,  particularly  when 
there  is  considerable  bronchitis,  as  they  lessen  the  danger  of  a  lobular  pneumonia. 

The  medicinal  treatment  of  whooping-cough  has  not  yet  shown  brilliant 
results  despite  the  large  number  of  remedies  recommended.  Internally,  quinine, 
belladonna,  and  bromide  of  potash  are  most  worthy  of  a  trial.  Quinine  is  given 
in  powders  of  one  and  a  half  to  eight  grains  (0*1  to  0*5)  several  times  a  day, 
either  in  capsules  or,  in  the  case  of  smaller  children,  with  chocolate.  The  earlier 
this  remedy  is  employed  the  more  prompt  is  said  to  be  its  beneficial  influence. 
Lately  the  treatment  of  whooping-cough  with  antipyrine  has  been  much  recom- 
mended. Belladonna  is  prescribed  in  powders  containing  one  twelfth  to  one 
sixth  grain  (0"005  to  0"01)  of  the  extract  of  belladonna,  giving  three  to  five  such 
powders  a  day.  This  remedy  has  often  seemed  to  the  author  to  diminish  the  num- 
ber and  violence  of  the  paroxysms.  The  largest  daily  dose  of  sulphate  of  atropine 
to  be  given  to  children  is  one  sixtieth  of  a  grain  (0"001),  and  even  this  amount 
demands  in  every  case  caution  and  watchfulness  for  the  possibility  of  symptoms 
of  poisoning,  such  as  enlargement  of  the  pupils  and  dryness  of  the  mouth.  Bro- 
mide of  potash  is  employed  in  an  aqueous  solution  in  the  dose  of  fifteen  to  forty- 
five  grains  per  diem  (1  to  3  grin.).  Its  benefit  is  probably  due  to  its  power  to 
diminish  reflex  excitability.  The  same  drug  employed  in  an  atomizer  often  has  a 
palliative  effect. 

If  the  paroxysms  are  very  violent  we  may  cautiously  administer  small  doses 
of  morphine  or  codeia.  Inhalations  of  chloroform  and  ether  have  also  been 
recommended.     The  following  mixture  is  a  suitable  one : 

IjS  Chloroformi §  j    (grm.  30) ; 

iEtheris §  ij  (grm.  60) ; 

01.  terebinthinaa , .  3  ijss.  (grm.  10).    M. 

Sig.  One  or  two  teaspoonfuls  to  be  poured  upon  a  pocket-handkerchief  for  inha- 
lation. 

Finally,  considerable  success  has  attended  the  application  of  cocaine  to  the 
throat  and  larynx  by  means  of  a  brush.  A  solution  of  ten  to  fifteen  per  cent, 
has  a  considerable  influence  in  modifying  the  frequency  and  violence  of  the 
paroxysms.  Michael  advocates  the  daily  insufflation  into  the  nostrils  of  pow- 
dered benzoin. 

Inhalations  of  various  antiseptic  remedies  have  been  frequently  employed 
because  of  the  infectious  nature  of  the  disease.  The  practitioner  must  not  expect 
too  much  from  them,  however,  although  they  sometimes  act  well.  A  one-per- 
cent, or  two-per-cent.  solution  of  carbolic  acid  is  most  frequently  employed  for 
inhalation.  It  may  be  given  several  times  a  day  for  periods  of  two  or  three 
minutes  at  a  time.  Next  to  this,  turpentine  and  benzine  are  most  to  be  recom- 
mended ;  of  these,  twenty  or  thirty  drops  are  poured  upon  a  sponge  previously 
moistened  with  hot  water.  [Parlow  and  others  report  marked  success  from  spray- 
ing the  upper  air-passages  with  a  two-per-cent.  solution  of  resorcin.] 

For  the  treatment  of  the  complications  and  sequel«  of  whooping-cough  the 
reader  is  referred  to  the  appropriate  chapters  of  this  book. 


164  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

CHAPTER  VI. 

BRONCHIECTASIS. 

{Bronchial  Dilatation.) 

Dilatation  of  the  bronchi  is  not  a  separate  disease,  but  it  is  a  result  of  various 
affections  of  the  lungs  and  bronchi.  Nevertheless,  we  will  speak  of  it  briefly  in 
this  connection  since  many  cases  of  bronchiectasis  present  the  appearance  of  quite 
a  characteristic  disease. 

We  distinguish  anatomically  the  cylindrical  and  saccular  bronchiectases. 

Cylindrical  bronchiectasis  consists  of  a  uniform  dilatation  of  a  bronchial  tube, 
and  occurs  most  frequently  in  the  medium-sized,  or  rarely  in  the  finer  bronchi  of 
one  or  more  lobes  of  the  lung.  It  is  usually  due  to  a  long-continued  bronchitis, 
and  develops  most  frequently  in  cases  of  emphysema,  and  also  in  whooping- 
cough,  measles,  and  sometimes  in  phthisis,  etc.  The  primary  process  is  probably 
always  the  atrophy  which  follows  the  catarrh,  and  the  diminished  resistance  of 
the  bronchial  walls  thus  occasioned.  The  dilatation  of  the  lumen  of  the  broncbes 
is  produced  gradually,  partly  by  the  traction  of  the  thorax  during  inspiration, 
and  still  more  by  the  increased  pressure  in  the  bronchi  due  to  the  frequent  and 
violent  fits  of  coughing,  and  finally,  perhaps,  by  the  constant  pressure  of  the 
stagnating  secretion. 

The  diagnosis  of  cylindrical  dilatation  of  the  bronchi  is  only  a  probable  one. 
We  suspect  that  a  bronchiectasis  has  formed  if  the  conditions  are  fulfilled 
which  we  know  lead  to  it.  In  the  chronic  bronchial  catarrh  of  emphysema  we 
judge  that  there  is  cylindrical  dilatation  of  the  bronchi  if  the  secretion  is  very 
abundant  and  comparatively  thin,  and  separates  on  standing  in  a  sputa-cup.  The 
dilatation  is  usually  emptied  by  a  severe  paroxysm  of  coughing,  such  as  is  apt  to 
occur  in  the  morning  if  the  secretion  collects  in  great  quantity  during  the  night. 
Physical  examination  usually  gives  numerous  small  and  medium  moist  rales, 
especially  in  the  lower  lobes.  The  respiratory  murmur  sometimes  loses  its  vesicu- 
lar character  in  marked  cylindrical  bronchiectasis,  and  has  a  more  indefinite  and 
tubular  quality. 

Saccular  bronchiectases  are  spherical  or  oval  dilatations  which  are  confined  to 
a  definite  portion  of  the  bronchial  tube.  They  may  attain  a  diameter  of  several 
centimetres.  The  bronchus  passes  suddenly  or  gradually  into  the  dilatation,  and 
it  is  often  obliterated  so  that  the  bronchiectasis  forms  a  completely  closed  cavity. 
The  wall  of  a  saccular  bronchiectasis  loses  in  great  measure  the  character  of  a 
normal  bronchial  wall.  As  a  rule  it  is  atrophied  to  a  high  degree,  the  atrophy 
involving  not  only  the  mucous  glands,  but  also  the  muscular  fibers,  the  elastic 
elements,  and  even  the  cartilages,  so  that  the  bronchiectasic  cavities  seem  lined 
with  nothing  but  a  thin  membrane.  In  other  cases,  however,  we  find  hyper- 
trophic processes,  which  involve  the  connective  tissue  of  the  mucous  membrane, 
and  lead  to  band-like  projections  and  swellings.  Finally,  ulcerative  processes 
may  develop  on  the  inner  surface  of  a  bronchiectasis  and  attack  the  surrounding 
lung-tissue,  and  change  the  bronchiectasis  to  a  typical  ulcerating  cavity. 

Only  rarely,  for  example  in  emphysema,  do  we  find  a  single  saccular  bron- 
chiectasis surrounded  by  tolerably  normal  lung-tissue.  Its  origin,  then,  is  to  be 
referred  to  causes  like  those  which  have  been  given  above  for  the  much  com- 
moner cylindrical  bronchiectases.  In  the  great  majority  of  cases  we  find  saccular 
bronchiectases,  singly  or  in  large  numbers,  surrounded  by  indurated  and  con- 
tracted lung-tissue.  They  form  one  of  the  complications  of  "pulmonary  con- 
traction" [fibroid  phthisis],  which  is  almost  always  associated  with  contraction  of 
the  pleura.     Since  Corrigan's  day  we  have  with  good  reason  looked  upon  this  con- 


BRONCHIECTASIS.  1G5 

traction  as  the  chief  cause  for  their  origin.  By  the  gradual  shrinking  and  retrac- 
tion of  the  lung,  which  as  a  rule  has  become  adherent  to  the  costal  pleura,  a  trac- 
tion is  exerted  upon  the  bronchial  walls  from  without  to  which  they  gradually 
yield.  Thus  arises  the  frequent  combination  of  pulmonary  contraction  with  the 
formation  of  bronchiectases.  This  combination  is  usually  unilateral,  and  involves 
the  whole  lung  or  only  one  of  the  upper  or  lower  lobes.  This  form  has  been 
described  from  a  histological  stand-point  as  a  chronic  interstitial  pneumonia, 
and  it  has  been  believed  possible  to  make  a  sharp  distinction  between  it  and  the 
chronic  tubercular  processes  in  the  lung. 

We  often  see  the  form  of  pulmonary  contraction  in  question  developing  as  a 
result  of  pleurisy.  Laennec  first  advanced  the  opinion  that  in  such  cases  the 
pleurisy  was  the  primary  trouble,  and  that  from  it  an  interstitial  inflammatory 
process  attacked  the  connective  tissue  of  the  underlying  lung  and  led  to  contrac- 
tion and  then  to  the  formation  of  bronchiectases.  In  our  opinion  we  must  indeed 
recognize  the  manifold  anatomical  and  clinical  peculiarities  of  the  combination 
of  pulmonary  contraction  and  formation  of  bronchiectases  in  question,  but  setio- 
logically  we  are  unable  to  separate  it  from  pulmonary  tuberculosis  (vide  infra),  at 
least  in  the  great  majority  of  cases.  But  on  the  other  hand  it  can  not  be  denied 
that  extensive  bronchiectasis  is  sometimes  observed  entirely  independent  of  any 
tuberculous  process.  In  these  rare  cases  the  bronchial  dilatation  seems  to  be  a 
sequel  in  most  instances  of  a  severe  antecedent  chronic  bronchitis.  It  is  seen,  for 
example,  in  workmen  who  are  obliged  to  inhale  a  great  deal  of  dust.  There  can 
be  no  doubt,  however,  that  the  process  here  finally  extends  to  the  lung-tissue,  for 
upon  autopsy  the  parenchyma  between  the  various  bronchiectasic  cavities  is  usu- 
ally not  normal,  but  transformed  into  a  firm  indurated  tissue.  As  a  rule  the  dis- 
ease is  mainly  limited  to  one  side,  involving  perhaps  the  whole  lung,  or,  if  only  a 
single  lobe,  usually  the  lower  one. 

The  symptoms  caused  by  saccular  bronchiectasis  alone  are  derived  in  part  from 
the  result  of  physical  examination  and  in  part  from  definite  peculiarities  of  the 
sputum.  If  great  bronchiectasic  cavities  lie  near  the  chest-wall,  they  may  give 
the  same  physical  signs  that  we  shall  learn  to  recognize  later  in  the  description  of 
tubercular  cavities.  Bronchiectases  lying  within  the  lung,  however,  are  often 
devoid  of  definite  physical  signs,  so  that  at  most  we  may  suspect  them  from  other 
symptoms,  like  the  peculiarities  of  the  sputum.  The  more  abundant  the  forma- 
tion of  bronchiectases  the  more  does  the  respiration  lose  its  vesicular  character 
and  become  harsh  and  finally  bronchial.  Inasmuch  as  there  is  usually  a  very 
considerable  secretion  of  mucus,  we  generally  find,  upon  auscultation,  abundant 
medium  and  even  coarse  moist  rales. 

The  expectoration  is,  as  a  rule,  very  abundant,  and  it  is  often  raised  "by 
mouthfuls."  On  standing,  it  exhibits  a  distinct  division  into  an  upper  layer  of 
serum  and  a  lower  of  pus.  It  usually  has  a  stale,  sweetish  odor,  but  it  may  be 
foetid.  The  diagnosis  of  the  extensive  formation  of  bronchiectases  in  the  lungs  is 
usually  quite  easy.  In  order  to  avoid  confounding  it  with  chronic  tuberculosis, 
the  following  should  be  especially  considered :  In  bronchiectasis  the  patient  does 
not  present  a  true  cachexia ;  he  is  usually  somewhat  cyanotic  and  often  pale  at  the 
same  time.  The  terminal  phalanges  of  the  fingers  are  often  clubbed,  as  in  foetid 
bronchitis.  Fever  is  usually  absent,  unless  there  are  some  special  complications. 
The  expectoration  is  more  abundant  and  more  distinctly  stratified  than  is  often 
seen  in  tuberculosis ;  and,  most  important  of  all,  it  contains,  of  course,  no  tubercle 
bacilli. 

Since  bronchiectasis  may  give  rise  to  a  foetid  bronchitis,  and  since,  on  the  other 
hand,  as  we  have  said,  foetid  bronchitis  itself  often  leads  to  the  formation  of 
bronchiectasis,  we  can  understand  the  manifold  relations  and  changes  which  the 


166  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

two  forms  of  disease  described  may  furnish.  If  ulcerative  processes  arise  in  the 
wall  of  a  bronchiectasis,  they  may  give  rise  to  haemoptysis. 

The  further  course  of  bronchiectases  depends,  of  course,  upon  the  nature  of  the 
primary  affection.  The  cylindrical  dilatations  which  arise  after  a  severe  bron- 
chitis, as  happens  in  whooping-cough,  measles,  or  typhoid,  may  in  many  cases 
gradually  get  well;  but  recovery  from  saccular  bronchiectasis  by  a  process  of 
obliteration,-  if  it  occurs  at  all,  is  extremely  rare.  Nevertheless,  the  course  of  the 
disease  may  be  comparatively  benign,  since  the  affection  often  remains  circum- 
scribed, and  the  patient's  general  strength  and  nutrition  suffer  comparatively  little 
from  it.  Finally,  of  course,  severe  symptoms  arise,  either  from  insufficiency  of 
the  heart,  when  there  is  cyanosis,  dyspnoea,  or  oedema,  or  as  a  result  of  emphy- 
sema, tuberculosis,  gangrene,  or  extensive  lobular  pneumonia. 

The  treatment  is  never  directed  against  the  bronchial  dilatation  as  such,  but 
toward  its  causes  or  sequelae.  The  treatment  of  bronchiectasis,  therefore,  coin- 
cides with  the  treatment  of  chronic  bronchitis,  emphysema,  foetid  bronchitis, 
chronic  tuberculosis,  etc. 


CHAPTER  VII. 
STENOSIS   OF   THE   TRACHEA  AND   BRONCHI. 

1.  Tracheal  Stenosis. 

iEtiology. — Stenosis  of  the  trachea  may  be  caused  either  by  diseases  in  the 
vicinity  of  the  trachea,  or  by  diseases  of  the  trachea  itself.  The  first-named 
mode  of  origin  is  the  more  frequent.  To  this  are  due  all  the  stenoses  of  the 
trachea  from  compression.  Enlargements  of  the  thyroid  gland  from  simple 
struma  and  new  growths,  aneurisms  of  the  arch  of  the  aorta  and  of  the  in- 
nominate artery,  tumors  and  abscesses  in  the  anterior  mediastinum,  swelling  of 
the  lymph-glands  at  the  bifurcation  of  the  trachea,  abscesses  on  the  antei'ior  sur- 
face of  the  cervical  vertebrae,  etc.,  may  exert  so  great  a  pressure  on  the  trachea 
from  without  that  its  lumen  is  made  narrower.  Besides  the  direct  action  of  press- 
ure, in  most  cases,  a  gradual  atrophy  from  the  pressure  and  a  softening  of  the 
rings  of  cartilage  sometimes  plays  an  important  part,  according  to  Rose,  in  the 
occurrence  of  stenosis.  A  collapse  of  the  trachea  may  arise  from  this  "  flaccid 
softening,"  which  may  come  on  quite  suddenly,  and  may  cause  many  of  the  cases 
of  sudden  "scrofula  death." 

Changes  in  the  trachea  itself  leading  to  stenosis  are  quite  rare.  Cicatricial 
stenosis  as  a  result  of  syphilitic  ulcerations  is  relatively  the  most  frequent.  New 
growths  in  the  trachea  are  also  to  be  mentioned,  such  as  polypi  and  carcinomata, 
the  latter  almost  always  having  invaded  the  trachea  from  the  adjacent  parts. 
Very  rarely  acute  and  chronic  inflammatory  processes  like  perichondritis  lead  to 
a  swelling  of  the  mucous  membrane  sufficient  to  cause  stenosis.  In  conclusion, 
we  may  mention  that  stenosis  of  the  trachea  may  be  due  to  the  presence  of  foreign 
bodies. 

Symptoms. — If  the  stenosis  is  so  extreme  that  there  is  a  real  hindrance  to  respi- 
ration, a  very  striking  modification  of  the  breathing  occurs.  It  is  difficult  and 
labored,  and  is  performed  only  by  the  help  of  the  accessory  muscles.  Both  expi- 
ration and  inspiration  are  protracted,  long  drawn,  and  accompanied  by  a  loud 
stridor.  In  many  cases  inspiration  is  more  difficult  than  expiration,  so  that  there 
is  accordingly  a  preponderating  inspiratory  dyspnoea,  and  the  number  of  respira- 
tions a  minute  is  diminished.     If  the  entrance  of  air  into  the  lungs  is  incomplete 


STENOSIS  OF  THE  TRACHEA  AND  BRONCHI.  Id 

in  spite  of  the  lengthening  of  the  respirations,  we  see  an  inspiratory  retraction  of 
the  lower  part  of  the  thorax,  and  sometimes  of  the  throat  and  the  supra-clavicular 
fossae.  In  tracheal  stenosis  the  larynx,  however,  shows  little  or  no  to-and-fro 
movement  on  respiration.  This  fact  is  of  value  in  diagnosis  in  distinguishing 
tracheal  from  laryngeal  stenosis,  for  in  the  latter  the  respiratory  movements  of 
the  larynx  are  quite  well  marked. 

We  sometimes  notice  in  the  pulse  during  inspiration  a  marked  fall  in  tension 
and  in  the  height  of  the  pulse-wave,  the  pulsus  paradoxus.  With  the  sphygmo- 
graph  we  can  show  still  more  plainly  the  changes  in  blood -pressure,  which  vary 
quite  markedly  with  the  respiration.  The  frequency  of  the  pulse  is  usually  a 
little  increased,  but  sometimes  it  is  diminished. 

The  symptoms  of  the  disease  just  described  may  form  so  characteristic  a 
picture  that  we  can  recognize  it  at  the  first  glance.  More  precise  information 
as  to  the  seat  of  the  stenosis,  or  the  accurate  differentiation  of  tracheal  stenosis 
from  the  very  similar  picture  presented  by  laryngeal  stenosis,  demands  a  direct 
laryngoscopic  examination  of  the  larynx  and  trachea,  which,  of  course,  is  hardly 
practicable  in  a  patient  with  a  high  degree  of  dyspnoea. 

2.  Bronchial  Stenosis. 

Narrowing  of  a  primary  bronchus,  which  is  the  only  form  to  be  mentioned 
here,  arises  most  frequently  as  a  result  of  the  presence  of  foreign  bodies.  These 
may  enter  the  air-passages  by  means  of  a  deep  inspiration  while  eating,  or  during 
sleep.  We  know  that  foreign  bodies  get  into  the  right  bronchus,  which  is  wider, 
somewhat  more  frequently  than  they  do  into  the  left.  Stenosis  of  the  main 
bronchi  from  pressure  also  arises  from  aneurisms  of  the  aorta,  mediastinal 
tumors,  enlarged  bronchial  lymph-glands,  etc.  Stenosis  of  the  left  bronchus 
from  the  pressure  of  the  greatly  dilated  left  auricle  has  been  observed  in  mitral 
stenosis. 

The  symptoms  are  not  equally  distinct  in  all  cases,  and  they  depend  upon  the 
shutting  off  of  the  corresponding  part  of  the  lung.  The  dyspnoea  is  usually  very 
evident,  especially  in  acute  cases.  The  respiratory  excursions  are  much  less  on 
the  affected  side  than  on  the  sound  side.  The  percussion-note,  indeed,  remains 
clear,  but  the  vesicular  respiratory  murmur  disappears,  and  instead  of  it  we  some- 
times hear  over  the  whole  side  a  loud  whistling  or  humming  sound,  the  vibration 
of  which  can  in  some  cases  be  felt  by  the  hand  applied  to  the  chest- wall.  The 
vocal  fremitus  is  diminished  on  the  affected  side.  A  vicarious  emphysema  soon 
develops  in  the  other  lung. 

Lobular  pneumonia  frequently  develops  as  a  result  of  the  entrance  of  foreign 
bodies  into  a  bronchus,  because  the  agents  of  inflammation  have  entered  at  the 
same  time  with  these  bodies,  and,  as  the  expectoration  can  be  evacuated  only  with 
difficulty,  and  hence  is  more  or  less  stagnant,  these  irritants  can  readily  establish 
themselves  in  it.  In  stenosis  from  pressiire  the  character  of  the  disease  may  of 
course  be  modified  in  many  ways  by  the  primary  disease. 

The  prognosis  and  treatment  of  tracheal  and  bronchial  stenosis  depend  entirely 
upon  the  nature  of  the  primary  disease.  General  statements  as  to  treatment, 
therefore,  need  not  be  given  here.  A  direct  mechanical  treatment  of  tracheal 
stenosis  in  appropriate  cases,  such  as  cicatricial  stenosis,  may  be  undertaken  ac- 
cording to  the  different  modes  of  dilatation  above  enumerated.  The  methods 
for  removing  foreign  bodies  from  the  larger  air-passages  belong  to  the  domain  of 
surgery.  The  employment  of  an  emetic  has  met  with  distinct  success  in  such 
cases,  but  it  is  not  without  danger,  for  the  foreign  body  may  wedge  itself  into  the 
glottis  during  the  act  of  vomiting  and  result  in  the  danger  of  instant  suffocation. 


168  DISEASES  OF  THE  EESPIEATOEY  ORGANS. 


CHAPTER  VIII. 

BRONCHIAL  ASTHMA. 

(Nervous  Asthma.) 

Bronchial  asthma  is  a  disease  clinically  well  chai'acterized,  but  astiologically 
it  is  probably  not  quite  a  distinct  affection.  Its  cbief  symptom,  consists  of  marked 
paroxysmal  attacks  of  dyspnoea.  The  cause  of  the  dyspnoea  is  not  to  be  sought 
in  any  coarse  factor  that  can  be  demonstrated  anatomically,  but  it  is  probably 
due,  at  least  in  part,  to  some  abnormal  condition  of  nervous  irritation.  The  chief 
theories  as  to  the  origin  of  the  asthmatic  attacks  will  be  given  further  on.  The 
disease  is  decidedly  more  common  in  men  than  in  women,  and  it  is  not  very  rare 
even  in  children. 

Symptoms  and  Course  of  the  Disease.—"  Nervous  "  bronchial  asthma  consists, 
in  its  purest  form,  of  attacks  of  shortness  of  breath,  which  come  on  in  persons  who 
are  otherwise  quite  well,  with  varying  frequency  and  varying  duration,  partly 
from  some  special  cause,  and  partly  without  any  discoverable  reason.  In  the 
intervals  between  the  attacks  the  patients  are  completely  well,  and  do  not  show 
the  slightest  signs  of  any  disease  of  the  respiratory  or  circulatory  organs. 

The  asthmatic  attack  either  begins  quite  suddenly,  or  it  is  preceded  for  a  shorter 
or  longer  period  by  prodromata.  These  consist  in  a  general  feeling  of  discomfort, 
in  abnormal  sensations  in  the  larynx  or  epigastrium,  sometimes  in  remarkably 
frequent  gaping,  and  often  in  a  marked  coryza  associated  with  a  good  deal  of 
secretion  and  frequent  sneezing  (compare  the  relation  between  many  attacks  of 
asthma  and  diseases  of  the  nose,  given  below).  The  attack  begins  in  most  cases 
at  night.  The  patient  wakes  up  with  an  intense  feeling  of  pressure  and  anxiety. 
Sometimes  he  complains  of  a  feeling  of  pain  in  the  chest.  He  has  to  sit  up 
straight,  and  in  severe  cases  even  to  get  out  of  bed.  He  often  hurries  to  an  open 
window  in  order  to  "get  air."  His  expression  is  anxious;  his  skin  becomes  pale 
and  cyanotic,  and  sometimes  is  covered  with  a  cold  sweat.  The  respiration,  too 
is  altered  in  a  very  peculiar  and  characteristic  way.  Both  inspiration  and  expira- 
tion are  almost  always  accompanied  by  a  high-pitched  whistling  sound,  audible  at 
a  distance.  Both  respiratory  acts  are  labored,  requiring  the  aid  of  the  accessory 
muscles.  On  inspiration,  only  the  upper  part  of  the  thorax  is  elevated  to  any 
extent.  We  see  in  the  neck  the  inspiratory  contraction  of  the  sterno-cleido- 
mastoids,  the  scaleni,  etc.  Still  more  striking,  however,  is  the  labored,  panting, 
long-protracted  expiration,  during  which  the  abdominal  muscles  are  contracted 
to  a  board-like  hardness.  We  therefore  recognize  the  disturbance  of  respiration 
in  asthma  as  essentially  an  expiratory  dyspnoea.  The  frequency  of  respiration  is 
in  many  cases  normal,  or  even  somewhat  diminished,  yet  we  have  repeatedly 
counted  thirty  or  forty  respirations  a  minute. 

On  physical  examination  of  the  lungs  during  the  paroxysm,  we  find  the  per- 
cussion-note over  them  normal  or  even  strikingly  loud  and  deep — the  "box-tone." 
The  lower  boundary  of  the  lung  is  usually  found  one  or  two  intercostal  spaces 
lower  than  normal.  We  accordingly  have  to  do  with  an  abnormally  low  position 
of  the  diaphragm,  with  an  acute  emphysema.  On  auscultation,  whistling  and 
creaking  sounds,  which  quite  obscure  the  vesicular  murmur,  are  heard  over  most 
of  the  lung,  especially  during  the  long  expirations.  In  many  places,  indeed,  the 
respiratory  murmur  is  entirely  absent,  or  we  hear  only  a  low  whistle  on  expira- 
tion. Toward  the  end  of  the  paroxysm  the  noises  become  deeper  and  more  boom- 
ing, and  sometimes  we  hear  a  few  moist  rales. 

In  brief  paroxysms  there  may  be  scarcely  any  cough  or  expectoration.     In 


BRONCHIAL  ASTHMA.  169 

most,  particularly  in  the  tedious,  cases,  there  is,  however,  a  scanty  tough  mucous 
expectoration.  In  this  are  found,  beside  the  ordinary  constituents  of  simple 
bronchitic  sputum,  larger  or  smaller  numbers  of  very  characteristic  clumps. 
These  may  be  yellow  or  greenish-yellow,  or,  on  the  other  hand,  gray.  The  yellow- 
ish clumps,  which  are  usually  very  tough,  and  often  consist  of  a  clump  of  thready 
matter,  represent  swollen  and  fatty-degenerated  pus  corpuscles,  between  winch 
are  very  frequently  interspersed  a  considerable  number  of  pointed  octahedral 
crystals.  These  crystals  were  first  described  by  Ley  den  in  the  sputum  of  asth- 
matic patients,  and  are  usually  termed  asthma  crystals  (see  Fig.  22).  Chemically 
they  are  identical  with  "  Charcot's  crystals,"  which  are  found  in  the  leukamiic 
spleen,  the  bone  marrow,  and  the  semen,  and  they  probably  represent  the  phos- 
phoric-acid salt  of  a  peculiar  base  (Schreiner's  base,  C2H5N).  As  soon  as  the 
paroxysms  cease  the  number  of  crystals  in  the  sputum  usually  begins  to  diminish 
rapidly,  and  it  is  often  possible  to  observe  in  them  evident  tokens  of  disintegra- 
tion. Often,  also,  numerous  ciliated  epithelial  cells  are  found,  in  addition  to  the 
crystals,  in  the  yellow  masses.  The  gray  plugs  in  the  sputum  of  asthmatic 
patients  consist  mainly  of  clumps  of  thready  mucus,  and  contain  the  peculiar 
"spirals"  which  were  first  described  by  Ungar  and  by  Curschmann.  Many  of 
these  spiral  threads  are  visible  to  the  naked  eye,  but  others  demand  the  micro- 
scope for  their  recognition,  through  which  they  are  seen  as  brilliant  forms  com- 
posed entirely  of  various  sized  bands  and  threads  collected  in  spirals  (see  Fig.  22). 
Sometimes  a  brilliant  central  thread  of  small  diameter  is  seen  in  the  midst  of  the 
spiral.  Around  the  spirals  are  found  round  cells,  drops  of  fat  and  myeline,  epi- 
thelium, and,  according  to  Lewy,  frequently  also  numerous  epithelial  cells  from 
the  pulmonary  alveoli.  As  to  the  precise  way  in  which  the  spirals  and  their 
central  thread  develop,  the  question  is  not  yet  settled,  but  it  is  certain  that  the 
spirals  represent  casts  of  the  minutest  branches  of  the  bronchi,  and  therefore 
indicate  the  existence  of  a  peculiar  disease  of  the  terminal  bronchial  twigs  (see 
below).  It  should  be  added  that  sometimes  also  the  microscope  reveals  in  the 
sputum  crystals  of  oxalate  of  lime  (Ungar)  and  of  phosphate  of  lime  (Lewy). 

The  pulse  is  usually  accelerated  during  the  asthmatic  paroxysm;  the  bodily 
temperature  is  normal,  or  sometimes  even  subnormal.  In  asthmatic  patients 
who  have  protracted  attacks  we  have  repeatedly  seen  a  slight  febrile  movement 
up  to  about  102°  (39°  C). 

The  duration  of  the  asthmatic  paroxysm  is  very  different  in  individual  cases, 
as  has  already  been  said.     Sometimes  it  lasts  only  a  few  hours,  but  sometimes 


Fig.  22.— Asthma  crystals  and  Cursehmann's  spirals  (a,  central  fiber). 

it  lasts  several  days,  and  even  weeks.     The  attacks  of  protracted  asthma  are  not 
very  rare.     Marked  exacerbations  and  remissions  of  the  disease  usually  alternate 


170  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

in  them.  The  frequency  of  the  paroxysms  in  ordinary  asthma  also  varies  exceed- 
ingly. Sometimes  they  come  on  almost  every  night,  and  then  there  are  long 
pauses  of  months  and  years,  so  that  we  can  not  make  any  general  statements  as 
to  the  course  of  the  disease.  Definite  recoveries  are  quite  rare ;  they  are  most 
frequent  in  children. 

Although  patients  with  the  form  of  pure  essential  asthma  which  we  have  so 
far  described  .seem  perfectly  well  in  the  intervals  between  the  attacks,  there  is 
also  a  symptomatic  asthma.  This  is  seen  chiefly  in  patients  with  emphysema  and 
chronic  bronchitis.  The  term  "  symptomatic  asthma,"  however,  can  be  used  only 
when  the  attacks  actually  show  the  symptoms  of  pure  asthma,  and  when  the 
dyspnoea  which  occurs  in  them  has  no  relation  to  the  anatomical  lesions  present. 
In  such  cases  it  is  often  hard  to  decide  whether  the  existing  emphysema  and 
chronic  bronchitis  are  really  the  primary  disease,  or  the  result  of  the  asthma. 
There  is  no  doubt  but  that  a  secondary  emphysema  of  the  lungs  may  develop  as 
a  result  of  frequent  and  protracted  asthmatic  attacks.  The  attacks  of  dyspnoea, 
which  come  on  in  chronic  affections  of  the  heart  and  blood-vessels — cardiac 
asthma  {vide  infra) — depend  upon  other  causes  than  the  peculiar  bronchial 
asthma,  and  should  not  be  classed  with  it. 

Theories  as  to  the  Origin  of  Asthma.— iEtiology.— The  peculiarity  of  the  asth- 
matic symptoms  has  given  rise  to  numerous  theories  as  to  the  origin  of  asthma, 
yet  none  of  them  have  obtained  general  recognition  up  to  the  present  time. 
Many  authors,  like  Weber,  Störck,  and  Fräntzel,  seek  the  underlying  cause  of 
asthma  in  an  acute  swelling  of  the  bronchial  mucous  membrane,  as  a  result 
either  of  a  sudden  dilatation  of  the  blood-vessels  arising  from  nervous  influences 
or  of  a  very  acute  catarrh.  Wintrich  and  Bamberger  have  advanced  the  theory 
that  asthma  consists  in  a  tonic  spasm  of  the  diaphragm,  by  which  the  diaphragm 
is  kept  motionless  in  a  fixed  inspiratory  position ;  but  it  is  at  once  plain  that  such 
a  condition  can  at  least  not  play  the  chief  part  in  the  occurrence  of  asthma,  for 
we  can  usually  feel  the  respiratory  movements  of  the  diaphragm  quite  plainly 
during  the  paroxysm.  It  should  be  stated  that  Riegel,  who  is  the  latest  champion 
of  the  theory  of  diaphragmatic  spasm,  is  of  the  opinion  that  there  is  not  a  com- 
plete tetanic  spasm  of  the  diaphragm,  but  merely  a  superexcitation  of  the  phrenic 
nerve,  and  that  the  excursions  of  the  diaphragm  are  not  completely  inhibited. 

The  theory  long  ago  advanced  by  Trousseau,  the  chief  advocate  of  which  of 
late  is  Biermer,  is  the  most  probable  one,  and  is  now  generally  accepted,  namely, 
that  the  spastic  nervous  element,  which  is  not  wholly  to  be  disregarded  in  any 
explanation  of  bronchial  asthma,  consists  of  a  tonic  spasm  of  the  muscles  of  the 
smaller  bronchi.  The  tonic  contraction  of  the  smaller  bronchi  explains  the 
whistling  sounds  that  are  heard.  A  marked  hindrance  to  respiration  is  set  up 
which  can  be  more  easily  overcome  by  the  inspiratory  suction  of  the  thorax  than 
by  the  expiratory  pressure.  Since  the  latter  acts  not  only  upon  the  alveoli,  but 
also  upon  the  lesser  bronchi  themselves,  the  closure  of  the  hronchi  upon  expira- 
tion is  still  more  marked.  The  air  which  is  drawn  into  the  alveoli  can  conse- 
quently get  out  again  only  imperfectly,  and  this  explains  the  expiratory  dysp- 
noea, the  emphysema  that  soon  occurs,  and  the  low  position  of  the  diaphragm. 
The  acceptance  of  this  theory  of  bronchial  spasm  also  readily  explains  the  often 
sudden  onset,  and  just  as  sudden  cessation,  of  the  asthmatic  attack. 

If  we  inquire  further,  however,  into  the  cause  of  the  occurrence  of  the  bron- 
chial spasm,  only  a  very  indefinite  answer  can  be  given;  for  little  is  said  by 
answering  that  asthma  is  a  neurosis  of  the  vagus.  Many  facts  make  it  very  prob- 
able that  the  spasm  is  of  reflex  origin,  at  least  in  many  cases.  Leyden  has 
expressed  the  suspicion  that  the  irritation  of  the  mucous  membrane  by  the  pointed 
crystals,  which  he  discovered,  gives  rise  to  the  spasm.     It  may  be  said  in  oppo- 


BBONCHIAL  ASTHMA.  171 

sition  to  this,  however,  that  the  "asthma  crystals"  are  sometimes  found  in  the 
sputum  of  patients  with  emphysema  who  have  no  asthmatic  symptoms,  and  also 
that  in  asthmatic  patients  the  severity  and  duration  of  the  attacks  stand  in  no 
constant  relation  to  the  number  of  the  crystals.  Nor  can  the  above-pictured 
spirals  be  regarded  as  the  cause  of  the  paroxysms  of  asthma,  since  they  likewise 
occur  in  other  diseases  of  the  minutest  branches  of  the  bronchi — for  example,  they 
are  not  very  rare  in  croupous  pneumonia. 

The  fact  lately  corroborated  by  numerous  observations  by  Voltilini,  B. 
Fränkel,  Hack,  and  others,  is  very  important — namely,  that  the  asthmatic  par- 
oxysm is  sometimes  of  reflex  origin,  starting  from  some  disease  of  the  nasal 
mucous  membrane.  "We  find  quite  often,  for  instance,  that  asthmatic  patients 
are  suffering  from  chronic  diseases  of  the  nose,  like  chronic  catarrh,  nasal  polypi, 
and  especially  the  enlargement  of  the  so-called  erectile  bodies  of  one  or  more 
turbinated  bones,  and  that  after  their  removal  the  asthma  disappears.  In  this 
connection  may  be  cited  the  noteworthy  fact  that  many  asthmatic  patients  have 
an  attack  brought  on  by  certain  odors,  for  example,  at  the  smell  of  freshly 
roasted  coffee,  or  of  ipecacuanha.  Trousseau,  who  suffered  from  asthma  himself, 
always  had  an  attack  on  smelling  violets.  It  is  doubtful  whether  a  pure  bron- 
chial asthma  can  have  a  reflex  origin  from  other  distant  organs.  The  connection 
between  asthma  and  diseases  of  the  pharynx,  or  hypertrophy  of  the  tonsils, 
is  extremely  probable  in  some  cases,  but  the  statements  as  to  the  occurrence 
of  asthmatic  paroxysms  in  diseases  of  the  stomach  ("dyspeptic  asthma"),  of 
the  intestine,  or  of  the  female  sexual  organs,  are  to  be  taken  only  with  great 
reserve.  We  usually  have  to  do  here  with  a  confusion  between  pure  asthma 
and  other  conditions  of  dyspnoea — nervous  dyspnoea,  conditions  of  cardiac  weak- 
ness, etc. 

In  a  large  number  of  cases — which  seem  to  us  to  be  most  characteristic — 
the  disease  can  be  explained,  in  our  opinion,  only  by  the  hypothesis  of  a  peculiar 
primary  disease  of  the  bronchial  mucous  membrane,  particularly  affecting  the  ter- 
minal twigs  of  the  smallest  bronchi,  and  whose  special  feature,  somewhat  like  the 
spasm  of  the  glottis  in  whooping-cough,  consists  in  the  occurrence  of  a  reflex 
bronchial  spasm.  The  whole  type  of  the  disease  and  the  peculiarities  of  the  ex- 
pectoration, the  spirals,  and  crystals,  furnish  unequivocal  testimony  for  this 
theory  of  asthma.  Curschmann  therefore  claims  that  the  anatomical  basis  of 
these  cases  is  an  exudative  bronchiolitis.  We  think  that  "  asthmatic  bronchiolitis  " 
is  the  most  fitting  name  for  such  cases  of  asthma  as  are  not  found  to  be  dependent 
upon  disorders  of  the  nose  or  similar  causes. 

The  observation,  often  made,  that  many  asthmatic  patients  have  attacks  only 
when  in  certain  places,  and  are  quite  free  from  them  in  others,  is  very  remarkable. 
They  sometimes  have  an  attack  at  every  change  of  place.  In  conclusion,  it  may 
be  mentioned  that  in  some  cases  a  distinct  hereditary  predisposition  to  asthma 
has  been  observed,  and  that  asthma  sometimes  occurs  in  families  with  a  general 
neurotic  tendency. 

Diagnosis.— This  is  usually  easy  if  we  pay  careful  attention  to  all  the  symp- 
toms and  to  the  whole  course  of  the  disease.  Other  conditions  which  may  lead  to 
dyspnoea  are  of  course  to  be  excluded  by  a  careful  examination  of  the  chest. 
Attacks  of  spasm  of  the  glottis  and  of  paralysis  of  the  openers  of  the  glottis  are  to 
be  differentiated  from  bronchial  asthma  by  the  predominance  of  inspiratory 
dyspnoea  as  well  as  by  other  signs.  And  in  cardiac  asthma  and  the  manifold 
varieties  of  respiratory  spasm  and  neurotic  angina,  such  as  are  seen  especially  in 
hysteria,  not  only  are  the  other  attendant  symptoms  different  from  those  seen 
in  genuine  bronchial  asthma,  but  the  very  dyspnoea  itself  is  usually  of  quite 
another  variety. 


172  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

Prognosis. — There  is  hardly  ever  any  immediate  danger  to  life  even  in  the 
most  intense  asthmatic  paroxysms,  hut  permanent  recovery  is  rare,  since  even 
after  long  intervals  the  attacks  may  finally  return.  The  chief  danger  in  severe 
and  protracted  cases  lies  in  the  development  of  a  pulmonary  emphysema  with  its 
further  consequences. 

Treatment. — In  every  case  of  asthma  the  first  thing  to  he  thought  of  is 
whether  there  is  not  a  definite  cause  whose  removal  may  cure  the  disease.  In  this 
connection  we  should  examine  the  nose  carefully,  since  numerous  observations 
have  recently  shown  that  a  previously  existing  asthma  may  permanently  disap- 
pear after  the  treatment  of  some  nasal  disease  which  may  be  present,  like  the 
removal  of  polypi,  the  destruction  of  the  erectile  bodies  by  the  galvano-cautery, 
etc. 

If  we  can  not  satisfy  the  causal  indication  in  this  way,  we  should  always  try 
next  a  remedy  which  must  pass  for  a  direct  specific  against  certain  forms  of 
asthma — iodide  of  potassium.  In  doses  of  twenty  to  forty-five  grains  a  day  (grm. 
l'ö-S'O),  which  can  be  increased  if  necessary,  this  usually  causes  a  rapid  improve- 
ment, which  of  course  is  not  always,  although  it  is  frequently,  permanent.  If 
iodide  of  potassium  has  been  used  in  vain,  we  must  turn  to  the  other  remedies 
which  have  been  employed  against  asthma,  although  their  action  is  often  quite 
uncertain.  We  may  mention  here  the  nitrite  of  sodium  (two  parts  in  one  hun- 
dred and  twenty  of  water,  two  to  three  teaspoonfuls  a  day),  and  nitro-glycerine, 
which  has  an  analogous  action  (twenty  drops  of  a  one-per-cent.  alcoholic  solution 
in  six  and  a  half  ounces  (grm.  200)  of  water,  a  tablespoonful  two  or  three  times  a 
day) ;  also  quinine,  bromide  of  potassium,  belladonna,  atropine,  arsenic,  etc.  In 
some  cases  pneumatic  treatment,  such  as  the  inhalation  of  compressed  air,  has 
been  successful,  and  sometimes,  too,  electricity  (galvanization  and  faradization  of 
the  neck),  or  hydrotherapy,  has  been  claimed  to  give  relief.  Change  of  climate 
may  be  of  distinct  service.  Many  patients  bear  the  sea-air  well,  while  with  others 
mountain  traveling  exerts  a  favorable  influence. 

In  severe  cases  a  special  symptomatic  treatment  of  the  attack  itself  is  often 
necessary.  Narcotics  are  without  doubt  the  most  effective,  especially  chloral  and 
morphine.  In  severe  attacks  we  can  not  avoid  injections  of  morphine,  but  we 
must  always  be  cautious  in  order  that  the  patient  may  not  form  the  habit  of 
using  this  to  excess.  Germain  See  has  lately  strongly  advocated  inhalations  of 
Pyridin.  Of  this,  about  one  drachm  (4  to  5  grm.)  is  shaken  into  a  saucer  and 
the  fumes  are  inhaled  three  times  a  day  for  fifteen  to  thirty  minutes.  Inhalations 
of  chloroform  and  ether  are  also  much  employed.  Among  other  useful  remedies 
and  devices  we  may  mention  mustard  plasters  to  the  chest  and  calves,  putting 
the  hands  and  feet  into  hot  water,  inhalations  of  nitrite  of  amyl,  inhalations  of 
turpentine  or  ammonia  vapor;  also  the  often-used  fumigation  with  saltpeter  paper 
— unsized  paper  dipped  in  a  concentrated  solution  of  nitrate  of  potassium  and 
dried.  The  stramonium  cigarettes  to  be  had  in  most  drug-stores  are  much  praised; 
or  the  patient  may  smoke  stramonium  or  belladonna  leaves  which  have  pre- 
viously been  dipped  in  a  solution  of  saltpeter  and  then  dried.  Among  internal  reme- 
dies we  may  mention  tincture  of  lobelia,  formerly  much  used,  and  also  the 
remedy  lately  employed  by  Penzoldt,  the  tincture  of  quebracho,  a  tablespoonful 
pure  or  in  some  mucilaginous  vehicle. 

[Potassic  iodide  is  more  likely  to  prevent  recurrence  if  it  is  given  continuously, 
for  several  months  at  least,  and  it  should  not  be  thrown  aside  as  useless  until  it 
has  been  pushed  to  the  limit  of  toleration  without  avail.  A  convenient  form  of 
administration  is  in  saturated  aqueous  solution,  a  minim  of  which  represents 
about  a  grain  of  the  drug. 

The  syrup  of  hydriodic  acid  may  be  substituted  for  potassic  iodide  in  cases 


PULMONAEY  EMPHYSEMA.  173 

of  intolerance  of  the  latter.  Grindelia  robusta,  a  drachm  of  the  fluid  extract 
three  or  four  times  a  day,  serves  sometimes  to  prevent  recurrence  of  attacks. 
Marked  alleviation  of  the  paroxysms  is  often  obtained  from  the  inhalation  of 
fifteen  to  thirty  drops  of  the  iodide  of  ethyl.] 


SECTION   IV. 

Diseases  of  the  Lungs. 


CHAPTER  I. 

PULMONARY    EMPHYSEMA. 

(Alveola?'  JEctasis.     Increased  Volume  of  the  Lungs.) 

Nature  and  JEtiology  of  the  Disease.— Pulmonary  emphysema,  the  abnormal 
inflation  of  the  lungs,  is  one  of  the  commonest  pulmonary  affections.  It  either 
develops  in  separate  parts  of  the  lung-,  in  which  case  it  is  subordinate  to  other 
pathological  changes  which  co- exist  in  the  lungs,  or  it  involves  almost  the  whole 
extent  of  both  lungs,  and  then  presents  the  symptoms  of  a  characteristic  affection, 
which  it  is  usually  easy  to  recognize. 

The  essence  of  pulmonary  emphysema,  the  condition  from  which  most  symp- 
toms are  immediately  derived,  is  the  loss  of  elasticity  in  the  lungs.  If  we  com- 
pare the  sound  lung  with  its  normal  elastic  force  to  a  new  and  very  tense  rub- 
ber band,  the  emphysematous  lung  must  be  compared  to  an  old  and  lax  band  that 
is  stretched  and  pulled  out.  We  therefore  see  why  the  emphysematous  lung  takes 
up  a  greater  space  than  the  sound  one,  for,  on  account  of  its  lack  of  elasticity,  it 
can  no  longer  contract  to  its  former  volume.  We  may  thus  call  emphysema  a 
permanent  inspiratory  distention  of  the  lung  from  which  it  can  no  longer  return 
to  its  expiratory  condition.  If  we  open  the  thorax  of  a  subject  with  normal  lungs, 
they  contract,  as  is  well  known,  but  the  emphysematous  lungs  remain  in  their 
inflated  condition  after  the  thorax  has  been  opened. 

If  we  inquire  into  the  factors  which  cause  this  loss  of  elasticity  in  the  lung,  we 
find  that  they  are  the  same  kind  of  influences  which  tend  to  diminish  the  elas- 
ticity of  any  other  elastic  body.  As  a  rubber  band,  by  much  pulling  and  stretching, 
gradually  gets  longer  and  less  elastic,  so  the  lungs,  as  a  result  of  then  abnormally 
frequent  and  severe  distention,  gradually  become  inelastic  and  emphysematous. 
The  normal  traction  of  inspiration,  which  is  continually  making  new  demands  on 
the  elastic  powers  of  the  lungs,  finally  leads  to  a  loss  of  elasticity  in  them.  In 
advanced  age  most  lungs  become  more  or  less  inelastic.  The  lungs  of  an  old 
man  are  like  an  elastic  band,  which  has  done  its  work  for  years  but  which  has 
finally  become  yielding.  We  therefore  class  the  emphysema  of  the  lungs  in  old 
age  rather  among  the  states  of  involution  such  as  develop  in  almost  all  organs  in 
advanced  life,  than  among  special  pathological  changes.  We  distinguish,  more- 
over, most  of  the  lungs  with  senile  emphysema  from  other  emphysematous  lungs 
by  the  fact  that  their  volume  as  a  whole  is  not  increased,  but  is  rather  diminished 
below  that  of  the  healthy  lung,  since  we  find  in  them  the  extensive  atrophic 
processes  of  old  age. 

The  condition  becomes  pathological,  however,  if  the  elasticity  of  the  lung  is 
deficient  in  earlier  years  and  without  exposure  to  the  action  of  the  special  in- 
jurious influences  which  will  soon  be  mentioned.     In  such  cases  of  emphysema, 


174  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

developing-  in  middle  life  or  even  in  youth,  the  idea  of  a  congenital  weakness  of 
the  elastic  elements  in  the  lungs  can  not  he  set  aside.  It  probably  consists  in  a 
quantitative  or  a  qualitative  defect  of  the  elastic  tissue.  Some  observations  seem 
to  corroborate  the  statement  that  a  disposition  to  emphysema  may  be  present  in 
several  members  of  the  same  family. 

If  a  lung  whose  elasticity  is  previously  subnormal  can  not  persistently  satisfy 
the  ordinary  demands  upon  it,  a  normal  lung,  on  the  other  hand,  also  loses  its 
elasticity  if  the  demands  made  upon  it  are  greater  than  it  can  perform.  This  is 
the  reason  why  pulmonary  emphysema  is  in  part  considered  a  disease  arising 
from  the  occupation.  We  mean  here  not  only  tbose  influences  which  lead  to 
chronic  bronchitis  and  thus  later  to  emphysema  (vide  infra),  but  more  especially 
the  abnormal  demands  upon  the  lungs  in  all  those  callings  which  necessitate 
severe  physical  labor.  We  must  not  only  regard  the  deeper  and  more  rapid  res- 
pirations, but  also  the  increased  pressure  on  expiration  to  which  the  lungs  are 
often  exposed  in  the  raising  of  heavy  weights,  etc.  This  explains  the  great  fre- 
quency of  emphysema  in  the  laboring  classes,  and  also  its  greater  frequency  in 
men  than  in  women.  Beside  this,  we  must  add  that  in  certain  callings,  like  glass- 
blowing  and  horn-blowing,  the  overstraining  of  the  lungs  is  much  more  direct. 
In  all  such  cases  emphysema  may  be  termed  simply  a  premature  exhaustion  of 
the  lungs. 

In  very  many  cases  emphysema  develops  as  a  result  of  other  diseases  of  the 
lung,  and  especially  as  a  result  of  chronic  bronchitis.  Dry  catarrh  of  the  middle 
and  finer  bronchi  when  of  long  duration  leads,  as  a  rule,  to  pulmonary  emphy- 
sema. The  abnormal  mechanical  influences  to  which  the  lungs  are  thus  exposed 
act  both  in  inspiration  and  in  expiration.  Since  the  entrance  of  air  to  the  alveoli 
is  rendered  more  difficult  by  the  swelling  of  the  mucous  membrane  in  the  smaller 
bronchi,  abnormally  deep  and  strong  inspirations  are  necessary,  with  a  marked 
expansion  of  the  alveoli,  in  order  to  draw  a  sufficient  quantity  of  air  into  the 
alveoli.  The  alveolar  walls  are  therefore  exposed  to  an  abnormal  traction  at  each 
inspiration.  On  expiration,  a  pressure  from  within,  which  is  perhaps  even  more 
injurious,  acts  on  the  alveoli.  The  ordinary  expiration,  which  usually  needs  only 
the  elastic  power  of  the  lungs,  is  not  sufficient  in  chronic  bronchitis  to  drive  the 
air  out  of  the  alveoli  through  the  narrowed  bronchi.  Thus  arise  the  difficulty 
and  delay  in  expiration  which  are  present  in  chronic  bronchitis,  and  which  lead 
to  the  active  participation  of  the  muscles  of  expiration,  the  abdominal  group  of 
muscles.  On  forced  expiration,  however,  the  pressure  does  not  act  simply  upon 
the  contents  of  the  alveoli,  but  much  more  upon  the  smaller  bronchi  themselves. 
The  channel  of  exit  for  the  air  from  the  alveoli,  therefore,  becomes  still  narrower. 
Since  the  air  can  not  escape,  the  pressure  within  the  alveoli  is  raised  by  the  efforts 
at  expiration,  and  the  alveolar  wall  is  thus  again  abnormally  expanded.  The 
cough,  which  is  often  present  in  chronic  bronchitis,  is  a  further  factor,  which 
acts  in  a  precisely  similar  injurious  fashion.  The  attacks  of  coughing  begin  with 
a  forced  contraction  of  the  muscles  of  expiration,  which  follows  the  closure  of  the 
glottis.  Until  the  glottis  opens,  therefore,  the  lower  parts  of  the  lung  especially 
are  put  under  strong  pressure.  The  air  in  them,  which  can  not  escape  outward, 
is  driven  into  the  upper  parts  of  the  lung,  and  there  leads  to  expansion  of  the 
alveoli,  and  finally  to  emphysema. 

We  accordingly  see  that  a  number  of  injurious  influences  co-operate  in  the 
gradual  development  of  emphysema  from  chronic  bi'onchitis,  and  that,  sooner  or 
later,  these  influences  have  as  their  result  the  gradual  dilatation  of  the  lungs. 
Here,  too,  we  must  bear  in  mind  the  individual  differences  in  tbe  resisting  power 
of  the  lungs. 

Conditions  precisely  similar  to  those  in  chronic  bronchitis  occur  in  other  dis- 


PULMONARY  EMPHYSEMA.  175 

eases,  and  lead  in  like  manner  to  pulmonary  emphysema.  We  very  often  see  the 
development  of  emphysema  in  severe  and  persistent  whooping-cough.  The  worst 
factor  here,  besides  the  existing-  bronchitis,  is  the  frequent  paroxysms  of  coughing'. 
We  have  already  mentioned,  in  the  description  of  bronchial  asthma,  both  the 
acute  emphysema,  which  occurs  during  the  attacks,  and  the  final  development  of 
a  permanent  emphysema. 

In  conclusion,  we  must  here  consider  a  theory  advanced  by  Freund,  which 
would  make  the  development  of  an  emphysema  dependent  upon  a  "  primary  rigid 
dilatation  of  the  thorax."  It  is  indeed  conceivable  that  from  certain  pathological 
changes  in  the  costal  cartilages,  as  Freund  claims,  a  thorax,  which  had  become 
rigid  in  the  position  of  inspiration,  might  exert  a  constant  abnormal  traction  on 
the  lungs,  and  so  give  rise  to  an  emphysema.  The  occurrence  of  this  hypothetical 
primary  disease  of  the  cartilages,  however,  has  up  to  the  present  time  not  been 
established.  It  is  rather  considered  by  the  majority  of  authors  as  a  second- 
ary change,  developing  as  a  result  of  emphysema  or  else  simultaneously  with 
it.  On  the  other  hand,  it  is  certainly  remarkable  that  we  sometimes  observe  in 
children  the  "  emphysematous  habit "  of  the  thorax  and  neck,  which  will  be  more 
fully  described  further  on,  and  that  in  fact  in  such  children  we  can  often  discover 
early  in  life  a  beginning  emphysema. 

Besides  the  already  described  essential  or  substantial  emphysema,  which  is  a 
special  disease  attacking  both  lungs  uniformly,  we  distinguish  a  so-called  vicarious 
or  complementary  emphysema.  If,  by  any  disease,  certain  portions  of  the  lungs 
are  incapacitated  in  their  functions,  the  parts  which  remain  healthy  must  then 
assume  the  whole  business  of  respiration.  They  become  excessively  expanded  on 
inspiration,  and  as  a  result  they  become  emphysematous.  Thus  we  see  emphysema 
of  the  upper  lobes  in  affections  of  the  lower  lobes.  Emphysema  of  one  lung  is 
most  frequently  observed  clinically  when  the  other  lung  is  extensively  diseased, 
especially  in  unilateral  chronic  contractions  of  the  lungs  and  pleura?,  usually  seen 
in  tuberculosis.  Vicarious  emphysema  may  also  be  confined  to  quite  small  por- 
tions of  the  lung,  but  then  it  is  merely  of  pathological  and  not  of  clinical  interest. 

Pathological  Anatomy.— As  we  have  seen,  the  actual  abnormality  of  the  lung 
in  emphysema  is  not  due  to  a  pathological  change,  but  to  a  change  in  its  physical 
conditions.  The  loss  of  elasticity  of  the  lung  is  shown  in  its  greater  volume,  in 
its  lack  of  contractility,  and  in  its  persistence  in  a  position  of  inspiration. 

The  single  alveoli  are  of  course  just  as  much  expanded  as  the  whole  lung,  but 
their  walls  show  at  first  no  histological  changes.  We  have  here,  then,  a  condition 
which  Traube  has  called  "  increased  volume  of  the  lungs,"  and  has  distinguished 
from  the  "  pulmonary  emphysema  "  proper.  This  distinction  is  without  doubt  justi- 
fied anatomically,  but  clinically  it  can  not  well  be  maintained.  As  the  distention  is 
constant,  the  alveolar  walls  can  not  withstand  the  constant  traction  and  pressure. 
This  leads  to  progressive  atrophy  of  their  tissue  from  pressure— that  is,  it  leads 
to  a  real  disappearance  of  the  elastic  elements  of  the  lung.  The  atrophy  be- 
gins quite  gradually.  The  partition- walls  of  the  alveoli  are  first  perforated"  and 
then  they  partly  or  wholly  break  down.  The  neighboring  alveoli  run  more  and 
more  into  one  another,  and  thus  finally  arise  alveolar  ectasis  and  infundibular 
ectasis,  which  can  be  made  out  with  the  naked  eye,  and  which  may  attain  a  diam- 
eter of  five  or  ten  millimetres  or  more.  If  single  air-bubbles  enter  the  interlobu- 
lar, interstitial,  or  subpleural  connective  tissue,  which  may  happen  perhaps  in 
severe  fits  of  coughing,  we  speak  of  an  interstitial  or  interlobular  emphysema,  in 
distinction  from  the  ordinary  vesicular  or  alveolar  emphysema. 

The  tissue  atrophy  in  the  septa  of  the  alveoli  affects  not  only  the  elastic  tissue, 
however,  but  it  also  affects  the  branches  of  the  pulmonary  capillaries  in  the  alveo- 
lar walls.     The  affection  of  the  elastic  tissue  adds  no  new  conditions  to  the  dis- 


176  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

turbed  functions  of  the  emphysematous  lung,  which  we  have  just  described.  The 
destruction  and  final  atrophy  of  the  pulmonary  capillaries,  however,  is  the  second 
important  factor  in  the  pathology  of  pulmonary  emphysema,  for,  with  the  destruc- 
tion of  so  great  a  part  of  the  vascular  area  in  the  lungs,  the  outflow  from  the 
right  side  of  the  heart  is  considerably  lessened.  There  must  therefore  necessarily 
be  a  stasis  in  the  pulmonary  arteries  and  the  right  side  of  the  heart,  and  the  right 
side  of  the  heart  can  overcome  the  increased  resistance  only  by  increased  work, 
and  thus  in  every  chronic  pulmonary  emphysema  there  finally  arise  a  dilata- 
tion and  consecutive  hypertmphy  of  the  right  ventricle  with  their  further  conse- 
quences. 

Symptoms  and  Course  of  the  Disease. 

General  Course  of  the  Disease. — Although  a  pulmonary  emphysema  may 
sometimes,  as  in  whooping-cough,  develop  in  a  comparatively  short  time,  still  its 
course  is  always  very  chronic.  In  most  cases  the  origin  of  the  disease  is  quite 
gradual,  as  in  all  those  cases  in  which  an  emphysema  develops  from  a  chronic 
bronchitis,  an  asthma,  or  as  a  result  of  some  injurious  occupation.  The  symp- 
toms gradually  and  insidiously  associate  themselves  with  those  of  the  chronic 
bronchitis. 

The  symptoms  of  emphysema  usually  begin  in  middle  or  advanced  life,  but 
marked  emphysema  may  occur  in  youth  and  childhood.  The  disease  always  lasts 
for  years,  unless  some  [fatal]  intercurrent  disease  arises. 

The  objective  and  subjective  symptoms  are  due  either  to  the  chronic  bron- 
chitis, which  very  often  co-exists,  or  to  the  emphysema  itself.  Not  only  is  the 
bronchitis,  as  we  have  seen  above,  very  often  the  cause  of  emphysema,  but,  on 
the  other  hand,  the  development  of  a  chronic  bronchitis  is  greatly  favored  by  the 
circulatory  disturbances  in  the  lung  associated  with  emphysema.  Thus  the  two 
diseases,  emphysema  and  chronic  bronchitis,  are  closely  connected  clinically. 

Bronchitis  causes  its  well-known  symptoms — cough,  expectoration,  moderate 
dyspnoea,  and  a  feeling  of  pressure  in  the  chest.  The  bronchiectases,  which  are 
often  gradually  formed,  especially  in  the  lower  lobes,  may  lend  a  peculiar  stamp 
to  the  cough  and  expectoration  (see  page  165).  Emphysema  increases  the  patient's 
dyspnoea  to  a  degree  which  can  never  be  caused  by  chronic  bronchitis  alone.  The 
emphysematous  lungs  soon  become  incapable  of  satisfying  any  extraordinary 
demands  of  respiration.  Many  patients  are  only  slightly  conscious  of  the  diffi- 
culty in  breathing  so  long  as  they  keep  quiet,  but  whenever  they  make  a  trifling 
physical  exertion,  go  up-stairs,  or  take  a  little  longer  walk  than  usual,  the  dyspnoea 
comes  on. 

The  variations  in  the  intensity  and  extent  of  the  bronchitis  correspond  to  the 
frequent  and  quite  marked  variations  in  the  patient's  feelings.  These  variations 
depend  upon  the  condition  of  the  patient,  his  external  circumstances,  and  the 
possibility  of  his  taking  care  of  himself ;  the  change  of  seasons,  too,  has  an  influ- 
ence on  him.  In  pleasant  weather  many  patients  live  in  tolerable  comfort,  but 
autumn  and  winter  bring  an  increase  of  all  their  symptoms  with  the  increase  in 
their  bronchitis. 

The  last  stage  of  the  disease  is  characterized  by  the  appearance  of  a  disturb- 
ance of  compensation  in  the  heart.  We  have  seen  above  that  the  cause  of  the 
impairment  of  the  pulmonary  circulation,  and  of  the  resulting  hypertrophy  of 
the  right  ventricle,  is  the  closure  of  numerous  pulmonary  capillaries.  A  further 
reason  for  the  impairment  of  the  circulation  comes  from  the  disturbance  of  res- 
piration itself,  since  the  influence  of  the  respiratory  movements  on  the  circulation 
is  well  known.  The  appearance  of  a  marked  disturbance  of  the  circulation  may 
be  deferred  for  some  time  by  the  increased  efforts  of  the  right  ventricle.     The 


PULMONARY  EMPHYSEMA.  177 

cyanosis  of  most  patients  is  due  solely  to  incomplete  oxidation  and  to  the  blood- 
stasis  which  extends  backward  from  the  right  side  of  the  heart  into  the  veins 
of  the  body.  Finally,  however,  the  right  ventricle  becomes  more  and  more 
feeble,  the  stasis  in  the  veins  increases,  oedema  of  the  extremities  and  transudation 
into  the  various  cavities  of  the  body  ensue,  and  after  long  suffering  the  patient 
succumbs  to  dropsy. 

Emphysema  is  frequently  combined  in  its  later  stages  with  other  chronic  dis- 
eases. Pulmonary  emphysema  with  its  sequela)  is  seldom  found  at  the  autopsy 
as  a  single  lesion,  but  we  discover  in  the  cadaver  co-existing  disease  of  the  heart, 
the  blood-vessels,  or  the  kidneys.  Pulmonary  tuberculosis  is  often  a  final  devel- 
opment in  emphysema,  but  it  is  usually  of  the  chronic  indurated  form,  and  is  not 
very  extensive. 

Physical  Examination.  1.  Inspection. — In  many  patients  we  can  detect  the 
disease  with  considerable  confidence  at  the  first  glance;  we  are  therefore  justified 
in  speaking  of  an  emphysematous  habit.  The  patients  are  usually  quite  well 
nourished,  at  least  in  the  early  stages  of  the  disease,  and  are  often  rather  corpulent. 
They  appear  plump  or  even  somewhat  bloated,  and  their  faces  are  more  or  less 
markedly  cyanotic.  The  configuration  of  the  neck  and  thorax  is  especially  char- 
acteristic. The  neck  is  usually  short  and  compressed;  the  sterno-cleido-mastoid 
muscles,  which  have  to  act  as  auxiliaries  in  inspiration,  are  tense  and  hyper- 
trophied.  The  inspiratory  contraction  of  the  scaleni  may  also  be  seen  and  felt. 
The  veins  in  the  neck  are  visibly  dilated,  and  in  severe  cases  are  swollen  to  thick 
blue  cords,  and  we  sometimes  see  in  them  evident  undulating  or  pulsating  move- 
ments. The  thorax  is  rather  short,  but  broad  and  strikingly  deep— the  "  barrel- 
shaped  thorax."  The  intercostal  spaces  are  narrow,  and  the  lower  ribs  move 
only  a  little  downward.  The  epigastric  angle  is  therefore  obtuse,  and  sometimes 
becomes  almost  a  straight  line.  The  respiratory  movements  are  almost  always 
accelerated  in  severe  cases.  Inspiration  becomes  short  and  labored.  The  excur- 
sions of  single  ribs  are  therefore  slight,  and  the  thorax  is  raised  rigidly  and  more 
as  a  whole.  Expiration  is  visibly  prolonged.  There  may  be  a  noticeable  retrac- 
tion of  the  intercostal  spaces  on  inspiration  in  the  lower  and  lateral  portions  of 
the  thorax. 

This  characteristic  form  of  the  thorax  in  emphysema  is  regarded  as  a  constant 
inspiratory  position  of  the  ribs,  and  corresponds  to  the  permanent  inspiratory  dila- 
tation of  the  lungs.  The  peculiar  rigidity  of  the  thorax  is  probably  due  to  the 
changes  in  the  costal  cartilages  already  described,  which,  according  to  Freund,  are 
primary.  In  many  cases  the  emphysematous  form  of  the  thorax  gradually  devel- 
ops in  the  course  of  the  disease,  but  in  other  cases  it  seems  to  depend  on  some 
original  predisposition  {vide  supra)  to  the  disease. 

In  conclusion,  we  must  state  that  the  above  description  corresponds  to  the  typi- 
cal form  of  emphysema,  from  which  we  may  have  many  deviations.  In  the  para- 
lyzed thorax,  for  instance,  we  may  meet  with  a  high  degree  of  essential  emphy- 
sema of  the  lungs,  which  has  often  given  rise  to  errors  in  diagnosis. 

2.  Percussion. — Percussion  gives  very  decided  results  in  the  diagnosis  of  pul- 
monary emphysema.  We  find  the  inferior  border  of  the  lungs  one  or  two  inter- 
costal spaces  lower  than  under  normal  conditions,  corresponding  to  their  perma- 
nent inspiratory  inflation.  Clear  pulmonary  resonance  on  the  right  front  in  the 
line  of  the  nipple  extends  to  the  lower  border  of  the  seventh,  and  sometimes  of  the 
eighth  rib.  On  the  left  front  it  extends  to  the  fifth  or  sixth  ribs,  so  that  the 
cardiac  dullness  is  lessened.  The  area  of  cardiac  dullness  can  often  not  be  made 
out  at  all ;  or  at  most,  on  strong  percussion,  it  is  made  out  in  a  limited  extent  as 
relative  dullness.  The  pulmonary  resonance  extends  on  both  sides  in  the  back  to 
the  first  or  second  lumbar  vertebra.  This  condition  on  percussion  in  emphysema, 
12 


178  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

however,  is  frequently  altered,  because  other  conditions,  like  passive  congestion 
of  the  liver,  meteorism,  and  ascites,  may  he  present  at  the  same  time,  and  push 
up  the  diaphragm.  Thus  the  detection  of  emphysema  by  percussion  is  made  decid- 
edly difficult. 

Qualitative  changes  in  the  percussion-note  may  be  entirely  wanting  in  emphy- 
sema. The  pitch  is  sometimes  remarkably  loud  and  deep — the  "  box-tone  "  [tym- 
panitic resonance] ;  but  in  other  cases,  especially  in  the  back,  we  find  it  somewhat 
raised.  This  may  depend  in  part  upon  the  poor  vibratory  conditions  in  the  rigid 
chest-walls,  but  in  other  cases  it  is  caused  by  the  retention  of  an  abundant  secre- 
tion in  the  lower  lobes. 

The  detection  of  dilatation  and  hypertrophy  of  the  right  ventricle  by  percus- 
sion is  in  many  cases  uncertain,  because  the  lungs  cover  the  heart.  A  positive 
result  can  be  obtained  only  by  carefully  defining  the  relative  cardiac  dullness. 
The  frequent  epigastric  pulsations  in  emphysema,  and  also  the  marked  undulating 
and  pulsating  movements  in  the  jugular  veins,  are  to  be  regarded  as  quite  certain 
signs  of  dilatation  of  the  right  side  of  the  heart. 

3.  Auscultation. — The  characteristic  auscultatory  sign  of  emphysema  is  the 
prolonged  expiration.  As  a  flabby  rubber  band,  when  it  is  stretched  and  then  let 
loose,  no  longer  snaps  back  quickly  and-  strongly,  so  the  emphysematous  lung, 
when  it  has  been  stretched  in  inspiration,  comes  back  again  only  slowly.  We  hear 
with  it  a  somewhat  aspirated,  sonorous  sound,  which  plainly  exceeds  the  vesicular 
inspiratory  sound  in  duration.  The  vesicular  murmur  itself  often  undergoes  a 
modification  in  pulmonary  emphysema.  It  sounds  exaggerated,  and  very  shuf- 
fling, or  in  other  cases  it  is  rougher  and  more  indefinite.  In  a  high  degree 
of  emphysema  the  vesicular  respiration  is  sometimes  very  low  and  obscure, 
because  the  inspiratory  current  of  air  is  reduced  to  a  small  amount  in  the  lungs, 
which  are  already  excessively  dilated.  In  many  cases  we  hear  rhonchi  beside  the 
respiratory  murmur,  dry  whistling,  buzzing,  and  creaking  sounds  on  inspiration 
and  expiration.  If  cylindrical  bronchiectases  have  already  formed,  we  hear,  espe- 
cially over  the  lower  lobes,  numerous  small  and  medium  moist  rales,  but  no  sono- 
rous rhonchi.  The  rhonchi  may  wholly  conceal  the  respiratory  sounds.  With  a 
marked  retention  of  secretion  we  sometimes  hear  nothing  but  a  low,  suppressed, 
rattling  sound. 

In  the  heart  the  sounds  are  usually  rather  low,  because  it  is  covered  by  the 
lung.  The  "  accidental  systolic  sound  in  emphysema  "  at  the  apex,  described  by 
some  writers,  we  have  heard  much  less  frequently  when  the  valves  were  intact 
than  we  should  expect  after  the  statements  relating  to  it.  The  pulmonic  second 
sound  is,  as  a  rule,  markedly  accentuated,  as  a  result  of  the  stasis  in  the  pulmo- 
nary circulation. 

The  diminution  of  the  expiratory  pressure  in  emphysema  may  be  measured 
with  the  manometer,  or  with  Waldenburg's  "  Pneumatometer."  The  normal  expi- 
ratory pressure  of  110  to  130  millimetres  sinks  in  emphysema  to  100  or  80  milli- 
metres. As  we  should  expect,  the  spirometer  shows  a  diminution  of  the  vital  lung 
capacity,  which  can  be  readily  explained.  The  normal  lung  capacity  of  about 
3,500  cubic  centimetres  falls  to  2,000  or  1,000  cubic  centimetres. 

Othek  Symptoms  in  the  Lungs  and  in  Other  Organs. 

In  regard  to  the  other  symptoms  in  the  lungs  we  have  only  a  little  to  add  to 
what  has  already  been  said.  The  intensity  of  the  cough  naturally  varies  in 
individual  cases  according  to  the  degree  of  the  existing  bronchial  catarrh.  Many 
patients  are  troubled  by  a  dry  cough,  while  others  have  abundant  expectoration. 
There  is  nothing  characteristic  of  emphysema  in  the  composition  of  the  latter. 


PULMONARY  EMPHYSEMA.  179 

All  the  kinds  of  sputa  which  are  found  in  the  different  forms  of  chronic  bronchitis 
are  also  found  in  pulmonary  emphysema.  The  dyspnoea,  whose  predominant 
expiratory  character  we  have  already  mentioned,  increases  in  advanced  cases  to  a 
most  marked  degree.  Sometimes  the  increase  shows  itself  by  the  appearance  of 
distinct  asthmatic  attacks.  These  are  often  really  to  be  regarded  as  a  symptomatic 
bronchial  asthma,  of  nervous  origin,  but,  on  the  other  hand,  we  must  not  overlook 
the  fact  that  a  temporary  increase  of  the  bronchitis,  retention  of  secretion,  and 
cardiac  failure,  may  also  excite  attacks  of  dyspnoea,  which  can  not  properly  be 
termed  asthma. 

The  important  changes  in  the  heart  resulting  from  emphysema  have  already 
been  described.  The  exhausted  right  ventricle  can  no  longer  overcome  the  in- 
creased resistance  in  the  pulmonary  circulation.  The  difficulty  of  respiration  is 
still  greater,  from  the  passive  congestion  of  the  pulmonary  vessels.  The  skin  be- 
comes still  more  cyanotic,  and  finally  oedema  and  general  dropsy  develop.  The 
failure  of  compensation  is  evident  by  the  lessening  of  the  pulse,  its  increased  fre- 
quency, and  sometimes  by  its  irregularity.  The  difficulty  of  an  objective  exam- 
ination of  the  heart  in  emphysema  has  been  spoken  of  above. 

The  appearances  of  blood  stasis  in  the  internal  organs  are  shown  especially  in 
the  liver  and  the  kidneys.  The  liver  is  swollen,  and  its  increase  in  size  (the  liver 
of  passive  congestion)  can  frequently  be  made  out  by  percussion  or  palpation. 
The  pains  in  the  region  of  the  liver,  of  which  many  patients  complain,  are  per- 
haps sometimes  clue  to  the  stretching  of  the  capsule  of  the  liver,  but  they  are  prob- 
ably more  often  muscular  pains  excited  by  the  frequent  coughing. 

In  the  kidneys  the  effect  of  stasis  is  first  shown  by  a  diminished  excretion  of 
urine.  The  urine  is  more  scanty 'in  amount,  more  concentrated,  of  a  higher  spe- 
cific gravity,  and  of  a  darker  color.  It  generally  gives  an  abundant  sediment  of 
urates,  and  may  contain  a  small  amount  of  albumen.  Microscopically,  are  dis- 
covered a  few  hyaline  casts,  and  a  few  red  and  white  blood-corpuscles.  It  is  evi- 
dent that  this  diminished  activity'of  the  kidneys  favors  the  development  of  dropsy. 

The  spleen  is  not  infrequently  found  congested  at  the  autopsy.  The  evidence 
of  this,  however,  is  often  uncertain  during  life,  for  percussion  of  the  spleen  is 
difficult  on  account  of  the  emphysema,  and  palpation  is  difficult  from  the  swelling 
of  the  body. 

Gastro-intestinal  symptoms  may  be  present  in  emphysema.  The  appetite 
seldom  remains  good  throughout  the  disease.  Many  patients  suffer  from  chronic 
constipation;  and  more  rarely  there  is  a  tendency  to  diarrhoea. 

Fever  is  not  present  in  simple  pulmonary  emphysema.  Every  fever  which 
exists  for  a  long  time  depends  on  other  complications,  like  severe  bronchitis, 
pneumonia,  or  tuberculosis. 

Complications  of  emphysema  with  other  chronic  diseases  are  frequent.  The 
old  opinion  that  emphysema  and  tuberculosis,  and  emphysema  and  chronic  heart 
disease,  were  antagonistic  to  each  other  is  entirely  false.  These  complications  are 
not  very  rare.  We  may  also  mention  the  complication  with  general  arterio- 
sclerosis and  with  chronic  nephritis,  especially  the  contracted  kidney.  Among 
acute  diseases  we  must  mention  croupous  pneumonia,  which  is  not  very  rare  in 
emphysema,  where  it  must  always  be  regarded  as  a  dangerous  combination. 

The  diagnosis  of  emphysema  can  be  made  directly  from  the  results  of  the 
physical  examination,  and  usually  presents  no  difficulties.  It  is  obscure  only 
when  the  patient  is  not  examined  till  the  final  stage  of  dropsy.  Then  it  may  be 
very  hard  to  avoid  confusing  it  with  forms  of  heart  disease,  like  primary  hyper- 
trophy, myocarditis,  or  mitral  stenosis,  or  with  contraction  of  the  kidney. 

Prognosis. — Pulmonary  emphysema  of  acute  origin,  like  that  resulting  from 
whooping-cough  and  analogous  affections,  may  be  recovered  from  in  many  cases, 


180  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

but  otherwise,  as  regards  the  final  curability  of  the  disease,  the  prognosis  is  wholly 
bad.  The  duration  of  the  disease  and  the  intensity  of  the  symptoms  are  of  course 
very  different  in  individual  cases.  Here  almost  everything  depends  upon  the 
circumstances  in  which  the  patient  is  placed.  With  sufficient  care  the  disease 
may  be  tolerably  well  borne  for  many  years,  but  without  it  the  first  symptoms  of 
respiratory  and  cardiac  insufficiency  appear  much  earlier. 

Treatment. — Since  emphysema  itself  is  only  slightly  amenable  to  treatment, 
most  of  our  therapeutic  remedies  are  directed  to  that  accompanying  condition 
upon  which  the  greater  part  of  the  symptoms  depend — to  the  chronic  bronchitis. 
If  we  succeed  in  improving  this,  or  even  in  wholly  removing  it,  we  always  obtain 
a  distinct  improvement  in  all  the  patient's  symptoms.  The  therapeutic  remedies 
mentioned  in  the  description  of  chronic  bronchitis  are  therefore  of  frequent  use 
in  emphysema. 

In  the  first  place,  we  must  seek  the  best  hygienic  conditions  for  the  patient,  and 
remove  him  from  all  injurious  influences,  such  as  dust,  bad  air,  and  work  requir- 
ing physical  exertion.  In  dry  catarrh  we  should  use  the  alkaline  mineral  waters, 
and  when  there  is  abundant  mucous  secretion  the  balsams,  such  as  turpentine 
internally  and  by  inhalation.  The  most  valuable  expectorants  are  apomorphine, 
liquor  ammonii  anisatus,  and  senega.  Their  action,  of  course,  too  often  fails  of 
the  desired  result,  so  that  we  frequently  have  to  change  our  remedies.  "When 
there  is  a  troublesome  cough,  disturbing  the  sleep,  we  can  not  dispense  with  nar- 
cotics, like  morphine  or  Dover's  powder.  If  sevei^e  dyspnoea  conies  on,  we  may 
try  to  obtain  relief  by  mustard  plasters  to  the  chest,  or  by  immersing  the  hands 
and  feet  in  hot  water.  With  asthmatic  attacks  we  may  try  iodide  of  potassium, 
beside  the  other  remedies  mentioned  for  asthma.  Here,  too,  we  must  finally 
resort  to  narcotics. 

We  must  carefully  watch  the  condition  of  the  heart,  and  use  digitalis  when 
there  are  signs  of  beginning  disturbance  of  compensation  and  the  pulse  grows 
small  and  irregular,  and  this  drug  may  prove  very  useful.  If  symptoms  of  dropsy 
set  in,  we  may  sometimes  prescribe  diuretic  remedies,  like  juniper-tea,  or  acetate 
of  potassium,  besides  digitalis.  We  also  try  to  strengthen  the  heart  by  wine, 
camphor,  benzoic  acid,  or  other  stimulants. 

Besides  the  purely  symptomatic  treatment  thus  described,  the  attempt  has  been 
made  to  meet  the  causal  indications  in  emphysema,  and  especially  to  aid  the 
patient  in  expiration,  and  thus  to  improve  the  power  of  the  lung  to  contract, 
where  it  is  possible.  To  this  end  Gerhardt  has  recommended  assisting  expiration 
mechanically  by  compression  of  the  thorax.  This  compression  must  be  done 
methodically  by  another  person,*  about  five  or  ten  minutes  every  day,  by  the  aid 
of  both  hands  laid  flat  on  the  lower  lateral  portions  of  the  thorax.  The  effect  of 
this  manipulation  in  diminishing  the  dyspnoea  and  making  expectoration  easier 
is  in  many  cases  very  satisfactory. 

The  employment  of  the  pneumatic  treatment  has  also  become  quite  general, 
especially  since  the  introduction  of  Waldenburg's  portable  apparatus.  The  expi- 
ration into  rarefied  air,  which  meets  the  causal  indication,  may  procure  great 
relief  for  the  patient  in  many  cases,  and  sometimes,  too,  result  in  an  improvement 
of  the  emphysema  which  can  be  demonstrated  on  physical  examination.     Inhala- 

*  One  of  my  patients  at  the  policlinic  in  Leipsic  made  himself  a  very  simple  but  very  effect- 
ive apparatus  for  producing  this  compression  of  the  thorax  on  himself  by  the  aid  of  two  small 
boards,  which  are  firmly  fastened  together  at  one  end  by  a  long  cord.  These  boards,  which  are  fur- 
nished with  a  piece  of  wood  at  this  end  fitted  to  the  wall  of  the  chest,  are  laid  flat  on  the  two  sides 
of  the  thorax  so  that  their  free  ends  can  project  forward  some  six  inches  or  a  foot,  and  serve  as  a  one- 
armed  lever.  By  pressing  them  together  the  patient  himself  can  thus,  without  any  strain,  exert  a  con- 
siderable pressure  on  his  thorax  with  each  expiration. 


PULMONARY  ATELECTASIS.  181 

tions  of  compressed  air  are  also  employed  when  there  is  severe  bronchial  catarrh. 
Still,  too  much  must  not  be  anticipated  from  pneumatic  treatment. 


CHAPTER  II. 

PULMONARY  ATELECTASIS. 

( Compression  of  the  Lungs.     Aplasia  of  the  Lungs  in  Cases  of  Kyphoscoliosis:) 

etiology.— Atelectasis  of  the  lungs  is  a  condition  directly  opposed  to  emphy- 
sema. While  in  the  latter  the  lungs  are  abnormally  inflated,  in  the  former  they 
are  abnormally  collapsed.  The  air  has  disappeared  from  the  alveoli  and  lesser 
bronchi,  and  in  the  most  advanced  cases  even  from  the  larger  bronchi.  The  atelec- 
tatic portions  of  the  lung  are  not  altered  histologically,  but  are  changed  to  a  firm 
tissue,  deprived  of  air— the  so-called  splenization  or  carnefaction. 

The  atelectasis  of  the  new-born  is  due  simply  to  deficient  respiration  and  to  the 
consequent  imperfect  entrance  of  air  into  the  lungs.  In  weak  children,  who  die 
soon  after  birth,  we  often  find  the  lower  lobes  wholly  or  in  part  in  a  foetal,  unin- 
flated  condition— that  is,  atelectatic.  By  artificial  inflation  we  can  readily  expand 
the  lungs  to  their  normal  extent. 

Acquired  atelectasis  occurs  in  two  ways.  We  may  mention,  as  the  first  and 
most  frequent  setiological  factor,  the  plugging  of  the  smaller  bronchi.  If  a  com- 
plete closure  of  a  bronchus  arises  from  the  accumulation  of  secretion,  as  may  easily 
happen  in  the  narrow  bronchi  of  children,  the  air  can  no  longer  enter,  on  inspira- 
tion into  that  portion  of  lung  supplied  by  the  plugged  bronchus.  The  air  which 
is  shut  up  in  it  is  gradually  absorbed  by  the  blood.  The  adjacent  parts  of  the 
lung  expand,  and  the  portion  that  is  excluded  from  respiration  collapses,  leaving 
a  circumscribed  pulmonary  atelectasis,  usually  rich  in  blood  but  devoid  of  air. 
Such  atelectases,  in  greater  or  less  number  and  extent,  are  very  often  found  in  the 
bodies  of  children  who  have  suffered  from  severe  bronchitis,  especially  after 
measles,  whooping-cough,  or  diphtheria.  Beside  the  direct  action  of  the  plugging 
of  the  bronchus,  the  weakness  of  the  respiratory  movements  and  the  cough,  condi- 
tional upon  the  general  state  of  the  disease,  play  a  significant  part. 

The  second  very  frequent  and  important  cause  of  pulmonary  atelectasis  is  com- 
pression of  the  lung.  In  all  the  diseases  which  diminish  the  space  for  the  expan- 
sion of  the  lungs,  the  lungs  are  pressed  together  from  without  to  a  greater  or  less 
extent,  whereby  the  air  is  pressed  out  of  them.  Thus  arise  the  atelectases  from 
pressure  in  pleuritic  effusion,  hydrothorax,  pneumothorax,  in  marked  cardiac 
hypertrophy,  pericardial  effusion,  and  aneurism  of  the  aorta.  Atelectasis  of  the 
lower  lobes  also  arises  in  the  same  way  from  great  upward  pressure  on  the 
diaphragm  by  ascites,  meteorism,  abdominal  tumors,  etc. 

That  form  of  pulmonary  atelectasis  which  arises  from  deformities  of  the  thorax 
is  of  great  practical  importance.  In  severe  kyphoscoliosis,  the  half  of  the  thorax 
corresponding  to  the  convexity  of  the  vertebral  column  is  much  narrowed.  The 
lungs  are  materially  hindered  in  their  expansion,  and  even  in  their  growth,  if  the 
deformity  occurs  in  youth.  This  is  called  "  aplasia  of  the  lungs,"  a  condition 
which  may  give  rise  to  grave  results  {vide  infra). 

Symptoms. — In  the  majority  of  cases  the  appearances  in  atelectasis  are  subordi- 
nate to  the  symptoms  caused  by  the  primary  disease.  This  is  especially  the  case 
in  most  of  the  atelectases  from  pressure,  although  the  most  dangerous  factor  lies 
in  the  compression  of  the  lung. 

The  atelectasis  of  the  lungs  developing  as  a  result  of  diffuse  capillary  bronchitis, 


182  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

especially  in  children,  can  of  course  not  be  detected  by  physical  examination 
imtil  it  is  of  great  extent.  The  respiration,  in  extensive  formation  of  atelectasis, 
often  chows  a  very  striking  and  characteristic  deviation  from  the  ordinary  type, 
especially  when  the  atelectasis  develops  in  the  lower  lobes.  It  is  accelerated  and 
labored,  and  is  performed  chiefly  by  the  upper  and  anterior  portions  of  the  thorax. 
In  the  lower  portions  we  see  marked  inspiratory  retractions,  which  are  caused  in 
part  by  the  external  pressure  of  the  air,  and  in  part  correspond  to  the  forced  con- 
traction of  the  diaphragm. 

Physical  examination  can,  of  course,  reveal  abnormal  conditions,  especially 
dullness  on  percussion,  only  when  the  atelectasis  is  extensive.  Dullness,  however, 
is  usually  hard  to  make  out  in  children.  Auscultation  gives  signs  of  existing 
bronchitis  ;  and  sometimes,  too,  with  more  extensive  consolidation,  there  is  bron- 
chial respiration.  In  other  cases,  as  may  be  easily  seen,  the  respiratory  murmur 
is  much  diminished  or  wholly  absent.  As  we  can  perceive,  the  physical  signs  of 
atelectasis  are  not  really  distinguishable  from  those  of  pneumonia,  especially  of 
lobular  pneumonia.  In  fact,  a  sharp  boundary  between  atelectatic  nodules  and 
nodules  of  lobular  pneumonia  in  the  lung  can  not  be  drawn  clinically. 

Aplasia  of  the  lungs  in  kyphoscoliosis  demands  a  special  description,  because  it 
is  of  great  practical  significance.  Many  patients  with  kyphoscoliosis  may  live  for 
years  without  special  respiratory  disturbance.  Moi*e  careful  observation,  of  course, 
usually  shows  a  somewhat  labored  and  hurried  respiration,  but  the  patients  have 
not  paid  much  attention  to  it.  In  other  cases  the  difficulty  in  breathing  is  more 
noticeable.  The  person  affected  is  incapable  of  any  severe  physical  exertion ;  he 
always  feels  short,  of  breath,  and  often  suffers  from  cough  and  expectoration.  In 
the  cases  first  mentioned,  however,  which  for  years  have  had  little  or  no  trouble, 
disturbances  in  respiration  sometimes  come  on  quite  suddenly.  They  may  de- 
velop as  a  result  of  a  mild  bronchial  catarrh,  and  they  also  frequently  arise  without 
any  special  cause,  and  may  attain  a  very  threatening  degree.  The  condition  may 
improve,  or  it  may  lead  to  comparatively  speedy  death.  Examination  of  the 
lungs  during  life  usually  shows  nothing  but  the  signs  of  an  extensive  bronchitis. 
By  careful  percussion  we  may  quite  frequently  detect  an  increased  area  of  cardiac 
dullness  to  the  right.  Sometimes  a  moderate  oedema  develops.  In  such  cases  the 
autopsy  shows  nothing  as  the  cause  of  death  but  the  changes  in  the  lungs.  The 
lungs  are  abnormally  poor  in  air,  small,  and  compressed,  but  in  circumscribed 
portions,  on  the  contrary,  emphysematous  and  expanded.  The  right  side  of  the 
heart  in  the  great  majority  of  cases  is  dilated  and  hypertrophied.  There  can 
scarcely  be  a  doubt,  therefore,  that  the  cause  of  the  onset  of  severe  symptoms  and 
the  final  cause  of  death  is  to  be  sought  in  the  cardiac  failure. 

Finally,  it  is  worthy  of  mention  that  there  is  a  frequent  form  of  mild  atelectasis 
in  the  lower  lobes,  which  occurs  in  very  sick  and  bed-ridden  patients  who  usu- 
ally keep  in  one  position — on  the  back — as  in  typhoid  fever.  On  making  such 
patients  sit  up  we  hear  during  the  first  inspirations  exquisite  crepitant  rales  over 
the  lower  lobes,  which  sometimes  disappear  after  a  few  deep  inspirations.  Here 
we  have  to  do  with  a  mild  atelectatic  condition,  with  a  temporary  adhesion  of  the 
walls  of  the  alveoli  and  smallest  bronchi. 

The  treatment  of  atelectasis  coincides  in  great  measure  with  the  treatment  of 
the  primary  disease,  and  is  therefore  to  be  looked  for  in  the  corresponding  chap- 
ters. The  prophylaxis  of  atelectasis,  by  constant  attention  to  the  respiration,  is  of 
great  practical  importance.  We  should  try  to  keep  the  patient  from  lying  con- 
tinually on  his  back,  and  we  should  make  him  take  deep  inspirations.  The  timely 
use  of  tepid  baths,  with  shower-baths,  is  a  special  preventive  of  the  development  of 
atelectasis,  and  it  may  bring  about  a  recovery  when  atelectasis  is  already  present. 

Tepid  baths  may  also  be  used  with  care  in  the  treatment  of  dyspnoea  caused  by 


PULMONAEY  CEDEMA.  183 

kyphoscoliosis.  The  condition  of  the  heart,  however,  deserves  especial  attention 
(stimulants  and  digitalis).  The  reader  is  referred  to  the  consideration  of  the 
general  treatment  of  circulatory  disturbances  under  Heart  Disease.  In  other 
respects  the  symptomatic  treatment  by  expectorants,  etc.,  is  the  same  as  in  other 
chronic  pulmonary  affections. 


CHAPTER  III. 
PULMONARY   CEDEMA. 

2Etiology  and  General  Pathology. — We  have  in  pulmonary  oedema  the  exuda 
tion  of  a  highly  albuminous  fluid,  usually  somewhat  hemorrhagic,  not  only  into 
the  interstitial  tissue,  but  also  into  the  alveoli  themselves.  The  danger  of  the 
condition  is  easily  understood  from  the  high  degree  of  dyspnoea  which  immedi- 
ately ensues  from  it.  In  fact,  pulmonary  oedema  is  in  many  cases  a  terminal 
symptom,  which  comes  on  in  all  forms  of  acute  and  chronic  disease.  Many  pa- 
tients are  said  to  die  with  the  signs  of  pulmonary  oedema,  especially  patients  with 
heart  disease,  pulmonary  and  renal  disease,  and  also  with  other  affections  of  the 
most  different  kinds. 

In  rare  cases  pulmonary  oedema  is  a  transitory  symptom.  Repeated  attacks 
of  it  may  occur,  especially  in  heart  disease  and  chronic  renal  disease,  and  for  a 
time  at  least,  the  patient  recover  from  them. 

Many  erroneous  notions  formerly  prevailed  as  to  the  particular  cause  of  pul- 
monary oedema.  The  theory  was  especially  wide-spread  that  arterial  congestion 
in  the  lungs  could  excite  an  oedema,  but  through  the  experiments  of  Cohnheim 
and  his  pupils  we  now  know  that  pulmonary  oedema  is  to  be  considered  the 
result  of  stasis.  It  takes  place  when  the  outflow  of  venous  blood  in  the  lung 
meets  an  obstacle  which  can  no  longer  be  overcome  by  the  mechanical  force  of 
the  right  ventricle.  The  obstacle  which  plays  the  most  significant  part  here,  and 
which  may  occur  in  all  possible  forms  of  disease — of  course  more  readily  in  those 
mentioned  above  than  in  others — is  the  paralysis  of  the  left  ventricle.  If  the 
further  progress  of  the  blood  is  much  hindered  by  this,  the  overfilling  of  the 
pulmonary  circulation  and  a  consequent  pulmonary  oedema  will  necessarily  fol- 
low, in  spite  of  the  most  vigorous  action  of  the  right  ventricle.  Every  terminal 
pulmonary  oedema  depends  upon  this  fact,  that  the  left  ventricle  is  paralyzed  in 
its  action  sooner  than  the  right. 

Inflammatory  pulmonary  oedema  must  be  distinguished  from  the  pure  oedema 
from  stasis  just  described.  It  is  found  in  the  vicinity  of  portions  of  lung  infil- 
trated with  pneumonia,  it  is  usually  of  limited  extent,  and  therefore  it  is  of  sub- 
ordinate importance  as  a  cause  of  disturbances  in  respiration  compared  with  the 
general  oedema  of  stasis. 

In  very  rare  cases,  as  we  have  seen,  an  apparently  primary  acute  pulmonary 
oedema,  with  a  speedily  fatal  termination,  develops  in  men  who  were  before  that 
apparently  perfectly  healthy,  and  the  autopsy  gives  no  further  explanation  of  its 
origin.  We  probably  have  to  do  in  these  cases  with  the  sudden  failure  of  the  left 
ventricle. 

Symptoms. — Marked  dyspnoea  is  the  most  striking  symptom  in  pulmonary 
oedema.  It  is  subordinate  only  when  the  patient  is  found  in  the  death  agony 
and  is  no  longer  fully  conscious. 

In  pulmonary  oedema  the  respiration  is  hurried,  labored,  and  rattling.  All 
the  accessory  muscles  of  respiration  are  called  into  play.     The  patient  usually  sits 


184  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

upright  in  bed.  "We  see  on  his  lips  and  cheeks  a  gradually  and  constantly 
increasing  cyanosis,  and  we  often  hear  at  a  distance  the  moist  rales  in  the  larger 
bronchi. 

On  examination  of  the  lungs,  the  percussion  is  essentially  normal,  if  there  is 
no  other  disease  of  the  lungs.  Sometimes  the  percussion-note  is  a  little  higher  in 
pitch,  and  often  it  is  slightly  tympanitic.  On  auscultation,  we  hear  everywhere 
many  small  and  medium  moist  rales.  If  the  patient  can  still  expectorate,  he 
raises  a  large  amount  of  frothy,  sero-hasmorrhagic  sputum.  The  whole  picture 
of  the  disease  is  so  characteristic  that  the  condition  can  scarcely  be  mistaken. 

Treatment. — Since  in  most  cases  pulmonary  oedema  is  not  so  much  the  cause 
as  a  symptom  of  approaching  death,  our  remedies  against  it  are  apt  to  prove  pow- 
erless, but  it  must  always  be  our  duty,  at  least  in  all  cases  that  are  not  absolutely 
hopeless,  to  try  to  relieve  the  pulmonary  circulation.  From  the  pathogene- 
sis of  pulmonary  oedema  it  follows  that  we  must  pay  particular  attention  to 
the  condition  of  the  heart,  especially  of  the  left  ventricle.  Hence  we  should 
use  energetic  stimulants,  especially  subcutaneous  injections  of  camphor  or  ether, 
every  half  hour  or  hour.  Internally  we  give  camphor,  musk,  wine,  and  strong 
cafe  noir.  Beside  that,  we  apply  strong  irritants  to  the  chest,  such  as  large  mus- 
tard plasters  or  hot  sponges.  Sometimes  an  actual  improvement  of  the  respira- 
tion, when  it  has  already  stopped,  may  be  obtained  by  a  bath  with  cold  douching, 
where  there  is  marked  general  cyanosis.  If  the  patient  is  on  the  whole  strong 
and  well  nourished,  venesection  is  sometimes  of  manifest  benefit.  Emetics,  how- 
ever, accomplish  little,  and  are  even  dangeroiis  on  account  of  the  collapse  which 
may  readily  come  on  after  them.  An  energetic  "  derivation  to  the  intestines," 
however,  by  senna,  calomel,  or  enemata  of  vinegar,  seems  sometimes  to  be  really 
of  service.  Acetate  of  lead  in  large  doses,  one  or  two  grains  (grm.  0"05-0-10),  in 
powder,  every  hour,  employed  empirically  by  Traube,  is  deserving  of  trial. 

In  this  way,  especially  in  acute  diseases  like  typhoid  and  pneumonia,  we  in 
fact  sometimes  succeed  in  averting  the  danger  of  pulmonary  oedema  by  rapid  and 
energetic  action.  In  the  cases  of  oedema  occurring  in  incurable  chronic  diseases 
of  the  heart  and  kidneys,  the  remedies  employed  are  of  course  unfortunately 
incapable  of  preventing  death. 


CHAPTER  IV. 

CATARRHAL  PNEUMONIA. 

{Bronclio-pneumonia.     Lobular  Pneumonia?) 

JEtiology. — Catarrhal  pneumonia  is  not,  like  croupous  pneumonia,  a  distinct 
and  independent  disease,  but  in  the  great  majority  of  cases  it  is  a  secondary 
phenomenon,  which  may  develop  in  the  course  of  acute  and  chronic  diseases  of 
various  kinds.  It  almost  always  follows  bronchitis.  The  same  process  which 
produces  catarrh  of  the  bronchial  mucous  membrane,  in  its  further  course  in- 
vades the  bronchioles  and  the  alveoli,  and  here  leads  to  catarrhal  pneumonia. 

In  every  acute  or  chronic  disease,  of  any  severity,  the  conditions  are  favorable 
for  the  development  of  an  inflammation  in  the  bronchi,  and  subsequently  in  the 
pulmonary  alveoli.  Everywhere  in  the  air-passages,  as  well  as  in  the  cavities  of 
the  mouth  and  pharynx,  saliva,  mucus,  etc.,  readily  collect  if  the  patient  is  very  ill. 
Expectoration  is  imperfect,  and  the  constant  dorsal  decubitus  favors  the  accumu- 
lation of  secretion,  especially  in  the  lower  lobes.  The  mouth  and  pharynx  arc 
harder  to  keep  clean  than  under  normal  conditions.  Fungi  and  bacteria  collect 
in  the  secretion  itself,  as  well  as  in  the  epithelium  and  particles  of  food  which 


CATARRHAL  PNEUMONIA.  185 

are  left  in  the  mouth,  and  these  excite  and  keep  up  processes  of  decomposition. 
The  inflammatory  agents,  which  are  carried  into  the  air-passages  with  the  inspired 
air,  find  everywhere  favorable  conditions  for  settling  and  further  development. 
From  the  upper  portions  they  are  drawn  farther  downward.  From  the  larger 
bronchi  the  process  invades  the  finer  bronchi,  and  finally  leads  to  catarrhal  pneu- 
monia. We  must  also  bear  in  mind  that  many  patients  who  are  very  ill  have 
difficulty  in  swallowing.  They  get  choked,  and  particles  of  food,  with  the  germs 
of  inflammation  clinging  to  them,  are  carried  into  the  air-passages.  That  which 
a  healthy  person  could  easily  cough  up  again  remains  there,  is  decomposed,  and 
gives  rise  to  bronchitis  and  lobular  pneumonia. 

This  is  the  explanation  of  the  frequent  development  of  lobular  pneumonia  in 
the  course  of  diseases  which  are  entirely  dissimilar.  We  observe  it  especially  in 
all  patients  with  stupor,  in  severe  typhoid,  in  meningitis,  and  also  in  cases  of  nerv- 
ous disease,  where  coughing  and  deglutition  are  impaired,  as  a  result  of  bulbar 
affections.  In  all  such  cases  lobular  pneumonia  is  to  be  considered  a  complica- 
tion, and  with  reference  to  its  origin  deserves  the  name  of  inhalation  pneumonia 
or  deglutition  pneumonia.  We  shall  soon  see  that  this  form,  under  some  circum- 
stances, may  pass  into  circumscribed  gangrene. 

Although  the  serological  factors  just  described,  which  come  into  notice  in  the 
development  of  lobular  pneumonia,  have  nothing  to  do  with  the  nature  of  the 
primary  disease  as  such,  there  are,  on  the  other  hand,  certain  infectious  diseases 
which  from  the  beginning  are  exclusively,  or  at  least  mainly,  localized  in  the 
air-passages.  Among  these  are  measles,  whooping-cough,  and  also,  to  a  certain 
degree,  diphtheria,  small-pox,  etc.  In  these  diseases  we  very  often  see  lobular 
pneumonia  following  bronchitis.  In  individual  cases,  of  course,  it  is  scarcely 
possible  to  decide  how  far  the  bronchitis  is  directly  dependent  upon  the  specific 
cause  of  the  disease,  or  whether  it  is  merely  a  complication  such  as  might  also 
occur  in  any  other  disease.  Lobular  pneumonia  in  diphtheria,  and  in  severe 
small-pox,  is  probably  for  the  most  part  a  deglutition  or  an  inhalation  pneu- 
monia, the  occurrence  of  which  in  these  diseases  may  be  readily  understood.  In 
measles  and  whooping-cough,  however,  we  may  consider  that  the  pneumonia  is 
directly  dependent  upon  the  specific  agents  of  the  disease,  although  here,  too, 
the  other  causes  for  the  development  of  lobular  pneumonia  should  be  borne  in 
mind. 

The  development  of  lobular  pneumonia  from  bronchitis  is  most  frequent,  as 
we  know,  in  children  and  old  people.  The  frequency  of  catarrhal  pneumonia  in 
childhood  depends  in  part  upon  the  limited  dimensions  of  the  bronchi.  Besides 
that,  however,  the  diseases  in  which  it  is  especially  frequent — namely,  measles 
and  whooping-cough — are  children's  diseases.  In  old  people  its  comparatively 
easy  development  is  due  to  imperfect  expectoration. 

The  mild  cases  of  primary  bronchitis  scarcely  ever  lead  to  lobular  pneumonia, 
but  sometimes  in  children,  and  less  often  in  adults,  a  severe  febrile  bronchitis 
may  occasion  the  formation  of  pneumonic  foci.  Here,  in  Erlangen,  the  author 
has  seen  cases  which  can  not  be  regarded  otherwise  than  as  primary  catarrhal 
pneumonia.  The  inhalation  of  irritating  chemicals  may  occasion  lobular  pneu- 
monia as  well  as  bronchitis. 

Pathological  Anatomy. — It  is  characteristic  of  catarrhal  pneumonia  that  the 
inflammation  is  circumscribed,  being  limited  to  the  territory  of  a  small  bronchus. 
Hence  the  name  of  "lobular"  pneumonia,  in  distinction  from  or  croupous  lobar 
pneumonia.  An  atelectasis  {vide  supra)  of  the  affected  lobule,  arising  from  the 
plugging  of  the  bronchus  leading  to  it,  often,  but  not  always,  precedes  the  inflamma- 
tion. The  inflammatory  process  itself  consists  of  the  exudation  of  a  scanty  fluid, 
which  does  not  coagulate,  and  of  numerous  pus-corpuscles  (white  blood-corpuscles) 


186  DISEASES  OF  THE  RESPIRATORY   ORGANS. 

into  the  lunien  of  the  alveoli.  The  alveoli  and  smallest  bronchi  are  completely 
filled  by  the  pus-corpuscles.  There  are  also  more  or  less  abundant  red  blood-cor- 
puscles. The  vessels  of  the  alveolar  walls  are  very  hyperaemic.  The  alveolar 
epithelium  is  much  swollen,  and  is  often  thrown  off  in  quite  large  amounts,  the 
"  desquamative  pneumonia.1'  It  is  doubtful  whether  it  also  takes  an  active  part  in 
these  changes  by  processes  of  division. 

The  inflamed  lobules  are  readily  apparent  to  the  eye  and  the  touch  by  their 
firm  consistence,  being  devoid  of  air.  Their  color  at  first,  from  the  blood  contained 
in  the  inflamed  part,  is  a  dark  red,  but  later  it  becomes  more  grayish.  Their 
lobular  boundary  is  usually  easily  recognized,  but,  by  confluence  of  adjacent  nod- 
ules, large  portions  of  the  lung,  and  even  whole  lobes,  may  become  infiltrated 
throughout — generalized  lobular  pneumonia. 

Symptoms. — The  primary  catarrhal  pneumonia  which  not  infrequently  occurs 
in  adults  usually  begins  with  the  same  phenomena  as  a  severe  attack  of  acute 
bronchitis.  The  patient  feels  prostrated,  has  cough,  dyspnoea,  and  pain  upon  that 
side  which  is  chiefly  affected.  The  fever  is  not  very  high,  say  101°  to  103°  (SS'ö0 
to  39'5°  C),  and  it  does  not  follow  any  regular  course.  The  expectoration  is  simply 
catarrhal,  not  bloody  as  in  croupous  pneumonia.  Upon  physical  examination  are 
found  moist  rales,  seldom  marked  bronchial  breathing,  and  a  dullness  upon  per- 
cussion which  is  usually  only  moderate,  or  else  a  tympanitic  percussion-note  over 
the  diseased  area.  The  illness  may  last  two  or  three  weeks,  or  even  longer.  There 
is  never  a  crisis,  the  fever  ending  gradually  by  lysis. 

Most  of  the  cases  of  catarrhal  pneumonia  develop,  as  we  have  already  said, 
secondarily  in  the  course  of  other  affections,  hence  the  symptoms  are  frequently 
overshadowed  by  those  of  the  other  disease.  There  are  often  found  at  autopsy  a 
few  foci  of  lobular  pneumonia  in  the  lower  lobes  which  gave  rise  to  no  clinical 
symptoms  whatever. 

In  other  cases,  however,  the  development  of  extensive  lobular  pneumonia  is 
of  the  greatest  clinical  significance.  The  disturbance  of  respiration,  during  the 
patient's  life,  forms  the  most  striking  symptom  of  the  disease,  and  lobular 
pneumonia  is  shown  at  the  autopsy  to  be  the  immediate  cause  of  death.  The 
largest  part  of  the  fatal  cases  of  measles  and  whooping-cough,  and  no  very  small 
part  of  those  of  diphtheria,  scarlet  fever,  typhoid,  or  small-pox,  are  due,  in  the 
last  instance,  to  the  disturbance  of  respiration  dependent  upon  lobular  pneu- 
monia. 

Since  a  diffuse  bronchitis,  extending  into  the  finer  bronchi,  almost  always  pre- 
cedes the  development  of  lobular  pneumonia,  and  since  it  may  also  give  rise  in 
itself  to  marked  disturbance  in  respiration,  there  is  no  sharp  boundary  to  be  drawn 
clinically  between  diffuse  capillary  bronchitis  and  lobular  pneumonia.  Only  the 
experience,  a  hundred  times  repeated,  that  every  extensive  capillary  bronchitis 
readily  leads  to  lobular  pneumonia*  permits  us  to  suspect  the  latter,  with  consider- 
able certainty,  even  if  there  is  no  direct  clinical  evidence  of  it. 

The  type  of  lobular  pneumonia  seen  in  childhood  is  the  most  characteristic  and 
the  most  important  clinically.  It  is  observed  in  measles  and  whooping-cough, 
and  also  in  weak,  atrophic,  and  rachitic  children.  The  increased  frequency  of 
respiration  is  most  striking.  The  breathing  is  superficial,  but  labored,  as  is  shown 
by  the  contraction  of  the  auxiliary  muscles  of  inspiration  and  the  play  of  the  nos- 
trils. We  also  notice  inspiratory  retraction  of  the  lower  lateral  portions  of  the 
thorax  as  a  result  of  the  incomplete  entrance  of  air.  The  number  of  respirations 
a  minute  increases  ha  children  to  sixty  or  eighty,  or  even  more.  In  most  cases 
the  child  has  a  frequent  and  apparently  painful  cough.  Expectoration  is  entirely 
absent  in  small  children.  When  it  is  present  it  shows  no  characteristic  peculiari- 
ties different  from  ordinary  catarrhal  sputum.     The  general  condition  is  always 


CATARRHAL  PNEUMONIA.  187 

bad.  The  child  is  restless,  apathetic,  and  more  or  less  stupid.  Its  face  is  usually- 
pale,  but  often  quite  cyanotic.  The  pulse  is  very  rapid,  and  in  small  children  may 
attain  a  frequency  of  140  to  180  a  minute.  Fever  is  almost  always  present.  It 
shows  no  typical  course,  it  is  now  remitting  and  now  intermitting,  and  toward 
evening  it  perhaps  rises  to  104°  or  105°  (39"5o-40'5°  C).  The  occurrence  of  such  a 
high  rise  in  temperature  is  not  without  value  in  the  diagnosis  of  catarrhal  pneu- 
monia. If  in  diffuse  capillary  bronchitis  a  high  fever  is  present  for  some  time, 
we  may  assume  with  considerable  certainty  that  the  formation  of  lobular  nodules 
has  already  begun. 

Physical  examination  furnishes  direct  evidence  of  the  affection  of  the  lungs, 
but  its  results  are  for  the  most  part  to  be  referred  to  the  diffuse  bronchitis  and 
not  to  the  lobular  infiltration.  Auscultation  gives  the  most  valuable  signs.  We 
hear  over  the  lungs,  in  a  greater  or  less  extent,  numerous  small  and  medium  moist 
rales,  often  quite  high-pitched.  From  these  signs,  strictly  interpreted,  we  can 
diagnosticate  merely  bronchitis,  but  we  may  suspect  pneumonia  with  the  greatest 
probability.  With  very  confluent  broncho-pneumonia  auscultation  sometimes 
gives  bronchial  breathing  and  bronchophony  beside  the  rales. 

It  goes  without  saying  that  little  lobular  nodules,  surrounded  by  normal 
lung-tissue  containing  air,  give  no  special  signs  on  percussion.  With  numer- 
ous nodules  running  into  one  another,  the  percussion-note  is  duller,  and  there 
is  sometimes  tympanitic  resonance.  The  dullness  is  often  first  to  be  made  out 
over  a  stripe  extending  along  the  vertebral  column — the  so-called  "  stripe-pneu- 
monia." 

Course  and  Termination. — An  attack  of  extensive  lobular  pneumonia  is  usu.- 
ally  quite  protracted.  Even  in  favorable  cases  the  disease  rarely  lasts  less  than 
two  or  three  weeks,  and  it  may  persist  much  longer.  The  course  of  the  disease  is 
apt  to  be  irregular,  relapses  succeeding  improvement.  The  chief  danger  of  the 
disease  lies  in  this  tendency  to  a  protracted  course,  extending  over  weeks  and 
months.  Many  children  finally  die,  not  of  the  lobular  pneumonia  itself,  but  from 
the  general  weakness  and  emaciation  following  the  tedious  febrile  disease.  We 
must  remember,  however,  that  complete  recovery  may  sometimes  take  place  quite 
late  in  the  disease. 

The  "transition  of  catarrhal  pneumonia  to  caseation  and  tuberculosis"  is  a 
clinical  fact  with  which  physicians  have  long  been  conversant.  In  fact,  we  often 
find  true  tubercular  changes  in  the  lungs  of  children  who  have  died  after  a  tedious 
illness,  as  a  result  of  measles,  whooping-cough,  etc.  There  can,  of  course,  be  no 
real  question,  however,  of  an  actual  transition  from  one  disease  to  the  other.  In 
such  cases  we  have  to  do  either  with  an  acquired  tubercular  infection,  which  has 
found  a  favoi'able  soil  in  an  already  diseased  lung,  or  (what  is  probably  more  fre- 
quently the  case)  the  disease  of  the  lung  has  promoted  the  development  of  a  pre- 
viously existing  tuberculosis.  It  is  usually  weak  children,  with  a  hereditary  pre- 
disposition to  tubercle,  who  succumb  to  tuberculosis  as  a  result  of  the  above-named 
diseases.  The  diagnosis  of  a  developing  tuberculosis  is  not  always  easy,  since  it 
is  only  rarely  that  marked  phthisical  changes — like  dullness  at  the  apex,  cavities, 
etc.,  which  can  be  made  out  by  a  physical  examination — are  found  in  the  lungs. 
We  can  usually  suspect  tuberculosis  only  from  the  general  conditions — emacia- 
tion, persistent  hectic  fever,  hereditary  predisposition,  or  some  secondary  tubercu- 
lar disease  like  meningitis,  etc. — especially  as  absolute  proof,  from  the  detection 
of  tubercle  bacilli  in  the  sputum,  is  only  rarely  possible  in  children. 

The  transition  of  inflammatory  lobular  nodules  to  purulent  foci  (abscesses),  or 
nodules  of  gangrene,  which  sometimes  happens,  especially  in  small-pox,  depends 
upon  the  specific  malignant  property  of  the  agents  of  inflammation  which  have 
entered  the  bronchi. 


1SS  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

If  the  lobular  nodules  extend  to  the  pleura,  a  secondary  sero-fibrinous  or  even 
purulent  pleurisy  may  develop. 

Treatment. — Since  we  have  already  mentioned  the  proper  treatment,  in  our 
description  of  the  various  diseases  in  which  secondary  pneumonia  is  especially 
prone  to  develop,  we  can  now  be  brief.  We  have  also  laid  repeated  stress  upon 
the  possibility  and  the  great  practical  importance  of  prophylaxis,  which  is  self- 
evident  from  a  just  comprehension  of  the  origin  of  lobular  pneumonia.  Besides 
keeping  the  cavities  of  the  nose,  the  mouth,  and  the  pharynx  as  clean  as  possible, 
tepid  baths,  with  cool  douching  later,  are  the  best  means  of  preventing  the  devel- 
opment of  lobular  pneumonia,  or  of  checking  its  further  extension  if  possible. 
Cold  packs  are  often  used  with  advantage,  but  they  are  more  disagreeable  to  many 
patients  than  baths.  It  is  an  advantage,  which  is  indeed  to  be  considered  in  the 
second  rank  in  comparison  with  the  improvement  in  respiration,  that  by  both  the 
bath  and  the  pack  the  febrile  temperature  is  at  the  same  time  reduced. 

In  the  treatment  of  the  lobular  pneumonia  of  children  a  wet  pack  including 
the  whole  body  is  the  best  remedy.  A  sheet  is  dipped  in  water,  wrung  out,  and 
wrapped  around  the  whole  of  the  patient  except  his  head  and  arms.  Outside  of 
this  is  to  be  placed  a  dry  woolen  blanket  or  a  layer  of  oiled  muslin.  The  temper- 
ature of  the  water  employed  should  be  68°  to  77°  (16°  to  20°  R).  The  higher  the 
fever  the  colder  should  the  water  be,  and  the  oftener,  say  every  hour,  must  the 
pack  be  renewed.  In  milder  cases  and  at  night  it  may  be  allowed  to  remain  for 
three  or  four  hours.  The  beneficial  influence  of  the  pack  is  shown  not  only  by 
the  temperature,  but  still  more  by  the  respiration.  If  the  breathing,  despite  this 
remedy,  remains  unsatisfactory,  and  the  patient  becomes  more  and  more  stupefied, 
the  treatment  must  be  changed  to  lukewarm  baths  of  a  temperature  of  77°  to  86° 
(20°  to  24°  R.),  with  douchings  of  colder  water.  It  is  sometimes  advisable  in 
severe  cases  to  add  to  the  water  employed  for  bathing  or  for  the  wet  pack  a  few 
handfuls  of  mustard.    The  stimulation  thus  exerted  upon  the  skin  is  quite  marked. 

Among  external  applications  to  the  chest,  beside  mustard  plasters  and  poul- 
tices, dry  cups  are  to  be  mentioned,  which  often  do  very  good  service  in  strong, 
older  children,  and  especially  in  adults.  We  never  need  to  use  local  blood-let- 
tings, however,  in  catarrhal  pneumonia. 

Of  internal  remedies,  expectorants  are  most  used.  Chief  among  these  are 
ipecac,  senega,  and  benzoic  acid.  This  last  is  particularly  useful  in  the  lobular 
pneumonia  of  children.  In  strong  children  the  abundant  collection  of  mucus  in 
the  bronchi  may  sometimes  be  relieved  by  the  administration  of  an  emetic.  We 
should  be  cautious  in  the  use  of  narcotics.  Stimulants  (camphor,  wine)  must  be 
used  in  severe  cases.  Inhalations  are  quite  valueless  in  lobular  pneumonia,  yet  it 
is  recommended  to  keep  the  air  in  the  sick-chamber  rather  moist  by  hanging  up 
wet  towels,  or  by  sprinkling  with  water.  The  room  should  also  be  as  large  and 
as  well  ventilated  as  possible.  The  general  hygienic  treatment  is  of  the  greatest 
importance.  One  of  the  most  important  duties,  of  which  the  physician  must 
always  be  mindful,  is  to  keep  up  the  patient's  strength  by  sufficient  and  proper 
food.  When  convalescence  sets  in,  complete  restoration  to  health  may  be  fur- 
thered by  a  suitable  residence  in  the  country. 


CROUPOUS  PNEUMONIA.  189 

CHAPTER  V. 

CROUPOUS   PNEUMONIA. 

{Lung  Fever.     Lobar  Pneumonia.     Fibrinous  Pat  umonia.     Pleuro-pneumonia.) 

Croupous  pneumonia  is  an  acute  febrile  disease  of  the  lungs,  very  sharply 
defined  both  anatomically  and  clinically.  It  is  one  of  the  most  important  and 
most  common  of  the  severe  acute  diseases.  It  is  generally  known  among  the 
laity  by  the  name  of  "  lung  fever."  Since  secondary  pneumonia  may  develop  in 
the  course  of  various  other  diseases,  like  typhoid,  small-pox,  or  diphtheria,  and 
may  anatomically  have  all  the  signs  of  croupous  pneumonia,  but  aetiologically  be 
quite  distinct  from  it,  we  speak  of  this  pneumonia  as  primary,  genuine  pneumonia, 
in  opposition  to  the  other  forms.  The  physical  signs  and  the  disturbances  of 
respiration  are  of  course  the  same  in  primary  pneumonia  as  in  secondary.  The 
whole  typical  picture  of  the  disease,  which  is  so  striking,  is  seen,  however,  only 
in  genuine  croupous  pneumonia,  of  which  we  will  make  exclusive  mention  in 
what  follows. 

iEtiology. — The  majority  of  pathologists  have  now  become  convinced,  from  a 
series  of  clinical  observations,  that  the  cause  of  pneumonia  is  to  be  sought  in  an 
infectious  agent  which  enters  the  lungs  and  there  gives  rise  to  the  development  of 
an  inflammatory  process.  This  conception  of  croupous  pneumonia  as  an  acute 
infectious  disease,  with  which  alone  all  the  pathological  appearances  readily  coin- 
cide, has  been  more  and  more  verified  by  all  the  recent  investigations.  The  pre- 
cise germ  of  the  disease  has  not  yet,  however,  been  fully  determined.  Friedländer, 
indeed,  has  almost  invariably  found  in  the  pneumonic  lung  a  special  kind  of 
micrococcus,  or,  to  speak  more  coi'rectly,  bacillus,  which,  singly  or  in  larger  num- 
bers, is  inclosed  in  a  characteristic  shell  or  capsule — "capsule  coccus" — and  on 
cultivation  shows  a  peculiar  "  nail-like"  growth  in  the  culture  gelatine;  but  since 
quite  similar  cocci  are  also  found  under  other  conditions,  there  is  no  definite  proof 
at  present  that  they  are  really  the  pathogenic  agents  in  pneumonia,  particularly 
as  the  results  of  experiments  upon  animals  have  not  been  unambiguous. 

[Friedländer  himself  has  now  agreed  that  the  capsule  is  simply  accidental, 
probably  due  to  imperfect  staining  or  decolorization.  Talamon  has  produced 
pneumonia  in  animals  by  the  injection  of  the  ovoid  coccus  in  pure  culture,  but 
has  obtained  also  a  similar  result  with  round  cocci.  Thus  the  question  of  the 
coccus  of  pneumonia  is  still  undetermined.] 

A.  Fränkel  has  lately  obtained  by  means  of  pure  cultivation  from  the  lungs 
in  pneumonia  a  lancet-shaped  diplococcus,  or,  more  correctly,  bacillus,  to  which 
he  ascribes  an  serological  significance.  This  bacillus  appears  to  be  identical  with 
that  sometimes  seen  in  the  saliva,  even  in  that  of  healthy  persons,  and  it  is  the 
cause  of  the  so-called  "  sputum  septicaemia"  which  can  be  artificially  produced  in 
animals,  particularly  in  rabbits.  Fränkel's  statements  have  been  confirmed  by 
Weichselbaum,  so  that  the  very  frequent  occurrence  of  Fränkel's  bacillus  in  lungs 
affected  with  pneumonia  is  indubitable,  but  an  absolute  proof  that  these  bacilli 
are  the  genuine  cause  of  croupous  pneumonia  has  not  yet  been  furnished.  Sup- 
posing the  infectious  nature  of  pneumonia  to  be  certain,  all  the  other  alleged 
causes  may  of  course  be  regarded  as  at  most  "predisposing  causes."  The  old 
opinion,  which  is  yet  current,  that  pneumonia  is  due  to  catching  cold,  is  to  be 
received  with  great  limitations,  for  croupous  pneumonia  is  very  frequently 
seen  independently  of  any  such  influence.  In  a  good  many  cases  it  will  be 
found  that  an  exposure  to  cold  immediately  preceded  the  commencement  of  the 
disease;  but  in  these  instances  the  cold  is  probably  to  be  regarded  merely  as  that 


190  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

circumstance  which,  promoted  the  occurrence  of  the  infection,  possibly  because 
of  the  resultant  injury  to  the  bronchial  and  pulmonary  epithelium.  This  explains 
the  fact  that  pneumonia  is  especially  frequent  in  certain  classes,  for  instance, 
among  day-laborers  and  soldiers.  With  regard  to  the  so-called  "  traumatic  pneu- 
monia," the  state  of  the  case  is  similar  to  that  of  pneumonia  due  to  cold.  Patients 
from  the  classes  who  work  hard  physically  sometimes  assert  that  they  were  taken 
ill  as  a  result  of  heavy  lifting  or  of  a  blow  on  the  chest,  but  in  such  cases  the 
subsequent  stitch  in  the  side  was  probably  not  the  result  of  the  injury,  but  a 
symptom  of  the  disease  which  had  previously  begun  to  develop. 

It  is  a  noteworthy  fact  in  favor  of  our  conception  of  pneumonia  as  an  acute 
infectious  disease  that  it  may  be  endemic ;  which  sometimes,  though  rarely,  seems 
to  be  quite  certain.  Extensive  endemics  of  pneumonia,  usually  of  quite  a  malig- 
nant character,  have  been  repeatedly  observed  in  single  buildings,  especially  in 
barracks  or  prisons,  as  well  as  in  tenement  houses  and  other  localities. 

Pneumonia  does  not  show  a  decided  epidemic  character.  In  a  large  popula- 
tion sporadic  cases  occur  at  any  season,  but,  on  the  other  hand,  we  may  notice  a 
striking  increase  of  pneumonia  at  many  times.  Most  attacks  occur  in  the  winter 
or  spring  months,  without  any  necessary  relation,  however,  between  the  frequency 
of  pneumonia  and  the  occurrence  of  especially  bad,  wet,  or  cold  weather. 

Individual  predisposition  plays  an  unmistakable  part  in  the  disease,  as  we  must 
suppose  that  it  does  in  all  infectious  diseases.  Like  facial  erysipelas  and  acute 
articular  rheumatism,  pneumonia  is  one  of  those  diseases  which  is  prone  to  attack 
the  same  individual  several  times.  There  are  persons  who  have  had  acute  pneu- 
monia four  or  five  or  even  more  times  in  their  lives. 

We  can  not  affirm  with  certainty  that  the  liability  to  pneumonia  is  due  to  a 
special  bodily  constitution.  The  strongest  and  most  robust  often  fall  ill  with  it, 
and,  on  the  other  hand,  weak  and  delicate  people,  with  a  tendency  to  phthisis,  are 
frequently  attacked.  Drunkards  seem  to  have  a  special  predisposition  to  the  dis- 
ease, but  of  course  it  is  exceedingly  hard  to  give  any  definite  statistics  upon  this 
point. 

Pneumonia  occurs  at  any  time  of  life,  most  frequently  in  youth  or  middle  age ; 
but  it  is  by  no  means  rare  in  early  childhood,  and  also  in  more  advanced  years  up 
to  sixty  or  seventy.  In  general  it  is  observed  rather  more  often  in  men  than  in 
women. 

[Defective  house  drainage  seems  to  be  a  predisposing  cause  of  pneumonia  in 
some  cases.  A  careful  inspection  of  the  local  sanitary  conditions  is  desirable, 
especially  where  more  than  one  case  occurs  in  a  house.] 

Pathological  Anatomy. — The  anatomical  process  in  croupous  pneumonia  con- 
sists in  the  formation  of  a  hsemorrhagic,  coagulable  "  fibrinous  "  or  "  croupous  " 
exudation  into  the  pulmonary  alveoli  and  the  smallest  bronchi.  The  develop- 
ment of  the  exudation  usually  extends  over  one  or  more  lobes  to  their  whole 
extent,  and,  as  the  alveoli  and  fine  bronchi  are  completely  filled  by  the  tough 
exudation,  the  spongy  lung,  filled  with  air,  is  changed  to  a  firm  tissue,  devoid  of 
air,  except  as  it  is  penetrated  by  the  large  bronchi. 

Since  Laennec's  day  we  distinguish  three  stages  in  the  development  of  the  pro- 
cess. In  the  first  stage  (stage  of  inflammatory  engorgement,  engouement)  the 
lung  is  very  hyperaemic,  dark  red,  and  the  air  contained  in  it  is  even  now  much 
diminished,  but  not  entirely  absent.  The  alveoli  are  filled  with  an  abundant 
exudation,  already  hasrnorrhagic,  but  still  fluid  and  not  coagulated. 

In  the  second  stage  (stage  of  red  hepatization)  the  coagulation  of  the  exudation 
is  complete,  and  the  lung  has  become  throughout  of  the  consistency  of  liver.  The 
hepatized  lung  shows  a  somewhat  increased  volume,  and  is  strikingly  hard.  The 
surface  of  the  section  has  a  red  and  manifestly  granular  appearance,  which  is  due 


CROUPOUS  PNEUMONIA.  l<jl 

to  the  projection  of  the  numerous  little  fibrinous  plugs  situated  in  the  alveoli. 
With  the  knife  we  can  scrape  off  a  tenacious,  creamy,  grayish-red  fluid  from  the 
surface  of  the  section.  In  the  small  bronchi,  divided  by  the  section  of  the  lung, 
we  find  characteristic  tubular  bronchial  casts. 

In  the  third  stage  (stage  of  yellow  or  gray  hepatization),  which  gradually 
develops  from  the  second,  the  red  color  of  the  surface  of  the  section  changes  to  a 
yellowish  gray,  while  the  contents  of  the  exudation  grow  poorer  in  red  but  richer 
in  white  blood-corpuscles.  The  consistency  of  the  lung  is  still  dense  but  more 
boggy.  The  fluid  scraped  from  the  surface  of  the  section  is  more  abundant,  milky, 
and  more  like  pus.  We  also  speak,'  therefore,  of  a  "stage  of  purulent  infiltra- 
tion." 

The  recovery  from  the  process  begins  as  the  exudation  becomes  fluid.  The 
fluid  is  in  part  absorbed  and  in  part  coughed  up. 

It  is  not  necessary  for  every  pneumonia  to  go  through  all  three  stages  com- 
pletely.    In  mild  cases  the  process  may  stop  sooner  and  go  on  to  recovery. 

Concerning  the  finer  histological  processes  in  croupous  pneumonia,  the  pri- 
mary change  is  probably  to  be  found  in  the  injury  and  partial  destruction  of  the 
epithelium  in  the  alveoli  and  smallest  bronchi,  produced  by  inflammation  due  to 
the  specific  causes  of  the  disease.  As  in  every  croupous  inflammation  of  a  mucous 
membrane  (see  the  chapter  on  diphtheria),  a  coagulable  exudation  is  formed  on  the 
surface  of  the  alveoli  and  smaller  bronchi  after  the  destruction  of  the  epithelium. 
With  the  microscope  we  see  the  fibrinous  net-work  of  the  exudation  filling  the 
alveoli.  Between  its  meshes  lie  numerous  red  blood-corpuscles — red  hepatization. 
Where  there  is  any  of  the  alveolar  epithelium  left,  we  often  notice  active  pro- 
liferation— increase  and  growth  of  cells.  Later  on  the  white  blood-corpuscles 
increase,  migrating  from  the  vessels  into  the  exudation — yellow  hepatization. 
The  red  blood-corpuscles  are  dissolved  unless  they  are  removed  by  expectoration. 
The  fibrinous  exudation  is  also  gradually  dissolved  as  the  result  of  chemical 
changes  not  yet  clearly  understood  (peptonization  of  the  albuminous  substances  ?), 
and  is  absorbed  like  the  cells.  The  regeneration  of  the  missing  epithelium  comes 
from  the  epithelium  that  has  remained  intact,  and  with  that  follows  a  gradual 
and  complete  restitutio  ad  integrum. 

The  whole  process  is  comparatively  brief,  usually  running  its  course  in  a  week 
or  ten  days.  The  most  frequent  termination  is  in  complete  recovery.  The  other 
methods  of  termination,  as  well  as  the  complications  in  other  organs,  will  be 
spoken  of  in  connection  with  the  clinical  symptoms.  We  may  here  mention 
simply  that  the  pleura  over  the  affected  portion  of  the  lung  takes  part  in  the 
inflammation,  without  exception,  as  soon  as  the  disease  reaches  the  periphery, 
and  a  fibrinous  pleurisy,  which  is  not  very  intense,  may  then  be  recognized ; 
hence  the  former  use  of  the  terms  " pleuro-pneumonia "  and  "peripneumonia." 

Croupous  pneumonia  usually  spreads  rapidly  over  a  great  part  of  the  lung.  It 
is  very  often  quite  sharply  limited  to  a  single  lobe — "  lobar  pneumonia  " — so  that 
the  septum  of  connective  tissue  between  two  lobes  also  forms  a  strict  boundary 
between  pneumonic  infiltration  and  healthy  lung  tissue ;  but  this  boundary  is  by 
no  means  insurmountable,  and  quite  frequently  several  lobes  are  wholly  or  in 
part  attacked  by  pneumonia.  According  to  all  statistics,  the  lower  lobes  are  more 
frequently  affected  than  the  upper.  Isolated  disease  of  the  right  middle  lobe  may 
occur,  but  it  is  much  rarer  than  pneumonia  of  the  upper  lobes.  Of  the  two  lungs, 
the  right  is  attacked  with  decidedly  greater  frequency  than  the  left.  We  have 
ourselves  seen,  in  244  cases,  137  on  the  right,  86  on  the  left,  and  21  in  which  both 
lungs  were  attacked  to  a  great  extent.  Simultaneous  affection  of  the  lower  lobe 
on  one  side  and  the  upper  lobe  on  the  other — quite  a  rare  occurrence — is  termed 
"  crossed  pneumonia." 


192  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

General  Course  of  the  Disease. — In  spite  of  the  numerous  modifications  which 
the  course  of  pneumonia  may  undergo  in  individual  instances,  we  can  still  call 
pneumonia  a  typical  disease,  considering  the  great  majority  of  cases.  The  sub- 
jective and  objective  symptoms  dependent  upon  the  local  affection  of  the  lung 
usually,  but  not  always,  take  the  chief  place  among  the  clinical  appearances. 
In  this,  pneumonia  differs  from  many  other  infectious  diseases,  like  typhoid,  in 
which  the  local  affection  is  subordinated  to  the  general  infection. 

Pneumonia  usually  begins  quite  suddenly.  In  the  majority  of  cases  it  starts 
with  a  pronounced  chill  of  half  an  hour  to  an  hour's  duration,  or  at  least  with  a 
marked  and  prolonged  chilliness.  The  initial  chill  may  attack  the  patient  while 
in  the  best  of  health.  It  comes  on  in  the  day-time,  in  the  evening,  or  even  in  the 
middle  of  the  night,  after  a  previously  quiet  sleep.  At  the  same  time  the  patient 
almost  always  feels  as  if  a  severe  illness  were  beginning. 

In  other  and  somewhat  rarer  cases  the  beginning  of  pneumonia  is  more  grad- 
ual. A  prodromal  stage  of  a  few  days,  or  even  longer,  precedes  the  severe  illness. 
The  symptoms  are  either  of  quite  a  general  and  indefinite  nature,  consisting  of 
malaise,  dullness,  loss  of  appetite,  and  headache,  or  the  signs  of  a  pulmonary 
affection  follow  the  prodromal  symptoms  more  closely.  The  patient  always  com- 
plains, for  some  days  or  weeks  before  the  special  severe  illness,  of  cough,  some 
pain  in  the  chest,  or  slight  trouble  with  breathing.  We  can  not  usually  be  sure 
whether  these  prodromata  belong  to  pneumonia  or  not:  a  pre-existing  simple 
bronchitis  may  often  furnish  the  most  favorable  soil  for  the  development  of  pneu- 
monia. 

In  the  cases  where  the  disease  begins  more  slowly,  the  onset  of  severe  symptoms 
is  sometimes  marked  distinctly  by  a  chill  or  by  sudden  thoracic  distress.  In  other 
cases  the  patient  grows  worse  gradually,  without  any  abrupt  change. 

The  subjective  symptoms  in  the  chest  begin,  as  a  rule,  a  short  time  after  the 
onset  of  the  disease,  on  the  first  day  or  only  a  little  later.  The  patient  feels  on 
every  deep  inspiration  a  stabbing  pain  in  one  side.  The  breathing  is  shallow, 
accelerated,  and  often  somewhat  irregular.  Later  on,  in  severe  cases,  there  is  very 
marked  dyspnoea  and  rapidity  of  respiration.  There  is  usually  an  irritating 
cough  from  the  beginning  of  the  disease.  The  cough  is  painful,  and  hence  short, 
half  suppressed,  and  quite  frequent  and  troublesome.  Prom  the  second  day  the 
expectoration  may  assume  its  characteristic  viscid,  rusty,  hemorrhagic  appear- 
ance. Physical  examination  gives  on  percussion  and  auscultation  the  signs  to 
be  described  more  fully  below.  These  are  rarely  to  be  found  on  the  first  day,  but 
more  frequently  on  the  second,  and  sometimes  not  till  later. 

Among  the  appearances  in  other  organs  we  may  mention,  as  the  most  impor- 
tant in  diagnosis,  the  very  frequent  occurrence  of  herpes  on  the  lips  or  on  the 
alas  of  the  nose.  In  severe  cases  there  are  sometimes  marked  symptoms  on  the 
part  of  the  nervous  system — headache,  sleeplessness,  and  delirium.  The  appetite 
is  usually  completely  lost.  Vomiting  is  not  infrequent,  especially  in  the  begin- 
ning of  the  disease.  The  bowels  are  usually  constipated,  but  diarrhoea  may  some- 
times be  present. 

Pneumonia  is  almost  always  associated  with  high  fever.  The  typical  character 
of  the  disease  may  be  best  demonstrated  by  the  behavior  of  the  temperature  curve. 
A  corresponding  increase  in  the  frequency  of  the  pulse  is  seen  with  the  increase 
of  the  temperature. 

The  course  varies  greatly  according  to  the  previous  individual  circumstances, 
the  severity  of  the  disease,  and  the  existence  of  complications.  In  the  majority  of 
cases,  after  a  comparatively  short  duration,  the  disease  takes  a  favorable  turn. 
The  beginning  of  improvement  is  often  sudden,  like  the  onset  of  the  disease. 
After  the  symptoms  have  lasted  for  some  five  to  seven  days,  or  in  rarer  cases  a 


CROUPOUS  PNEUMONIA.  L93 

shorter  or  a  longer  time,  at  a  constant  height  or  with  increasing  intensity,  there 
occurs  in  the  regular  course  of  the  disease  a  critical  decline  of  the  fever,  fre- 
quently associated  with  quite  a  copious  perspiration,  and  with  that  a  very  rapid 
improvement  of  all  the  other  symptoms.  In  a  short  time  complete  recovery 
follows. 

In  other  cases,  however,  the  course  is  not  so  favorable.  The  disease  may  have 
a  fatal  termination.  In  a  third  small  class  of  cases  the  disease  finally  takes  a  pro- 
tracted course,  which  is  usually  due  to  the  occurrence  of  abnormal  seouela:  in  the 
lungs. 

Description  of  Single  Symptoms  and  Complications. 

1.  Symptoms  on  the  Part  of  the  Lungs.— The  chief  subjective  symptom  in  pneu- 
monic patients  is  the  characteristic  painful  feeling  in  the  affected  side — the  "  stitch 
in  the  side."  This  probably  always  has  its  origin  in  the  dry  pleurisy  which  accom- 
panies the  pnetimonia.  It  is  therefore  absent  in  the  cases  of  central  pneumonia 
(vide  infra).  In  pneumonia  of  the  lower  and  right  middle  lobes  the  pain  is  visu- 
ally more  severe  than  in  pneumonia  of  the  upper  lobes.  One  result  of  the  stitch 
in  the  side  is  the  difficulty,  or  even  the  impossibility,  of  deep  inspiration.  Hence 
the  patient's  dyspnoea  is  considerably  increased,  and  this  explains  the  incongruity 
between  the  shortness  of  breath  and  the  relatively  slight  extent  of  the  pneumonia 
in  many  cases.  The  subjective  feeling  of  difficulty  of  breathing  is  present  in  the 
majority  of  cases,  and  it  may  become  most  distressing. 

Cough  is  one  of  the  most  constant  symptoms  in  pneumonia,  and  is  usually  very 
painful ;  hence  the  patient  often  tries  to  suppress  it.  Expectoration  is  apt  to  be 
very  difficult  at  the  onset  of  the  disease,  from  the  viscidity  and  scanty  amount  of 
the  sputum;  hence  very  severe  and  distressing  paroxysms  of  coughing  are  some- 
times observed.  The  cause  of  the  cough  is  probably  not  to  be  found  in  the  affec- 
tion of  the  alveoli,  but  in  the  co-existing  bronchitis.  The  irritation  of  the  pleura 
may  also  set  up  a  reflex  cough.  In  rare  cases  cough  is  entirely  absent  in  pneu- 
monia. Except  in  the  cases  of  limited  or  late  localization  (vide  infra),  we  observe 
this  absence  of  cough  chiefly  in  the  pneumonia  of  old  or  very  weak  people,  and 
also,  what  is  of  practical  importance,  in  the  drunkard's  pneumonia  associated  with 
delirium  tremens. 

The  pneumonic  expectoration  is  so  characteristic  that  we  can  often  make  the 
diagnosis  of  croupous  pneumonia  from  this  alone.  It  consists  of  a  very  tough 
mucus,  which  sticks  fast  to  the  bottom  of  the  vessel,  and  is  mixed  with  blood,  and 
therefore  has  a  more  or  less  intense  red  or  yellow  haemorrhagic  color.  In  indi- 
vidual cases  there  are  numerous  gradations.  We  usually  call  the  pneumonic  spu- 
tum "rusty,"  or  "brick-red,"  or  of  a  "prune-juice  color."  etc.  Sometimes  it  has 
only  a  slight  reddish  or  yellowish  tint,  and  sometimes  it  consists  almost  entirely  of 
blood.  In  some  cases  it  assumes  a  peculiar  grass-green  color,  which  is  clue  to  a 
change  in  the  blood  coloring-matter,  or  to  a  mixture  with  bile  pigment  in  "  bilious 
pneumonia." 

The  red  color  of  the  sputum,  as  microscopic  examination  shows,  is  due  to 
numerous  red  blood-corpuscles,  still  well  preserved,  mixed  with  it.  Thev  are 
however,  in  part  dissolved,  and  hence  cause  the  uniform  red  color  of  the  sputum. 
Separate  spots  containing  much  blood  are  often  seen  in  it.  Besides  the  red  blood- 
corpuscles,  the  microscope  shows  numerous  partly  swollen  or  fatty  degenerated 
pus-corpuscles.  We  also  see  long  threads  of  mucus;  sometimes  large,  round,  pig- 
mented cells  (alveolar  epithelium  ?) ;  and  finally,  in  rare  cases,  ciliated  epithelium 
and  crystals  of  haematoidin.  Micrococci  always,  and  capsule-cocci  frequently 
{vide  supra),  are  to  be  found  in  stained  preparations,  but  these  have  at  present  no 
diagnostic  value,  since  nothing  certain  is  known  as  yet  as  to  their  significance. 
13 


194  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

We  have  still  to  mention  the  bronchial  casts  as  important  constituents  of  pneu- 
monic sputum.  Since  they  are  usually  rolled  up  together,  we  may  not  find  them 
except  by  spreading  out  the  sputum  in  water.  They  consist  of  the  most  beautiful 
casts  of  the  small  bronchi,  with  many  dichotomous  divisions,  and  are  a  product  of 
the  croupous  inflammation  extending  into  the  bronchi.  The  casts  of  the  smallest 
bronchi  are  sometimes  found  in  the  form  of  "spirals,"  like  those  in  asthmatic 
bronchitis  (see  page  169). 

The  amount  of  the  pneumonic  sputum  is,  as  a  rule,  not  very  considerable,  but 
it  differs  a  good  deal  in  different  cases.  The  chemical  examination  of  the  sputum 
has  so  far  given  no  remarkable  results.  The  amount  of  common  salt  contained  in 
it  is  quite  considerable. 

In  many  cases  the  pneumonic  expectoration  is  absent.  Sometimes  it  is  very 
tough  and  slimy,  but  without  any  admixture  of  blood;  in  other  cases  the  sputum 
is  simply  catarrhal,  when  present  at  all,  and  then,  of  course,  it  comes  not  from  the 
parts  infiltrated  with  pneumonia,  but  from  the  catarrh  of  the  larger  bronchi.  We 
often  find  simple  catarrhal  sputum,  too,  beside  the  characteristic  pneumonic 
sputum. 

The  pneumonic  sputum  sometimes  is  seen  in  the  first  or  second  day  of  pneu- 
monia, but  perbaps  not  till  later.  With  the  beginning  of  resolution  it  gradually 
loses  its  characteristic  appearance.  The  expectoration  then  becomes  less  tenacious 
and  simply  muco-purulent,  and  finally  disappears  entirely. 

Physical  Examination. — Inspection  shows  no  especial  anomaly  in  the  general 
contour  of  the  thorax.  A  marked  bulging  of  the  affected  side  occurs  only  when 
there  is  also  abundant  effusion  into  the  pleural  cavity.  The  action  of  the  thorax 
in  respiration  is  very  important.  With  a  limited  pneumonia  we  often  notice  a 
very  marked  delay  and  limitation  of  motion  of  the  affected  side  on  inspiration. 
This  is  due  in  part  to  the  pain  in  the  side,  which  comes  on  with  every  deep  inspi- 
ration, and  also,  in  extensive  pneumonia,  of  course,  to  the  physical  conditions 
resulting  from  the  anatomical  changes.  The  unaffected  portions  of  the  lung  act 
all  the  more  forcibly. 

The  acceleration  of  respiration  is  very  striking,  its  frequency  increasing  to 
thirty  or  forty,  or  even  more,  a  minute.  We  have  repeatedly  counted  sixty  respira- 
tions in  adults,  even  in  cases  that  finally  resulted  favorably.  The  breathing  is 
shallow,  but  yet  in  all  severe  cases  very  labored.  ■  We  see  the  inspiratory  con- 
traction of  the  sterno-cleido-mastoicls  and  scaleni  in  the  neck,  aud  often  in  the  face 
a  marked  dilatation  of  the  nostrils  on  inspiration.  The  patient  usually  reclines 
in  bed  with  the  upper  half  of  the  body  raised.  The  cheeks  and  lips  are  cyanotic. 
The  pale  parts  about  the  corners  of  the  mouth  are  often  sharply  contrasted  with 
the  circumscribed  bluish-red  coloring  of  the  cheeks. 

The  results  of  percussion  are  directly  dependent  upon  the  changed  physical 
condition  in  the  lung,  due  to  the  anatomical  processes.  In  the  beginning  of  pneu- 
monia, so  long  as  the  total  amount  of  air  in  the  lung  remains  unaltered,  the  per- 
cussion-note remains  clear,  but  when  the  elasticity  and  tension  of  the  tissue  in  the 
diseased  portion  of  the  lung  diminish,  the  resonance  often  becomes  quite  tym- 
panitic. With  increased  exudation  into  the  alveoli  and  smallest  bronchi  the 
amount  of  air  in  the  lung  constantly  grows  less,  and  therefore  the  percussion  reso- 
nance becomes  very  dull,  but  it  usually  retains  its  tympanitic  timbre.  Since  the 
pneumonic  lung  is  only  rarely  absolutely  deprived  of  air — for  a  certain  amount  is 
always  left  in  the  larger  bronchi — tbe  percussion  resonance  seldom  becomes  so 
completely  dull—"  flat  " — as  it  does,  for  example,  with  a  large  pleuritic  effusion. 
As  soon  as  the  absorption  of  the  exudation  begins,  the  volume  of  air  in  the  lung 
increases,  and  the  percussion-note  becomes  clearer,  and  remains  for  some  time  still 
markedly  tympanitic,  until  the  lung  has  regained  its  normal  tension  and  elas- 


CROUPOUS  PNEUMONIA.  195 

ticity.  We  have  also  to  note  that  the  intensity  of  the  dullness  in  croupous  pneu- 
monia is  sometimes  subject  to  quite  marked  variations,  since  the  secretion  retained 
in  the  bronchi  is  at  one  time  abundant  and  at  another,  after  expectoration,  scanty. 

The  extent  of  the  dullness  or  of  the  tympanitic  resonance  is  naturally  depend- 
ent upon  the  extent  of  the  anatomical  process.  Small  and  central  infiltrations 
may  entirely  escape  detection  by  percussion. 

Auscultation  is  of  greater  importance  than  percussion  in  the  detection  of  a 
beginning1  or  limited  pneumonic  infiltration.  The  auscultatory  signs  depend  in 
part  upon  the  presence  of  the  pneumonic  exudation  and  in  part  upon  the  change 
of  the  lung  into  a  firm  tissue  containing  air  only  in  the  larger  bronchi.  In  the 
beginning  of  the  disease  we  hear  over  the  affected  portions  large  or  small  rales, 
and  very  often,  too,  the  characteristic  crepitant  rale  on  inspiration  discovered  by 
Laennec.  This  arises  because  the  walls  of  the  alveoli  and  smallest  bronchi,  which 
are  cemented  together,  are  torn  apart  at  each  inspiration.  The  crepitation,  how- 
ever, is  neither  pathognomonic  of  pneumonia,  nor  is  it  heard  in  every  case  of 
pneumonia.  With  increasing  infiltration,  bronchial  breathing  replaces  the  vesic- 
ular. The  bronchial  breathing  in  pneumonia  is,  as  a  rule,  very  loud  and  sharp, 
and  sounds  close  to  the  ear.  Beside  this,  we  may  detect  more  or  less  numerous 
sonorous  rhonchi.  We  may  hear  a  pure,  loud  bronchial  breathing  when  there  is 
marked  infiltration,  without  any  adventitious  sounds.  With  the  beginning  of 
the  "  resolution  of  pneumonia  " — that  is,  as  soon  as  the  exudation  becomes  more 
fluid — abundant,  loud,  moist  rales  occur,  which  are  usually  rather  large,  and  they 
more  or  less  obscure  the  bronchial  breathing.  At  this  time  we  frequently  hear  the 
characteristic  crepitant  rale  again — crepitatio  redux.  The  rales  gradually  disap- 
pear, the  respiratory  murmur  loses  its  bronchial  character,  becomes  harsh  and  in- 
definite, and  finally  is  normally  vesicular  once  more. 

We  often  hear  a  few  rhonchi  over  the  unaffected  portions  of  the  lungs,  but  the 
respiratory  murmur  is  completely  normal  over  them. 

The  auscultatory  signs  just  described  undergo  an  important  change  if  the  larger 
bronchi  leading  to  the  affected  portion  of  the  lung  are  completely  plugged  by  the 
secretion,  as  they  are  quite  liable  to  be.  The  respiratory  murmur  may  then  almost 
entirely  disappear,  and  we  hear,  perhaps,  only  here  and  there  a  few  obscure  rales. 
Since  such  a  plugging  may  be  very  transitory,  we  understand  why  in  one  day, 
over  the  same  portion  of  the  lung,  we  hear  first  loud  bronchial  breathing  and 
rales,  and  then  quite  obscure  and  diminished  breathing. 

Wherever  there  is  bronchial  breathing,  we  hear  marked  bronchophony.  The 
vocal  fremitus  persists  or  is  somewhat  increased  over  a  pneumonic  lung  so  long  as 
the  large  bronchi  are  open,  but  when  they  become  plugged,  the  vocal  fremitus  is 
weakened  or  wholly  absent. 

We  have  yet  to  add  a  few  remarks  about  the  parts  of  the  lung  in  which  we 
may  expect  first  to  perceive  the  physical  signs  of  pneumonia,  especially  the  aus- 
cultatory signs. 

In  the  first  place,  we  should  never  neglect  to  examine  carefully  the  lateral  por- 
tions of  the  thorax  and  the  axillary  region  when  we  suspect  a  developing  pneu- 
monia. We  often  find  the  first  rales  here  in  pneumonia  of  the  lower  lobes.  The 
first  signs  of  infiltration  may  be  found  in  the  posterior  middle  portion  of  the  tho- 
rax, and  extend  downward  from  this  point.  Pneumonia  of  the  upper  lobes  be- 
gins just  as  frequently  behind  in  the  apices  as  in  front  in  the  infra-clavicular  fossae. 
Isolated  pneumonia  of  the  right  middle  lobe  also  occurs,  to  be  made  out  in  front, 
on  the  right,  between  the  fourth  and  sixth  ribs. 

Few  general  statements  can  be  made  about  the  nature  or  the  rapidity  of  the 
extension  of  pneumonia,  since  in  these  respects  the  greatest  differences  are 
observed.     The  infiltration  may  remain  confined  to  a  small  portion  of  the  lung, 


196  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

and  again  it  may  spread  over  a  whole  lobe  or  more  in  a  short  time,  even  in  one 
or  two  days.  We  call  the  pneumonia,  whose  constant  extension  by  contiguity 
we  can  follow  from  day  to  day,  wandering  pneumonia  (pneumonia  migrans),  or, 
from  a  purely  superficial  resemblance,  which  has  given  rise  to  many  wrong  ideas, 
"  erysipelatous  pneumonia."  In  these  cases  all  the  signs  of  resolution  are  present 
in  the  parts  first  attacked,  while  the  parts  affected  later  are  found  still  at  the  height 
of  the  disease,  or  in  the  beginning  of  infiltration;  but  we  may  also  find  in  the 
autopsies  of  wandering  pneumonia  the  parts  of  the  lung  affected  later  in  a  more 
advanced  stage  (gray  hepatization)  than  the  parts  first  attacked,  which  are  still  in 
the  stage  of  red  hepatizatiou.  Wandering  pneumonia  is  almost  always  severe  and 
quite  protracted. 

Pneumonia  in  rare  cases  progresses  by  leaps.  Such  cases  have  been  termed 
erratic  pneumonia. 

2.  Symptoms  on  the  Part  of  the  Pleura. — As  we  have  already  mentioned,  every 
pneumonia  which  reaches  the  periphery  of  the  lung  is  associated  with  a  fibrinous 
pleurisy,  but  in  many  cases  this  causes  no  objective  symptoms.  The  stitch  in 
the  side  in  pneumonia,  however,  is  due  to  the  affection  of  the  pleura.  In  other 
cases  the  dry  pleurisy  is  marked  by  a  distinctly  audible,  and  often  a  very  loud, 
pleuritic  friction-sound,  and  a  rub,  which  may  sometimes  be  felt  by  laying  the 
hand  on  the  chest  wall.  We  rarely  hear  the  pleuritic  friction  sound  in  the  begin- 
ning of  pneumonia,  but  more  frequently  in  the  later  stages,  and  perhaps  not  till 
many  days  after  the  crisis  has  taken  place. 

The  cases  in  which  pleurisy  with  effusion  develops  as  a  sequel  to  pneumonia, 
which  may  occur  quite  early,  are  more  important.  We  usually  have  to  do  with 
a  serous  effusion,  but  in  rare  cases  purulent  pleurisy  also  comes  on  after  pneu- 
monia. Purulent  effusions  of  this  kind  have  been  repeatedly  found  to  con- 
tain the  above-described  lancet-shaped  pneumonia  coccus.  In  one  case,  which 
ended  fatally,  we  saw  a  haemorrhagic  pleurisy,  leading  to  an  abundant  effusion  of 
blood  into  the  pleural  cavity. 

The  diagnosis  of  pleurisy  with  effusion,  complicating  pneumonia,  is  seldom 
difficult.  The  percussion  resonance  is  duller  than  we  find  it  in  pure  pneumonia 
(vide  supra).  The  respiratory  murmur  and  the  vocal  fremitus  are  constantly 
diminished  and  finally  entirely  absent.  The  symptoms  of  pressure  on  the  neigh- 
boring organs  and  cavities,  the  heart,  the  liver,  and  the  semilunar  space  (see  page 
260),  are  especially  important  because  they  are  most  unequivocal.  An  explora- 
tory puncture  with  a  Pravaz's  [hypodermic]  syringe,  that  has  been  carefully 
cleansed  and  disinfected,  gives  a  very  certain  and  safe  method  of  recognizing 
pleurisy  in  doubtful  cases. 

A  moderate  degree  of  pleurisy  may  somewhat  delay  the  course  of  the  disease, 
but  it  has  no  special  significance.  Large  effusions,  however,  may  decidedly 
increase  the  difficulty  in  respiration.  Otherwise  the  pneumonia  may  recover, 
leaving  the  pleuritic  effusion  quite  undisturbed.  In  pneumonia  of  an  upper  lobe, 
too.  the  pleurisy  may  develop  below  and  lead  to  an  effusion  there,  while  the  lower 
lobe  itself  remains  quite  free  from  pneumonia. 

3.  Circulatory  Apparatus. — The  pulse  is  accelerated  from  the  beginning  of  the 
disease.  In  cases  of  moderate  severity  its  frequency  reaches  100  or  120,  and,  in 
very  severe  cases,  a  still  higher  rate  up  to  140  or  160  is  seen,  and  is  always  a 
dangerous  symptom.  This  high  rate  of  the  pulse  does  not  have  as  bad  a  signifi- 
cance in  children  as  it  does  in  adults.  The  consideration  of  the  quality  of  the 
pulse  is  important.  Small ness,  weakness,  and  irregularity  of  the  pulse  are  of  bad 
omen  as  symptoms  of  the  onset  of  cardiac  weakness.  The  attacks  of  collapse, 
which  sometimes  come  on  quite  suddenly  in  severe  cases  of  pneumonia  as  in  other 
acute  diseases,  are  especially  dangerous.     They  consist  of  sudden  attacks  of  weak- 


CROUPOUS  PNEUMONIA.  10  7 

ness  of  the  heart  with  a  very  small  and  frequent  pulse.  The  temperature  sinks  to 
subnormal,  95°  to  93°  (35°-34°  C).  The  peripheral  parts,  the  nose  and  extremities, 
become  cool,  pale,  and  somewhat  cyanotic.  The  general  weakness  is  extremely 
marked.  The  collapse  may  be  recovered  from,  esfjecially  with  timely  assistance, 
but  patients  may  die  in  it. 

The  pericarditis  that  sometimes  accompanies  a  fibrinous  or  sero-fibrinous  exu- 
dation is  one  of  the  most  important  anatomical  changes  in  the  heart.  This  can 
always  be  explained  by  a  direct  conduction  of  the  inflammatory  process  from  the 
neighboring  pleura,  and  is  therefore  somewhat  more  frequent  in  left-sided  pneu- 
monia than  in  right.  It  is  a  complication  to  be  borne  in  mind.  Its  diagnosis  is 
seldom  difficult  if  we  make  a  careful  physical  examination  of  the  heart,  but  with 
very  severe  and  extensive  symptoms  in  the  lungs  a  complicating  pericarditis  may 
be  overlooked. 

A  slight  fresh  endocarditis  is  sometimes  found  on  autopsy,  but  it  has  no  clinical 
significance.  Diseases  of  the  cardiac  muscle,  especially  fatty  and  parenchymat- 
ous degeneration,  may  be  discovered  post  mortem,  but  they  are  by  no  means 
frequent.  In  very  weak  people,  drunkards,  etc.,  who  die  of  pneumonia,  we 
sometimes,  indeed,  find  the  heart  remarkably  flabby,  with  the  right  ventricle 
dilated,  but  in  many  cases  of  pneumonia  we  find  the  muscle  of  the  heart  at  the 
autopsy  perfectly  normal.  A  constant  relation  between  the  finer  histological 
changes  in  the  cardiac  muscle  and  the  condition  of  the  heart's  action  during  life 
is,  at  any  rate,  not  proved. 

4.  Digestive  Apparatus. — In  severe  cases  of  pneumonia  the  tongue  is  dry, 
coated,  and  quite  like  the  tongue  in  typhoid.  The  appetite  is  also  almost  wholly 
lost  from  the  beginning.  Vomiting  is  not  infrequent,  especially  in  the  begin- 
ning of  pneumonia,  and  it  also  occurs  later.  It  is  observed  with  especial  fre- 
quency in  the  pneumonia  of  children.  Severe  symptoms  on  the  part  of  the  in- 
testinal canal  are  rare.  The  bowels  are  ordinarily  somewhat  constipated,  but 
quite  severe  diarrhoea  is  also  observed. 

The  complication  of  pneumonia  with  jaundice  has  a  certain  significance,  but 
its  causes  are  not  always  very  clear.  It  is  sometimes  due  to  an  accompanying 
catarrh  of  the  duodenum.  In  other  cases  the  veins  of  the  liver,  dilated  from 
stasis,  may  exert  a  pressure  on  the  bile-ducts.  Slight  jaundice  has  no  special  sig- 
nificance, and  is  frequent,  even  in  mild  cases;  a  marked  jaundice,  however,  is 
seen  only  in  severe  cases,  especially  in  drunkards'  pneumonia.  We  call  such 
cases,  associated  with  jaundice,  "bilious  pneumonia."  They  have  often  other 
severe  gastro-intestinal  symptoms,  like  vomiting,  diarrhoea,  and  meteorism,  and 
severe  nervous  symptoms,  like  stupor  and  delirium. 

The  liver  sometimes  shows  the  signs  of  passive  congestion.  The  spleen  is 
moderately  enlarged,  especially  in  severe  cases — acute  splenic  tumor — as  in  other 
acute  infectious  diseases. 

5.  Kidneys  and  Urine. — The  infectioiis  character  of  pneumonia  is  also  shown 
by  the  occurrence  of  a  genuine  acute  nephritis,  which  is  not  especially  common,  but 
which  still  has  been  repeatedly  observed.  It  begins  most  frequently  on  the  third 
to  the  sixth  day  of  the  disease.  It  is  recognized  by  the  presence  of  albumen,  casts, 
and  blood  in  the  urine.  The  nephritis  usually  gets  perfectly  well,  but  we  have 
once  seen  it  pass  into  the  chronic  form.  The  slight  albuminuria  which  is  found 
in  severe  pneumonia  is,  in  our  opinion,  also  due  to  a  mild  disease  of  the  kidneys, 
and  not  to  the  fever  as  such  (see  the  section  on  diseases  of  the  kidney,  pages 
825  and  837). 

Great  weight  was  formerly  laid  upon  the  diminution  of  the  chlorides  in  the 
urine  in  pneumonia.  In  fact,  the  precipitate  of  chloride  of  silver,  when  we  put  a 
drop  of  solution  of  nitrate  of  silver  into  the  urine,  may  be  very  slight  or  entirely 


198  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

absent.  The  chief  cause  of  this  diminution  of  the  chlorides  is  the  small  amount 
of  nourishment  taken  by  the  patient,  but  we  must  also  bear  in  mind  the  large 
amount  of  chloride  of  sodium  contained  in  the  pneumonic  exudation. 

Great  significance  was  also  formerly  laid  upon  the  abundant  sediment  of  uric 
acid  (sedimentum  lateritium — brick-dust  sediment)  which  is  often  noticed  on  the 
day  of  the  crisis.  This  is  in  part  due  to  a  real  increase  in  uric  acid,  but  in 
greater  part  to  the  fact  that  the  conditions  for  the  deposition  of  the  sediment 
are  especially  favorable  on  that  day.  The  urine  is  scanty  in  amount  from  the 
abundant  perspiration,  and  is  concentrated  and  relatively  very  acid.  The  uric 
acid  contained  in  it  can  therefore  readily  be  precipitated  in  the  form  of  a  sedi- 
ment. 

Pneumonia,  in  common  with  most  of  the  other  acute  febrile  diseases,  is  attended 
with  an  increased  secretion  of  urea  during  the  disease. 

6.  Nervous  System. — As  in  every  severe  febrile  disease,  nervous  symptoms  of  a 
mild  type  are  very  rarely  absent  in  any  case  of  pneumonia.  Among  the  nervous 
symptoms  are  the  general  weakness  and  dullness,  and  especially  the  headache, 
which  is  often  very  intense,  and  is  usually  increased  by  coughing.  The  onset  of 
more  severe  cerebral  symptoms,  especially  delirium,  is  of  great  importance.  We 
see  this  chiefly  in  individuals  who  have  a  peculiar  predisposition  to  delirium,  and 
particularly  in  drunkards.  Delirium  gives  the  drunkard's  pneumonia  {vide 
infra)  its  characteristic  stamp. 

While  no  anatomical  basis  has  as  yet  been  discovered  for  the  above-named 
symptoms,  nor  for  the  worst  form  of  delirium  in  drunkards,  there  is  an  anatomi- 
cal disease  of  the  brain  which  is,  to  be  sure,  a  rare  complication  of  pneumonia, 
but  which  yet  is  undoubtedly  related  to  it:  this  is  purulent  meningitis.  This 
complication  has  been  repeatedly  observed,  especially  at  times  when  an  epidemic 
of  cerebro-spinal  meningitis  was  prevailing,  and  also  at  other  times.  It  is  usually 
hard  to  make  the  diagnosis  of  a  complicating  meningitis,  since  its  appearances 
are  hidden  under  the  other  severe  symptoms.  The  chief  points  for  diagnosis  are 
intense  headache,  rigidity  of  the  neck,  and  a  stupor  increasing  to  deep  coma.  In 
many  cases  these  symptoms  are  very  slightly  developed.  The  termination  of 
meningitis  is  probably  always  fatal. 

7.  Skin. — Tbe  frequent  appearance  of  herpes  in  the  course  of  pneumonia  is 
characteristic,  and  is  sometimes  of  diagnostic  importance.  It  appears  from  the 
second  to  the  fourth  day  of  the  disease,  or  sometimes  later.  Its  ordinary  seat  is 
on  the  lips,  especially  at  the  corners  of  the  mouth,  also  on  the  alse  of  the  nose,  and 
more  rarely  on  tbe  cheeks  or  the  ear  (herpes  labialis,  nasalis,  etc.).  It  has  been 
seen  only  very  rarely  on  other  portions  of  the  body  beside  the  face,  for  example 
on  the  forearm  and  the  buttock,  and  in  some  cases  on  the  mucous  membrane 
of  the  tongue.  We  once  saw  two  eruptions  of  herpes  separated  by  an  interval  of 
several  days.  In  repeated  instances,  under  our  own  observation,  herpes  labialis, 
with  a  fresh  rise  of  temperature,  appeared  some  days  after  the  crisis  had  taken 
place.  The  especial  cause  of  the  development  of  herpes  in  pneumonia  is  unknown 
to  us.  It  is  connected,  at  all  events,  with  the  infectious  nature  of  the  disease,  and 
it  is  accordingly  quite  analogous  to  the  occurrence  of  herpes  in  intermittent  and 
recurrent  fever,  epidemic  meningitis,  etc.  Other  affections  of  the  skin  are  of  rare 
occurrence.  We  have  seen  urticaria  in  some  cases.  The  jaundice  occurring  in 
pneumonia  has  already  been  described. 

8.  Course  of  the  Fever  (see  Figs.  23  and  24).— Pneumonia  is,  almost  without 
exception,  accompanied  by  a  more  or  less  high  fever  with  a  very  typical  course. 
In  the  beginning  of  the  fever  the  temperature  rises  very  rapidly  to  a  high 
point.  Even  during  the  initial  chill  the  bodily  heat  increases  from  normal  to 
about  104°  (40°  C)  and  over.    There  are  at  present  no  observations  to  show  whether, 


CROUPOUS  PNEUMONIA. 


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Pseudo-crisis. 

Fig.  23. — Example  of  the  temperature  curve  in  croupous 
pneumonia.    (Personal  observation.) 


in  the  cases  of  pneumonia  that  begin  gradually,  there  is  also  a  gradual  increase  of 
the  fever.  During  the  course  of  the  disease  the  fever  shows  on  the  whole  a  con- 
tinuous or  remitting  character,  but  there  is  with  this  a  decided  tendency  to  single 
deep  falls  of  temperature.  Since 

these  at  first  may  easily  be  tak-  12       3       4       5       6       7       8       9       10 

en  for  the  actual  occurrence  of 
crises,  although  later  they  are 
proved  by  the  renewed  rise  in 
temperature  to  be  a  mere  tem- 
porary decline  in  the  bodily 
heat,  they  are  termed  pseudo- 
crises.  Pseudo-crises  are  usu- 
ally seen  in  the  first  days  of 
the  disease,  but  in  some  cases 
they  appear  later.  They  may 
be  repeated  once  or  offener,  so 
that  then  the  fever  has  a  de- 
cidedly intermitting  course. 
These  intermitting  pneumonias, 
so  called  from  the  course  of 
the  fever,  have  nothing  at  all 
to  do  with  malaria,  which  fact 
must  be  especially  noted  be- 
cause of  the  frequency  of  erro- 
neous statements. 

The  fever  may  be  decidedly  high  in  pneumonia,  often  reaching  104°  or  106° 
(40°-41°  C).  The  highest  temperature  observed  by  us  was  107'8°  (42'1°  C).  In 
general  there  is  a  correspondence  between  the  height  of  the  fever  and  the  severity 

of  the  case,  but   sometimes 
2       3       4      5      6       7       8       9      10      li      12       the   most  severe  and  even 

fatal  cases  run  their  course 
with  a  comparatively  low 
fever,  varying  between  101° 
and  103°  (38-5°-39'5°  C). 
We  expect  the  greatest  in- 
crease in  temperature  in  the 
first  days  of  the  disease.  We 
have  certainly  not  seen  such 
a  special  increase  immedi- 
ately before  the  crisis — the 
so-called  perturbatio  critica 
— as  many  statements  would 
lead  us  to  expect.  We  have 
seen  a  gradual  decline  in 
temperature  quite  frequent- 
ly in  the  closing  days  in  fa- 
tal cases,  but  the  opposite 
condition  also  obtains.  A 
marked  rise  before  death  is 
not  peculiar  to  pneumonia,  but  it  does  occur  when  there  is  a  complicating  men- 
ingitis. 

The  decline  of  the  fever  is  the  most  characteristic  portion  of  the  pneumonia 
curve.     The  fall  in  temperature  usually  comes  on  in  the  form  of  a  decided  crisis. 


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-Example  of  the  temperature  curve  in  "  intermitting ' 
pneumonia.    (Personal  observation.) 


200  DISEASES   OF  THE  RESPIRATORY  ORGANS. 

During-  the  night  there  is  generally  a  sinking  of  the  temperature  with  a  more  or 
less  abundant  perspiration,  in  which  as  a  rule  the  temperature  may  reach  a  sub- 
normal point— 96°  to  95°  (36°-35°  C).  The  critical  decline  is  often  broken  by 
new  and  slight  elevations  of  temperature,  so  that  on  the  morning  of  the  next  day 
there  may  be  a  definite  increase  of  fever,  the  so-called  protracted  crisis.  Only  in 
a  comparatively  small  number  of  cases  does  the  fever  end  by  lysis,  in  which  the 
temperature  goes  down  like  steps.  The  duration  of  lysis  is  seldom  more  than 
three  or  four  days  at,  most.  A  decline  of  temperature  by  lysis  is  most  frequent  in 
severe  and  protracted  cases,  in  so-called  typhoid  pneumonia  {vide  infra),  or  in 
pneumonia  migrans. 

Although  the  pathological  process  in  the  lungs  by  no  means  ends  with  the 
crisis,  we  usually  consider  the  day  of  the  crisis  as  the  last  day  of  the  disease.  The 
pneumonia  makes  no  advance  after  that,  but  resolution  and  absorption  of  the 
exudation  and  the  return  of  the  patient's  strength  still  take  time.  Hippocrates 
knew  when  the  time  of  the  crisis  occurs,  and  that  the  odd  clays,  especially  the  fifth 
and  the  seventh,  have  a  special  significance  in  regard  to  it.  In  an  infectious  dis- 
ease that  has  a  typical  course  there  can  be  nothing  strange  in  the  fact  that  the 
cessation  of  fever,  to  a  certain  degree,  is  associated  with  a  definite  period  of  time ; 
but  Hippocrates's  rule  has  frequent  exceptions.  The  crisis  sometimes  occurs  on 
the  ninth,  the  twelfth,  or  the  thirteenth  day,  and  even  later,  and,  on  the  other 
hand,  there  are  quite  short  pneumonias  of  but  one  or  two  days'  duration. 

In  the  days  following  the  crisis  the  temperature,  which,  as  we  have  said,  falls 
to  subnormal,  regains  its  normal  height.  The  pulse,  which  usually  sinks  to 
fifty  or  sixty  during  the  ci'isis,  when  it  often  shows  a  slight  irregularity,  reaches 
its  normal  frequency  again  in  a  few  days.  We  are  quite  apt  to  see,  in  the  days 
immediately  following  the  crisis,  a  slight  increase  of  temperature  again,  100°  to 
102°  at  most  (38°-39°  C),  but  this  has  no  special  significance. 

The  general  revolution  which  the  whole  condition  of  the  patient  undergoes 
after  the  crisis  is  often  astonishing.  The  rapid  decline  in  the  respiratory  symptoms 
is  especially  striking.  The  return  of  the  affected  portion  of  the  lung  to  normal 
follows  in  quite  a  short  time.  The  expectoration  is  more  abundant  but  less  viscid. 
It  loses  its  bloody  character  and  is  simply  catarrhal.  In  cases  which  run  their 
course  regularly,  the  signs  in  the  lung  on  auscultation  and  percussion  become 
normal  again  in  about  five  to  eight  days  after  the  crisis.  Abnormally  delayed 
resolution  will  be  mentioned  below. 

Special  Peculiarities  and  Anomalies  in  the  Course  of  Pneumonia. 

1.  Pneumonia  in  Children. — Beside  the  common  lobular  pneumonia  there  is 
also  a  pure,  lobar,  croupous  pneumonia  in  children,  which  is  by  no  means  so  rare 
as  some  authors  formerly  supposed.  An  initial  chill  is  seen  only  in  older  chil- 
dren; initial  vomiting,  however,  is  very  common  in  children.  In  many  cases 
severe  cerebral  symptoms,  like  delirium,  drowsiness,  or  convulsions,  obscure  the 
pulmonary  symptoms  at  first.  The  further  course,  the  development  of  physical 
signs,  the  fever,  and  the  complications,  are  quite  analogous  to  the  appearances  in 
adults.  The  pneumonic  sputum  is  only  exceptionally  to  be  observed  in  children 
under  eight  years  of  age. 

2.  Pneumonia  in  old  people  is  always  dangerous.  It  may  begin  suddenly, 
as  in  people  of  middle  age,  but  often  it  begins  more  slowly  and  insidiously.  Its 
course  is  marked  by  the  speedy  onset  of  great  weakness  and  debility.  Nervous 
symptoms,  like  delirium,  are  not  infrequent. 

3.  Drunkard^s  Pneumonia. — We  see  croupous  pneumonia  in  drunkards  with 
remarkable  frequency.      The  clinical   course  is   characterized    by  the  develop- 


CROUPOUS  PNEUMONIA.  201 

merit  of  delirium  tremens,  usually  in  the  first  days  of  the  disease.  The 
patient's  mind  is  disturbed,  he  is  very  restless,  constantly  tries  to  get  out  of 
bad,  and  he  fumbles  night  and  day  with  his  bed-clothes  or  articles  of  cloth- 
ing. The  alcoholic  character  of  the  delirium  is  shown  by  the  patient's 
whole  manner,  the  tremor  of  the  hands  and  tongue,  and  the  usually  happy 
character  of  the  delirium.  The  delirium  refers  to  his  favorite  beverages, 
his  previous  boon  companions,  etc.  He  becomes  tearful  or  raving  only  when 
forcibly  restrained.  He  may  think  himself  involved  in  the  tavern  brawls. 
The  alcoholic  delirium  is  almost  always  associated  with  hallucinations.  The 
hallucinations  of  little  moving  black  figures  are  especially  characteristic. 
They  are  either  animals,  rats  or  beetles,  or  little  black  men,  and  they  give  him 
much  trouble.  The  subjective  symptoms  of  pneumonia  are  wholly  in  the  back- 
ground. No  delirious  patient  with  pneumonia  complains  of  cough,  pain  in  the 
chest,  or  dyspnoea.  Careful  objective  examination  is  the  only  thing  that  con- 
firms the  diagnosis.  Very  often  patients  with  a  happy  delirium  serve  to  enter- 
tain those  about  them,  until  suddenly  very  severe  symptoms  arise,  and  they  become 
somnolent  and  succumb,  with  the  symptoms  of  pulmonary  cedema.  The  prognosis 
of  every  case  of  drunkard's  pneumonia,  therefore,  is  to  be  regarded  as  very  un- 
favorable. 

4.  Pneumonia  in  Pre-existing  Chronic  Diseases. — Croupous  pneumonia  is 
occasionally  seen  in  all  forms  of  chronic  disease.  It  is  especially  dangerous  in 
persons  who  are  already  enfeebled,  or  afflicted  with  chronic  cardiac  or  pulmonary 
disease,  like  phthisis  or  emphysema.  The  pneumonia  which  often  attacks  patients 
with  emphysema  is  clinically  important,  since  emphysema  may  render  the  object- 
ive evidence  of  pneumonia  very  difficult.  The  croupous  exudation  does  not  com- 
pletely fill  the  dilated  alveoli ;  hence  decided  dullness  and  bronchial  breathing  are 
absent. 

5.  Pneumonia  with  Late  or  Slight  Localization — Central  Pneumonia. — Cases 
are  quite  often  seen  whose  beginning,  course,  and  subjective  symptoms  correspond 
throughout  to  a  croupous  pneumonia,  but  in  which  the  objective  evidence  of 
pneumonic  infiltration  evades  the  most  careful  examination.  The  disease  be- 
gins with  a  chill,  the  fever  is  high,  the  patient  complains  of  pain  in  the  chest, 
which  is  usually  slight,  there  is  perhaps  herpes,  but  only  on  the  fourth,  fifth,  or 
sixth  days  can  we  make  out  anywhere  any  bronchial  breathing  or  crepitant  rales. 
In  other  cases  even  the  cinsis  may  set  in  before  we  are  able  to  localize  the 
pneumonia  with  certainty.  In  most  of  these  cases  we  probably  have  to  do  less 
with  an  actual  late  localization  than  with  a  central  infiltration  which  no- 
where approaches  the  periphery,  and  hence  is  made  out  objectively  only  late  or 
not  at  all.  A  careful  examination  of  the  sputum  is  of  the  greatest  diagnostic 
importance,  since  it  sometimes  has  a  perfectly  characteristic  appearance  in  spite 
of  the  absence  or  the  indefinite  character  of  the  physical  signs.  If  there  is  no 
sputum,  the  diagnosis  must  of  course  remain  very  uncertain.  In  such  a  case 
under  our  own  observation  a  slight  pleuritic  friction-sound  was  the  only  thing 
heard  and  that  not  until  the  day  after  the  crisis,  but  this,  added  to  the  rational 
signs,  made  the  diagnosis  of  pneumonia  certain. 

6.  Typhoid  Pneumonia — Asthenic  Pneumonia. — By  typhoid  pneumonia  we 
mean  those  cases  in  which,  beside  the  local  pulmonary  symptoms,  which  may  be 
either  slight  or  well  marked,  there  are  remarkably  severe  general  symptoms. 
The  cases  do  not  often  begin  as  suddenly  as  ordinary  pneumonia,  but  more 
gradually,  like  typhoid.  Even  at  first  the  general  symptoms,  such  as  great  dull- 
ness, loss  of  appetite,  or  headache,  predominate  over  the  thoracic  symptoms.  At 
the  height  of  the  disease  there  is  a  decided  typhoidal  state,  stupor,  delirium,  a  very 
dry  tongue,  great  general  weakness,  and  also  enlargement  of  the  spleen,  and  fre- 


202  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

quently  mild  jaundice,  albuminuria,  etc.  Sucli  cases  are  to  be  regarded  as  pneu- 
monia with  an  unusually  severe  general  infection.  They  sometimes  occur  in  epi- 
demics. It  is  said  that  pneumonia  of  the  upper  lobes  shows  a  somewhat  more 
frequent  tendency  to  severe  nervous  symptoms  tban  pneumonia  of  the  lower  lobes. 
Recovery  from  this  typhoid  or  asthenic  pneumonia,  which  may  last  two  weeks 
or  more,  often  follows  by  lysis.  Typhoid  pneumonia  is  by  no  means  a  sharply 
defined  disease.  The  term  serves  merely  as  a  short  name  for  the  grave  constitu- 
tional disturbance..  Clinically  it  is  impossible  to  distinguish  it  sharply  from 
pneumonia  migrans,  bilious  pneumonia,  and  other  forms. 

The  croupous  pneumonia  which  comes  on  in  the  course  of  genuine  typhoid 
is  astiologically  quite  different,  but  in  diagnosis  it  is  often  very  hard  to  distinguish 
it.  Here  we  have  typhoid  with  a  secondary  localization  in  the  lungs — "  pneumo- 
typhoid  "  (see  page  13) — which  is  rare.  In  the  cases  first  described,  however,  we 
had  a  pneumonia  with  very  marked  general  infection — "  typhoid  "  symptoms. 
The  only  things  which  render  an  accurate  differentiation  of  the  two  diseases  pos- 
sible in  such  cases  are  observation  of  the  whole  course  of  the  disease,  attention 
to  all  the  single  symptoms,  such  as  the  intestinal  symptoms,  and  roseola,  and  the 
astiological  relations,  so  far  as  we  can  learn  them. 

7.  Pneumonia  with  Delayed  Resolution. — While  the  resolution  of  pneumonia 
is  complete,  as  a  rule,  in  three  days  to  a  week  after  the  occurrence  of  the  crisis, 
there  are  cases  in  which  this  process  demands  a  much  longer  time.  Not  infre- 
quently, and  particularly  in  severe  cases  of  pneumonia,  one  sees  after  the  crisis 
a  surprisingly  rapid  disappearance  of  all  the  physical  signs,  while,  on  the  other 
hand,  recovery  is  sometimes  remarkably  slow  in  apparently  mild  cases ;  but  this 
rule  is  of  course  not  universal,  and  not  without  exceptions.  The  course  of  the 
disease  is  often  enough  precisely  the  opposite.  Just  what  are  the  conditions  upon 
which  the  rapidity  or  the  slowness  of  resolution  depends  we  do  not  know.  Some- 
times unfavorable  constitutional  conditions,  such  as  anaemia,  debility,  phthisical 
tendencies,  and  kyphoscoliosis  appear  to  delay  resolution.  Sometimes,  on  the 
other  hand,  no  such  explanation  can  be  found.  It  seems  to  us  that  at  certain 
times  all  the  cases  of  pneumonia  exhibit  more  of  a  tendency  to  delayed  resolu- 
tion than  at  others,  so  that  it  is  not  impossible  that  there  are  variations  in  the 
pathological  process  itself.  Perhaps,  however,  secondary  pulmonary  diseases  play 
a  part  in  the  phenomenon. 

With  regard  to  the  symptoms  of  delayed  resolution,  there  are  various  forms. 
In  the  first  place,  we  see  cases  where  the  crisis  takes  place  in  the  usual  way,  and 
the  temperature  thereafter  remains  permanently  normal.  The  patients  perhaps 
feel  quite  well,  and  are  troubled  little  by  thoracic  symptoms;  nevertheless,  the 
dullness  upon  percussion  remains  unchanged,  or  diminishes  at  best  very  gradually, 
and  the  bronchial  breathing  or  subcrepitant  rales  can  still  be  heard.  All  the 
signs  diminish  very  slowly,  sometimes  occupying  several  weeks  in  their  disap- 
pearance, and  then  complete  recovery  ensues.  In  other  cases  there  is  no  distinct 
crisis,  but  the  fever  continues,  although  lower  than  at  first,  and  the  physical  signs 
remain  to  a  greater  or  less  extent.  At  the  end  of  two  or  three  weeks,  or  even  still 
later,  the  fever  slowly  ceases,  and  thereupon  normal  resonance  and  vesicular 
breathing  gradually  return.  Still  another  course,  which  differs  somewhat  from 
those  already  described,  and  of  which  we  have  repeatedly  observed  typical  in- 
stances, is  the  following:  The  patients  remain  free  from  fever  for  about  a  week 
after  the  crisis  appears.  During  this  time  the  dullness  i*emains,  and  the  bronchial 
breathing,  although  not  very  loud,  is  constant.  Then  a  moderately  intermitting 
fever  comes  on  again,  with  an  increase  of  temperature  to  about  102°  or  103°  (39°- 
39 "5°  C).  This  fever  may  last  from  two  to  four  weeks,  or  even  longer.  Only 
occasionally,  if  ever,  do  we  hear  a  rale  over  the  affected  portion  of  the  lung.     A 


CROUPOUS  PNEUMONIA. 


203 


moderate  contraction  of  the  affected  side  gradually  appears.  Then  the  reso- 
nance slowly  becomes  clearer,  and  the  respiration  becomes  louder  and  vesicular 
again.  The  fever  disappears,  and  complete  recovery  finally  takes  place.  In  many 
other  cases  of  delayed  resolution  there  is  also  a  marked  absence  of  rales  and  a 
mild  degree  of  contraction.  The  differentiation  from  secondary  pleurisy  is  here 
often  very  difficult,  except  by  tapping  the  chest.  Again,  it  is  not  very  excep- 
tional to  observe  delayed  resolution  and  secondary  pleurisy  (simultaneously  in 
the  same  patient. 

If  there  is  really  merely  delay  in  the  resolution  and  no  distinct  secondary 
disease  (see  below),  complete  recovery  will  almost  always  come  at  last. 

8.  Termination  of  Pneumonia  in  Phthisis,  Contraction  of  the  Lungs,  Pul- 
monary Gangrene,  or  Pulmonary  Abscess. — Three  terminations  of  pneumonia 
are  ordinarily  mentioned  as  unusual  and  anomalous — the  termination  in  "  chronic 
pneumonia,"  in  gangrene,  and  in  abscess. 

Concerning  the  termination  in  chronic  pneumonia,  we  have  already  mentioned 
a  process  belonging  here,  the  termination  in  contraction  with  ultimate  recovery ; 
but  in  rare  cases  the  contraction  is  persistent.  From  the  complete  lack  as  yet  of 
careful  post-mortem  examinations,  we  can  not  give  fuller  details  as  to  the  anatom- 
ical process  in  these  cases  (hyperplasia  and  retraction  of  the  inter-alveolar  con- 
nective tissue  ?). 

By  the  "  termination  in  chronic  pneumonia  "  we  usually  mean  a  termination 
in  phthisis — that  is,  tuberculosis.  With  our  present  conception  of  the  two  diseases 
there  can,  of  course,  be  no  question  of  an  actual  transition  from  one  to  the  other. 
Accordingly,  where  a  clear  case  of  phthisis  develops  as  a  sequel  to  genuine  croup- 
ous pneumonia — which,  however,  is  quite  rare — either  the  pneumonia  develops 
upon  a  pre-existing  tuberculosis,  or  tuberculosis  develops  after  the  pneumonia  in 
a  person  predisposed  to  tubercle. 

The  transition  from  pneumonia  to  pulmonary  gangrene  is  sometimes  seen, 
especially  in  old  and  weak  individuals.  Here,  too,  in  our  opinion,  a  new  infec- 
tion, with  a  foul  and  putrid  substance,  must  always  take  place,  and  this  excites 
the  gangrene.  The  previous  pneumonia  furnishes  only  the  occasion  for  the  de- 
velopment of  gangrene,  and  perhaps  prepares  the  soil  for  the  agents  of  decompo- 
sition. The  development  of  gangrene  is  appreciated  clinically  from  the  change 
in  the  sputum. 

The  transition  from  pneumonia  to  pulmonary  abscess  is  very  rare.  We  can 
not  decide  whether  a  specific  further  cause  is  also  needed  for  this,  or  whether  the 
pneumonic  process  may  exceptionally  go  on  into 
the  formation  of  abscess.  The  transition  to  an 
abscess  may  be  recognized  by  the  character  of 
the  sputum,  which  contains  fragments  of  pul- 
monary tissue,  such  as  elastic  fibers,  beside  abun- 
dant pus.  Besides  that,  we  find,  on  microscopic 
examination  of  the  sputum  in  abscess,  some- 
times scales  of  Cholesterine  (Fig.  25)  and  haema- 
toidine  crystals ;  the  latter  may  be  so  abundant 
as  to  give  the  expectoration  a  brownish  color. 
Sometimes  we  have  seen  a  peculiar  greenish 
color  of  the  sputum.  The  signs  of  a  pulmonary 
cavity  are  found  if  the  abscess  bursts. 

Diagnosis. — No  special  remarks  on  diagnosis 
need  to  be  added  to  the  description  we  have 
given  of  all  the  important  symptoms  which  may  occur  in  croupous  pneumonia. 
We  should  pay  particular  attention  to  the  sudden  onset,  the  characteristic  spu- 


Ftg.  25. — Cholesterine  crystals. 


204  DISEASES   OF  THE  RESPIRATORY  ORGANS. 

tum,  the  physical  signs,  the  frequent  occurrence  of  herpes  on  the  face,  and  finally 
to  the  whole  course  of  the  disease,  especially  to  the  temperature  curve.  We  will 
discuss  the  differential  diagnosis  between  pneumonia  and  pleurisy  with  effusion 
more  fully  in  the  description  of  the  latter  affection. 

Prognosis. — Croupous  pneumonia  belongs  in  general  to  the  benignant  infec- 
tious diseases.  The  great  majority  of  cases,  in  previously  strong  and  healthy 
individuals,  run  a  favorable  course,  and  end  in  complete  recovery.  On  the  other 
hand,  pneumonia  brings  a  number  of  perils  with  it,  the  knowledge  of  which 
should  always  make  us  cautious  in  giving  a  prognosis. 

A  grave  danger  lies  in  the  extension  of  the  process.  If  the  advance  of  the 
pneumonia  can  not  be  stopped,  if  the  whole  of  one  lung  is  involved,  and,  besides 
that,  a  great  portion  of  the  other  lung,  the  diminution  of  the  respiratory  surfaces 
forms  a  factor  which  may  give  rise  to  a  fatal  termination. 

A  further  danger  lies  in  the  onset  of  certain  complications.  An  intense  pleu- 
risy, with  effusion,  especially  if  purulent,  causes  greater  difficulty  in  respiration, 
and  thus  increases  the  danger.  Still  worse  is  a  sero-fibrinous  or  purulent  peri- 
carditis, which,  in  not  very  rare  cases,  is  revealed  at  the  autopsy  as  the  special 
cause  of  death.  We  must  note,  however,  that  recovery  sometimes  finally  takes 
place  in  spite  of  an  empyema  or  of  a  purulent  pericarditis.  The  complication 
with  a  purulent  meningitis,  which  is  fortunately  very  rare,  is  probably  invariably 
fatal. 

The  dangers  of  general  infection  (or  perhaps  a  more  correct  expression  would 
be  general  intoxication)  occupy  a  subordinate  place  in  pneumonia,  on  the  whole, 
in  comparison  with  other  infectious  diseases,  like  typhoid,  but  the  constitutional 
state  is  important  in  the  so-called  typhoid,  asthenic  pneumonia.  Sometimes  un- 
usually severe  and  malignant  forms  of  pneumonia,  with  a  high  mortality,  occur 
in  epidemics  and  endemics,  but  these  cases  are  often  characterized  by  the  extent 
of  the  local  process,  or  by  the  development  of  the  dangerous  complications  men- 
tioned above. 

The  individual  circumstances  of  the  patient  play  the  most  important  part  in  the 
prognosis  of  pneumonia.  While  a  constitution  that  was  previously  healthy  and 
uninjured  usually  survives  the  disease,  one  that  was  previously  weak  and  diseased 
readily  succumbs.  In  this  fact  lies  the  danger  of  pneumonia  in  old,  weak,  badly 
nourished  persons,  and  in  persons  with  a  pre-existing  emphysema,  kyphoscoliosis, 
heart  disease,  etc.  In  this,  too,  lies  the  great  danger  of  every  pneumonia  in  drunk- 
ards. Since  the  nervous  system  is  much  affected  by  chronic  alcoholism,  we  very 
often  see  outbreaks  of  delirium  tremens  in  pneumonia,  which  come  on  very  read- 
ily. In  like  manner  the  other  nerve-centers  are  weakened  and  incapable  of  resist- 
ance, especially  the  regulatory  centers  for  the  heart  and  respiration.  Hence  we 
can  understand  why  even  moderate  drinkers,  though  previously  strong  and  well 
to  all  appearance,  succumb  to  pneumonia  from  insufficiency  of  the  heart  and 
lungs. 

If  we  ask  upon  what  symptoms  our  prognosis  in  any  given  case  should  depend, 
we  must  reply  that  no  single  factor  can  be  given  especial  prominence.  Chief 
stress  must  always  be  laid  upon  the  state  of  the  lungs  and  the  respiration,  but 
attention  must  also  be  given  to  the  general  condition,  the  heart's  action,  the  height 
of  the  fever,  etc.     The  worst  dangers  of  pneumonia  have  just  been  mentioned. 

Of  the  abnormal  terminations  of  pneumonia,  contraction  gives  the  best  prog- 
nosis, but  recovery,  or  at  least  a  marked  subsidence  of  all  the  symptoms,  may 
sometimes  take  place  after  gangrene  and  abscess. 

Treatment. — Many  of  tbe  milder  cases  of  typical  pneumonia  need  no  special 
active  treatment  when  the  disease  on  the  whole  takes  a  favorable  course.  Most 
cases  get  well  under,  or,  we  can  almost  say,  in  spite  of  any  treatment.     From  the 


CROUPOUS  PNEUMONIA.  205 

method  of  treatment  by  large  bleedings,  which  was  formerly  customary,  and  also 
by  certain  drugs  which  are  even  now  occasionally  used — we  refer  especially  to 
veratrine— we  should  expect  an  injurious  effect,  and  not  a  favorable  one;  and  yet 
even  with  such  treatment  many  cases  of  pneumonia  recover. 

[In  robust  individuals,  with  a  full,  hard  pulse  and  great  oppression  of  breathing, 
venesection  affords  a  prompt  relief  to  be  obtained  in  no  other  way. 

In  general,  the  main  indications  for  treatment  are,  as  in  other  acute  self-limited 
diseases,  to  support  life  until  the  disease  has  run  its  course.] 

We  do  not  know  a  remedy  which  can  in  any  way  exert  a  favorable  influence 
upon  the  pneumonic  process  itself.  The  treatment  of  pneumonia  must  therefore  be 
purely  hygienic  and  symptomatic,  but  in  this  respect  it  can  accomplish  very  much. 

The  symptoms  which  are  usually  prominent  in  every  pneumonia,  even  in  the 
milder  cases,  and  of  which  the  patient  is  especially  desirous  to  be  relieved,  are  the 
pain  in  the  side,  the  troublesome  cough,  and  the  difficulty  and  distress  in  breath- 
ing. Since  the  respiratory  symptoms,  as  we  have  seen,  are  partly  due  to  the  pain, 
as  this  improves  the  patient's  breathing  often  undergoes  a  decided  improvement. 
For  the  pain,  we  may  first  mention  a  number  of  external  applications  to  the 
skin  on  the  affected  side.  An  ice-bag  sometimes  gives  marked  relief.  Many 
patients  can  not  bear  this,  but  prefer  warm  poultices  or  cold  wet  compresses.  The 
application  of  mustard  plasters  or  dry  cups  to  the  skin  may  be  of  advantage.  Sub- 
cutaneous injections  of  morphine,  however,  are  the  most  effective  remedy,  and 
are  often  indispensable.  There  is  no  reason  why  we  should  not  use  this  remedy, 
with  care  and  in  moderate  doses,  for  the  relief  of  pain ;  and,  as  the  disease  is  of 
short  duration,  we  need  not  particularly  fear  the  morphine  habit.  Small  doses 
of  morphine,  subcutaneously  or  by  the  mouth,  may  also  be  required  to  alleviate 
the  cough. 

Local  blood-letting  is  a  remedy  the  action  of  which  can  not  be  explained 
physiologically,  and  yet  experience  has  shown  that  it  is  of  undoubted  advantage. 
The  relief  which  many  patients  feel  after  the  application  of  ten  or  twelve  leeches 
to  the  affected  side  is  very  striking;  but  we  should  prescribe  them  only  when 
there  are  severe  symptoms  at  the  beginning  of  the  disease,  and  in  persons  who 
were  strong  and  healthy  before  the  attack.  '  Wet  cups  accomplish  the  same  thing, 
but  the  effect  is  somewhat  more  powerful,  and  hence  they  should  be  reserved  for 
strong  and  robust  persons,  such  as  laborers. 

The  tepid  bath  serves  as  the  most  effective  means  of  impi'oving  the  restoration, 
of  aiding  expectoration,  and  of  stimulating  and  refreshing  the  whole  system. 
We  hold  it  useless,  if  not  injurious,  to  give  a  patient  baths  if  the  disease  is 
progressing  favorably,  for  almost  every  bath  has  some  disagreeable  feature. 
These  disadvantages,  however,  are  always  less,  in  severe  cases,  than  the  bene- 
fit and  improvement  which  baths  give  the  patient,  and  which  most  patients 
recognize  with  gratitude.  The  main  point  is  that  the  patient  should  make  no 
physical  exertion  while  in  the  bath,  that  he  should  be  lifted  into  it,  held  and  sup- 
ported while  in  it,  and  lifted  into  bed  again  after  it.  Since  the  baths  are  given 
primarily  not  on  account  of  the  fever,  but  to  improve  the  respiration,  and 
because  of  their  favorable  influence  on  the  nervous  system,  their  temperature 
need  not  be  especially  low.  We  give  them  from  85°  to  90°  (24°-26°  R);  some- 
what warmer  with  sensitive  and  weak  people,  and  cooler,  down  to  77°  or  even 
72-5°  (20°-18°  R),  with  strong  people,  or  with  very  high  fever  or  severe  nervous 
symptoms.  We  need  not  employ  more  than  two  or  three  baths  a  day,  and  at 
night  we  employ  them  only  when  there  are  threatening  symptoms.  The  favor- 
able action  of  the  baths  is  especially  seen  in  the  great  relief  and  refreshment  that 
the  patient  feels.  The  respiration  is  quieter  and  slower,  but  deeper.  The  patieut 
often  falls  into  a  quiet  sleep  after  the  bath. 


206  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

Antipyretics  are  seldom  useful  in  pneumonia.  Even  if  the  temperature  rises 
very  high,  up  to  106°  (41°  C),  cool  baths  are  sufficient  to  avert  the  dangers  of  an 
increase  of  bodily  heat.  If  any  antipyretic  must  be  used,  antipyrine  is  to  be  pre- 
ferred. 

Expectorants  are  much  used,  especially  siuce  in  practice  we  seldom  can  avoid 
giving  some  internal  remedy.  Among  the  most  useful  are  infusion  of  ipecac- 
uanha, benzoin,  liquor  ammonii  anisatus,  and  tartar  emetic,  once  held  to  be  a  neces- 
sary specific  against  pneumonia  (!).  Finally,  digitalis  may  be  indicated  under 
some  circumstances  with  a  weak  and  frequent  pulse,  either  in  powder  or  in  an 
infusion  of  about  1  to  100. 

We  must  give  the  greatest  attention  in  all  severe  cases  to  keeping  up  the  pa- 
tient's strength.  We  must  therefore  take  care  to  furnish  an  easily  digestible  but 
nutritious  diet.  Meat  in  small  pieces,  cut  up  fine  or  scraped,  may  be  freely  al- 
lowed if  the  patient  has  an  appetite  for  it,  but  during  the  first  days  of  the  disease 
we  are  usually  confined  to  giving  soups,  milk,  and  eggs.  As  soon  as  the  signs  of 
more  marked  general  weakness  appear,  and  the  pulse  becomes  smaller,  we  must 
order  stimulants,  wine,  strong  cafe  noir,  or,  still  better,  ether  or  camphor.  The  lat- 
ter is  best  given  subcutaneously  in  severe  cases,  dissolved  in  olive-oil,  in  a  ratio  of 
one  to  four.  If  the  patient  swallows  well,  we  may  give  it  in  wine,  two  grains 
(grm.  O'l)  every  one  or  two  hours. 

We  have  yet  to  make  some  remarks  upon  the  very  extensive  use  of  large 
amounts  of  alcohol  in  pneumonia.  Without  doubt  a  free  use  of  alcohol  is  neces- 
sary in  drunkards,  esj>ecially  when  delirium  tremens  is  beginning  or  is  already 
pronounced.  Since  the  withdrawal  of  any  poison  that  is  taken  habitually,  like 
nicotine  or  morphine,  may  excite  the  severest  symptoms,  the  sudden  withdrawal 
of  alcohol  from  drunkards  may  have  the  worst  results,  while,  if  we  give  an  abun- 
dant supply  of  the  stimulant  to  which  the  nervous  system  is  accustomed,  we  some- 
times succeed  in  avoiding  the  onset  of  severe  nervous  symptoms,  like  collapse  and 
failure  of  the  heart  and  respiration.  It  is  quite  a  different  matter  with  patients 
who  before  their  illness  have  not  been  accustomed  to  take  alcohol  at  all,  or  who 
took  it  only  in  small  amounts.  It  may  be  true  that  in  these  cases  small  amounts 
of  wine  may  have  a  stimulating  and  exciting  action,  although  we  never  could 
satisfy  ourselves  of  the  often  praised  influence  of  alcohol  upon  the  action  of  the 
heart.  We  hold  it,  however,  unjustifiable  to  force  large  amounts  of  alcohol  indis- 
criminately upon  every  patient  with  pneumonia,  perhaps  in  spite  of  great  resistance 
on  his  part.  Why  should  we  expect  sick  persons  to  bear  closes  of  alcohol  which 
have  only  bad  results  on  healthy  men  unaccustomed  to  them  ? 

[Few  Amei'ican  physicians  of  any  experience  will  accept  the  reasoning  of 
the  author  on  the  employment  of  alcoholic  stimulants  in  those  not  accustomed 
to  their  use. 

The  toxic  effects  of  alcohol  are  as  undesirable  in  pneumonia  as  in  any  other 
disease,  but  there  are  few  affections  in  which  so  great  tolerance  is  shown  for  this 
agent.  The  chief  indications  for  its  exhibition  are  derived  from  the  pulse  and 
the  first  cardiac  sound  at  the  apex.  A  flagging  heart  calls  for  alcohol,  the  effect 
of  which  on  the  symptoms  and  on  the  circulation  is  to  be  carefully  watched ;  the 
quantity  is  to  be  diminished,  increased,  maintained,  or  the  agent  is  to  be  omitted 
entirely,  according  to  the  conditions  present  in  the  individual  case.  I  am  no  ad- 
vocate of  indiscriminate  alcoholic  stimulation ;  but  I  believe  that  lives  have  been 
frequently  saved  in  the  past,  and  will  be  saved  in  the  future,  by  the  judicious  and 
sometimes  extremely  free  use  of  this  class  of  remedies  in  acute  pneumonia.  In- 
halation of  oxygen  has  won  a  prominent  place  in  the  treatment  of  severe  pneu- 
monia of  late  years,  and  cases  are  reported  in  which  life  seems  unquestionably  to 
have  been  saved  by  it.     In  a  considerable  number  of  cases  the  editor  has  seen  only 


TUBERCULOSIS  OP  THE  LUNGS.  201 

one  which  could  come  under  this  class.  He  has  seen,  however,  marked  tempo- 
rary improvement  in  pulse  and  respiration,  with  diminution  of  cyanosis  and  in- 
duction of  relatively  quiet  sleep.  But  the  oxygen  must  he  given  in  large  quan- 
tities, sometimes  continuously.  If  its  inhalation  fatigues  the  patient,  the  gas  may 
he  allowed  to  escape  hefore  the  mouth  or  under  the  nose  of  the  patient.  The  ob- 
jection to  the  efficient  use  of  oxygen  in  some  cases  is  the  expense  of  perhaps  some 
hundreds  of  gallons  a  day  at  five  cents  a  gallon.] 

The  treatment  of  complications  follows  the  ordinary  rules  which  have  heen 
given  under  the  individual  affections.  We  must  also  mention  that,  in  delir- 
ium tremens,  tepid  baths  with  cold  douches  sometimes  have  a  very  good  effect. 
Besides  this,  we  may  try  subcutaneous  injections  of  strychnine,  seven  to  fifteen 
minims  of  a  one-per-cent.  solution,  once  or  twice  a  day.  We  can  not  wholly  dis- 
pense with  narcotics,  such  as  morphine  and  chloral,  but  we  must  warn  against  the 
imprudent  use  of  large  doses  of  chloral,  above  thirty-five  grains  (grm.  2'5). 


CHAPTER  VI. 

TUBERCULOSIS   OF   THE   LUNGS. 

{Pulmonary  Phthisis.     Pulmonary  Consumption.) 

General  Pathology  and  ^Etiology  of  Tuberculosis. 

Ever  since  Bayle,  in  1810,  demonstrated  the  extensive  distribution  of  peculiar 
nodules  in  the  various  organs,  and  their  relation  to  pulmonary  consumption,  few 
questions  have  so  taxed  clinical  observers  and  pathologists  as  those  relating  to  the 
cause  and  nature  of  tuberculosis.  Harmony  could  not  be  reached,  however,  so 
long  as  the  criterion  for  the  decision  of  the  questions  was  sought  in  the  presence 
of  definite  anatomical  changes,  which  were  regarded  as  specific  of  tuberculosis. 
Laennec  considered  the  peculiar  change  in  the  tubercular  products,  which  later 
was  named  caseation  by  Virchow,  to  be  characteristic,  and  called  everything 
tubercular  where  it  was  found.  He  distinguished  the  isolated  tubercle  from 
diffuse,  tubercular,  cheesy  infiltration.  Thus  Laennec  recognized  that  many 
processes  were  allied  whose  affinity  was  often  disputed  afterward,  and  has  only 
recently  been  established,  such  as  the  affinity  between  "scrofulous"  enlargement 
of  the  glands  and  tuberculosis.  Another  opinion  became  quite  prevalent,  after 
Virchow  discovered  that  precisely  the  same  anatomical  process  as  tubercular  casea- 
tion was  also  found  in  inflammatory  products,  which  were  certainly  not  tubercular, 
and  in  cancerous  ulcerations.  Hence  Virchow  made  a  sharp  distinction  between 
tubercle  and  those  new  growths  and  inflammatory  processes  which  had  become 
cheesy.  The  anatomical  criterion  of  tuberculosis  was,  in  his  view,  the  presence  of 
the  miliary  tubercle,  a  gray  nodule,  the  size  of  a  millet-seed  at  the  largest,  made 
up  of  cells  like  lymph-corpuscles.  The  study  of  the  finer  structure  of  the  miliary 
tubercle  was  now  pushed  most  eagerly  by  Wagner,  Schüppel,  Langhans,  and 
others,  but  they  were  unable  to  reach  perfect  harmony  regarding  its  origin  and 
significance. 

As  long  ago  as  1865,  however,  a  discovery  was  made  which  pointed  unequivo- 
cally to  the  only  way  which  could  lead  to  a  correct  knowledge  of  tuberculosis.  It 
was  the  fact,  discovered  by  Villemin,  that  tuberculosis  can  be  produced  artificially 
by  inoculating  healthy  animals  with  small  amounts  of  tubercular  and  cheesy  sub- 
stances. Although  doubted  and  misinterpreted  at  first  in  various  quarters,  the  fact 
that  tuberculosis  can  be  transmitted,  and  consequently  the  fact  of  its  infectious 


208  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

character,  must  now  be  regarded  as  proved  beyond  a  doubt.  In  the  general 
change  which  our  opinions  upon  the  nature  of  infectious  diseases  have  undergone, 
especially  in  the  last  few  years,  the  existence  of  a  specific,  organized  cause  of  tuber- 
culosis, too,  had  to  be  assumed.  Klebs,  and  later  Cohnheim,  had  already  without 
reserve  defined  tuberculosis  as  a  specific,  infectious  disease  and,  sooner  than  we 
dared  to  hope,  R.  Koch  discovered  the  special  carriers  of  the  disease  in  the  shape 
of  the  tubercle  bacilli,  in  the  year  1881.  The  definition  of  tuberculosis  no  longer 
rests  upon  any  external  anatomical  chai^acter.  Every  disease  is  tubercular  which 
is  excited  by  the  pathogenic  action  of  a  specific  kind  of  bacteria,  the  tubercle 
bacilli  discovered  by  Koch. 

The  pathogenic  bacteria  of  tuberculosis  belong  to  the  group  of  bacilli.  The 
tubercle  bacilli  are  rod-like,  of  small  diameter,  slightly  rounded  at  their  extremi- 
ties, and  either  straight  or  somewhat  bent.  Their  length  is  perhaps  a  fourth  or  a 
half  that  of  the  diameter  of  a  red  blood-corpuscle.  Iu  the  interior  of  these  rods  it 
is  not  seldom  possible  to  distinguish  very  minute  colorless  spots  which  are  proba- 
bly to  be  regarded  as  endogenous  spores.  The  tubercle  bacilli  have  no  independ- 
ent motion  whatever.  Their  reaction  to  certain  coloring  matters  is  very  charac- 
teristic, and  of  the  highest  importance  with  regard  to  their  recognition  (see  below). 
We  know  with  absolute  certainty  that  the  tubercle  bacilli  are  always  present  in 
all  the  different  forms  of  pulmonary  tuberculosis,  both  in  the  lung  itself  and  in 
the  expectoration  {vide  infra),  and  also  iu  tubercular  diseases  of  other  organs, 
like  the  brain,  the  intestines,  the  spleen,  the  liver,  and  the  kidneys,  and  also  in 
"  scrofulous  lymph-glands,"  in  ''  fungous  "  diseases  of  the  bones  and  joints,  and  in 
the  so-called  lupus,  which  is  nothing  but  a  local  tuberculosis  of  the  skin.  Pre- 
cisely the  same  bacilli  are  also  found  in  the  "  spontaneous  "  tuberculosis  of  animals» 
such  as  monkeys,  puppies,  and  guinea-pigs,  and  in  every  tuberculosis  that  is  arti- 
ficially produced  in  animals  by  inoculation.  Finally,  by  the  discovery  of  tubercle 
bacilli  in  the  "  pearly  distemper  "  of  cattle,  the  identity  of  this  disease  with  tuber- 
culosis— an  identity  which  had  already  been  established  by  experiments  in  inocu- 
lation— was  confirmed  anew. 

Koch,  by  his  successful  "  pure  cultures  "  and  inoculations  with  the  cultivated 
bacilli,  has  established  the  fact  that  these  bodies,  known  as  tubercle  bacilli,  are  to 
be  regarded  as  organized,  and  as  the  special  cause  of  tuberculosis.  Bacilli  coming 
from  any  fresh  product  of  tubercular  disease  may  be  cultivated  at  a  constant  tem- 
perature of  98°  to  100°  (37°-38°  C.)  upon  blood-serum  which  has  been  stiffened  by 
heating,  and  upon  several  other  artificially  prepared  soils.  In  this  cultivation 
they  show  certain  characteristic  properties  in  their  growth,  which  can  not  be 
fully  described  here,  and  they  multiply  to  an  unlimited  extent.  In  this  way  we 
can  keep  up  perfectly  "  pure  cultures  "  of  tubercle  bacilli.  Inoculation  experi- 
ments tried  with  them  on  all  sorts  of  creatures  always  give  a  positive  result.  The 
animals  fall  ill,  lose  flesh,  and  finally  die,  and  at  the  autopsy  we  find  undoubted 
tubercular  disease  of  the  internal  organs,  which  may  be  more  or  less  extensive. 
The  most  instructive  inoculations  are  those  into  the  anterior  chamber  of  the  eye 
in  puppies  or  guinea-pigs,  which  were  first  tried  by  Cohnheim  and  Salomonsen. 
After  an  incubation  of  two  or  three  weeks  we  see  here  very  plainly  an  eruption  of 
the  first  nodules  of  tubercle  in  the  iris,  and  the  tuberculosis  spreads  to  the  other 
organs  of  the  body  later. 

iETTOLOGY  OF  TUBERCULOSIS  IN  MAN. 

The  distribution  of  tubercle  bacilli  must  be  remarkably  extensive,  for  tuber- 
cular diseases  occur  in  almost  every  country  on  earth.  The  predisposition  of 
mankind  to  the  disease  is  also  very  great,  and  thus  we  understand  the  frightful 


TUBERCULOSIS  OF  THE  LUNGS.  209 

fact,  which  statistics  show,  that  nearly  one  seventh  of  all  deaths  are  from  tuber- 
culosis I  It  has  neither  been  proved,  nor  is  it  probable,  that  tubercle  bacilli  multi- 
ply outside  of  the  human  body,  like  the  bacilli  of  splenic  fever,  since  they  can 
develop  only  in  a  constant  and  uniformly  warm  temperature  between  85°  and 
104°  (30°-40°  C),  We  must  therefore  regard  them  as  true  parasites,  which  can 
live — that  is,  which  can  propagate  and  multiply — only  in  the  bodies  of  animals, 
but  they  seem  to  preserve  their  virulence  and  their  ability  to  multiply  outside  of 
the  body  for  a  long  time.  Phthisical  sputum  may  be  used  for  inoculation  with 
success,  even  if  it  has  been  dried  for  several  weeks.  The  tubercle  bacilli  also 
resist  most  chemical  reagents,  like  nitric  acid,  very  decidedly. 

If  the  body  becomes  infected,  then,  with  tubercle  bacilli,  it  is  always  probable 
that  they  have  come  from  some  other  individual — man  or  beast — with  tubercular 
disease.  We  need  not  mention  how  numerous  the  opportunities  for  infection  may 
be,  considering  the  present  general  distribution  of  tuberculosis.  The  chief  stress  in 
this  respect  is  to  be  laid  upon  the  expectoration  of  phthisical  patients,  which  con- 
tains the  bacilli.  This  dries  on  the  floor,  on  the  linen,  and  on  other  objects,  and 
then  the  small  particles  which  contain  the  germs  of  infection  are  carried  off  by 
the  air.  The  view  most  generally  held  is  that  the  material  which  contains  the 
bacilli  or  spores  is  taken  into  the  body,  in  the  majority  of  cases,  along  with  the 
inspired  air.  This  is  probable,  because,  in  most  cases,  tuberculosis  has  its  starting- 
point  in  the  air-passages,  the  lungs,  or  larynx.  Inoculation  experiments  show 
that  the  first  extension  of  the  process  depends  upon  the  point  of  inoculation.  If 
it  be  in  the  anterior  chamber  of  the  eye,  the  first  nodules  appear  in  the  iris,  as  we 
have  said ;  if  it  be  in  the  abdominal  cavity,  we  have  first  a  tuberculosis  of  the  peri- 
tonaeum ;  if  the  infectious  matter  be  inhaled,  we  have  first  a  tuberculosis  of  the 
lungs.  For  several  years  Tappeiner  and  others  have  experimented  with  inhala- 
tions of  powdered  tuberculous  sputa  at  the  Munich  Pathological  Institute.  Pul- 
monary tuberculosis  could  always  be  pi'oduced  by  these  inhalations  in  the  animals 
experimented  upon.  Hence  it  seems  very  probable  that,  in  tuberculosis  in  man, 
the  infectious  matter  is  taken  directly  into  the  air-passages  by  the  breath.  In  this 
way  it  sometimes,  though  rarely,  attacks  the  upper  air-passages,  as  in  primary 
tuberculosis  of  the  nose,  the  pharynx,  and  the  larynx,  but  more  frequently  it  af- 
fects the  deeper  portions  of  the  respiratory  apparatus,  as  in  primary  tuberculosis 
of  the  lungs  and  bronchi. 

We  must  also  consider  other  methods  of  infection,  first  among  which  is  the 
possibility  of  infection  of  the  intestinal  canal,  from  swallowing  the  infectious 
material.  The  transmission  of  tuberculosis  from  domestic  animals  to  man  plays 
a  part  in  this  connection  which  perhaps  is  not  unimportant.  Since  the  pearly 
distemper  in  cattle  is  identical  with  tuberculosis  in  man,  the  use  of  the  flesh  of 
such  animals  as  food  furnishes  a  possible  means  of  infection.  It  is  a  still  more 
important  circumstance,  however,  that,  when  pearly  nodules  are  present  on  the 
udder,  the  milk  of  the  diseased  animal  may  be  polluted  by  tubercle  bacilli,  and 
that  the  use  of  such  milk  as  food,  when  it  is  uncooked,  certainly  involves  the 
danger  of  the  transmission  of  tuberculosis.  Primary  tuberculosis  of  the  intes- 
tines, however,  does  not  seem  to  be  very  frequent,  probably  because  the  tubercle 
bacilli  which  have  been  swallowed  are  usually  destroyed  in  the  stomach. 

In  some  cases  the  tubercular  infection  may  probably  arise  from  little  fissures 
and  excoriations  of  the  skin.  In  this  way  we  get  either  a  local  tuberculosis  of  the 
skin,  like  lupus,  or  the  bacilli  are  carried  by  the  lymphatics  to  the  neighboring 
glands  of  the  neck  or  axilla,  establish  themselves  there,  and  set  up  a  tubercidar 
disease  in  them.  In  conclusion,  we  have  still  to  mention  that  the  apparently 
primary  appearance  of  tuberculosis  in  the  genito-urinary  apparatus  leads  us  to 
think  of  the  possibility  of  an  infection  of  the  genital  or  urinary  organs. 
14 


210  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

Considering  the  wide  distribution  of  the  tubercle  bacilli,  and  the  many  chances 
for  infection,  it  seems  wonderful  that  in  spite  of  it  so  many  men  escape  the  dis- 
ease. Oue  factor,  which  has  been  already  mentioned  by  Koch,  must  be  borne  in 
mind,  however,  and  that  is  the  extremely  slow  growth  of  the  tubercle  bacilli. 
This  is  the  reason  why  the  bacilli  do  not  always  remain  in  the  body,  but  in  many 
cases  are  eliminated  again  before  they  have  gained  a  definite  foothold. 

Individual  predisposition,  however,  is  another  factor  which  perhaps  is  still 
more  importaut^a  factor  which  we  can  not  well  explain,  but  which  we  can  not 
get  on  without,  at  the  present  time,  in  the  pathology  of  many  infectious  diseases. 
In  our  conception  of  most  of  the  other  infectious  diseases,  as  well  as  of  tubercu- 
losis, we  must  assume  provisionally  an  unequal  predisposition  to  disease  in  differ 
ent  individuals.  Only  a  part  fall  ill  of  all  who  are  exposed  to  the  action  of  the 
poison.  These  are  persons  in  whom  it  is  particularly  easy  for  the  poison  to  estab- 
lish and  propagate  itself. 

We  have  long  considered  people  with  a  generally  feeble  physical  constitution 
as  especially  liable  to  tubercular  disease.  We  speak  of  a  "tubercular  habit"  (vide 
infra).  In  this  connection  we  must,  of  course,  remember  that  much  that  we 
once  regarded  as  merely  the  signs  of  a  special  predisposition  to  disease  is  really 
the  expression  of  a  disease  that  already  exists.  If,  for  example,  we  once  affirmed 
that  ''scrofulous"  children  had  a  special  predisposition  to  tuberculosis,  we  know 
now  that  the  so-called  scrofulous  diseases  of  the  mucous  membranes,  the  lymph- 
glands,  and  the  bones,  are  the  results  of  an  existing  tuberculosis ;  or,  at  least,  that 
this  is  so  in  a  large  number  of  cases. 

We  now  believe  that  many  evil  influences  which  were  once  thought  to  be 
causes  of  tuberculosis  act  only  in  increasing  the  predisposition  to  the  disease.  In- 
sufficient food,  bad  air,  severe  illness,  childbirth,  want,  and  care— these  alone,  of 
course,  can  never  produce  tuberculosis ;  but  we  can  easily  imagine  that  the  body 
which  has  become  weakened  affords  less  resistance  to  the  injurious  influence  of 
the  tubercular  poison  than  does  the  strong  and  healthy  body.  Thus  it  seems  to 
us,  from  our  own  observations,  to  be  in  the  highest  degree  probable  that  chronic 
alcoholism  increases  the  liability  of  the  individual  to  tuberculosis. 

People  used  often  to  speak  of  the  transition  of  other  affections  of  the  lungs 
into  pulmonary  consumption — that  is,  into  tuberculosis.  It  was  imagined  that 
an  old  bronchial  catarrh,  croupous  inflammation  of  the  lungs,  or  catarrhal  pneu- 
monia in  measles,  or  whooping-cough,  could  readily  become  "tubercular."  It 
goes  without  saying  that  such  an  idea  is  no  longer  tenable,  after  the  demonstra- 
tion of  the  specific,  infectious  nature  of  tuberculosis.  If  we  see  a  pulmonary 
tuberculosis  develop  as  a  sequel  of  any  other  affection  of  the  lungs,  we  can 
express  the  relation  between  the  two  diseases  only  in  this  way,  that  the  first  dis- 
ease furnished  a  favorable  soil  for  infection  with  tubercular  virus,  and  that, 
consequently,  the  tubercle  bacilli  could  more  easily  take  root  upon  a  previously 
diseased  mucous  membrane  than  under  normal  conditions;  moreover,  there  is  no 
doubt  that  many  of  the  affections,  whose  "  transition  into  tuberculosis  "  we  once 
assumed,  are  themselves  tubercular.  This  is  the  case,  as  we  shall  see,  in  many 
cases  of  pleurisy.  No  one  will  now  admit  the  truth  of  the  theory,  which  Nie- 
meyer  once  vigorously  defended,  that  a  primary  pulmonary  haemorrhage  could 
cause  the  development  of  pulmonary  phthisis.  Certainly,  in  the  cases  which 
apparently  support  such  an  opinion,  the  pulmonary  haemorrhage  is  not  the  cause, 
but  a  symptom,  of  pulmonary  tuberculosis. 

No  single  factor,  however,  of  those  which  favor  the  predisposition  to  tuber- 
culosis, plays  so  manifest  and  so  visible  a  part  as  does  heredity.  The  fact  of 
the  heredity  of  phthisis  meets  us  with  such  uncommon  frequency  that  it  must 
have  forced  itself  upon  the  notice  of  the  older  physicians.     In  the  great  majority 


TUBERCULOSIS  OF  THE  LUNGS.  211 

of  all  cases  of  phthisis  we  can  make  out,  by  close  questioning,  that  in  the  family, 
either  among  the  older  members  or  among  the  brothers  and  sisters,  one  or  more 
cases  of  tubercular  disease  have  already  occurred.  The  closer  we  investigate,  and 
the  more  we  search  for  some  one  of  the  different  forms  in  which  tuberculosis 
can  show  itself,  like  pleurisy,  or  affections  of  the  bones  and  joints,  the  more 
frequently  we  can  make  out  this  hereditary  predisposition. 

While  there  can  be  no  doubt  of  the  facts  themselves,  their  explanation  is  by  no 
means  a  simple  one.  At  all  events,  the  question  of  the  heredity  of  tuberculosis 
now  needs  to  be  studied  with  renewed  care.  The  hereditary  character  of  tuber- 
culosis may  very  well  harmonize  with  its  infectious  character.*  We  might  as- 
sume in  this  case  a  perfect  analogy  with  syphilis— namely,  a  transition  of  the 
infectious  material  from  the  parent  to  the  child  before  birth.  There  is  only  one 
striking  difference  between  syphilis  and  tuberculosis — that  the  children  of  syph- 
ilitic parents  very  often  come  into  the  world  with  definite  signs  of  infection,  while 
congenital  tuberculosis  in  this  sense  is  an  extremely  rare  occurrence.  We  must 
accordingly  compare  tuberculosis  to  that  form  of  hereditary  syphilis  (lues  heredi- 
taria tarda)  in  which  the  first  symptoms  of  the  affection  come  on  at  a  late 
period. 

Since  certain  considerations,  however,  constantly  oppose  such  a  theory,  we  are 
of  late  disposed  to  assume  that,  as  a  rule,  tuberculosis  in  itself  is  not  inherited,  but 
only  the  predisposition  to  tubercular  disease.  This  opinion  agrees  with  the  facts 
that  members  of  a  family  in  which  tuberculosis  prevails  very  often  show  the  so- 
called  tubercular  habit  even  without  any  real  tubercular  disease;  and  that  they 
often  have  "  weak  lungs  " — that  is,  that  they  easily  get  out  of  breath,  and  manifest 
a  distinct  tendency  to  catarrh  of  the  respiratory  organs.  Another  fact,  which  to  a 
certain  extent  may  be  regarded  as  an  argument  against  the  assumption  of  a  direct 
hereditary  transmission  of  the  disease,  is  that,  in  cases  of  apparently  hereditary 
tuberculosis,  as  a  rule  those  organs  first  show  evidences  of  disease  which  are  most 
exposed  to  an  infection  from  the  outer  world — namely,  the  lungs  and  larynx. 

Meanwhile  there  is  a  third  possibility  to  be  considered  with  regard  to  the  "  in- 
heritance of  tuberculosis."  Many  cases  of  apparently  inherited  tuberculosis  are, 
in  all  probability,  to  be  explained  by  the  fact  that  children  or  relatives  who  are 
constantly  in  the  company  of  a  patient  with  phthisis  are  decidedly  more  exposed 
to  the  danger  of  infection  than  other  persons,  This  is  also  the  reason  why  tuber- 
culosis is  very  often  conveyed  from  husband  to  wife,  or  vice  versa,  of  which  we 
might  furnish  a  series  of  examples  from  our  own  experience. 

The  age  of  the  patient  has  an  important  influence  upon  the  predisposition  to 
tubercular  disease.  Pulmonary  tuberculosis  occurs  with  special  frequency  in 
youth,  between  fifteen  and  thirty.  It  is  not  rare  in  children.  After  forty  it  is 
much  rarer  in  its  pronounced  forms,  but  it  is  seen  even  in  the  most  advanced  age. 
Slight  tuberculous  changes  are  very  frequently  found  at  autopsy  in  the  lungs  of 
old  persons.     These  changes  have,  as  a  rule,  no  clinical  significance. 

It  has  not  yet  been  shown  that  sex  has  a  special  influence  upon  the  predisposi- 
tion to  the  disease. 

*  Jani  has  made  the  very  interesting  observation,  that  a  few  tubercle  bacilli  may  be  found  in 
phthisis  in  the  vas  deferens  and  the  prostate,  or  in  the  folds  of  the  lining  membrane  of  the  tubes, 
without  apparent  disease  of  these  parts.  "Whether  this,  however,  explains  the  hereditary  transmission 
of  tuberculosis,  is  as  yet  doubtful. 


212  DISEASES  OF  THE  RESPIRATORY  ORGANS. 


Pathological  Anatomy  of  Tuberculosis,  especially  of  Pulmonary 

Tuberculosis. 

If  now  we  inquire  wherein  consists  the  injury  which  the  tubercle  bacilli  in- 
flict upon  the  body,  the  first  point  to  emphasize  is  that  the  action  of  the  tubercle 
bacilli  is  at  first  invariably  purely  local.  Tuberculosis  does  not  belong-  to  the 
"  general  infectious  diseases,"  in  which  the  infection  of  the  whole  organism,  the 
''general  infection"  of  the  body,  predominates  over  the  local  disturbances.  The 
essence  of  tuberculosis,  at  least  in  the  great  majority  of  cases,  is  the  local  disease. 
The  tubercle  bacilli  give  rise  to  definite  anatomical  changes  in  the  organs  where 
they  settle,  aud  the  consequent  disturbance  of  function  in  the  organ  has  an  effect 
on  the  rest  of  the  body.  In  many  cases  the  whole  body  may  be  so  little  affected 
that  we  may  be  justified  in  saying  that  there  is  a  purely  " local  tuberculosis." 

The  danger  of  tubercular  diseases,  however,  consists  in  the  fact  that  the  local 
affection  often  attacks  the  most  important  organs,  as  the  lungs  and  the  brain, 
and  sets  up  such  extensive  anatomical  changes  in  them  that  because  of  these 
changes  alone  it  becomes  impossible  for  life  to  continue  longer.  Besides  this,  the 
infection  in  many  cases  does  not  always  confine  itself  to  one  organ,  but  the  infec- 
tious material  extends  over  the  body  by  ways  and  means  which  we  shall  learn 
in  part  later  on,  and  attacks  one  organ  after  another,  or  even  many  at  once. 
Finally,  it  is  to  be  said  that  the  peculiar  character  of  the  changes  caused  by  tuber- 
culosis explains  why  these  are  often  the  cause  of  manifold  secondary  processes, 
such  as  toxic  effects  and  secondary  infections.  Thus  arise  fever  and  other  impor- 
tant symptoms,  which  will  be  minutely  considered  later. 

The  entire  local  action  of  the  tubercle  bacilli — that  is,  the  pathological  anat- 
omy of  tuberculosis  —  is  almost  wholly  independent  of  the  organ  attacked. 
Tuberculosis  belongs  to  the  group  of  so-called  "  infectious  tumors  " — that  is,  the 
local  action  of  the  tubercle  bacilli  consists  chiefly  in  the  production  of  a  prolifera- 
tion and  accumulation  of  cells  at  their  place  of  settlement,  which  is  termed  a 
tubercular  new  growth. 

According  to  the  later  investigations  of  Arnold,  Baumgarten,  and  others,  the 
process  begins  with  hyperplasia  of  the  normal  tissue,  both  of  the  interstitial  and 
of  the  epithelial  cells.  In  this  way  are  developed  the  so-called  epithelioid  cells 
and  the  giant  cells.  The  next  step  in  the  process  is  the  migration  of  numerous 
leucocytes  from  the  surrounding  blood-vessels.  The  leucocytes,  or  round  cells, 
collect  about  the  above-mentioned  new-formed  cells,  and  may  finally  completely 
cover  them.  A  network,  or  reticulum,  is  found  between  the  individual  new- 
formed  cells  and  the  wandering  cells.  This  probably  represents  the  remains  of 
the  original  interstitial  tissue,  crowded  apart  by  the  increased  number  of  cells. 
There  is  no  new  formation  of  vessels.  The  tubercle  contains  no  blood-vessels. 
The  tubercle  bacilli  lie  especially  inside  the  giant  cells,  but  also  in  their  vicinity. 

If  these  changes  have  progressed  far  enough,  they  become  visible  to  the  naked 
eye  as  a  small,  circumscribed  grayish  point,  which  is  called  a  miliary  tubercle. 
From  these  minute  nodules  the  disease  itself  obtained  its  name  of  tuberculosis. 
By  approximation  and  coalescence  of  neighboring  tubercles — for  these  keep  devel- 
oping because  of  the  spread  of  the  local  infection — the  tuberculous  formation 
continually  extends  itself,  and  thus  are  gradually  formed  the  large  tubercular 
nodules,  and  finally  the  diffuse  tuberculous  new  growth  or  the  diffuse  tubercu- 
lous infiltration. 

The  tuberculous  new  growth,  as  such,  can  scarcely  ever  be  distinguished  histo- 
logically from  other  infectious  tumors,  such  as  those  seen  in  syphilis  aud  leprosy. 
Tuberculosis,  however,  has  a  characteristic  difference  iu  its  final  stages  of  cheesy 
degeneration  and   eventual   disintegration  of  the   new-formed  tissue,  processes 


TUBERCULOSIS  OF  THE  LUNGS.  213 

which  are  apparently  connected  with  the  absence  of  blood-vessels  and  the  conse- 
quent deficiency  of  nutrition  of  the  new  formation.  Both  the  tuherculous  infil- 
tration and  also  the  portions  of  the  original  tissues  inclosed  by  it  perish,  lose  their 
nuclei,  and  finally  become  disintegrated.  The  manner  in  which  they  are  destroyed 
— namely,  "fatty  degeneration''1 — belongs  in  the  group  of  the  so-called  coagu- 
lation necroses.  This  process  is  recognizable  to  the  naked  eye,  because  the  tuber- 
culous infiltration  when  it  becomes  thus  degenerated  takes  on  a  pronounced  yel- 
lowish color.  Wherever  the  necrotic  portions  of  tissue  are  superficially  situated 
they  are  cast  off,  giving  rise  to  tuberculous  ulcers. 

Alongside  the  tuberculous  new  formation  there  are  found  in  the  organs  af- 
fected with  tuberculosis  various  inflammatory  processes,  either  simple  or  sup- 
purative or  hemorrhagic.  We  may  therefore  surmise  that  the  tubercle  bacilli, 
besides  their  characteristic  effects,  act  simultaneously  in  another  role  as  excitants 
of  inflammation ;  but  it  is  very  probable,  and  especially  so  in  pulmonary  tubercu- 
losis, that  many  of  the  inflammatory  changes  which  arise  are  not  peculiar  to  the 
tuberculosis  as  such,  but  are  to  be  regarded  as  secondary  processes  {vide  infra). 

As  regards  the  special  anatomical  processes  and  appearances  in  pulmonary 
tuberculosis,  the  tubercular  change  usually  begins  in  the  walls  of  the  smallest 
bronchi,  or  not  rarely  in  the  alveoli  themselves.  The  disease  does  not  begin, 
however,  in  many  different  parts  of  the  lung  at  once,  but  probably  in  one  or  two 
circumscribed  spots  only,  and  in  a  great  majority  of  cases  in  one  apex.  We  do 
not  know  why  the  apices  are  so  often  the  starting-point  of  phthisis,  but  perhaps 
it  is  because  of  their  relatively  slighter  expiratory  power,  which  renders  them  a 
favorable  lodging-place  for  the  tubercle  bacilli. 

The  tubercular  infiltration  begins  in  the  bronchial  wall  and  extends  gradually 
to  the  periphery.  A  tubercular  peribronchitis  arises  as  a  result  of  the  original 
tubercular  bronchitis.  The  infectious  material,  as  soon  as  there  is  any  super- 
ficial ulceration,  is  readily  carried  from  the  original  focus  of  the  disease  to  other 
bronchi,  by  means  of  the  current  of  air,  and  thus  the  disease  gradually  extends. 
Tubercular  peribronchitis  is  usually  easily  recognized  with  the  naked  eye.  We 
notice  the  little  lumen  of  the  bronchus  in  the  middle  of  the  "cheesy  "  nodule, 
which  at  first  is  gray  and  later  yellowish.  Many  of  the  adjacent  nodules  run 
together  in  part,  and  even  entirely.  The  lumen  of  the  bronchus  is  either  wholly 
plugged  by  the  infiltration,  or  the  destruction  of  the  necrotic  cells  begins  in  the 
midst  of  the  peribronchitis.  In  the  latter  case  the  lumen  is  enlarged  to  a  little 
irregular  hole — the  first  beginning  of  the  formation  of  a  cavity. 

The  alveolar  tissue  of  the  lung  can  not  long  remain  unaffected,  with  such  a 
disease  of  the  smaller  bronchi.  Lobular  atelectasis,  the  necessary  result  of 
every  permanent  bronchial  obstruction,  must  arise,  but  this  soon  passes  into  a 
lobular  pneumonia,  which  from  its  specific  nature  later  becomes  caseous.  We 
can  not  go  into  the  histological  details  here.  The  alveoli  are  filled  with  pus- 
corpuscles  and  large  epithelioid  cells,  which  are  considered  by  many  authors 
to  be  the  offspring  of  the  alveolar  epithelium.  The  alveolar  walls  are  also  infil- 
trated. This  finally  results  in  the  destruction  of  the  cheesy  and  necrotic  tissue, 
and  consequently  in  the  formation  of  cavities.  At  other  times  the  neighboring 
nodules  run  together,  and  the  tubercular  infiltration  thus  extends,  giving  rise  to 
a  diffuse  caseous  pneumonia.  These  processes  may  all  be  readily  recognized  by 
the  naked  eye.  The  earlier  stages  of  atelectasis  and  infiltration  correspond  to  the 
jelly-like,  gray  coloring  seen  in  the  so-called  gelatinous  infiltration  of  Laennec, 
and  the  transition  to  caseation  is  recognized  by  the  eye  from  the  yellowish  color. 

Although  all  the  processes  thus  far  described  are  destructive  in  their  nature, 
changes  are  also  found  in  the  lungs,  in  tuberculosis,  which  seem  to  have  a  tendency 
toward  circumscribing  the  disease  and  toward  healing.     Prominent  among  these 


214  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

are  the  chronic  interstitial  processes.  We  meet  with  the  formation  of  new  con- 
nective tissue,  partly  ahout  the  tubercular  infiltration,  but  especially  where  there 
is  already  destruction  of  tissue,  and  this  leads  to  contraction  and  the  formation  of 
a  firm  cicatrix.  The  encapsulated  cheesy  masses  may  then  be  in  part  reab- 
sorbed; in  part  they  undergo  calcification.  The  possibility  of  such  a  halt  in  the 
tuberculous  process  depends,  however,  upon  certain  conditions.  The  tuberculous 
new  growth  and  its  destruction  must  not  advance  too  rapidly,  and  the  new-formed 
tissue  must  not  itself  be  destroyed  before  it  becomes  cicatrized.  We  see  the 
cicatricial  formation,  therefore,  more  especially  in  chronic  cases;  we  find  it  in 
places  which  have  been  affected  the  longest,  aud  where  the  tubercular  process, 
perhaps,  has  finally  come  to  a  standstill  of  its  own  accord.  Macroscopically,  this 
cicatricial  connective  tissue  is  composed  of  a  thick,  firm  substance,  usually  pig- 
mented— the  so-called  pigment  induration.  If  the  cicatricial  formation  follows  a 
previous  extensive  destruction  of  the  pulmonary  tissue,  the  affected  portion  of  the 
lung  may  thus  be  diminished  to  less  than  half  its  original  bulk.  Cavities  and 
firm  cicatricial  tissue  form  the  anatomical  basis  of  such  an  extensive  "  pulmonary 
contraction."  The  cavities  are  either  formed  in  the  usual  way  from  the  destruction 
of  lung  tissue,  or  they  may  be  simple  bronchial  dilatations  due  to  the  traction  of 
the  contracted  tissue — bronchiectasic  cavities. 

The  contractile  changes  in  pulmonary  tuberculosis  teach  us  that  the  tuber- 
cular process  is  in  itself  capable  of  healing.  The  incurability  of  most  cases  of 
phthisis  is  due  to  the  fact  that  the  infectious  material  from  every  existing  tuber- 
cular nodule  is  carried  into  other  bronchi,  and  there  sets  up  a  new  tuberculosis. 
Thus  the  disease  is  constantly  extended.  The  original  tuberculosis,  which  was 
localized  in  one  apex  only,  gradually  spreads  to  the  lower  portion  of  the  lung. 
The  infectious  material  is  carried  by  coughing  into  the  trachea,  and  from  this 
point  may  be  carried  by  inspiration  into  the  other  lung.  This  becomes  diseased, 
and  finally  there  is  such  an  extensive  destruction  of  the  lungs  as  to  make  the 
further  continuance  of  life  impossible. 

Besides  the  spots  of  specific  tubercular  disease,  we  very  often  find  in  phthisical 
lungs  simple  inflammatory  processes,  bronchitis,  lobular  catarrhal  pneumonia,  and 
sometimes  even  croupous  pneumonia.  This,  of  course,  is  rarely  extensive.  These 
changes  may  be  partly  due  to  the  influence  of  the  tubercle  bacilli  themselves 
in  exciting  inflammation,  but  it  is,  of  course,  easily  conceivable  that  many  other 
excitants  of  inflammation  may  easily  settle  in  the  secretions  of  the  bronchi  and 
the  cavities,  and  lead  to  complicating  diseases  of  the  bronchial  mucous  membrane 
and  the  alveoli.  Thus  in  pulmonary  tuberculosis  a  local  gangrene  may  occasion- 
ally arise.  An  especial  importance  attaches  to  the  secondary  inflammatory  pro- 
cesses in  the  lungs,  because  they  furnish  a  suitable  spot  for  the  subsequent  inva- 
sion of  the  tubercle  bacilli.  Thus,  in  phthisical  patients,  foci  of  simple  inflamma- 
tion very  frequently  assume  a  tuberculous  character. 

If  we  consider  the  list  of  anatomical  processes  which  are  found  in  tuberculosis 
of  the  lungs,  and  which  may  be  combined  in  the  most  manifold  ways,  we  can 
understand  the  great  diversity  in  the  anatomical  picture  in  different  cases.  Sim- 
ple bronchitis,  tuberculosis  of  the  bronchial  wall  and  tubercular  peribronchitis, 
diffuse  cheesy  pneumonia,  and  destruction  of  the  tubercular  new  growths,  with 
the  formation  of  cavities,  on  the  one  hand,  contracting  interstitial  pneumonia, 
cicatricial  formation,  and  pigment  induration  on  the  other — these  are  the  com- 
paratively simple  anatomical  lesions  from  which  the  whole  process  in  its  most 
varied  forms  is  composed.  Besides  this,  we  often  And  here  and  there  one  or 
more  miliary  tubercles  scattered  through  the  lungs  which  are  probably  due  very 
largely  to  an  extension  of  the  infectious  material  by  means  of  the  blood  or  lymph 
current. 


TUBERCULOSIS  OF   THE  LUNGS.  215 

The  secondary  tubercular  diseases  of  the  pleura,  the  bronchial  glands,  and 
other  organs,  will  receive  a  special  description. 

Clinical  History  of  Tuberculosis  in  General  and   of  Pulmonary  Tuber- 
culosis in  Particular. 

In  judging  of  the  various  appearances  in  the  clinical  picture  of  tuberculosis 
we  must  especially  consider  the  following  points :  The  place  of  the  first  infec- 
tion is  of  the  chief  importance— that  is,  the  place  where  a  local  affection,  set 
up  by  the  tubercular-  poison,  first  arises.  As  has  been  said,  the  lungs  are  the 
organs  first  attacked  in  a  large  number  of  cases,  and  such  cases  are  termed  pri- 
mary pulmonary  tuberculosis.  In  other  cases,  the  tubercular  poison  first  fixes 
itself  in  the  larynx,  as  in  primary  laryngeal  tuberculosis,  or  it  reaches  the  intes- 
tine, as  in  primary  intestinal  tuberculosis,  or  the  genito-urinary  organs,  as  in 
primary  tuberculosis  of  the  genito-urinary  apparatus,  etc.  In  other  cases  still,  we 
apparently  have  to  do  with  a  primary  tuberculosis  of  the  serous  membranes  (vide 
infra)  or  of  the  lymph-glands,  particularly  the  bronchial  lymph-glands  (vide 
infra) ;  and  finally,  we  very  often  see  primary  tubercular  diseases  of  the  bones 
and  joints,  to  which  the  most  part  of  the  formerly  so-called  chronic  scrofulous  and 
fungous  inflammations  of  the  bones  and  joints  belong.  It  is  obvious  that  all  these 
diseases,  although  identical  setiologically,  must  have  a  very  different  clinical  ap- 
pearance. 

Another  reason  for  the  great  variation  in  the  course  of  tuberculosis  is  found  in 
the  fact  that  the  extension  of  the  local  tubercular  process  may  vary  very  greatly 
as  regards  time.  Tuberculosis  in  one  case  may  produce  the  most  extensive  destruc- 
tion in  both  lungs  in  a  few  months  or  even  weeks,  and  in  another  case  it  may 
remain  almost  quiescent  for  years,  or  advance  only  very  slowly.  We  do  not 
know  fully  on  what  these  differences  depend,  but  much  is  certainly  due  to  the 
hygienic  influences  under  which  the  patient  lives.  In  the  last  instance,  however, 
we  are  often  led  to  think  of  individual  differences  of  constitution,  which  now 
check  and  now  favor  the  rapid  extension  of  the  disease. 

A  third  and  final  reason  for  the  differences  in  the  course  of  tubercular  infec- 
tion is  the  manner  of  the  further  extension  of  the  tubercular  poison  in  the  body. 
As  we  shall  see  in  the  description  of  tuberculosis  in  single  organs,  there  are  differ- 
ent ways  in  which  tuberculosis  may  pass  from  one  organ  to  another.  Many  con- 
tingencies are  involved  here,  and  we  can  easily  comprehend  how  greatly  the 
whole  clinical  course  of  the  disease  must  be  modified  by  the  rapidity  and  the 
degree  in  which  individual  organs  are  affected. 

After  these  preliminary  remarks,  which  we  have  thought  necessary  to  a  right 
understanding  of  tubercular  disease  in  general,  we  will  pass  on  to  the  description 
of  the  clinical  course  of  pulmonary  tuberculosis. 

The  onset  of  pulmonary  tuberculosis  is  quite  slow  and  gradual  in  the  majority 
of  cases.  The  patient  can  give  only  an  approximate  idea  of  the  time  when  he 
began  to  be  ill.  The  symptoms  which  he  notices  are  referred  directly  to  the  res- 
piratory organs.  The  cough  and  its  attendant  expectoration  are  the  chief  things 
which  affect  him.  Besides  that,  there  is  often  pain  in  the  chest,  either  the  pleu- 
ritic stitch,  or  a  pain  in  the  sternal  region,  or  pain  between  the  shoulder-blades. 
The  patient  is  also  apt  to  complain  of  shortness  of  breath,  especially  on  severe 
physical  exertion. 

Besides  these  symptoms,  which  point  pretty  directly  to  disease  of  the  lungs, 
there  are  often  quite  striking  general  symptoms.  The  patient's  emaciation  is 
especially  noticeable,  which  may  be  partly,  though  not  wholly,  explained  by  his 
loss  of  appetite.    Besides  the  emaciation  there  is  a  steadily  increasing  pallor  of  the 


216  DISEASES  OF  THE  RESPIRATORY  ORGANS, 

skin.  The  patient  also  shows  a  general  dullness,  weakness,  and  disinclination  to 
work.  There  is  not  infrequently  a  slight  rise  of  temperature  in  the  first  stages 
of  the  disease,  which  causes  chilliness  and  subjective  feelings  of  heat.  Severe 
night-sweats  may  also  be  noticed  early. 

All  such  general  symptoms  should  determine  the  physician  not  to  regard  the 
mild  thoracic  symptoms,  which  are  also  present,  as  insignificant,  but  to  think  of 
the  possibility  of  incipient  tuberculosis.  It  is  very  important  to  remember  that 
the  pulmonary  symptoms  may  be  entirely  subordinate  to  the  general  symptoms 
mentioned,  and  that  the  patient  himself  is  apt  to  pay  little  or  no  attention  to  them. 
Incipient  phthisis  is  therefore  frequently  diagnosticated  as  simple  "  chlorosis  "  or 
"gastric  catarrh  "  for  a  long  time,  and  is  treated  as  such.  An  early  and  careful 
physical  examination  of  the  lungs  and  of  the  expectoration  is  the  only  protection 
against  such  an  error. 

Both  the  pulmonary  and  the  general  symptoms  assume  significance,  if  we 
have  to  do  wifh  a  patient  in  whom  we  suspect  a  "  tubercular  predisposition."  We 
very  often  meet  people  in  whose  family,  either  in  the  parents  or  the  brothers  and 
sisters,  several  cases  of  phthisis  have  occurred.  They  are  persons  who  are  always 
pale  and  weak,  and  who  have  previously  shown  a  special  liability  to  disease, 
particularly  to  disease  of  the  respiratory  organs.  They  have  perhaps  had  diseases 
which  our  present  theories  bring  into  direct  relation  with  tubercular  infection. 
We  refer  to  those  quite  frequent  cases  of  pulmonary  tuberculosis  in  persons  who 
have  previously  suffered  from  "  scrofulous  diseases,"  like  chronic  swelling  of  the 
lymph-glands,  chronic  affections  of  the  eye  or  ear,  or  fungous  diseases  of  the 
bones  and  joints.  This  fact  does  not  signify  that  scrofula  passes  into  tuberculosis. 
It  is  much  more  probable  that  many  scrofulous  diseases  are  really  tubercular,  as 
has  been  proved  by  the  result  of  inoculations  in  animals,  and  recently  by  the  dis- 
covery of  tubercle  bacilli  in  "  scrofulous  "  lymph-glands  and  in  the  fungus  nodules 
in  the  bones  and  joints. 

As  we  have  said,  pulmonary  tuberculosis  often  develops  in  persons  who  have 
suffered  before  from  diseases  of  the  respiratory  mucous  membrane,  in  whom,  as 
the  expression  is,  the  lungs  have  always  been  the  locus  minoris  resistentice. 
The  predisposition  to  tuberculosis  may  really  perhaps  coincide  at  times  with  the 
predisposition  to  other  pulmonary  affections;  thus  we  see  tubercular  patients  who 
have  previously  had  several  attacks  of  croupous  pneumonia.  In  other  cases,  how- 
ever, the  predisposition  to  tuberculosis  is  probably  caused  by  some  disease  of  the 
respiratory  mucous  membrane,  although  sometimes  these  previous  diseases  of 
the  respiratory  organs  are  themselves  of  a  tubercular  nature.  This  is  especially 
true  of  pleurisy,  but  we  shall  have  to  take  up  its  relation  to  pulmonary  tuberculo- 
sis somewhat  more  in  detail  in  our  description  of  pleurisy. 

Although  the  first  symptoms  of  pulmonary  tuberculosis  often  develop  in  people 
who  were  not  quite  well  before,  this  is  true  in  only  a  part  of  the  cases.  We  often 
see  precisely  the  same  symptoms,  both  the  pulmonary  and  the  general,  occurring 
in  persons  who  previously  seemed  quite  well  and  strong.  No  constitution  is  per- 
fectly protected  against  the  disease.  We  have  even  seen  the  herculean  athletes  of 
a  circus  die  of  phthisis. 

In  distinction  from  the  slow  and  gradual  method  of  the  development  of  tuber- 
culosis which  has  just  been  described,  the  first  symptoms  in  other  cases  may  be 
more  sudden.  A  definite  exposure  is  often  given  as  a  cause,  after  which  the  first 
symptoms  of  the  disease  have  speedily  developed.  It  goes  without  saying  that  we 
must  consider  these  harmful  influences — a  chilling  of  the  body,  a  cold  draught, 
over-exertion,  or  marked  mental  excitement — at  most,  as  exciting  causes. 

Some  cases  in  our  own  observation  seem  to  us  worthy  of  note,  in  which  young 
people  have  fallen  ill  quite  suddenly,  with  rather  severe,  general  febrile  symp- 


TUBERCULOSIS  OF  THE  LUNGS.  217 

toms.  At  first  no  cause  for  the  fever  could  be  made  out,  so  that  the  diagnosis 
was  in  doubt,  or  the  attack  was  even  falsely  regarded  as  typhoid  or  some  other 
disease.  Some  time  later  thoracic  symptoms  developed,  and  it  became  possible  to 
detect  the  physical  signs  of  phthisis.  Most  of  these  cases  took  quite  a  rapidly 
progressive  course. 

In  conclusion,  those  cases  are  to  be  mentioned  in  which  the  first  signs  of 
tuberculosis  appear,  not  in  the  lungs  but  in  the  larynx.  The  full  description  of 
these  cases  has  already  been  given  in  the  chapter  on  laryngeal  tuberculosis  (see 
page  136). 

The  further  course  of  pulmonary  tuberculosis  may  vary  so  much  that  it  is  im- 
possible to  give  a  complete  enumeration  of  all  the  possibilities. 

In  some  cases  it  advances  rapidly.  We  can  make  out  the  extension  of  the  dis- 
ease objectively,  almost  from  week  to  week.  At  first  the  apex  of  one  lung  alone 
is  attacked,  soon  after  the  lower  lobe  of  the  same  lung,  then  the  other  lung,  either 
at  the  apex  first  or  in  the  lower  part.  Besides  the  pulmonary  symptoms,  there  is 
quite  a  high  fever,  rapidly  increasing  emaciation,  and  general  loss  of  strength. 
Death  ensues  in  a  few  months.  We  term  such  cases  florid  phthisis,  or  ''galloping 
consumption." 

In  other  cases,  however,  the  disease  has  a  remarkably  chronic  course.  Its 
onset  is  very  gradual,  or  else,  after  rather  an  acute  onset,  there  is  a  comparative 
cessation  of  all  symptoms.  The  thoracic  symptoms  do  not  disappear,  but  they  are 
only  trifling,  and  do  not  disturb  the  patient.  Physical  examination  of  the  lungs 
does  not  show  any  extension  of  the  process  for  months.  The  fever  which  accom- 
panies it  is  slight,  if  there  be  any.  The  patient  remains  quite  well  nourished,  but 
in  some  cases  there  is  a  good  deal  of  weakness.  He  feels  better  and  worse  by  turns, 
his  condition  being  greatly  influenced  by  the  care  and  nursing  he  receives. 

Unilateral  contracting  phthisis  especially  has  this  comparatively  favorable 
course  {vide  supra).  The  affection  remains  confined  to  one  lung  for  a  long  time. 
The  occurrence  of  contraction  shows  the  slight  tendency  of  the  tubercular  process 
to  advance,  and  with  satisfactory  care  the  patient  may  remain  quite  well  for  years. 

In  cases,  too,  which  have  had  severe  symptoms  for  a  long  time,  a  temporary 
standstill  of  the  affection  may  take  place,  or  an  actual  improvement  in  all  the 
symptoms.  At  other  times,  in  cases  which  have  made  no  advance  for  a  long  time, 
the  symptoms  suddenly  grow  worse. 

There  are  all  possible  varieties  between  the  extremes  of  florid  phthisis  and  the 
very  chronic  cases  wThich  last  for  years.  If  we  recall  the  further  modifications 
which  the  course  of  the  disease  may  assume  if  complications  arise,  we  can  appre- 
ciate the  manifold  character  of  the  clinical  picture  of  phthisis. 

Most  cases  terminate  fatally.  Death  ensues,  either  with  the  signs  of  general 
exhaustion,  or  as  a  result  of  the  final  failure  of  respiration ;  or  it  is  due  to  the 
occurrence  of  complications,  like  tubercular  meningitis,  miliary  tuberculosis,  pul- 
monary haemorrhage,  or  pneumothorax.  A  recovery  from  the  tubercular  pro- 
cess is  certainly  possible.  The  comparatively  great  rarity  of  recovery  in  pulmonary 
tuberculosis,  however,  is  due  chiefly  to  the  possibility  of  the  continual  spread  of 
the  tubercular  poison  in  the  lungs  themselves,  and  also  in  other  oi-gans.  From 
clinical  and  pathological  experience,  however,  we  can  not  deny  the  possibility  of 
definite  recovery  in  pulmonary  tuberculosis.  We  do  not,  of  course,  mean  a  resti- 
tutio ad  integrum  of  the  lung-tissue,  but  a  recovery  with  a  cessation  of  the  tuber- 
cular process,  and  with  the  formation  of  a  cicatrix,  or  contraction.  Such  recov- 
eries, as  we  have  said,  are  rare,  and  they  occur  only  where  the  changes  in  the 
lungs  are  of  limited  extent.  The  possibility  of  recovery  depends  mainly  upon 
the  general  physical  constitution  and  upon  the  external  circumstances  of  the 
patient. 


218  DISEASES  OF  THE  RESPIRATORY   ORGANS. 

Special  Symptoms  and  Complications. 

1.  Symptoms  on  the  Part  of  the  Lungs. — Pain  in  the  Chest. — Extensive  destruc- 
tion in  the  lungs  may  exist  without  any  feeling-  of  pain.  Many  cases  of  phthisis 
are  painless  throughout  their  course.  In  other  cases,  however,  the  patient's  chief 
complaint  is  of  severe  pains  in  the  side  or  in  the  front  of  the  chest.  These  are 
prohahly  always  due  to  co-existing  affections  of  the  pleura,  like  pleurisy,  or 
pleuritic  adhesions.  .In  patients  who  suffer  from  severe  cough,  pains  sometimes 
arise  in  the  abdominal  muscles  and  at  the  insertion  of  the  diaphragm,  due  to  the 
excessive  muscular  contraction.  Stabbing  pains  between  the  shoulder-blades 
are  held  by  some  to  be  not  wholly  unimportant  as  a  diagnostic  symptom  of  in- 
cipient phthisis. 

Cough. — In  the  majority  of  instances  cough  is  one  of  the  most  distressing 
symptoms  in  phthisis,  but  its  severity  varies  very  much  in  different  individuals, 
and  at  different  times  in  the  same  patient.  We  sometimes  see  cases  in  which,  in 
spite  of  advancing  phthisis,  cough  is  remarkably  slight,  or  entirely  absent.  In 
these  we  usually  have  to  do  with  patients  who  are  very  slightly  sensitive.  In 
cases  with  severe  cough,  it  is  often  worst  at  night,  but  paroxysms  of  coughing  of 
long  duration  are  also  apt  to  come  on  in  the  morning  or  evening  hours,  which 
are  painful  and  very  distressing,  and  unpleasant  for  the  patient.  The  cough  is 
usually  associated  with  a  more  or  less  abundant  expectoration,  but  sometimes 
there  is  chiefly  a  dry  cough.  The  cough  becomes  very  severe  if  the  tubercular 
affection  attacks  the  larynx  and  trachea  (see  laryngeal  tuberculosis). 

Expectoration. — The  amount  of  expectoration  differs  very  much  in  different 
cases.  It  is  most  abundant  where  there  is  extensive  formation  of  cavities  in  the 
lungs.  In  such  cases  it  is  often  evacuated  in  the  morning  by  persistent  coughing. 
The  consistency  of  the  great  part  of  the  sputum  is  muco-purulent,  and  it  does  not 
differ  from  that  of  simple  bronchitis;  in  fact,  a  large  part  of  the  phthisical  expec- 
toration comes  from  the  catarrhal  inflammation  of  the  bronchial  mucous  mem- 
brane. Another  part  comes  from  the  purulent  secretion  of  the  walls  of  the  cavities. 
The  sputum  has  a  characteristic  tendency  to  roll  itself  together  in  single  large 
lumps,  into  the  ball-like  or  so-called  nummular  sputa.  This  is  noticed  especially 
where  there  are  cavities. 

The  admixture  of  blood  with  the  sputum  is  of  great  diagnostic  and  practical 
importance.  Since  no  other  disease  so  often  gives  rise  to  the  presence  of  blood  in 
the  expectoration,  coughing  of  blood  (haemoptysis)  is  almost  synonymous  with 
consumption  among  the  laity.  Little  streaks  of  blood  in  the  expectoration  are 
quite  frequent.  They  have  no  great  significance,  but,  of  course,  they  may  some- 
times be  the  precursors  of  severe  haemorrhages.  Profuse  haemoptysis  takes  place 
when  the  wall  of  a  little  pulmonary  vessel— almost  always  a  branch  of  the  pul- 
monary artery— is  infiltrated,  destroyed,  and  finally  eroded,  by  the  tubercular  new 
growth.  The  reason  why  haemoptysis  is  not  more  frequent  is  because  the  contents 
of  the  vessels  usually  undergo  thrombosis.  Severe  haemorrhages  very  often  have 
their  origin  in  the  perforation  of  little  aneurisms  of  the  branches  of  the  pulmonary 
artery,  which  penetrate  into  the  interior  of  the  cavities.  In  the  cases  of  fatal 
haemoptysis  we  frequently  succeed  in  finding  the  little  aneurism  and  its  point  of 
rupture. 

Pulmonary  haemorrhages  occur  in  all  stages  of  phthisis.  The  amount  of  blood 
coughed  up  sometimes  amounts  to  only  one  or  two  tablespoonfuls,  sometimes  to 
one  or  two  pints.  The  blood  is  bright-red  in  color,  usually  quite  frothy,  only 
slightly  coagulated,  and  partly  mixed  with  the  other  constituents  of  the  sputum. 
If  the  patient  recovers  from  the  first  severe  haemoptysis,  the  expectoration  usually 
contains  some  blood  for  several  days.     Recurrences  of  severe  haemorrhages  are 


TUBERCULOSIS  OF  THE  LUNGS. 


219 


frequent.  The  haemoptysis  sometimes  comes  on  quite  suddenly,  often  at  night, 
without  any  occasion,  but  it  may  return  from  some  definite  cause,  such  as  physical 
exertion,  severe  paroxysms  of  coughing,  straining  at  stool,  or  mental  excitement. 
Many  cases  of  phthisis  are  characterized  by  a  special  tendency  to  haemorrhage, 
while  in  many  others  haemoptysis  never  occurs.  Severe  haemoptyses  are,  of 
course,  always  an  undesirable  and  dangerous  complication,  since  they  weaken  the 
patient  very  much,  and  also  depress  his  spirits.  Many  patients  maintain  their 
peculiar,  careless  indifference,  which  is  almost  characteristic  of  the  disease,  despite 
the  spitting  of  blood.  The  haemoptysis  may  sometimes  be  the  direct  cause  of 
death,  but,  as  a  rule,  the  patients  survive  it.  We  can  not  make  the  general  state- 
ment that  the  further  course  of  phthisis  is  materially  hastened  by  haemoptysis.  In 
not  rare  instances,  however,  it  is  observed  that  after  a  haemoptysis  the  pulmonary 
disease  extends  more  rapidly,  the  fever  becomes  higher  and  more  persistent,  and 
the  general  condition  of  the  patient  grows  worse. 

A  purulent  sputum  intimately  mixed  with  blood  is  quite  frequent  and  charac- 
teristic in  many  cases  of  phthisis  with  extensive  formation  of  cavities.  This  is 
formed  in  the  cavities  from  the  mixture  of  the  purulent  secretion  with  little 
capillary  haemorrhages.  In  this  way  the  sputum,  which  is  often  nummular, 
assumes  a  greasy  chai^acter  and  a  reddish-brown  or  chocolate  color. 

If  foetid  or  gangrenous  processes  develop  in  the  lungs,  the  sputum  becomes 
foetid.  In  some  cases  we  see  temporarily  in  phthisis  the  characteristic  sputum 
of  croupous  pneumonia,  which  comes  from  portions  of  the  lung  attacked  with 
pneumonia. 

Microscopic  examination  of  the  sputum  may  show — besides  the  ordinary  ele- 
mentary forms,  such  as  pus-corpuscles,  red  blood-corpuscles,  pavement  epithelium, 
drops  of  myeline,  and  sometimes,  perhaps,  pulmonary  epithelium — two  constitu- 
ents which  are  of  decided  diagnostic  importance:  elastic  fibers  and  tubercle 
bacilli. 

The  demonstration  of  elastic  fibers  in  the  expectoration  permits  us  to  decide 
with  certainty  that  there  is  a  destructive  process  in  the  lungs,  and  thus  it  usually 
is  direct  proof  of  tuberculosis.  Elastic  fibers  are  also 
found  in  pulmonary  gangrene,  and  in  the  very  rare 
cases  of  pulmonary  abscess,  as  well  as  in  tuberculosis, 
but  gangrene  is  easily  recognized  by  the  other  peculiari- 
ties of  the  sputum.  The  search  for  elastic  fibers  in  the 
expectoration  of  tubercular  patients  demands  a  certain 
amount  of  practice.  We  are  most  sure  to  find  them  if 
we  look  in  the  sputum,  when  it  is  spread  out,  for  little 
lentiform  particles,  which  can  easily  be  made  out  with 
the  naked  eye.  These  consist  of  necrotic  shreds  of  tis- 
sue torn  off  from  the  walls  of  cavities.  If  we  press  one 
of  these  "  kernels  "  under  a  cover-glass  we  find,  in  the 
midst  of  the  granular  detritus,  beautifully  twisted  elas- 
tic fibers,  which  often  have  quite  a  definite  alveolar  ar- 
rangement (see  Fig.  26).  The  elastic  tissue  is  the  only 
one  spared  in  the  general  destruction.  There  is  a  spe- 
cial method  of  looking  for  elastic  fibers,  but  we  have 
found  it  unnecessary.  The  sputum  is  boiled  in  sodic 
hydrate  dissolved  in  watei\  and  we  look  for  elastic  fibers 
in  the  precipitate  which  then  forms.  We  are  never  jus- 
tified, however,  iu  deciding  that  pulmonary  tuberculosis 

is  absent  because  we  do  not  find  elastic  fibers  in  the  sputum.  Their  presence  is 
the  only  thing  that  has  real  diagnostic  significance. 


Fig.  26.— Elastic  fibers. 


220 


DISEASES  OF  THE  RESPIRATORY  ORGANS. 


Fig.  27. — Tubercle  bacilli  in  the  sputum. 


The  discovery  of  tubercle  bacilli  in  the  expectoration  of  phthisical  patients  is 
of  much  greater  importance,  and  often  this  alone  is  decisive  (see  Fig.  27).     They 

were  first  demonstrated  by  Koch,  but  Ehrlich 
devised  the  first  simple  method  for  their  dis- 
covery, which  can  be  easily  employed  by  any 
physician. 

The  sputum  is  spread  in  the  thinnest  possi- 
ble film  on  a  cover-glass,  and  permitted  to  dry 
on  it.  The  best  way  to  do  this  is  to  rub  some 
of  the  sputum  between  two  cover-glasses,  and 
to  slide  one  slowly  off  of  the  other.  We  pass 
the  cover-glass  through  the  gas-flame  three 
times  slowly  to  fix  the  sputum,  and  then,  after 
cooling  it  for  a  little  time,  we  let  it  float  in  the 
staining  fluid.  The  latter  is  made  in  this  way : 
One  part  of  aniline  oil  and  six  parts  of  water 
are  mixed  in  a  test-tube,  filtered,  and  to  the 
filtrate,  known  as  aniline-water,  a  portion  of 
which  is  placed  in  a  watch-glass,  about  eight  or  ten  drops  of  a  concentrated  alco- 
holic solution  of  methyl  violet  or  gentian  violet  are  added.  The  cover-glass  on 
which  the  sputum  has  been  placed  is  allowed  to  remain  in  the  watch-glass  as  long 
as  possible — one  or  two  hours,  or  more.  If  it  is  desired  to  shorten  the  process,  the 
staining  liquid  is  warmed,  but  not  to  the  boiling-point.  The  bacilli  will  in  this  case 
usually  be  stained  with  sufficient  distinctness  in  as  short  a  time  as  ten  or  fifteen 
minutes.  When  the  cover-glass  is  taken  out  of  the  staining  fluid  it  is  immersed 
in  a  solution  of  one  part  of  nitric  acid  in  three  parts  of  water,  and  in  this  way  the 
preparation  is  almost  completely  bleached  in  a  very  short  time.  The  tubercle 
bacilli  alone  have  the  property  of  retaining  the  stain  which  they  have  taken  on, 
despite  the  action  of  the  nitric  acid.  When  the  cover-glass  is  taken  out  of  the 
nitric  acid,  it  is  rinsed  in  water,  dried  between  two  layers  of  blotting-paper,  then 
stained  for  about  a  minute  in  a  one-  or  two-per-cent.  solution  of  Bismarck-brown 
in  water,  then  dried,  and  examined  in  water,  or,  better,  in  Canada  balsam.  A  dry 
lens  of  the  strength  of,  say,  objective  number  eight  of  Hartnack  (330  to  440 
diameters)  answers  perfectly  for  the  examination.  The  pus-cells  and  any  other 
bacteria  that  may  be  present  are  colored  brown.  The  tubercle  bacilli,  however, 
are  stained  dark  blue.  Ziehl  and  Neelsen's  staining  fluid  is  also  to  be  highly 
recommended.  It  is  composed  of  one  hundred  parts  of  distilled  water,  five  parts 
of  carbolic-acid  crystals,  and  one  part  of  fuchsin.  After  these  are  mixed  and 
filtered,  ten  parts  of  alcohol  are  added.  A  solution  thus  prepared  lasts  for  quite  a 
long  while,  and  stains  the  tubercle  bacilli  a  bright  red  even  in  a  few  minutes, 
provided  warmth  is  employed.  For  bleaching  the  other  components  of  the  prepa- 
ration, a  five-per-cent.  solution  of  sulphuric  acid  may  be  employed,  and  the  best 
means  of  secondary  staining  of  the  pus-corpuscles  is  to  use  a  watery  solution  of 
methyl  blue.  If  a  solution  is  made  up  containing  fifty  parts  of  water,  thirty  of 
alcohol,  twenty  of  nitric  acid,  and  as  much  methyl  blue  as  the  liquid  will  take 
up,  the  bleaching  and  the  secondary  staining  may  be  accomplished  simultane- 
ously. This  is  a  very  practical  method,  which  was  first  recommended  by  ,B. 
Fränkel. 

The  number  of  bacilli  varies  a  good  deal  in  different  cases,  and  at  different 
times  in  the  same  case.  The  more  bacilli  there  are,  the  more  readily  can  we  decide 
that  there  are  extensive  processes  of  ulceration.  We  can  found  no  definite  prog- 
nostic conclusions  upon  the  behavior  of  the  bacilli,  but  their  presence  is  of  the 
greatest  significance  in  a  diagnostic  point  of  view,  especially  as  they  can  be 


TUBERCULOSIS   OF  THE  LUNGS.  221 

found  upon  careful  examination  in  incipient  cases.     At  so  early  a  period  all  the 
other  symptoms  by  themselves  would  very  often  not  warrant  an  absolute  diagnosis. 

Dyspnoea. — A  marked  subjective  feeling  of  dyspnoea  is  a  symptom  which  is  of 
relatively  rare  occurrence  in  phthisis. 

Many  patients  hardly  ever  complain  of  their  breathing  in  spite  of  extensive 
destruction  in  the  lungs.  A  patient  who  is  much  emaciated  manifestly  needs 
little  oxygen,  and  the  increased  frequency  of  respiration,  which  is  almost  constant, 
can  satisfy  his  needs.  If  there  is  a  greater  demand  upon  the  respiration,  a  sub- 
jective feeling  of  dyspnoea  may  of  course  very  readily  occur,  especially  on  a  slight 
bodily  exertion.  In  many  cases,  however,  the  patient  complains  of  a  difficulty  in 
breathing  even  when  quiet,  especially  if  pleuritic  pains  or  adhesions  between  the 
surfaces  of  the  pleura  prevent  him  from  taking  a  deep  breath,  and  in  the  final 
stages  the  dyspnoea  may  be  extreme. 

2.  Symptoms  on  Physical  Examination,— In  many  cases  inspection  gives  us 
that  general  impression  of  the  patient  which  we  term  the  "  phthisical  habit. "  The 
special  signs  of  this  are  as  follows :  A  slender  but  often  quite  a  tall  frame,  weak 
muscular  developmeiit,  a  thin  layer  of  fat,  a  pale  and  perhaps  very  delicate  skin 
with  a  bluish  translucence,  sometimes  a  circumscribed  "  hectic  "  flush  in  the  cheeks, 
a  long  and  slender  neck,  a  long  and  narrow  thorax,  small,  thin  hands,  etc.  There 
are,  of  course,  many  variations  from  this  type  in  individual  cases. 

The  inspection  of  the  thorax  is  of  special  value.  The  phthisical  or  "  paralytic" 
thorax  is  generally  noticeable  from  its  length,  but  it  is  narrow  and  flat.  Unusual 
width  of  single  intercostal  spaces,  and  acuteness  of  the  epigastric  angle,  are  asso- 
ciated with  a  long  thorax.  The  sternum  is  also  long  and  narrow,  and  the  sternal 
angle— Louis's  angle — is  often  prominent.  The  supra-clavicular  and  infra-clavicular 
fossae  are  sunken,  the  neck  is  wasted,  and  the  shoulder-blades  stand  out  from  the 
thorax.  On  comparing  the  two  halves  of  the  body,  we  very  likely  see  unilateral 
contractions,  most  frequently  in  the  upper  and  anterior  portion  of  the  thorax,  but 
also  in  the  lower  portions. 

The  paralytic  form  of  thorax  is  very  often  seen  in  phthisis,  but  it  may  be  en- 
tirely absent. 

The  respiration  is  usually  somewhat  accelerated,  and  sometimes  quite  markedly 
so  in  women  with  disease  of  the  apices.  The  feminine  type  of  high  thoracic 
breathing  is  largely  changed  to  low  thoracic  or  diaphragmatic  breathing.  A 
unilateral  impairment  of  respiration  is  of  greater  importance ;  in  such  a  case  one 
apex,  or  one  side,  if  there  be  phthisis  of  the  lower  lobe,  holds  back  in  inspiration. 
The  respiration  is  sometimes  irregular,  especially  if  there  be  pleuritic  pains. 

The  results  of  percussion  are,  of  course,  entirely  dependent  upon  the  sort  of 
anatomical  changes  in  the  lungs,  and  hence  differ  very  greatly  in  different  cases. 
Since  the  phthisical  process  begins  in  the  apices  in  the  majority  of  cases,  our  chief 
attention  is  turned  to  the  condition  of  the  upper  portions  of  the  lungs  on  percus- 
sion. Slight  changes  in  percussion  may  wholly  escape  discovery.  Only  when 
the  air  contained  in  the  lung-tissue  in  the  part  affected  is  replaced  to  a  certain 
degree  by  the  tubercular  infiltration  does  the  percussion-note  become  dull.  Uni- 
lateral dullness  at  the  apex  is  therefore  one  of  the  most  frequent  physical  signs 
of  phthisis.  We  can  usually  make  it  out  most  plainly  in  the  upper  anterior  inter- 
costal spaces  first,  and  in  incipient  cases  often  in  the  supra-clavicular  fossae  only, 
but  it  is  also  observed  sometimes  in  the  back  in  the  supra-scapular  fossae.  As  the 
infiltration  advances  the  dullness  becomes  more  extensive.  It  frequently  assiunes 
a  tympanitic  quality,  as  a  result  of  diminished  tension  or  partial  retraction  of  the 
lung-tissue. 

The  formation  of  cavities  in  tuberculosis  has  a  great  influence  on  the  percus- 
sion-note.   The  dullness  on  percussion  may  thus  become  decidedly  less,  the  degree 


222  DISEASES  OF  THE  RESPIRATORY   ORGANS. 

of  resonance  depending,  of  course,  upon  the  fullness  of  the  cavity  aud  the  char- 
acter of  the  surrounding  tissue.  We  often  find  a  decided  tympanitic  resonance 
or  a  combination  of  dullness  and  tympany  over  a  cavity.  The  different  modifica- 
tions of  the  percussion-note  in  cavities  are  given  below.  The  "  cracked-pot  reso- 
nance," or  buckram  sound,  is  met  with  in  percussing  over  cavities,  but  we  also 
find  it  in  many  other  pathological  conditions. 

Auscultation  also  gives  no  special  pathognomonic  signs  of  phthisis.  Varying 
with  the  character  and  extent  of  the  tubercular  changes,  abnormal  respiratory 
sounds  and  adventitious  sounds  are  heard  in  place  of  the  normal  vesicular  mur- 
mur. With  slighter  changes  the  vesicular  breathing  is  merely  modified ;  it  seems 
remarkably  diminished  or  interrupted,  or  sometimes  exaggerated,  with  prolonged 
expiration.  When  the  infiltration  of  the  lungs  increases,  we  find  bronchial  res- 
piration in  place  of  the  vesicular  breathing ;  but,  on  the  other  hand,  the  formation 
of  a  cavity  is  a  frequent  cause  of  bronchial  respiration. 

The  most  constant  auscultatory  signs  of  phthisis,  and  the  most  important  for 
diagnosis,  are  the  different  kinds  of  rales,  which  are  due  to  the  accumulation  of 
the  secretion  in  the  bronchi  or  in  the  cavities.  They  are  heard  at  one  apex  only, 
or  over  a  larger  space,  according  to  the  extent  of  the  affection. 

Physical  Diagnosis  of  Incipient  Phthisis.— On  account  of  the  importance 
of  the  diagnosis  of  incipient  phthisis,  we  will  here  mention  connectedly  the  phys- 
ical signs  which  are  chiefly  met  with  in  it.  The  auscultatory  signs  in  the  begin- 
ning of  the  disease  are  generally  more  certain  and  easier  to  recognize  than  those 
from  percussion.  He  who  lays  too  much  weight  on  the  so-called  "  slight  dullness 
at  the  apex  "  will  often  make  a  false  diagnosis.  We  will  mention  particularly  the 
following  symptoms:  1.  Constant  and  evident  diminution  of  the  respiratory  mur- 
mur at  one  apex,  especially  if  it  is  associated  with  marked  deficiency  of  the  respira- 
tory movement  on  the  affected  side.  In  some  cases  the  respiratory  murmur  on 
the  diseased  side  is  not  weaker,  but  it  has  a  more  indefinite  and  harsher  character; 
or  again  it  may  be  rude,  sharp,  and  "puerile."  2.  Markedly  interrupted  respira- 
tion at  one  apex.  3.  A  prolonged  expiratory  murmur,  which  has  a  harsh  charac- 
ter. 4.  The  discovery  of  dry  rhonchi  or  moist  rales  at  one  apex  is  most  important, 
since  we  know  by  experience  that  "  apex  catarrhs  "  are,  as  a  rule,  tubercular.  5. 
Definite  dullness,  apparent  on  repeated  examinations,  or  tympanitic  dullness  at 
one  apex.  6.  Evident  contraction  at  one  apex,  as  revealed  by  inspection  or  per- 
cussion above  the  clavicles.  7.  Some  authors  lay  stress  upon  a  systolic  murmur 
in  the  subclavian  artery,  especially  loud  on  expiration.  This  may  occur  in  the 
beginning  of  phthisis,  if  the  caliber  of  the  vessel  is  narrowed  by  processes  of  con- 
traction in  the  neighboring  apex,  but  this  symptom  is  neither  frequent  nor  of  great 
practical  importance. 

The  chief  rule  in  the  diagnosis  of  incipient  phthisis  must  be  held  to  be  this 
—not  to  give  a  definite  opinion  until  repeated  examinations  have  been  made. 
The  other  portions  of  the  lungs  are  to  be  carefully  examined  as  well  as  the 
apices,  since  in  not  very  rare  cases  tuberculosis  may  begin  in  the  lower  lobes. 
We  must  always  consider  the  patient's  general  symptoms  as  well  as  the  phys- 
ical signs. 

Symptoms  op  Cavities. — The  diagnosis  of  a  cavity  in  the  lungs  by  means  of 
the  physical  signs  is  often  very  difficult.  We  may  mention  as  the  chief  symptoms 
of  a  cavity:  1.  Loud  bronchial  respiration,  perhaps  of  an  amphoric  character,  in 
places  where  the  percussion-note  is  only  slightly  or  not  at  all  dull.  Such  a  con- 
dition means  that  the  bronchial  respiration  is  not  due  to  an  infiltration  of  lung- 
tissue.  Bronchial  respiration,  however,  may  of  course  be  heard  over  cavities 
which  are  surrounded  by  thickened  lung-tissue,  and  hence  give  dullness  on  per- 
cussion.    2.  The  so-called  metamorphosing  respiration,  which  begins  as  vesicular 


TUBERCULOSIS  OF  THE  LUNGS.  223 

and  suddenly  becomes  bronchial,  is  heard  especially  over  cavities,  and  hence  L:is 
a  diagnostic  value.  3.  The  different  kinds  of  "changes  in  tbe  percussion  note" 
over  cavities  are  important  signs.  Wintricb's  change  in  pitch  is  when  the  tym- 
panitic resonance,  which  is  obtained  over  the  cavity,  becomes,  on  opening  the 
mouth,  more  decidedly  tympanitic,  louder,  and  especially  much  higher.  The  res- 
piratory change  of  pitch  of  Friedreich  usually  consists  of  a  higher  pitch  on  in- 
spiration, but  here  there  are  numerous  variations.  Gerhardt's  change  of  pitch 
(Weil)  consists  in  a  change  of  the  tympanitic  resonance  when  the  patient  change-; 
his  position,  the  pitch  usually  being  higher  when  the  patient  sits  up  than  when 
he  is  lying  down.*  4.  Loud,  bubbling  rales  are  one  of  the  most  frequent  signs  of 
a  cavity.  They  are  definite  indications  of  the  occurrence  of  rales  in  a  larger  space 
than  is  normally  present  in  the  apices  of  the  lungs. 

Contraction  of  the  Lungs  [Fibroid  Phthisis].— Unilateral  contraction  of 
the  lungs,  more  frequent  on  the  left  than  on  the  right,  is  a  form  of  tuberculosis 
which  is  made  apparent  both  by  special  physical  signs  and  also  by  cei'tain  clinical 
peculiarities.  It  is  usually  recognized  at  once  by  inspection  of  the  thorax,  one 
side  of  the  thorax  being  remarkably  retracted.  The  upper  anterior  portions  of 
the  thorax,  and,  in  all  cases  of  a  high  degree  of  disease,  the  lower  lateral  and 
posterior  portions,  are  much  less  tense  than  the  corresponding  parts  on  the  other 
healthy  side.  The  fossae  and  intercostal  spaces  on  the  affected  side  are  deeper, 
the  shoulder-blade  is  drawn  nearer  the  vertebral  column,  and  the  latter  is  even 
sometimes  drawn  over  to  the  contracted  side  (scoliosis).  The  resonance  is  dimin- 
ished to  a  greater  or  less  degree,  over  the  affected  side,  which  either  lags  behind 
or  remains  almost  wholly  at  rest  on  respiration.  The  respiratory  murmur  is  quite 
loud,  and  bronchial ;  and  we  also  hear  many  rales,  which  are  usually  bubbling. 
Anatomically,  we  have  to  do  with  a  marked  process  of  contraction  of  the  intersti- 
tial connective  tissue  in  the  lungs,  which  is  almost  always  associated  with  extensive 
formation  of  cavities,  partly  of  an  ulcerative,  partly  of  a  bronchiectasic  character. 
The  pleura  is  involved  in  the  process  almost  without  exception,  but  almost  always 
secondarily;  it  is  also  thickened  and  contracted.  If  the  pleuritic  thickening  is 
mai'ked,  the  respiratory  murmur  and  the  vocal  fremitus  are  decidedly  weakened. 

The  influence  of  the  contraction  on  the  neighboring  organs  is  very  decided, 
and  usually  it  is  easy  to  discover.  The  heart  especially,  whose  external  peri- 
cardium is  in  most  cases  very  adherent  to  the  pleura,  is  drawn  well  over  to  the  side 
of  the  contraction.  The  apex-beat  and  the  cardiac  dullness  are  correspondingly 
displaced.  With  left-sided  contraction  the  heart  may  be  drawn  over  to  the  line 
of  the  left  axilla,  and  with  right-sided  contraction  it  may  be  drawn  to  the  median 
line,  or  ever  to  the  right  of  the  sternum.  With  contraction  of  the  left  upper 
lobe  the  anterior  surface  of  the  heart  comes  into  immediate  contact  wnth  the  an- 
terior chest-wall  over  a  larger  area  than  normal.  We  therefore  see  the  motions 
of  the  heart  over  an  abnormal  extent,  and  we  can  often  feel  very  plainly  in  the 
second  left  intercostal  space  the  pulsation  and  the  closure  of  the  valves  in  dias- 
tole of  the  pulmonary  artery.  The  upward  traction  of  the  diaphragm  may  he 
recognized  by  the  position  of  the  liver,  or,  in  left-sided  contraction,  by  the  increase 
of  the  "  semilunar  "  tympanitic  space  on  the  left.  We  usually  find  the  sound  lung 
on  the  other  side  quite  emphysematous,  as  shown  by  the  downward  displacement 
of  the  lower  boundary  of  the  lung,  and  also  by  the  drawing  over  of  the  anterior 
median  edge  of  the  lung  to  the  contracted  side.  In  a  part  of  the  cases  we  can 
make  out  by  percussion  the  development  of  consecutive  dilatation  and  hyper- 
trophy of  the  right  ventricle. 

*  Fuller  details  of  the  significance  of  the  different  changes  in  the  pitch  are  found  in  Weil's  "  Hand- 
buch der  topographischen  Percussion."    Leipzig  :  Vogel,  1880. 


224  DISEASES  OF  THE  EESPIRATORY  ORGANS. 

These  are  the  chief  physical  signs  of  the  so-called  unilateral  form  of  chronic 
pulmonary  contraction.  We  would  add  here  a  few  clinical  remarks.  The  cases 
often,  but  of  course  not  always,  run  a  very  chronic  course,  lasting  for  years.  The 
general  condition  and  the  nutrition  of  the  patient  may  thus  remain  comparatively 
undisturbed  for  a  long  time.  The  patient  looks  somewhat  pale  and  cyanotic,  yet 
he  is  so  well  nourished  as  to  present  a  very  marked  contrast  to  the  appearance  of 
the  ordinary  cases  of  phthisis.  The  appetite  remains  good,  the  fever  is  entirely 
absent,  or  else  a  slight  degree  of  fever  may  be  at  times  discovered  by  careful  ex- 
amination. The  cough  and  expectoration,  too,  though  often  very  severe,  are  at 
other  times  very  slight,  especially  when  the  patient  has  good  care  and  nourish- 
ment. We  need  not  wonder,  then,  that  many  physicians  do  not  consider  that 
these  cases  have  anything  to  do  with  phthisis — "consumption";  and  yet  we  are 
convinced  by  many  clinical  and  anatomical  observations  that,  aetiologically,  they 
are  in  by  far  the  greatest  part  tubercular.  They  represent  a  very  slow  form  of 
tuberculosis,  which  has  time  to  develop  interstitial  processes  which  lead  to  contrac- 
tion— that  is,  to  local  healing.  If  such  cases  come  to  autopsy,  their  tubercular  char- 
acter is  usually  definitely  confirmed.  We  find  undoubted  tubercular  lesions  in  the 
other  lung  and  also  in  the  remaining  organs — e.  g.,  the  intestines.  Furthermore, 
sudden  changes  for  the  worse  may  occur  iu  every  "  pulmonary  contraction,"  even 
those  cases  which  seem  favorable;  the  other  lung  may  become  highly  tubercular, 
a  miliary  tuberculosis  or  a  tubercular  meningitis  may  develop,  etc.  On  the  whole, 
however,  the  slow  course  of  this  form  of  chronic  tuberculosis  is  characteristic  and 
of  practical  significance,  and  its  prognosis  is  therefore  comparatively  favorable. 

We  can  not  absolutely  deny  that  a  non-tubercular  unilateral  contraction  of 
the  lung  may  occur.  As  a  result  of  foetid  bronchitis  and  pulmonary  gangrene, 
processes  of  contraction  develop,  which  are  associated  with  the  formation  of 
bronchiectases,  and  certainly  have  nothing  to  do  with  tuberculosis.  In  rare  cases 
also  croupous  pneumonia  is  followed  by  unilateral  contraction  of  the  lung;  and 
finally  there  is  a  rare  and  by  no  means  satisfactorily  investigated  form  of  unilat- 
eral chronic  interstitial  pneumonia,  with  contraction,  often  associated  with  the 
formation  of  bronchiectases.  The  differential  diagnosis  of  these  conditions  from 
tuberculous  contraction  rests  in  part  upon  the  clinical  history,  but  mainly  upon 
the  absence  of  tubercle  bacilli  in  the  expectoration. 

In  conclusion,  we  must  mention  that  there  are  very  many  transitional  forms 
between  pulmonary  contraction  and  the  other  varieties  of  pulmonary  tuberculosis. 
We  find  more  or  less  extensive  processes  of  contraction  in  one  apex  in  most  cases 
of  phthisis. 

Disseminated  Pulmonary  Tuberculosis. —There  is  a  form  of  pulmonary 
tuberculosis  which  it  is  very  hard  to  make  out  on  physical  examination.  In  this 
we  have  to  do  with  numerous  peribronchial  nodules  disseminated  over  the  whole 
lung.  As  there  is  still  a  good  deal  of  normal  tissue,  containing  air,  between  these 
nodules,  percussion  affords  no  dullness,  and  auscultation  gives  at  most  diffuse 
rhonchi;  hence  this  form  is  often  confused  with  chronic  bronchitis  or  pulmonary 
emphysema.  The  diagnosis  can  seldom  be  made  from  the  physical  signs,  but  only 
from  the  other  symptoms,  such  as  fever,  emaciation,  striking  pallor  of  the  skin, 
and  the  sputum. 

This  form  of  phthisis  sometimes  runs  a  chronic  course,  but  usually  it  is  quite 
rapid.  It  occurs  in  elderly  people,  and  also  in  children.  Many  forms  of  "  dis- 
seminated, coarse  granular  "  tuberculosis  are  transitional  forms  between  this  and 
genuine  acute  miliary  tuberculosis. 

3.  General  Symptoms  in  Pulmonary  Tuberculosis. — In  the  description  of  the 
general  course  of  pulmonary  tuberculosis  we  have  already  mentioned  the  value 
of  the  general  symptoms  in  diagnosis  and  prognosis. 


TUBERCULOSIS  OF  THE  LUNGS.  225 

Fever. — Only  a  few  cases  of  phthisis  run  their  course  entirely  without  fever, 
but  it  may  he  absent  for  a  time,  even  for  weeks  and  months.  This  is  especially 
the  case  in  the  very  chronic  forms,  like  unilateral  contraction.  The  more  care- 
fully we  take  the  temperature,  the  more  frequently  shall  we  find  a  slight  even- 
ing rise  of  temperature  up  to  100°  or  101°  (38°-38'5°  0.),  or  at  least  between  99° 
and  100°  (37"5°-38°  C),  even  at  times  when  the  patient  is  doing  favorably.  Such 
subfebrile  conditions  may  last  a  long  time,  but  many  cases  of  phthisis  are  associ- 
ated with  high  fever. 

The  fever  in  tubei'culosis  is  generally  noticeable  from  its  very  monotonous 
character.  For  months  the  temperature  curve  may  be  like  this:  in  the  morning 
a  normal  or  approximately  normal  temperature,  and  at  evening  a  rise  to  103°  or 
104°  (39°-40°  C),  rarely  higher.  The  fever  in  phthisis,  then,  shows  a  decidedly 
intermitting  or  remitting  character,  the  so-called  ':  hectic  fever." 

More  rarely  we  see  very  irregular  temperature  curves,  where  elevations  of 
temperature,  which  last  a  shorter  or  a  longer  time,  alternate  in  an  irregular  fash- 
ion with  periods  that  are  free  from  fever.  It  often  happens  that  toward  the  end 
of  the  disease,  when  the  general  weakness  increases,  the  curve,  that  previously 
was  regular  in  its  intermissions,  becomes  irregular.  The  intermissions  then 
become  deeper,  and  we  often  see  genuine  temperatures  of  collapse,  94°  to  92°  (35°- 
34°  0.).  At  other  times  the  fever  may  temporarily  assume  a  more  continuous 
chai'acter,  probably  from  an  increase  of  the  tubercular  process.  In  some  cases 
with  an  acute  onset  {vide  supra)  we  have  also  seen,  at  the  beginning  of  the  dis- 
ease, quite  a  high  and  approximately  continuous  fever,  which  later  went  over 
gradually  to  the  ordinary  hectic. 

We  must  probably  look  for  the  cause  of  the  fever  not  in  the  tuberculosis  itself, 
but  in  the  absorption  of  septic  substances  from  the  decomposition  of  the  secretion 
of  the  bronchi  and  cavities. 

In  general,  it  may  be  said  that  continuous  fever  points  to  an  advance,  com- 
plete absence  of  fever,  on  the  other  hand,  to  a  halt  (at  least  a  temporary  one),  of 
the  tuberculous  process ;  hence  is  evident  the  great  prognostic  importance  of  the 
temperature  in  pulmonary  tuberculosis. 

Emaciation. — The  great  emaciation  of  the  patient  is  very  striking  in  most 
cases  of  phthisis.  The  muscular  system  and  the  fatty  tissue  are  affected  in  equal 
degree.  The  soft  parts  of  the  thorax  are  often  especially  involved.  The  emacia- 
tion is  due  in  part  to  the  patient's  loss  of  appetite,  and  to  the  small  amount  of  food 
which  he  takes  in  consequence  thereof,  but  the  chief  cause  lies  in  the  persistent 
fever  and  the  increased  metamorphosis  of  tissue.  Quite  a  high  degree  of  emacia- 
tion, however,  may  appear  in  the  beginning  of  the  disease  with  no  fever.  This 
we  are  wont  to  ascribe  to  the  "general  illness,"  but  the  special  cause  of  it  is  un- 
known. Under  favorable  external  conditions  phthisical  patients  may  make  quite 
a  decided  gain  in  weight,  especially  at  the  times  when  they  are  free  from  fever. 
In  very  chronic  cases,  which  run  their  course  from  the  first  without  fever,  the 
nutrition  of  the  patient  may  remain  good  for  a  long  time.  Toward  the  end  of 
the  disease  emaciation  sometimes  reaches  its  highest  degree,  and  many  phthisical 
patients  die  "  wasted  to  a  skeleton  "  in  the  true  sense  of  the  word. 

Ancemia — Color  of  the  Skin. — In  most  cases  anaemia  appears  in  the  course  of 
the  disease,  which  can  be  recognized  by  the  pale  and  sallow  color  of  the  skin  and 
the  visible  mucous  membranes.  The  anaemia  only  rarely  reaches  that  degree  of 
peculiar  waxy  pallor  that  is  found  in  idiopathic  pernicious  anaemia.  The  exist- 
ence of  the  anaemia  is  also  the  reason  why  the  phthisical  patient  does  not  look 
cyanotic,  in  spite  of  the  respiratory  disturbance.  In  the  more  chronic  forms, 
where  the  general  nutrition  suffers  less,  we  often  see  a  cyanotic  coloring  of  the 
lips  and  cheeks.  Sometimes  the  skin  of  phthisical  patients  assumes  a  dirty;  dusky 
15 


226  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

hue.  We  have  already  spoken  of  the  circumscribed  "  hectic  flush  of  the  cheeks  " 
seen  with  the  fever. 

General  Weakness — Night-Siceats — Nervous  Disturbances. — We  need  not  say 
that  the  general  emaciation  and  anaemia  are  accompanied  by  a  marked  decline  in 
the  patient's  power  of  endurance.  He  finally  becomes  so  helpless  that  he  can 
scarcely  move  alone  in  the  bed. 

The  tendency  which  very  many  patients  have  to  severe  night-sweats  is  not 
wholly  explained.  ,  It  may  have  some  connection  with  the  fall  from  the  evening 
febrile  temperature  to  the  morning  remission,  and  perhaps  it  is  due  to  the  greater 
accumulation  of  carbonic  acid  in  the  blood  from  the  disturbance  of  respiration. 

The  disease  has  remairkably  little  influence  upon  the  higher  nervous  functions, 
especially  those  of  the  mind.  Most  patients  have  a  perfectly  clear  intellect  to 
their  latest  breath.  We  all  know  the  contented,  hopeful  disposition  of  many 
patients,  who  do  not  recognize  their  own  danger  until  the  last  stages  of  the  dis- 
ease. Occasionally  the  anaemia  and  the  general  disturbance  of  the  nutrition  of 
the  brain  lead  to  mental  alterations,  such  as  confusion,  distraction,  or  melancholic 
conditions. 

We  find,  more  frequently,  disturbances  in  the  peripheral  nerves  and  muscles. 
Among  these  are  neuralgic  pains,  and  pains  of  an  indefinite  character,  which  have 
their  seat  in  the  legs,  or  sometimes  in  the  arms,  especially  in  the  ulnar  region,  and 
which  may  be  very  distressing.  Marked  hyperaesthesia  of  the  skin  and  deeper 
parts  is  also  not  uncommon.  The  cause  of  such  disturbances  is  probably  often  to 
be  looked  for  in  degenerative  changes  in  the  peripheral  nerves  (Vierordt  and 
others).  Well-marked  multiple  neuritis  has  been  repeatedly  observed  in  tubercu- 
lous patients  (see  section  on  nervous  diseases). 

We  very  often  see  an  increased  reaction  upon  direct  mechanical  irritation  in 
the  emaciated  muscles,  and  great  liveliness  of  the  so-called  idiomuscular  contrac- 
tions, which  is  shown,  for  example,  on  percussing  the  pectoral  muscles  on  the  an- 
terior wall  of  the  chest.  The  phenomena  grouped  under  the  name  of  tendon  re- 
flexes are  also  much  increased  in  phthisis. 

4.  Symptoms  and  Complications  on  the  Part  of  Other  Organs.— 1.  Pleura.— 
In  pulmonary  tuberculosis  the  pleura  is  also  involved  as  a  rule.  The  affection  is 
almost  always  the  result  of  a  direct  extension  of  the  process  from  the  lung  to  the 
pleura.  At  the  autopsy,  we  find  in  the  pleura  a  few  or  many  miliary  tubercles, 
besides  the  simple  inflammatory  process — tubercular  pleurisy. 

In  many  cases,  in  which  we  have  to  do  only  with  an  adhesive  pleurisy  and 
with  pleuritic  contraction,  we  can  merely  suspect  the  disease  of  the  pleura,  but  it 
can  not  be  directly  made  out  and  differentiated  clinically  from  the  pulmonary 
affection.  In  other  cases  we  can  diagnosticate  a  dry  pleurisy  in  phthisis  from  the 
occurrence  of  the  pleuritic  friction-rub.  The  symptoms  of  pleurisy  become  more 
marked  if  there  is  a  pleuritic  effusion,  which  is  usually  readily  discovered  by  a 
physical  examination.  The  patient's  pain  and  dyspnoea  are  usually  much  in- 
creased by  such  a  complication.  Besides  a  simple  sero-fibrinous  effusion  we  quite 
frequently  find  purulent  and  even  haemorrhagic  effusions  in  tuberculosis  of  the 
pleura. 

The  formation  of  pneumothorax  is  an  important  complication  in  the  pleura  in 
phthisis.  This  is  due  to  the  rupture  of  a  superficial  pulmonary  cavity  into  the 
pleural  cavity,  and  the  entrance  of  air  into  the  latter.  The  different  forms  of 
pneumothorax  and  its  symptoms  will  be  described  under  diseases  of  the  pleura. 

2.  Larynx,  Pharynx,  and  Trachea. — The  symptoms  of  laryngeal  tuberculosis 
and  their  relation  to  pulmonary  tuberculosis  have  already  been  given  under  dis- 
eases of  the  larynx.  We  saw  there  thatj  although  there  is  a  primary  laryngeal 
tuberculosis,  most  cases  are  secondary  in  their  development  to  a  pulmonary  tuber- 


TUBERCULOSIS  OF  THE  LUNGS.  227 

culosis.  The  constant  passage  of  tubercular  sputa  from  the  lungs,  through  the 
trachea  and  larynx,  naturally  leads  to  a  direct  infection  of  the  mucous  membrane 
of  the  parts  mentioned. 

The  same  holds  true  in  regard  to  the  much  rarer  tuberculosis  of  the  pharynx. 
In  some  cases  this  may  be  of  primary  origin,  but  it  is  usually  a  result  of  re-inocu- 
lation with  tuberculosis  by  means  of  the  sputum,  or  of  a  direct  extension  of  the 
tubercular  process  from  the  larynx  to  the  pharynx.  Tubercular  ulcers  of  the 
pharynx  are  found  most  frequently  on  the  soft  palate,  on  the  tonsils,  on  the  root 
of  the  tongue,  and  on  the  boundary  between  the  pharynx  and  the  larynx;  they 
are  rare  in  other  parts  of  the  pharynx.  In  exceptional  cases  tubercular  affections 
are  seen  in  the  mouth — on  the  tongue.  The  local  discomforts  which  all  these 
ulcers  cause  is  usually  very  considerable.  Disseminated  miliary  tubercles,  too, 
have  been  repeatedly  seen  in  the  mucous  membrane  of  the  pharynx. 

3.  Stomach  and  Intestinal  Canal — Peritoneum. — Tubercular  ulcers  in  the 
mucous  membrane  of  the  stomach  are  exceedingly  rare,  but  we  very  often  notice 
some  symptoms  on  the  part  of  the  stomach.  Loss  of  appetite  is  a  particularly 
common  symptom  in  phthisis.  Vomiting  occurs  often  in  phthisical  patients, 
especially  when  the  larynx  is  involved:  It  is  usually  brought  on  by  paroxysms 
of  coughing.  Less  frequently  the  cause  of  the  vomiting  is  gastric  catarrh,  occa- 
sioned by  the  irritation  of  the  phthisical  sputa  which  have  been  swallowed ;  but 
in  some  cases  the  gastric  symptoms  depend  upon  the  general  condition,  like 
anaemia. 

Although  the  tubercle  bacilli  swallowed  with  the  sputum  hardly  ever  infect 
the  stomach,  probably  from  the  acid  reaction  of  its  contents,  they  very  often  at- 
tack the  intestinal  canal.  In  the  majority  of  the  cases  of  phthisis  we  find  tuber- 
cular ulcers,  either  singly  or  in  considerable  numbers,  in  the  vicinity  of  Bauhin's 
valves  [the  ileo-csecal  valve],  in  the  lower  part  of  the  ileum,  and  the  upper  part 
of  the  large  intestine. 

Intestinal  tuberculosis  does  not  always  cause  very  marked  clinical  symptoms, 
but  as  a  rule  we  find  diarrhoea  in  patients  with  tubercular  ulcers  of  the  intestine. 
They  may  have  three  or  four  stools  in  the  twenty-four  hours,  and  even  more,  but 
the  stools  have  nothing  chai'acteristic.  We  rarely  see  a  slight  admixture  of  pus 
or  blood  in  them.  Tubercle  bacilli  have  been  repeatedly  discovered  in  the  de- 
jecta, but  the  search  for  them  is  rather  difficult.  We  must  call  attention,  how- 
ever, to  the  fact  that  many  patients  have  diarrhoea  during  life  in  whom  we  find 
at  the  autopsy  no  intestinal  tuberculosis,  but  only  a  simple  intestinal  catarrh,  or 
amyloid  of  the  intestine.  On  the  other  hand,  we  quite  frequently  find  at  the  au- 
topsy tubercular  ulcers  of  the  intestine  which  during  life  caused  no  diarrhoea. 

In  cases  of  severe  intestinal  tuberculosis  we  sometimes  meet  with  meteorism. 
With  deep  ulcers,  extending  to  the  peritoneum,  we  often  see  marked  tenderness 
of  the  abdomen. 

The  peritoneum  may  be  affected  by  the  tubercular  ulcers  of  the  intestine  in  a 
twofold  manner.  Genuine  peritonitis  from  perforation,  with  a  purulent  or  even 
a  sanious  exudation,  is  quite  rare,  and  is  excited  by  the  rupture  of  an  ulcer  and 
the  entrance  of  the  contents  of  the  intestine  into  the  abdominal  cavity.  An  infec- 
tion of  the  peritoneum  with  the  tubercular  poison  is  more  frequent.  This  may 
arise  from  deep-seated  ulcers,  which  do  not  reach  actual  perforation,  so  that  we 
have  a  peritoneal  tuberculosis,  or  a  tubercular  peritonitis.  During  life  peritonitis 
from  perforation  and  that  from  tuberculosis  are  not  always  to  be  distinguished. 
We  must  also  mention  that  simple  ascitic  fluid  is  sometimes  found  in  the  abdomi- 
nal cavity  in  phthisis,  which  may  lead  to  a  false  diagnosis  of  peritoneal  tuber- 
culosis. 

Another  way  in  which  we  may  have  a  peritoneal  tuberculosis  in  the  course  of 


228  DISEASES  OP  THE  RESPIRATORY  ORGANS. 

phthisis  is  from  the  extension  of  the  process  in  a  tubercular  pleurisy,  through  the 
diaphragm  to  the  peritoneum. 

4.  Liver  and  Spleen. — We  very  often  find  a  few  or  even  many  tubercles  in  the 
liver  in  phthisis,  but  they  have  no  clinical  significance.  The  liver  is  almost  always 
infected  with  the  tubercular  poison  from  tubercular  ulcers  in  the  intestines,  from 
which  the  poison  passes  to  the  branches  of  the  portal  vein  and  then  to  the  liver. 
Fatty  liver  and  amyloid  or  lardaceous  liver  are  more  important  clinical  changes. 
We  can  sometimes  recognize  the  former  by  making  out  on  physical  examination 
the  increase  in  the  size  of  the  organ,  and  by  feeling  its  characteristic  blunt  lower 
edge. 

Amyloid  liver  is  almost  always  associated  with  the  development  of  amyloid  in 
other  organs.  In  marked  cases  the  liver  is  evidently  enlarged,  and  its  firm,  sharp 
lower  edge,  and  often  its  dense  anterior  surface,  may  usually  be  plainly  felt. 

Miliary  tubercles  or  single  large  tubercular  nodules  in  the  spleen  have  a  patho- 
logical interest  only.  Great  splenic  enlargement  is  found  in  amyloid  degen- 
eration. 

5.  Kidneys,  Urinary  Passages,  and  Sexual  Organs. — The  presence  of  miliary 
tubercles  in  the  kidneys  is  the  first  change  in  them  to  be  mentioned,  but  it  has  no 
clinical  significance.  Extensive  tuberculosis  of  the  genito-urinary  apparatus, 
however,  may  produce  marked  symptoms,  like  pyuria,  which  will  be  described 
later.  In  regard  to  the  symptoms  of  amyloid  kidney,  which  may  develop  in  the 
course  of  phthisis  in  connection  with  amyloid  disease  in  other  organs,  we  will 
refer  to  the  section  on  renal  diseases. 

Genuine  cases  of  nephritis,  both  acute  and  chronic,  are  also  found  quite  fre- 
quently in  phthisis,  usually  combined  with  amyloid  disease.  These  can  not  escape 
notice  if  the  urine  is  carefully  examined.  Cases  of  genuine  amyloid  kidney  of 
moderate  severity  are  seen,  however,  in  which  the  urine  remains  normal,  or  at 
any  rate  free  from  albumen. 

6.  Circulatory  Organs. — Not  only  is  the  frequency  of  the  pulse  increased  in 
many  patients  in  proportion  to  the  existing  fever,  but  even  where  there  is  no  fever 
we  often  find  it  accelerated.  The  greater  or  less  increase  of  the  pulse,  which 
readily  comes  on  from  comparatively  trifling  external  causes,  is  especially  note- 
worthy. It  may  be  seen  after  slight  physical  exertion,  or  upon  mental  excitement, 
as  during  the  physician's  visit. 

Anatomical  changes  in  the  heart  are  rare,  except  that  it  is  often  remarkably 
small  and  flaccid.  Moderate  fatty  degeneration  of  the  heart,  slight  endocarditis 
of  the  valves,  or  occasional  tubercles  in  the  heart,  cause  no  symptoms.  The  occur- 
rence of  tubercular  pericarditis,  however,  is  important.  This  almost  always  arises 
from  the  extension  of  the  tubercular  process  from  the  adjacent  pleura,  but  in 
exceptional  cases  pericarditis  has  been  seen  as  a  result  of  rupture  of  a  pulmonary 
cavity  into  the  pericardium. 

7.  Lymph-glands. —  The  lymph-glands  are  a  favorite  seat  for  tubercular 
changes.  We  have  stated  above  that  the  so-called  scrofulous,  cheesy  lymph- 
glands,  which  are  seen  chiefly  in  the  neck  and  the  axilke,  are  affected  with  tuber- 
cle in  the  majority  of  cases.  The  tubercular  infection  probably  develops  here 
from  slight  injuries  and  excoriations  of  the  skin,  by  which  the  bacilli  enter  the 
body  and  reach  the  neighboring  glands  by  means  of  the  lymph-current.  In 
other  cases  the  infection  perhaps  comes  from  the  mucous  membrane  of  the  phar- 
ynx. In  tuberculosis  of  internal  organs,  too,  we  very  often  find  the  corresponding 
lymph-glands  enlarged  and  more  or  less  cheesy.  The  bronchial  lymph-glands 
are  swollen  as  a  result  of  pulmonary  tuberculosis,  the  mesenteric  and  retroperito- 
neal glands  as  a  result  of  intestinal  tuberculosis.  The  tuberculosis  of  the  bron- 
chial lymph-glands  is  of  especial  importance  in  children.     Indeed,  the  tubercular 


TUBERCULOSIS  OF  THE  LUNGS.  229 

virus  which  has  gained  access  to  the  lungs  may  apparently  reach  the  bronchial 
glands  by  means  of  the  lymph-channels  even  without  affecting  the  lungs  them- 
selves, and  occasion  a  tuberculous  disease  of  the  glands.  Glands  thus  diseased 
break  down  and  discharge  into  the  lungs,  and  in  this  way  generate  a  secondary 
pulmonary  tuberculosis.  This  is  one  reason  why  the  pulmonary  tuberculosis  of 
children  so  often  begins  not  in  the  apex  but  in  the  middle  and  lower  portion  of 
the  lung. 

Pressure  from  the  enlarged  glands  may  affect  the  air-passages,  the  branches  of 
the  pulmonary  artery,  the  veins,  the  recurrent  nerve,  and  even  the  aorta.  Per- 
foration of  the  cheesy  bronchial  glands  into  the  oesophagus,  the  blood-vessels,  etc., 
has  also  been  observed.  Tuberculosis  of  the  bronchial  glands  in  children  does  not 
present  any  definite  type  of  disease,  however,  and,  although  we  may  sometimes 
suspect  it  when  there  is  pulmonary  tuberculosis,  we  can  only  rarely  diagnosticate 
it  with  certainty. 

8.  Nervous  System.— We  have  already  mentioned  various  nervous  symptoms 
in  the  description  of  the  general  symptoms.  We  must  also  add  that  tubercular 
meningitis  is  seen  in  the  course  of  phthisis  (see  page  702),  and  also  that  large 
solitary  tubercles  may  occasionally  develop  in  the  central  nervous  system  (see 
page  749). 

9.  Skin. — We  have  spoken  of  the  great  tendency  which  many  patients  have  to 
severe  sweats,  especially  at  night.  The  frequent  appearance  of  pityriasis  versi- 
color, especially  on  the  skin  over  the  thorax,  is  also  worthy  of  note.  We  often 
see  moderate  oedema  of  the  legs  and  ankles,  which  is  due  to  weakness  of  the 
heart.  More  marked  oedema  of  one  leg  sometimes  arises  from  thrombosis  of  the 
femoral  vein.  We  must  also  mention  here,  in  conclusion,  the  specific  tubercular 
disease  of  the  skin — lupus.  This  occurs  alone,  as  a  rule,  without  a  co-existiug 
pulmonary  tuberculosis;  but,  on  the  other  hand,  the  old  term  "  scrofulous  lupus  " 
had  reference  to  the  fact  that  we  often  find  other  tubercular  affections  in  lupus 
besides  the  disease  of  the  skin.  Thus  it  does  not  seem  strange  that  lupus  and 
phthisis  have  been  repeatedly  observed  to  co-exist.  Cutaneous  tuberculosis  may 
develop  not  only  in  the  ordinary  form  of  lupus,  but  also  in  nodules  of  consider- 
able size,  or  in  rather  extensive  ulcers.  Perhaps  some  of  the  cases  of  so-called 
corpse-tubercle  belong  to  true  tuberculosis.  We  have  seen  a  similar  tuberculous 
cutaneous  disease  in  a  woman  who  for  a  long  time  had  washed  the  soiled  handker- 
chiefs of  a  consumptive  patient. 

Diagnosis. — The  diagnosis  of  pulmonary  tuberculosis  has  become  absolutely  cer- 
tain, since  the  discovery  of  the  tubercle  bacilli,  by  the  demonstration  of  their  pres- 
ence in  the  sputum  (vide  supra).  In  all  incipient  cases,  in  which  the  other  symp- 
toms of  the  disease  have  not  yet  made  themselves  manifest,  but  where  the  suspicion 
of  incipient  phthisis  has  been  aroused  by  a  persistent  cough,  by  marked  pallor  and 
emaciation,  by  slight  hoarseness,  by  an  evening  rise  of  temperature,  by  the  appear- 
ance of  night-sweats,  by  the  presence  of  a  hereditary  predisposition,  and  similar 
symptoms,  the  finding  of  tubercle  bacilli  in  the  sputum  is  often  the  sole  deciding 
factor.  We  must  not  forget,  however,  that  in  most  cases  the  diagnosis  may  be 
made  from  the  other  symptoms  alone,  and  also  that  we  can  actually  judge  of 
the  severity  of  the  individual  case,  and  of  the  exact  extension  and  form  of  the 
tubercular  process,  only  by  considering  the  other  symptoms,  and  especially  by 
considering  the  data  of  the  physical  examination.  The  latter,  therefore,  has  lost 
none  of  its  importance  by  the  discovery  of  the  tubercle  bacilli. 

Confusion  between  phthisis  and  other  diseases  is  twofold.  Where  the  consti- 
tutional symptoms  are  predominant,  and  there  are  no  marked  pulmonary  symp- 
toms, an  existing  tuberculosis  may  be  overlooked.  In  the  beginning,  especially, 
many  cases  of  phthisis  are  considered  to  be  merely  anaemia,  chronic   gastric 


230  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

catarrh,  or  simple  bronchitis.  If  an  intermittmg  fever  appears  in  an  early  stage 
of  phthisis,  before  any  marked  pulmonary  symptoms  have  developed,  the  disease 
may  be  mistaken  for  malaria  or  the  like.  On  the  other  hand,  it  is  by  no  means 
rare  to  consider  patients  phthisical  who  are  suffering  from  some  entirely  different 
affection.  He  who  lays  too  great  stress  on  the  uncertain  results  of  percussion 
will  often  make  a  false  diagnosis.  Severe  latent  diseases  of  the  stomach,  or  certain 
general  diseases,  such  as  anaemia,  diabetes,  or  chronic  nephritis,  may  falsely  be 
taken  for  phthisis»  Other  pulmonary  affections,  too,  may  be  confounded  with 
tuberculosis,  especially  chronic  bronchitis,  emphysema,  bronchiectasis,  foetid  and 
gangrenous  processes,  and  carcinoma  of  the  lungs.  A  careful,  unprejudiced,  and 
complete  examination  of  the  patient  is  the  only  possible  protection  against  such 
errors. 

Prognosis. — In  the  present  condition  of  our  therapeutic  knowledge  the  prog- 
nosis of  phthisis  must  unfortunately  still  be  regarded  as  extremely  unfavorable. 
There  can  be  no  doubt  that  the  tubercular  process  in  the  lungs  is  in  itself  cur- 
able, but,  in  all  cases  where  we  get  certain  objective  evidence  of  tuberculosis, 
a  definite  extinction  of  the  disease  is  very  improbable,  because  the  conditions  for 
a  further  extension  of  the  disease  in  the  lungs  are  extremely  favorable.  In 
individual  cases,  however,  with  the  best  hygienic  surroundings,  circumscribed 
tubercular  affections  of  the  lungs  have  been  certainly  found  to  heal.  Indeed, 
it  is  possible  that  recovery  from  pulmonary  tuberculosis  is  more  frequent  than 
was  formerly  supposed ;  for  it  is  precisely  in  the  earliest  stages,  when  the  disease 
is  still  curable  and  tubercle  bacilli  have  not  yet  been  discovered,  that  the  diagnosis 
is  difficult  and  often  uncertain.  In  advanced  cases  of  phthisis  the  prognosis,  of 
course,  is  almost  absolutely  fatal. 

In  individual  cases  the  prognosis  with  regard  to  the  duration  of  the  disease  is 
very  difficult.  Here  we  must  always  be  mindful  of  the  great  differences  in  differ- 
ent persons,  and  hence  we  must  be  very  cautious  in  expressing  an  opinion.  How 
many  patients  with  phthisis  give  us  the  impression  on  the  first  examination  that 
they  can  not  live  a  fortnight  longer,  and  later  on  we  see  the  disease  lasting  for 
many  months,  most  of  the  symptoms  improving,  and  the  patient  recovering 
again !  In  other  cases,  on  the  contrary,  we  think  we  have  to  do  with  an  incipient 
case,  and  give  great  encouragement — and  the  patient  dies  in  a  few  weeks  with 
florid  phthisis.  Even  disregarding  the  constant  possibility  of  an  unforeseen 
fatal  haemoptysis,  pneumothorax,  or  tubercular  meningitis,  a  conjecture  as  to  the 
duration  of  the  disease  is,  therefore,  very  uncertain  in  most  cases  which  have  not 
yet  reached  the  last  stage,  and  should  be  made  only  after  long  observation  of  the 
patient.  Very  much,  of  course,  depends  upon  the  circumstances  of  the  patient, 
and  upon  the  possibility  of  good  care,  suitable  food,  and  good  air. 

Of  the  single  factors  which  influence  the  prognosis,  our  chief  attention  must  be 
paid  to  the  general  nutrition,  the  patient's  weight,  the  extent  of  the  pulmonary 
affection,  the  fever,  and  certain  complications,  especially  laryngeal  and  intestinal 
tuberculosis.     We  need  not  repeat  the  special  points  which  relate  to  these. 

[Flint,  especially,  has  called  attention  to  the  fact  that  phthisis  is  sometimes  self- 
limited  ;  that  recovery  or  arrest  takes  place  without  any  special  treatment,  and  in 
spite  of  relatively  unfavorable  surroundings.  The  clinical  evidence  is  greatly 
strengthened  by  the  frequency  with  which,  after  death  from  any  cause,  the  remains 
of  an  old  phthisical  affection  are  found. 

In  1857,  39 "50  deaths  from  consumption  were  returned  in  the  State  of  Massa- 
chusetts for  each  ten  thousand  of  the  population;  in  1883,  29-90.  This  decrease 
is  too  large  to  credit  to  greater  accuracy  in  diagnosis  and  to  the  transference  of 
consumptives  to  other  States,  and  is  mainly  attributable  to  the  prevention  of 
phthisis  by  improved  hygiene.     Still,  it  seems  fair  to  carry  some  of  the  improve- 


TUBERCULOSIS  OF  THE  LUNGS  231 

merit  to  the  account  of  the  arrest  and  cure  of  actually  developed  disease  through 
early  diagnosis  and  more  rational  treatment,  hygienic  as  well  as  medicinal.] 

Treatment. — 1.  Prophylaxis. — The  question  of  what  prophylactic  measures 
may  effectually  prevent  the  extension  of  the  disease  has  entered  upon  a  new 
stage  since  our  definite  knowledge  as  to  the  infectious  nature  of  tuberculosis. 
We  can  no  longer  doubt  the  contagious  character  of  phthisis,  in  support  of  which 
isolated  examples  were  previously  brought  forward.  Even  if,  according  to  all 
experience,  the  dauger  of  contagion  is  not  very  great,  still  it  is  foolish  to  ignore 
it  entirely.  We  must  therefore  call  the  attention  of  the  relatives  of  phthisical 
patients  to  the  possibility  of  this  danger,  and  we  should  not  permit  the  children 
of  such  patients  to  be  uselessly  exposed  to  it.  We  should  take  satisfactory  pre- 
cautions for  isolation,  and  also  for  disinfection  of  the  sputum,  which  can  best  be 
done  by  a  strong  solution  of  carbolic  acid.  The  future  will  teach  us  whether 
many  evils  may  not  be  averted  by  such  measures,  although  now  these  measures 
are  greatly  neglected. 

The  "prophylaxis"  at  present  employed  is  almost  exclusively  confined  to 
hardening  and  strengthening  the  threatened  individual  as  much  as  possible.  We 
should  try  to  strengthen  the  bodies  of  children  of  a  weak  habit,  with  "  scrofulous  " 
symptoms,  and  children  from  families  in  which  cases  of  tuberculosis  have  already 
occurred,  and  thus  to  arm  them  against  the  enemy  that  threatens  them.  Good 
food,  fresh  air,  and  a  diminution  of  the  sensitiveness  of  the  body  by  cold  sponging 
and  cold  baths — these  are  the  factors  whose  favorable  influence  is  generally 
recognized. 

The  removal  of  certain  foci  of  tubercular  disease,  already  existing,  from  the 
body  may  prove  of  great  prophylactic  importance.  We  refer  to  the  timely  treat- 
ment or  extirpation  of  scrofulous — that  is,  tubercular — swellings  of  the  lymph- 
glands,  healing  or  resection  of  tubercular  bones  and  joints,  etc.  Although  in 
individual  cases  we  can  of  course  never  know  whether  the  part  removed  is  the 
sole  focus  of  disease  in  the  body,  still  we  are  undoubtedly  justified  in  trying  to 
remove  at  least  one  possible  source  of  some  later  general  infection.  A  fuller 
discussion  of  this  important  point  must  be  left  to  the  works  on  surgery. 

2.  Treatment. — We  do  not  yet  know  any  actual  treatment,  corresponding  to 
the  causal  indication,  whose  point  of  attack  is  aimed  directly  against  the  tuber- 
cular poison.  The  inhalations  employed  with  this  idea,  containing  antiseptic  sub- 
stances, like  carbolic  acid,  benzoate  of  sodium,  and  lately  iodoform,  have  so  far 
all  proved  unsatisfactory,  chiefly  because  the  substances  inhaled  have  not  reached 
the  bronchi  in  sufficient  amount.  Inhalations  of  iodoform,  made  by  a  special 
apparatus  invented  by  Küssner,  have  been  the  most  successful  in  tuberculosis 
of  the  larynx.  We  have  already  spoken  of  inhalations  with  astringents  and 
narcotics. 

We  must  make  especial  mention  of  arsenic  among  the  internal  remedies  to 
which  a  specific  action  in  tuberculosis  has  been  attributed.  Our  own  experiments, 
which  were  suggested  by  quite  a  number  which  were  made  by  Büchner,  have  in 
general  given  no  favorable  result.  In  some  cases,  however,  the  remedy  seems  to 
have  a  marked  therapeutic  action,  so  that  we  are  always  justified  in  trying  arsenic 
in  incipient  cases,  the  more  especially  since  it  has  lately  been  observed  to  have  a 
favorable  influence  in  other  tubercular  affections,  like  tuberculosis  of  the  lymph- 
glands,  caries,  and  lupus.  It  is  better  not  to  prescribe  arsenic  in  solution,  but  in 
pills  of  a  twentieth  of  a  grain  (grm.  0-003)  of  arsenious  acid,  giving  two  or  three 
a  day,  and  later  four  or  five  if  possible,  always  after  eating.  Good  results  can  be 
obtained  only  after  using  the  remedy  for  at  least  some  months.  Another  internal 
remedy  which  has  been  much  talked  about  of  late  years  is  creasote.  It  may  be 
given  in  pills,  or  combined  with  cod-liver  oil,  as  in  the  following  formula : 


232  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

]J   Creasoti gr.  xv  (grm.  1)  ; 

Olei  morrhuae 3  ü j  3  ijss.  (grm.  100)  ; 

Olei  menthae  piperita? gtt.  2.     M. 

Three  or  four  teaspoonfuls  daily. 

Or  it  may  be  given  in  gelatine  capsules,  which  usually  contain  five  sixths  of  a 
grain  of  creasote  (0"05)  combined  with  a  third  of  a  grain  of  balsam  of  tolu  (0-02). 
The  patient  should  take  six  to  twelve,  or  even  more,  of  these  capsules  a  day.  Crea- 
sote may  also  be  administered  in  milk.  A  certain  improvement  of  the  symptoms 
under  the  use  of  creasote,  especially  with  regard  to  cough  and  expectoration,  can 
not  be  denied.  The  exaggerated  expectations  which  many  physicians  cherished 
concerning  this  remedy  will  scarcely,  however,  be  fulfilled. 

The  hygienic  and  symptomatic  treatment  of  phthisis  is  more  important  than 
the  remedies  so  far  mentioned. 

The  hygienic  treatment,  in  the  broadest  sense  of  the  word,  aims,  on  the  one 
hand,  to  increase  the  power  of  resistance  of  the  body  to  the  disease,  and,  on  the 
other,  to  put  the  body  under  conditions  which  we  know  can  combat  the  further 
extension  of  the  disease.  We  try  to  aid,  so  far  as  possible,  the  process  of  spon- 
taneous recovery  in  phthisis.  First  to  be  mentioned  here  is  the  diet  of  the  patient, 
which  must  be  as  nutritious  and  abundant  as  possible.  Meat,  milk,  eggs,  farina- 
ceous food,  and  butter  are  to  be  used  chiefly,  special  care  being  taken  that  the  body 
gets  hydrocarbons  and  fat  in  sufficient  amount,  as  well  as  plenty  of  albumen. 
Many  of  the  special  "  cures  "  for  phthisis  have  their  only  value  in  the  fact  that  in 
these  places  the  patient  takes  a  large  amount  of  easily  assimilated  nutriment,  like 
milk,  and  also  koumyss— which  is,  properly  speaking,  mare's  milk  fermented  in  a 
peculiar  fashion,  although  with  us  it  is  artificially  made  from  cow's  milk — and 
also  kefir,  which  is  similar  to  koumyss.  French  physicians  have  lately  brought 
forward  forced  feeding  as  a  special  "  method  "  of  treating  consumption.  It  con- 
sists in  giving  the  largest  possible  amounts  of  nourishment  (pulverized  meat  and 
the  like),  and  sometimes  the  food  is  even  poured  down  through  a  stomach-tube. 
In  ordering  milk-cures  we  must  not  forget  that  milk  soon  becomes  repugnant  to 
many  patients,  and  then  it  can  no  longer  be  taken  in  sufficient  amount.  In  such 
cases  we  sometimes  succeed  in  making  the  milk  palatable  to  the  patient  by  adding 
common  salt,  cognac,  or  coffee.  It  is  also  a  good  way  to  have  an  infusion  of  tea 
or  coffee  made  with  hot  milk.  Many  patients  prefer  this  to  pure  milk.  As  regards 
alcohol,  we  should  chiefly  prescribe  those  forms  of  malt  liquor  which  are  relatively 
rich  in  nutriment — e.  g.,  porter.  Small  amounts  of  good  wine  may  aid  in  im- 
proving the  appetite  and  the  general  condition.  Many  physicians  indeed  believe 
that  the  stronger  alcoholic  beverages,  such  as  brandy  and  the  like,  are  of  special 
benefit  in  the  treatment  of  consumption,  but  we  doubt  it.  Cod-liver  oil,  two  to 
four  tablespoon  fuls  a  day,  is  a  prescription  which  furthers  the  patient's  nutrition, 
and,  if  it  be  well  borne,  it  may  be  of  distinct  service,  especially  in  emaciated 
patients.  Still,  we  believe  that  one  may  obtain  the  same  success  by  the  regular 
daily  administration  of  several  tablespoonfuls  of  pure  fresh  cream. 

We  must  also  pay  attention  to  the  patient's  manner  of  living,  as  well  as  care 
for  his  nutrition.  Here  we  must  endeavor,  on  the  one  hand,  to  remove  all  the 
injurious  influences  connected  with  his  occupation,  like  staying  in  badly  venti- 
lated counting-rooms  and  work-shops,  inhaling  dust,  or  excessive  speaking,  and, 
on  the  other  hand,  must  give  him  such  directions  as  will  have  a  favorable  action 
on  the  whole  body,  and  especially  on  the  respiratory  organs — the  enjoyment  of 
good  air,  free  from  dust,  sponging  the  chest  with  cold  water,  and  baths;  but  since 
we  often  can  not  satisfy  all  these  demands  under  the  patient's  ordinary  household 
conditions,  it  has  long  been  the  custom  to  send  patients  with  thoracic  diseases  to 


TUBERCULOSIS  OF  THE  LUNGS.  233 

certain  special  health-resorts,  where  the  conditions  for  a  prescrihed  manner  of  liv- 
ing may  be  fulfilled  more  completely  than  at  home.  On  this  depends  the  so-called 
climatic  treatment  of  phthisis.  Many  physicians  assert  that  certain  climatic  fac- 
tors, like  temperature,  moisture,  and  atmospheric  pressure,  exert  a  specific  thera- 
peutic influence;  hut  this  view  does  not  seem  very  probable. 

In  regard  to  the  choice  of  a  temporary  resort  for  the  summer,  in  many  cases  we 
must  content  ourselves  with  recommending  a  country  residence  for  the 'patient,  in 
a  region  as  healthy  as  possible,  protected,  dry,  and  well  wooded,  paying  attention 
at  the  same  time  to  the  character  of  the  board  and  lodging  there.  A  good  country 
boarding-place  may  do  just  as  well  as  many  expensive  health-resorts.  We  may 
mention  in  particular,  among  the  special  health-resorts,  springs,  and  places  for 
inhalations  in  Germany,  (1)  the  acidulous  saline  waters  at  Ems,  Gleichenberg, 
Neuenahr,  Obersalzbrunn,  Reinerz,  and  others ;  (2)  the  chloride-of -sodium  waters 
at  Reichenhall,  Salzungen,  Soden,  and  others;  (3)  the  springs  containing  the 
earthy  salts  at  Inselbad,  Lippspringe,  and  Weissenburg.  The  favorable  influence 
of  these  baths  is  best  seen  in  cases  where  there  is  anorexia  or  other  gastric  dis- 
turbance. Besides  these  we  may  also  mention  some  of  the  well-known  high  cli- 
matic health-resorts  in  the  Alps:  Aussee,  Beatenberg,  Berchtesgaden,  Engelberg, 
Gmunden,  Heiden,  St.  Moritz,  Seelisberg,  and  others;  and  in  the  Black  Forest: 
Baden weiler,  St.  Blasien,  Rippoldsau,  and  others. 

The  choice  of  a  winter  health-resort  is,  under  some  circumstances,  of  still 
greater  importance,  since  the  colder  season  with  us  brings  with  it  many  dangers 
for  the  patient.  The  first  to  be  mentioned  here  are  the  high  health-resorts,  where 
the  weather  is  usually  clear  and  sunny.  Among  these  Davos  enjoys  the  greatest 
reputation.  This  place  is  especially  suited  for  patients  who  are  still  quite  strong 
and  free  from  fever,  and  who  do  not  suffer  from  laryngeal  symptoms.  Among 
the  winter  health-resorts  in  Germany  we  must  mention  first  Görbersdorf,  and  also 
St.  Blasien.  The  southern  climate  is  better  for  delicate,  "  erethistic  "  patients,  and 
also  for  those  with  laryngeal  affections.  Of  course  only  the  very  distant  health- 
resorts  in  Algiers,  Egypt,  Malta,  and  the  much-praised  Madeira,  can  furnish  a 
certain  guarantee  of  constant  mild  weather.  The  Sicilian  health-resorts  (Catania 
and  Palermo),  and  also  Ajaccio  and  Pau,  afford  favorable  climatic  conditions; 
while  the  health-resorts  of  the  Riviera  (see  p.  153),  Meran,  Areo,  Lugano,  and 
Montreux,  are  much  more  uncertain  in  this  respect,  and  therefore  are  to  be  used 
merely  as  stopping-places  by  the  way  during  the  spring  and  autumn  months. 

We  can  not  go  into  a  full  description  here  of  all  the  health-resorts  men- 
tioned. We  can  not  omit,  however,  calling  special  attention  to  the  fact  that  we 
should  always  ask  ourselves,  in  choosing  a  health-resort,  whether  the  expense  and 
inconvenience  thus  imposed  upon  the  patient  can  be  balanced  by  the  possible 
benefit.  The  earlier  the  stage  of  the  disease  and  the  better  the  general  condition 
of  the  patient,  the  more  will  his  physician  be  justified  in  urging  him  to  make 
every  sacrifice  in  order  to  regain  his  health.  It  is  blameworthy,  from  a  profes- 
sional and  humane  stand- point,  to  send  patients  in  the  last  stages  of  phthisis 
among  strangers,  to  die  far  from  their  home  and  relatives.  For  severe  cases, 
when  we  wish  to  send  them  from  home,  the  special  institutions  are  the  only 
suitable  places,  where  the  patient  may  at  least  be  under  the  constant  care  and 
attention  of  a  physician.  Especial  asylums  for  lung  patients  are  Falkenstein  on 
the  Taunus,  Görbersdorf,  Inselbad  at  Paderborn,  and  Reiboldsgrlm. 

[Our  own  health-resorts  for  consumptives  are  too  well  known  to  demand  ex- 
tensive consideration  here.  The  prime  object  is  to  secure  for  the  patient  a  pure 
air,  with  such  climatic  conditions  that  he  can  pass  the  largest  amount  of  time  out 
of  doors,  at  the  same  time  that  within  doors  his  comfort  is  provided  for,  and  a 
sufficiency  of  suitable  and  well-cooked  food  is  attainable.     In  Colorado,  New 


234  DISEASES  OF  THE  RESPIRATORY   ORGANS. 

Mexico,  and  California,  large  numbers  of  former  consumptives  are  leading  active 
lives.  Florida,  Aiken,  Thomasville,  Asheville,  and  some  other  southern  resorts 
are  good  winter  asylums  for  many  cases,  but  patients  should  not  return  to  New 
England  before  June  1st.  An  out-door  life  in  the  Maine  or  Adirondack  woods 
during  the  warmer  months  is  highly  to  be  recommeuded  for  early  and  otherwise 
suitable  cases.  Saranac,  N.  Y.,  affords  every  comfort  during  the  colder  months 
combined  with  the  very  best  medical  attendance,  and  many  people  do  well  there. 
A  relative  disadvantage  under  which  nearly  all  American  health-resorts  labor  as 
compared  with  those  of  Europe,  consists  in  the  greater  difficulty  in  providing  oc- 
cupation and  thus  securing  a  mental  attitude  most  favorable  to  recovery.  In  gen- 
eral, the  northern  sea-board  is  much  less  favorable  than  the  intei'ior,  and  early 
cases  often  do  well  during  the  winter  removed  from  the  dampness  of  the  coast, 
with  its  alternations  of  freezing  aud  thawing.  A  change  of  climate  is  a  very  im- 
portant step,  and  should  receive  the  most  careful  consideration  of  the  physician— 
the  circumstances  of  the  patient,  the  stage  and  character  of  his  disease,  his  tastes, 
etc.,  being  carefully  weighed  before  a  decision  is  reached.] 

We  must  also  state  that,  in  incipient  cases,  a  residence  by  the  sea,  or  a  long 
sea-voyage,  may  sometimes  be  of  great  help.  We  have  ourselves  known  several 
young  physicians  who  have  become  ship-surgeons  on  account  of  incipient  phthisis, 
and  who  have  returned  from  the  voyage  much  stronger,  and  some  of  them  appar- 
ently entirely  well. 

The  symptomatic  treatment  of  phthisis  is  directed  in  the  first  place  against  the 
pulmonary  symptoms.  We  use  much  the  same  remedies  to  help  the  cough  as  in 
chronic  bronchitis.  We  try  inhalations  with  a  solution  of  common  salt,  or  of  the 
alkaline  carbonates,  or,  where  there  is  much  secretion,  with  solutions  of  tannin 
and  the  balsams,  like  turpentine,  or  balsam  of  Peru.  Where  there  is  severe,  spas- 
modic cough,  inhalations  with  narcotic  solutions  sometimes  give  some  relief,  such 
as  cherry-laurel  water,  opium,  or  bromide  of  potassram.  It  is  doubtful  whether 
the  inhalation  of  nitrogen,  recommended  by  many  physicians,  has  any  real  thera- 
peutic value.  Pneumatic  treatment,  by  inhalations  of  compressed  ah,  may  some- 
times give  good  results  in  cases  of  incipient  phthisis. 

Morphine  stands  first  among  the  drugs  employed  to  check  the  cough.  We 
should  be  cautious  and  sparing  in  its  use  at  first,  but  it  is  an  indispensable  remedy 
in  severe  and  hopeless  cases.  It  relieves  the  irritation  of  coughing,  the  pain  and 
the  oppression  in  the  chest,  and  at  least  gives  the  patient  for  a  time  the  desired 
sleep.  In  chronic  cases,  with  moderately  severe  symptoms,  we  may  use  for  a  long 
time  the  milder  narcotics  with  advantage,  like  extract  of  hyoscyamus  (extracti 
hyoscyami  1,  aqua?  lauro-cerasi  20,  fifteen  to  twenty  drops  every  two  hours),  one 
to  three  grains  (grm.  0-05-0-20)  of  lactucarium  in  powder,  or  half  a  grain  to  a  grain 
(grm.  0-03-0-05)  of  extract  of  belladonna  in  powder.* 

If  the  patient  complains  of  difficulty  in  loosening  the  expectoration,  we  pre- 
scribe expectorants,  the  action  of  which  often  fails  to  meet  our  desires,  but  which 
can  not  be  dispensed  with  in  practice.  The  expectorants  most  frequently  used 
are  cai'bonate  of  ammonia,  ipecacuanha,  apomorphine,  and  sulphuret  of  anti- 
mony, t  We  very  often  combine  expectorants  with  narcotics,  as  in  Dover's  powder. 

If  severe  pain  in  the  chest  comes  on,  we  often  use  local  applications  :  mustard 
plasters,  warm  poultices  and  cold  compresses,  painting  with  iodine,  or  embro- 
cations of  chloroform.  Narcotics,  like  morphine,  are  indispensable  in  severe 
dyspoena,  which  usually  occurs  only  in  the  last  stages  of  the  disease  or  as  a  result 
of  pneumothorax. 

*  Extractum  belladonna,  U.  S.  P.,  is  about  twice  the  strength  of  the  German  preparation.— Trans. 
t  We  should  use  tartar  emetic  instead  of  the  sulphuret. — Trans. 


TUBERCULOSIS  OF  THE  LUNGS.  235 

The  treatment  of  haemoptysis  is  important.  As  a  slight  admixture  of  blood 
in  the  expectoration  often  precedes  a  severe  haemoptysis,  such  an  event  always 
demands  caution.  The  patient  must  keep  as  quiet  as  possible,  and  avoid  hot 
drinks  and  alcohol.  When  there  is  a  severe  haemoptysis,  absolute  rest  in  hod  is 
especially  necessary.  We  should  avoid  any  careful  examination  of  the  lungs, 
especially  any  severe  percussion.  We  should  lay  a  flat  and  not  too  heavy  ice- 
bag  over  the  lung  on  the  side  from  which  we  suspect  the  haemorrhage;  the  cold 
is  usually  well  borne,  but  sometimes  it  aggravates  the  cough,  and  must  then 
be  omitted.  We  would  also  recommend  swallowing  bits  of  cracked  ice.  Nar- 
cotics, like  morphine,  are  the  most  suitable  internal  remedies,  since  they  aid  the 
cessation  of  the  haemorrhage  by  suppressing  the  attacks  of  coughing.  Among 
the  remedies  which  may  be  employed  to  check  the  bleeding  are  ergotine,  two  or 
three  one-grain  pills  (grm.  0'05)  every  hour ;  also  sclerotinic  acid,  thirty  to  forty-five 
minims  of  a  four-per-cent.  solution  subcutaneously  in  the  twenty-four  hours ;  and 
one  or  two  grains  (grm.  0 -05-0-10)  of  acetate  of  lead  in  powder  every  two  hours, 
sometimes  combined  with  morphine.  The  liquor  fern  chloridi  (a  tablespoonful  of 
a  two-per-cent.  solution  every  one  or  two  hours)  is  also  recommended,  but  in  this 
form  it  is  probably  entirely  useless.  Common  salt  is  a  remedy  which  sometimes 
seems  to  be  of  service,  and  which  is  almost  always  at  hand.  We  give  one  or  more 
teaspoonfuls  of  it  in  water.  Acids,  lemonade,  and  Haller's  acid  elixir  [mixtura 
sulf urica  acida  (P.  G.)]  are  favorite  household  remedies  in  haemoptysis. 

After  the  haemorrhage  ceases,  the  patient  must  be  extremely  careful  for  a  long 
time,  since  it  often  recurs. 

The  hectic  fever  of  phthisis  is  characterized  by  its  great  resistance  to  antipy- 
retic remedies.  It  is  usually  utterly  useless  to  try  to  combat  it  with  large  doses  of 
quinine  or  salicylate  of  sodium.  The  action  of  antipyrine,  too,  is  only  temporary. 
Cold  sponging  of  the  whole  body  is  to  be  highly  recommended  at  the  times  of  rise 
of  temperature.  It  is  usually  well  borne,  and  gives  the  patient  visible  relief  and 
refreshment. 

Cold  sponging  often  diminishes  the  troublesome  sweats  in  phthisis,  but  if  this 
does  not  check  them,  we  may  often  prescribe  atropine  to  advantage,  gr.  t|-ö  to  -rV 
(grm.  0-0005-0 '001)  at  night,  but  its  action  does  not  usually  last  very  long.  Lately 
agaricine  in  Ty  to  ^-grain  pills  (grm.  0-005-0 -01)  has  been  recommended  for  the 
night-sweats  in  phthisis;  also picrotoxin,  of  which  gr.  |  to  -Jr  (grm.  O-008-O'Ol)  is 
given  in  pill  or  solution  at  bed-time.  Dusting  the  body  with  a  powder  of  five 
parts  of  salicylic  acid  to  ninety-five  of  French  chalk  is  also  a  good  thing.  Sage 
tea  is  a  favorite  remedy  for  night-sweats— two  or  three  cups  of  it  cold  at  night— 
and  so  is  milk  and  cognac. 

If  there  is  loss  of  appetite,  small  doses  of  quinine,  compound  tincture  of  cin- 
chona, wine  of  cinchona,  and  other  bitter  remedies,  like  tinctura  amara  (P.  G.), 
are  sometimes  of  service.  It  is  also  frequently  a  good  thing  to  prescribe  "a  little 
muriatic  acid,  five  to  ten  drops  of  the  dilute  acid,  with  the  meals.  It  is  often  very 
hard  to  check  diarrhoea  in  phthisis.  Opium,  combined  with  tannin  or  acetate  of 
lead,  is  most  effective.  This  subject  will  be  discussed  more  fully  in  the  chapter  on 
intestinal  tuberculosis. 

We  often  prescribe  preparations  of  iron,  combined  sometimes  with  quinine  or 
arsenic  (vide  supra),  in  the  beginning  of  the  disease  to  improve  the  general  con- 
dition and  the  anaemia,  but,  as  experience  shows,  iron  is  contra-indicated  in 
patients  who  are  feverish  or  who  have  a  tendency  to  haemoptysis. 

The  treatment  of  the  diseases  complicating  phthisis  is  to  be  found  in  the  appro- 
priate chapters. 


236  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

CHAPTER  VII. 
ACUTE    GENERAL   MILIARY   TUBERCULOSIS. 

iEtiology. — Acute  miliary  tuberculosis  is  a  form  of  tuberculosis  wbicb  we  are 
justified  in  describing  particularly  because  of  its  auatomical  relations  and  of  its 
peculiar  clinical  bistory.  Tbe  disease  is  characterized  anatomically  by  tbe 
extremely  .abundant  development  of  miliary  tubercles  in  a  comparatively  short 
time  in  many  organs  of  the  body.  We  can  not  liken  this  process  to  anything 
but  an  overfilling  of  the  body  with  tubercle  bacilli,  which  in  some  way  reach  the 
different  organs  at  the  same  time,  and  there  give  rise  to  the  eruption  of  tubercles. 
Buhl  advanced  the  hypothesis  a  long  time  ago,  that  a  cheesy  focus  could  be 
found  somewhere  in  the  body  in  every  case  of  acute  miliary  tuberculosis,  and  that 
the  general  infection  of  the  body  resulted  from  the  absorption  of  these  cheesy 
masses  by  the  blood.  Later  investigations,  however,  have  given  us  a  much  more 
definite  explanation  of  the  nature  and  manner  of  this  general  infection.  Ponfick 
first  found,  in  some  cases  of  acute  miliary  tuberculosis,  an  extensive  tuberculosis 
of  the  thoracic  duct,  with  destruction  of  the  tubercular  new  growth.  It  is  easy  to 
see  how,  in  this  way,  a  large  amount  of  tubercular  material  could  be  brought 
directly  into  the  circulation,  from  the  free  communication  of  the  lymph-duct  with 
the  subclavian  vein,  and  thus  be  "  disseminated  "  through  tbe  different  organs  in 
a  short  time.  Still  more  frequently,  however,  the  tuberculosis  of  the  large  venous 
trunks,  discovered  by  Weigert,  especially  the  pulmonary  veins,  seems  to  be  the 
starting-point  for  an  acute  general  miliary  tuberculosis.  Usually  there  are  tuber- 
cular lymph-glands,  or  sometimes  other  foci  of  tubercular  disease,  which  unite 
with  the  wall  of  a  neighboring  vein,  gradually  break  through  it,  and  project  into 
its  lumen.  If  caseation  and  ulceration  result  in  this  spot,  the  infectious  material 
is  of  course  constantly  washed  off  by  the  blood-current  and  carried  away,  and 
thus  it  reaches  the  other  organs. 

Since  such  a  tubercular  focus — e.  g.,  a  tubercular  bronchial  gland — may  remain 
for  a  long  time  entirely  without  symptoms,  we  can  understand  how  miliary  tuber- 
culosis may  break  out  in  an  acute  form  in  persons  who  previously  seemed  perfectly 
well.  In  other  cases  the  patient  has  already  suffered  from  some  tubercular  affec- 
tion, until  suddenly  the  conditions  occur  somewhere  in  the  body  which  lead  to 
the  development  of  miliary  tuberculosis.  Thus  we  sometimes  see  it  break  out  in 
a  patient  who  has  ordinary  phthisis,  but  acute  miliary  tuberculosis  is  one  of  the 
rarities  in  advanced  phthisis.  If  we  find,  at  the  autopsy  of  a  case  of  acute  general 
miliary  tuberculosis,  old  phthisical  changes  in  the  lungs,  which  is  by  no  means 
very  common,  they  consist  of  old,  partly  cicatrized  foci,  pigment  indurations,  etc. 
We  see  miliary  tuberculosis  rather  frequently  as  a  sequel  to  pleuritic  effusion.  We 
have  already  previously  called  attention  to  the  fact  that  in  such  cases  the  pleurisy 
itself  is  a  tubercular  disease.  Miliary  tuberculosis  is  also  seen  in  people  with  old 
tubercular  affections  of  the  bones  and  joints,  like  coxitis  and  vertebral  caries,  with 
tubercular  swellings  of  the  lymph-glancls,  as  in  the  neck  and  the  axilla?,  or  with 
tuberculosis  of  the  genito-urinary  organs.  In  such  cases,  of  course,  the  tubercular 
affection,  which  is  discovered  during  life,  is  not  always  the  source  of  the  general 
miliary  tuberculosis,  but  the  discovery  of  the  existence  of  such  an  affection  is  of 
the  greatest  significance  in  diagnosis,  as  in  this  way  our  attention  is  strongly 
directed  to  the  possibility  of  a  general  tubercular  affection. 

In  some  cases  an  outbreak  of  miliary  tuberculosis  has  been  seen  to  follow  other 
acute  diseases,  like  typhoid,  or  measles. 

Pathological  Anatomy. — Except  for  the  presence  of  some  old  tubercular  affec- 
tion in  some  organ,  and  except  for  the  tuberculosis  of  a  vein  or  of  the  thoracic 


ACUTE  GENERAL  MILIARY  TUBERCULOSIS.  237 

duct,  which  are  as  a  rule  apparent,  and  which  have  heen  described  above,  the 
anatomical  lesion  in  acute  miliary  tuberculosis  consists  in  the  dissemination  of 
miliary  tubercles  through  a  large  number  of  the  organs  of  the  body.  The  lungs, 
the  liver,  and  the  spleen  are  constantly  affected;  almost  as  constantly  the  kid- 
neys, the  thyroid  gland,  the  marrow  of  the  bones,  the  heart,  and  the  choroid;  less 
constantly,  but  still  quite  frequently,  the  serous  membranes  and  the  meninges. 
The  miliary  nodules  may  be  found  in  large  numbers  in  all  the  organs  mentioned. 
They  may  in  part  be  easily  recognized  by  the  naked  eye,  and  in  the  lungs  tbey 
may  be  very  plainly  perceived  by  the  touch.  In  many  organs,  however,  especially 
in  the  liver  and  often  in  the  spleen,  they  are  hard  to  recognize  with  the  naked  eye, 
but  they  are  easily  discovered  by  the  microscope.  In  regard  to  the  histological 
structure  of  miliary  tubercles,  and  the  discovery  of  tubercle  bacilli  in  them,  we 
must  refer  to  what  has  been  said  in  the  chapter  on  pulmonary  tuberculosis,  but 
we  must  also  mention  that,  in  some  of  the  more  chronic  cases,  some  of  the  nodules 
may  grow  to  be  large  tubercular  foci,  from  the  size  of  a  lentil  to  that  of  a  pea. 
Less  developed  cases  of  miliary  tuberculosis  are  also  found,  in  which  only  a  lim- 
ited number  of  organs  are  attacked,  and  these  with  less  severity. 

Clinical  History. — The  clinical  symptoms  of  miliary  tuberculosis  depend  upon 
two  factors,  the  first  being  the  general  infection  of  the  body,  and  the  second  the 
local  tubercular  affection  of  certain  organs.  Although  in  many  organs  miliary 
tuberculosis  is  entirely  without  symptoms,  as  in  the  liver,  the  kidneys,  the  heart, 
and  the  marrow  of  the  bones,  in  two  organs — the  lungs,  and  more  especially  the 
brain — it  leads  to  the  most  marked  local  symptoms.  The  miliary  tuberculosis  of 
the  choroid,  discovered  by  Cohnheim  and  Manz,  is  also  without  symptoms,  but  it 
can  be  made  out  with  the  ophthalmoscope,  and  is  therefore  of  great  diagnostic 
value. 

Miliary  tuberculosis  affords  quite  different  pictures,  according  to  the  predom- 
inance of  one  or  the  other  of  the  groups  of  symptoms  mentioned.  We  distin- 
guish the  four  following  forms : 

1.  Miliary  Tuberculosis,  with  Predominant  Symptoms  of  General  Infection : 
the  so-called  Typhoid  Form. — This  form  may  in  part  greatly  resemble  typhoid 
fever.  The  patient,  who  previously  seemed  quite  well,  or  in  whom  some  local 
manifestation  of  tuberculosis  was  suspected,  falls  ill  with  gradually  increasing 
general  symptoms,  dullness,  loss  of  appetite,  headache,  and  fever.  Since  there  is 
no  local  affection  to  be  discovered  to  explain  the  symptoms,  the  disease  at  first 
may  well  be  taken  for  typhoid.  The  general  condition  grows  worse  constantly, 
the  fever  is  high  and  continually  rises,  and  cerebral  symptoms  appear.  In  some 
cases  an  exanthematous  eruption,  like  roseola,  may  increase  the  resemblance  to 
typhoid.  With  careful  observation,  however,  symptoms  are  almost  always  de- 
tected later  in  the  disease  which  are,  to  a  certain  degree,  characteristic  of  miliary 
tuberculosis,  and  are  due  to  the  existence  of  that  disease  either  in  the  lungs  or  in 
the  brain.  The  patient's  complexion  assumes  a  peculiar  pallor,  and  with  it  a  defi- 
nite cyanotic  hue.  The  respiration  becomes  remarkably  deep,  and  there  is  dysp- 
noea, or  signs  of  a  tubercular  meningitis  arise,  like  rigidity  of  the  neck,  loss  of 
consciousness,  disturbances  in  the  innervation  of  the  ocular  muscles,  etc.,  and 
death  follows  with  these  symptoms.  These  cases  last  from  ten  days  to  three 
weeks,  reckoning  from  the  beginning  of  the  severe  symptoms. 

2.  Miliary  Tubercidosis  with  Predominant  Pulmonary  Symptoms.— These 
cases,  too,  may  begin  quite  suddenly,  almost  like  an  acute  croupous  pneumonia, 
or  they  may  develop  gradually  with  quite  a  long  prodromal  stage.  From  the 
onset  the  symptoms  point  especially  to  disease  of  the  lungs  or  the  pleura.  The 
patient  complains  of  a  stitch  in  the  side,  cough,  and  dyspnoea,  and  there  is  also 
usually  much  general  weakness  and  fever.     Later  on,  the  pulmonary  symptoms 


238  DISEASES  OF  THE  RESPIRATORY   ORGANS. 

constantly  increase.  The  patient  has  extreme  dyspnoea,  and  we  can  often  make 
out  an  intense  diffuse  hronchitis  on  examining  the  lungs.  The  patient's  face  is 
pale,  cyanotic,  and  anxious.  Death  ensues  with  all  the  signs  of  insufficiency  of 
respiration.  The  course  is  usually  somewhat  more  protracted  than  in  the  typhoid 
form,  lasting  for  three  or  four  weeks  and  more. 

.  3.  Miliary  Tuberculosis  ivith  Predominant  Cerebral  Symptoms,  due  to  Tuber- 
cidar  Meningitis. — Tuberculosis  of  the  meninges  does  not  belong  among  the  reg- 
ular lesions  of  general  miliary  tuberculosis.  It  develops  in  about  half  the  cases, 
according  to  our  estimation ;  but  where  it  occurs  it  almost  always  gives  the  whole 
case  the  characteristic  imprint  of  tubercular  meningitis,  hy  which  the  other  symp- 
toms are  entirely  concealed.  The  predominant  symptoms  are  headache,  fever, 
stupor  increasing  to  deep  coma,  rigidity  of  the  hack  and  neck,  and  disturbances 
in  the  innervatiou  of  the  ocular  muscles.  In  such  cases  the  tubercular  menin- 
gitis is  often  the  only  thing  diagnosticated,  and  the  general  miliary  tuberculosis 
is  not  made  out  at  all.  In  the  cases  of  this  sort  which  we  have  seen,  a  remark- 
able, peculiarly  deep  and  accelerated  respiration,  even  in  the  deepest  coma,  was 
the  only  symptom  which  pointed  to  a  co-existing  miliary  tuherculosis  of  the 
lungs. 

The  symptoms  of  tubercular  meningitis  in  many  cases  predominate  in  this 
type  of  the  disease  from  the  onset,  but  in  other  cases  they  come  on  during  the 
attack  and  form  its  final  period.     The  duration  of  the  disease  varies  accordingly. 

4.  Miliary  Tuberculosis  with  a  Protracted  Course  and  Indefinite  Symptoms 
for  a  Long  Time — Intermitting  Form. — Besides  the  forms  already  mentioned, 
cases  occur  which  usually  take  quite  a  protracted  course,  lasting  for  eight  or  ten 
weeks,  and  having  such  indefinite  symptoms  that  a  definite  diagnosis  is  for  a  long 
time,  or  even  throughout  the  disease,  quite  impossible.  The  patient  complains  of  a 
number  of  general  symptoms,  such  as  headache  and  dullness,  and  also  of  thoracic 
symptoms,  for  which,  however,  we  can  find  on  examination  no  sufficient  basis. 
There  is  almost  always  fever,  usually  not  very  high,  and  with  a  very  irregular 
course;  hut  we  have  seen  a  regular  daily  rise  of  temperature  for  a  time  in  some 
cases,  and  attacks  of  fever  with  quite  a  severe  chill,  so  that  at  first  we  thought  of 
an  irregular  intermittent  fever— the  intermitting  form.  Later  on  the  symptoms 
gradually  increase.  The  apparently  inexplicable  loss  of  strength,  and  the  patient's 
anaemia  and  emaciation,  are  marked,  and  they  are  important  in  diagnosis.  Fi- 
nally, either  severe  pulmonary  symptoms  or  the  signs  of  tubercular  meningitis  set 
in,  to  which  the  patient  succumbs. 

We  must  mention  particularly  that  the  four  forms  of  miliary  tuberculosis  just 
described  are  only  the  types  of  the  disease.  In  individual  cases  we  often  meet 
with  variations  and  transitional  forms  between  these  types. 

Single  Symptoms.— 1.  General  Symptoms.— In  all  cases  of  acute  miliary  tuber- 
culosis the  general  condition  of  the  patient  is  very  serious.  Most  patients  have  a 
subjective  feeling  of  severe  illness,  although  they  make  little  special  complaint  of 
it  from  the  painless  character  of  the  disease.  As  the  disease  increases,  there  is 
often  a  marked  feeling  of  anxiety  and  oppression  besides  the  dyspnoea.  There  is, 
especially  in  the  face,  quite  a  peculiar  pallor,  characteristic  of  the  disease,  and 
associated  with  a  marked  cyanosis  of  the  lips  and  cheeks. 

2.  Fever. — Acute  miliary  tuberculosis  almost  always  runs  its  course  with  a 
more  or  less  high  fever,  a  course  without  fever  having  been  observed  in  only  a 
few  instances.  It  often  happens,  in  more  protracted  cases,  that  the  temperature 
may  be  nearly  normal  for  a  time,  or  only  slightly  elevated.  There  is  nothing  char- 
acteristic or  typical  in  the  course  of  the  fever.  In  the  cases  with  typhoid  symp- 
toms the  fever  is  usually  quite  high,  between  103°  and  105°  (39'5°-40-5°  C),  and 
rises  continually,  so  that  the  temperature  curve  may  be  exactly  like  that  of  ty- 


ACUTE  GENERAL  MILIARY  TUBERCULOSIS.  239 

plioid.  In  other  oases  the  fever  is  irregular  and  is  broken  by  ninny  remissions, 
remitting  or  intermitting  quite  regularly  for  some  time.  Death  ensues  with  a 
moderately  high  temperature  or  in  collapse.  In  cases  with  tubercular  menin- 
gitis there  is  also  a  marked  rise  of  temperature  at  the  close,  up  to  108°  (42°  C.j 
and  over. 

3.  Respiratory  Apparatus. — It  goes  without  saying  that  physical  examination 
of  the  lungs  may  give  no  definite  results.  Almost  every  positive  evidence  is 
often  wanting,  and  the  contrast  between  the  labored  breathing  and  dyspnoea  and 
the  insignificance  of  the  physical  signs  in  the  lungs  is  an  important  feature;  in 
diagnosis.  Auscultation,  as  a  rule,  gives  the  signs  of  an  intense  bronchial  catarrh ; 
we  hear  rhonchi  or  numerous  small  and  medium  moist  rales  all  over  both  lungs. 
The  respiratory  murmur  itself  is  usually  higher  in  pitch  than  normal,  and  in 
many  cases  it  is  obscure,  i*ough,  or  harsh.  In  one  of  our  cases  there  was  heard, 
over  a  circumscribed  area  of  the  lung,  a  wholly  peculiar,  sharp,  "lapping  "  sound 
on  inspiration,  which  we  have  never  heard  under  any  other  circumstances.  Jür- 
gensen  describes  a  soft  friction  sound,  due  to  miliary  tuberculosis  of  the  pleura. 
Percussion  usually  gives  no  objective  changes.  At  times  the  resonance  is  rather 
tympanitic,  or  slightly  dull  in  some  places. 

In  some  cases  circumscribed  pneumonic  infiltration  has  been  observed  in  the 
lungs  in  acute  miliary  tuberculosis,  which  may  give  rise  to  a  confusion  between 
miliary  tuberculosis  and  croupous  pneumonia,  from  the  presence  of  marked  dull- 
ness, crepitant  rales,  and  bronchial  respiration. 

We  must  mention,  finally,  that  in  some  of  the  cases  physical  examination  of 
the  lungs  shows  old  changes  in  them,  a  phthisical  affection  of  the  apex,  a  former 
pleurisy,  and  the  like.  Positive  evidence  of  such  old  tubercular  affections  may 
be  of  great  diagnostic  value  in  doubtful  cases. 

Dyspnoea  has  been  repeatedly  mentioned  among  the  symptoms  in  the  lungs. 
The  respiration  is  usually  very  much  accelerated,  especially  during  the  more 
advanced  stage  of  the  disease,  so  that  we  see  in  adults  forty,  sixty,  and  even 
seventy  respirations  a  minute.  The  respiration  is  also  very  deep,  and  is  sometimes 
associated  with  a  loud  noise.  As  a  rule  there  is  cough,  but  it  is  usually  trouble- 
some only  in  the  cases  with  severe  bronchitis.  It  is  often  very  slight.  The 
expectoration  is  usually  scanty,  and  it  is  not  characteristic.  Special  mention 
must  be  made  of  the  fact  that  tubercle  bacilli  are  absent  in  it,  unless  old  ulcerated 
tubercular  foci  are  present  at  the  same  time  in  the  lungs. 

4.  Circulatory  Apparatus.— The  pulse  is  frequent,  about  100  to  120  a  minute, 
often  weak  and  small,  and  sometimes  irregular,  especially  if  tubercular  menin- 
gitis co-exists.  The  miliary  tubercles,  which  anatomically  are  almost  always  to 
be  made  out  in  the  heart,  especially  in  the  endocardium,  cause  no  symptoms.  The 
presence  of  tubercle  bacilli  in  the  blood  will  be  mentioned  below. 

5.  Digestive  Apparatus.  —Vomiting  is  frequent  at  the  onset  of  the  disease. 
The  bowels  are  usually  constipated,  but  in  many  cases  there  is  a  moderate  diar- 
rhoea. The  loss  of  appetite,  the  thirst,  and  the  dry  tongue  are  due  to  the  general 
disease  and  the  fever.  The  spleen  is  usually  somewhat,  but  not  very  much, 
enlarged. 

6.  Nervous  Sy stein. — In  many  cases  where  the  pulmonary  symptoms  predomi- 
nate the  intellect  remains  quite  clear  until  the  last,  but  in  other  cases  cerebral 
symptoms,  like  headache,  dizziness,  stupor,  and  delirium,  come  on  quite  early,  and 
are  a  part  of  the  general  infection.  As  has  already  been  said,  the  nervous  symp- 
toms in  the  cases  combined  with  tubercular  meningitis  become  quite  prominent, 
but  in  individual  instances  it  may  be  hard  to  decide  whether  they  are  due  to  such 
a  complication,  or  are  merely  severe  general  symptoms. 

7.  Eyes. — The  ophthalmoscopic  examination  of  the  retina  is  of  special  diag- 


240  DISEASES   OF  THE  RESPIRATORY   ORGANS. 

nostic  importance,  since  the  diagnosis  may  be  niade  absolutely  certain  by  finding 
miliary  tubercles  in  the  choroid.  A  negative  result,  however,  is  never  decisive 
against  the  diagnosis,  since  the  tubercles  are  sometimes  absent,  or  at  least  are 
very  scanty.  Their  discovery  is  almost  always  difficult,  and  demands  much  prac- 
tice in  the  method  of  examination.  In  cases  with  tubercular  meningitis  we  some- 
times find  an  optic  neuritis. 

Diagnosis.— The  diagnosis  of  acute  general  miliary  tuberculosis  is  ordinarily 
and  justly  considered  very  difficult.  It  quite  often  happens  that  at  the  autopsy  a 
miliary  tuberculosis  is  found  which  was  not  even  suspected  during  life.  It  must 
be  confessed  that  frequently,  in  such  cases,  we  might  very  well  have  thought  of 
acute  tuberculosis.  If,  therefore,  the  possibility  of  acute  miliary  tuberculosis  is 
brought  to  our  attention  during  the  patient's  life,  we  can  occasionally  make  quite 
a  certain  diagnosis. 

The  severe  general  condition,  usually  associated  with  fever,  is  most  important, 
and  for  this  no  local  cause  can  be  found.  Then  come  the  pulmonary  symptoms, 
especially  the  peculiar  dyspnoea,  for  which  there  is  also  no  adequate  corresponding 
physical  change  to  be  discovered.  It  gives  decided  support  to  our  suspicion  if  we 
can  make  out  a  distinct  predisposition  to  tuberculosis,  either  hereditary  or  consti- 
tutional, or  the  history  of  a  previous  tubercular  affection,  especially  pleurisy,  and 
also  chronic  affections  of  the  bones.  The  peculiar  cyanotic  pallor  of  the  patient 
is  very  characteristic. 

On  these  factors  rests  the  differential  diagnosis  between  the  "  typhoid  "  form  of 
miliary  tuberculosis  and  typhoid  fever.  Marked  roseola  is  a  distinct  argument 
for  typhoid,  although  it  sometimes  occurs  in  miliary  tuberculosis,  and  so  are  the 
characteristic  intestinal  symptoms  of  typhoid,  like  meteorism  and  the  peculiar 
stools ;  but  we  must  not  forget  that  both  the  roseola  and  the  intestinal  symptoms 
may  be  absent  in  typhoid.  The  course  of  the  fever  must  always  be  considered 
in  the  differential  diagnosis.  It  is  much  more  frequently  irregular  and  atypical 
in  tuberculosis  than  in  typhoid.  Of  course,  the  temperature  curve  is  not  an  abso- 
lutely decisive  factor.  The  occasional  unequivocal  evidence  of  the  ophthalmo- 
scopic appearances  has  already  been  mentioned. 

In  many  cases  the  onset  of  meningeal  symptoms  may  aid  the  diagnosis.  Of 
course,  if  the  patient  is  not  seen  until  the  last  stages  of  meningitis,  especially 
where  there  is  an  incomplete  history,  the  diagnosis  is  next  to  impossible. 

Acute  tuberculosis  is  often  confounded  with  severe  bronchitis,  especially  in  old 
people  who  are  considered  emphysematous.  The  very  severe  general  condition, 
the  pallor,  the  rapid  loss  of  strength,  and  the  fever,  are  the  only  things  here  which 
call  our  attention  to  acute  tuberculosis,  and  render  the  diagnosis  possible. 

Finally,  the  discovery  of  tubercle  bacilli  in  the  blood  is  of  the  greatest  diag- 
nostic significance.  Their  detection  is  a  difficult  matter,  but  "Weichselbaum  and 
others  have  repeatedly  succeeded  in  finding  them. 

Prognosis.— The  cases  described  in  literature  as  "cured  miliary  tuberculosis " 
are  so  uncertain  in  their  diagnosis  that  they  can  not  be  regarded  as  convincing. 
We  must  therefore  consider  the  prognosis  as  absolutely  fatal.  The  differences  in 
the  course  of  the  disease  have  been  mentioned  above. 

Treatment. — Although  drugs  are  absolutely  powerless,  still  the  case  in  hand 
must  always  receive  treatment,  since  the  diagnosis  often  can  not  be  made  out  with 
absolute  certainty.  Our  prescriptions  are  purely  symptomatic.  The  cases  with 
a  typhoid  course  are  to  be  treated  just  like  typhoid,  with  baths,  stimulants,  etc. 
Tepid  baths,  and  also  local  applications  to  the  chest,  expectorants,  and  narcotics, 
are  indicated  when  the  thoracic  symptoms  predominate.  If  meningeal  symptoms 
set  in,  we  may  try  ice,  and  also  local  blood-letting,  with  iodide  of  potassium  inter- 
nally. 


GANGRENE  OF  THE  LUNGS.  241 

CHAPTER  VIII. 
GANGRENE  OF  THE  LUNGS. 

JEtiology. — The  sole  cause  of  pulmonary  gangrene — that  is,  the  death  and 
putrid  decomposition  of  the  lung-tissue — is  the  entrance  of  the  bacteria  of  putre- 
faction into  the  lungs.  The  opportunity  for  inhaling  them  is  certainly  very 
great,  but  the.  normal  organism  apparently  possesses  the  property  of  nullifying 
them  and  making  them  powerless.  Under  certain  conditions,  however,  they  take 
root  in  the  lung  and  cause  the  death  of  the  pulmonary  parenchyma,  which  then, 
as  a  result  of  the  presence  of  these  specific  bacteria  of  putrefaction,  succumbs  to 
that  peculiar  form  of  putrid  decomposition  known  as  "moist  gangrene." 

The  factor  which  most  frequently  gives  rise  to  the  development  of  pulmonary 
gangrene  is  the  entrance  of  organic  foreign  substances,  especially  bits  of  food,  into 
the  lungs.  The  bacteria  of  putrefaction  either  enter  the  lungs  with  the  foreign 
substance,  or  they  settle  there  later  and  set  up  a  putrid  decomposition,  first  in  that 
portion  of  the  lungs,  and  then  in  the  neighboring  lung-tissue.  The  entrance  of 
organic  foreign  substances  into  the  lungs  occurs  in  different  ways.  It  often  hap- 
pens from  swallowing  the  wrong  way,  or  from  an  accidental  inhalation.  In  this 
way  pulmonary  gangrene  may  arise  in  previously  healthy  people,  but  it  occurs 
especially  in  patients  who  are  very  low,  very  stupid,  and  soporose,  and  also  in  the 
insane,  in  patients  who  can  not  swallow  or  cough  well,  and  in  patients  with  paral- 
ysis of  deglutition,  as  in  bulbar  paralysis.  Bits  of  food  may  also  reach  the  lungs 
from  eructations  and  vomiting.  Thus  are  explained  the  cases  of  pulmonary  gan- 
grene which  occur  in  patients  with  cancer  of  the  stomach,  and,  still  more  fre- 
quently, with  cancer  of  the  oesophagus.  Putrid  organic  material  may  also  reach 
the  lungs  from  ulcerative  and  ichorous  processes  in  the  mouth,  the  pharynx,  and 
the  larynx.  In  cancer  of  the  tongue,  the  pharynx,  and  the  larynx,  in  other  ulcer- 
ative processes,  and  in  injuries  or  wounds  from  operations  in  the  mouth  and  phar- 
ynx that  have  become  septic,  pulmonary  gangrene  may  develop  quite  readily. 
Finally,  septic  foci  in  the  vicinity  may  extend  to  the  Kings  or  perforate  into  a 
bronchus.  In  this  way  a  pulmonary  gangrene  may  arise  from  the  perforation 
through  the  pleura  into  the  lungs  of  an  ulcerated  cancer  of  the  stomach  or  a 
gastric  ulcer,  or  in  rare  cases  from  vertebral  caries,  or  from  sanious  lymph-glands. 

In  some  cases  the  cause  of  the  piilmonary  gangrene  can  not  be  made  out,  since 
the  entrance  of  a  foreign  substance  has  perhaps  been  wholly  unnoticed,  as  may 
happen  in  children,  or  during  sleep.  We  had  a  grown-up  young  woman  under 
observation  for  a  long  time  with  pulmonary  gangrene,  and  one  day  she  coughed 
up  several  fragments  of  chicken-bones,  but  she  could  give  no  account  of  how  they 
entered  the  lungs. 

Experience  teaches  us  that  pulmonary  gangrene  is  more  apt  to  develop  in 
persons  with  a  general  weak  nutrition,  in  old,  marantic  people  and  drunkards, 
than  in  those  who  are  healthy.  The  tendency  of  patients  with  diabetes  mellitus 
to  pulmonary  gangrene  is  remarkable. 

Pulmonary  gangrene  often  develops  secondarily  to  some  other  pulmonary 
affection.  We  have  already  spoken  of  the  relations  between  it  and  foetid  bron- 
chitis. Foetid  bronchitis,  on  the  one  hand,  often  leads  to  pulmonary  gangrene 
through  an  extension  of  the  process  to  the  alveoli ;  and,  on  the  other  hand,  where 
there  is  a  gangrenous  focus  in  the  lungs,  the  bronchi  are  often  infected  to  a  wide 
extent  by  the  putrid  secretion  coming  from  it,  and  then  there  arises  foetid  bron- 
chitis. Both  diseases  often  run  into  each  other  without  any  sharp  boundary ;  but 
gangrene  may  develop  secondarily  in  other  affections  of  the  lungs.  A  new  infec- 
tion with  putrid  material,  however,  is  always  requisite,  and  the  affection  of  the 
16 


242  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

lungs  that  already  exists  furnishes  merely  a  favorahle  soil.  This  is  the  only 
explanation  of  the  process  when  croupous  pneumonia  "runs  into  gangrene,"  or 
when  gangrene  develops  in  catarrhal  pneumonia,  in  bronchiectasis,  or  in  phthisis. 

Although  the  agents  of  putrefaction  enter  the  lungs  through  the  bronchi  in 
most  of  the  methods  of  origin  of  pulmonary  gangrene  that  have  been  mentioned, 
they  may  also  be  transported  into  the  lungs  by  the  blood-current.  We  call  these 
forms  embolic  gangrene.  We  find  such  gangrenous  nodules  in  the  lungs  in 
connection  with  extensive  gangrenous  bed-sores,  puerperal  processes,  suppurative 
caries  of  the  bones,  etc.  In  these  cases  the  putrid  material  enters  a  vein  from  the 
seat  of  the  primary  process  and  is  brought  to  the  lungs,  and  here  we  find,  as  a 
result  of  the  putrid  character  of  the  embolus,  not  a  simple  infarction,  but  an 
embolic  gangrene. 

Pathological  Anatomy. — We  more  frequently  find  pulmonary  gangrene  in  the 
lower  lobes  than  in  the  upper,  corresponding  to  its  mode  of  origin.  Either  both 
lungs  are  affected  or  only  one,  and  the  right  somewhat  more  frequently  than  the 
left.  We  distinguish  a  diffuse  and  a  circumscribed  form,  according  to  the  extent 
of  the  gangrene.  Embolic  gangrene  belongs  to  the  latter  form,  and  its  nodules, 
by  preference,  lie  near  the  pleural  surface. 

We  can  easily  recognize  the  anatomical  changes  in  gangrene.  The  lung-tissue 
is  changed  to  a  discolored,  dirty,  greenish-gray  mass,  which  gradually  and  pro- 
gressively becomes  dissolved,  forming  a  most  foul-smelling  ichor.  We  find,  left 
in  it,  necrotic  fragments  of  tissue  and  vessels.  Gangrene  cavities,  with  irregular, 
ragged  walls,  are  formed  from  the  partial  expectoration  of  the  softened  gangre- 
nous nodule.  The  lung-tissue  in  the  vicinity  of  the  peculiar  nodule  is  to  a  greater 
or  less  extent  inflamed,  partly  in  the  form  of  catarrhal  pneumonia,  partly  in  the 
form  of  circumscribed  croupous  pneumonia.  The  inflamed  parts  in  the  vicinity 
are  gradually  involved  in  the  gangrene,  so  long  as  the  process  extends,  but  finally 
a  suppurating  line  of  demarkation  may  be  formed  about  the  gangrene,  the  whole 
gangrenous  fragment  is  in  a  measure  sequestrated,  encapsuled,  and  gradually 
expelled,  and  so  healing  becomes  possible.  We  have  already  stated  that  foetid 
bronchitis  may  arise  from  a  gangrenous  nodule. 

Whenever  a  gangrenous  nodule  reaches  the  pleura,  a  purulent  and  usually  a 
sanious  pleurisy  follows  from  direct  infection.  Pneumothorax  may  arise  from 
perforation  of  a  gangrenous  cavity. 

Clinical  History. — The  symptoms  of  gangrene  depend  for  the  most  part  upon 
the  local  affection  in  the  lung.  The  condition  of  the  expectoration  is  characteris- 
tic, and  it  alone  may  decide  the  diagnosis. 

In  many  of  its  conditions  the  expectoration  greatly  resembles  that  of  foetid 
bronchitis,  and  indeed  a  great  part  of  it  does  not  come  directly  from  the  gangre- 
nous nodule,  but  is  the  secretion  of  the  diseased  bronchi.  The  penetrating  stench 
of  the  sputum,  a  most  repulsive,  putrid  odor,  is  very  striking.  The  patient's  breath 
and  cough  also  have  this  bad  smell,  which  infects  the  whole  vicinity.  The  amount 
of  the  sputum  is  usually  large;  it  may  reach  ten  or  twenty  ounces  (200-500  c.  c.) 
in  twenty-four  hours.  If  the  sputum  is  collected  in  a  glass  it  forms  three  layers, 
as  in  the  sputum  of  foetid  bronchitis — an  upper  layer,  muco-purulent,  greasy,  con- 
sisting in  part  of  nummular  sputa,  and  covered  with  much  froth  ;  a  middle  serous 
layer,  in  which  some  firm  masses  from  the  upper  layer  float ;  and  a  lower  layer, 
almost  wholly  of  pus,  but  greasy  and  greenish-yellow,  which  usually  contains 
many  large  and  small  plugs  and  shreds  of  tissue.  We  find  in  these  plugs,  on 
microscopic  examination,  beautifully  twisted  needles  of  the  fat  acids  (see  Fig.  21, 
p.  156)  imbedded  in  countless  bacteria,  fat-drops,  and  detritus,  and  often  collected 
in  large  bundles ;  but  besides  these  we  find  in  it  the  constituents  of  the  paren- 
chyma of  the  lungs,  and  this  alone  is  the  decisive  factor  in  distinguishing  between 


GANGRENE  OF  THE  LUNGS.  243 

pulmonary  gangrene  and  simple  foetid  bronchitis.  Traube's  theory — that  elastic 
fibers  are  not  found  in  the  expectoration  in  pulmonary  gangrene,  or  that  they  are 
rare,  because  the  elastic  tissue  also  is  destroyed  by  the  gangrene — is  untrue.  We 
have  almost  always  found  elastic  tissue  in  abundance  in  the  expectoration,  and 
also  other  fragments  of  parenchyma,  lung-pigment,  etc.  Which  of  the  coarse, 
rod-like  bacteria,  described  by  Leyden  and  Jaffe  as  leptothrix  pulmonalis,  are  the 
special  bacteria  of  gangrene  is  not  decided.  The  chemical  examination  of  the 
sputum  shows  the  presence  of  those  substances  which  may  always  be  found  in  the 
putrefaction  of  organic  matter— tyrosine,  leucine,  ammonia,  sulphuretted  hydro- 
gen, butyric  acid,  valerianic  acid,  caprylic  acid,  etc.  The  fresh  sputum  usually 
has  an  alkaline  reaction,  but  on  standing  it  becomes  acid. 

Many  cases  of  gangrene  lead  to  erosion  of  the  vessels  and  severe  haemoptysis. 
Slight  admixtures  of  blood  in  the  sputum  are  not  infrequent. 

The  other  symptoms  on  the  part  of  the  lungs  are  not  especially  characteristic 
of  gangrene.  Most  patients  complain  of  cough,  pain  in  the  side,  and  more  or  less 
severe  dyspnoea.  Physical  examination,  as  a  rule,  permits  us  to  make  out  the  seat 
of  the  nodule,  but  not  always,  since  the  physical  signs,  of  course,  depend  upon  the 
situation  and  extent  of  the  gangrene.  Small  nodules,  situated  centrally,  often 
give  no  objective  evidence  of  their  presence.  Every  extensive  infiltration,  however, 
must  cause  dullness  on  percussion.  Over  the  area  of  dullness  we  hear  bronchial 
respiration,  and  usually  quite  numerous  moist  rales.  If  a  gangrenous  cavity  is 
formed,  the  physical  examination  may  show  plain  symptoms  of  a  cavity — tym- 
panitic resonance  on  percussion,  amphoric  respiration,  large  moist  rales,  etc. 

The  physical  signs  are  sometimes  due  to  the  accompanying  pleurisy ;  the  dull- 
ness is  more  intense,  the  respiratory  murmur  and  the  vocal  fremitus  are  dimin- 
ished, and  the  adjacent  organs  are  displaced  by  the  abundant  effusion ;  but  an 
absolute  diagnosis  of  an  accompanying  pleurisy  is  often  to  be  made  only  by  an 
exploratory  puncture.  We  have  already  spoken  of  the  occasional  development 
of  pneumothorax. 

In  many  cases  there  is  fever,  of  quite  an  irregular  character  and  of  very  vary- 
ing intensity.  In  the  cases  where  the  gangrenous  nodule  is  sequestrated,  and 
where  the  secretion  can  be  freely  emptied  through  the  bronchi,  and  where,  accord- 
ingly, there  is  no  absorption  of  septic  material  into  the  blood,  the  fever  also  may 
be  entirely  absent. 

We  often  see  gastric  and  intestinal  symptoms  in  pulmonary  gangrene,  the  dis- 
turbance being  without  doubt  due  to  swallowing  some  of  the  foetid  sputum.  Many 
patients  complain  of  loss  of  appetite,  and  sometimes  of  vomiting  or  diarrhoea. 
We  also  see  rheumatic  pains  in  the  joints  and^muscles,  as  in  foetid  bronchitis.  It 
is  also  worthy  of  note  that  secondary  abscess  of  the  brain  has  been  repeatedly 
observed  in  pulmonary  gangrene  (see  page  741).  We  must  bear  this  in  mind  if 
very  severe  cerebral  symptoms,  like  somnolence  or  paralysis,  develop  in  the  course 
of  a  gangrene. 

The  general  course  of  the  disease  shows  very  great  variations.  In  all  cases 
where  the  pulmonary  gangrene  is  secondary  to  some  other  affection,  the  course 
and  the  general  type  of  the  disease  depend  very  largely  upon  the  primary  attack, 
but  the  cases  of  idiopathic  gangrene  also  present  great  variations.  The  onset  is 
either  quite  gradual  and  slow,  or  quite  acute,  and  associated  with  fever  and  tho- 
racic symptoms.  The  stinking  expectoration  and  the  bad  odor  from  the  patient's 
mouth  first  direct  the  attention  to  the  existence  of  putrid  processes  in  the  lungs. 
The  disease  is  usually  very  chronic,  lasting  for  months  or  even  years.  Many 
remissions  and  intermissions  occur.  With  proper  care  and  treatment  we  may  see 
a  clear  improvement,  and  often  apparently  a  complete  cessation  of  the  disease. 
The  bad  odor  ceases,  the  expectoration  diminishes  or  disappears  entirely,  and  the 


244  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

patient's  strength  and  nutrition  become  almost  normal ;  but  relapses  may  occur 
after  long  intervals.  Where  the  affection  is  of  slight  extent  we  may  even  see  a 
complete  recovery. 

Pulmonary  gangrene  always  takes  a  worse  course  in  previously  weak  and 
marantic  persons,  and  an  unfavorable  termination  may  follow  in  a  comparatively 
short  time.  Death  ensues  either  from  a  general  loss  of  strength,  as  a  result  of  the 
disease,  or  from  complications,  such  as  pulmonary  haemorrhage,  ichorous  pleurisy, 
pneumothorax,  or  abscess  of  the  brain.  Rupture  of  an  ichorous  empyema  out- 
wardly, or  into  the  peritoneum,  or  into  other  cavities,  is  rare. 

Special  mention  must  be  made  of  the  fact  that  the  symptoms  of  pulmonary 
gangrene  are  not  always  so  very  pronounced.  In  people  who  are  weak  and  run 
down  we  often  see  pulmonary  gangrene  at  the  autopsy,  although  during  life  there 
have  been  no  marked  symptoms,  not  even  offensive  sputum  nor  the  fcetor  from 
the  mouth 

Diagnosis.— The  diagnosis  can  be  made  with  certainty  only  when  the  charac- 
teristic sputum  is  present.  We  can  decide  whether  the  sputum  comes  from  a 
foetid  bronchitis  or  from  the  foetid  contents  of  a  bronchiectasis,  or  from  actual 
gangrene,  only  by  finding  under  the  microscope  the  remains  of  lung-tissue  in  the 
expectoration.  Physical  examination  in  gangrene,  at  least  in  part  of  the  cases, 
also  gives  the  signs  of  infiltration  or  of  cavity-formation  in  the  lungs. 

Prognosis. — The  prognosis  depends  first  upon  the  nature  of  the  underlying 
disease,  and  then  upon  the  extent  of  the  affection,  the  strength  of  the  patient,  and 
the  possibility  of  sufficient  care  and  proper  treatment.  If  the  process  in  the  lung 
becomes  sequestrated,  marked  improvement  may  follow,  even  in  the  severest  con- 
ditions; but  we  must  always  remember  that  a  i^elapse  is  possible.  We  have 
already  mentioned  the  dangers  which  may  cause  a  fatal  termination  in  pulmo- 
nary gangrene. 

Treatment. — Prophylaxis  plays  an  important  part  in  those  cases  where  there 
is  danger  of  the  entrance  of  bits  of  food  into  the  air-passages  from  defective  deglu- 
tition. We  must  think  of  the  possibility  of  this  with  all  patients  who  show  great 
stupor,  and  also  with  patients  who  have  paralysis  of  deglutition,  in  order  to  watch 
them  while  taking  food,  and  eventually  to  try  artificial  feeding  with  the  oesopha- 
geal tube. 

The  treatment  of  already  existing  pulmonary  gangrene  has,  as  its  chief  aim,  to 
check  the  putrid  processes  of  decomposition  in  the  lungs.  Unfortunately,  the 
remedies  at  our  command  are  not  in  all  cases  sufficient  for  this.  The  different 
disinfecting  inhalations  are  the  most  effective.  They  are  used  in  the  same  way  as 
in  foetid  bronchitis  (vide  supra).  Turpentine  deserves  the  most  confidence,  and 
it  may  also  be  given  internally  with  good  results.  According  to  Lepine,  however, 
terpine  acts  still  better  than  does  turpentine.  We  may  also  call  attention  to 
inhalations  with  carbolic  acid,  Curschmann's  carbolic  mask,  inhalations  with 
salicylic  and  boracic  acids  (4  parts  of  salicylic  and  20  of  boracic  acid  to  1,200  of 
distilled  water),  bromine  (bromine  and  bromide  of  potassium,  2  parts  of  each  to 
1,000  of  water),  and  similar  substances. 

Besides  oil  of  turpentine,  other  internal  remedies  are  recommended:  half  a 
grain  to  a  grain  (grm.  0'03-0-06)  of  acetate  of  lead  every  two  hours,  creasote,  car- 
bolic acid,  etc.  Their  action  is  uncertain.  Of  late,  myrtol  has  been  greatly 
extolled.  It  is  given  in  capsules  containing  grains  ijss.  (0"15),  of  which  two  or 
three  are  to  be  taken  every  two  hours. 

The  general  treatment  of  the  patient  is  very  important — he  should  have  good 
food,  and  live  in  as  good  air  as  possible.  We  must  treat  the  pain  in  the  chest  and 
the  cough  symptomatically,  local  applications  and  morphine  being  most  useful. 
The  fever  seldom  gives  occasion  for  direct  interference.     In  general,  cold  spong- 


DISEASES  FROM  THE  INHALATION  OF  DUST.  245 

ing,  or  else  tepid  baths,  suffice,  so  that  quinine  is  only  rarely  to  be  used.  We 
may  try  to  relieve  the  gastric  and  intestinal  symptoms  by  giving  antiseptics  in- 
ternally, especially  by  Small  doses  of  muriatic  acid,  salicylic  acid,  or  creasote,  as 
well  as  by  the  ordinary  remedies,  such  as  bitters  and  opium. 

If  a  secondary  ichorous  pleurisy  develops,  with  or  without  pneumothorax, 
removal  of  the  fluid  by  operation  is  necessary,  if  the  patient  has  sufficient  strength 
to  bear  it. 


CHAPTER  IX. 

DISEASES  FROM   THE   INHALATION   OP  DUST. 

( Pneumonoconiosis.) 

Although  there  are  a  number  of  important  contrivances  in  the  respiratory 
apparatus  to  impede  the  entrance  of  foreign  substances  contained  in  the  air  into 
the  lungs,  still,  if  a  person  remains  in  a  dusty  atmosphere,  so  many  particles  of 
dust  may  be  inhaled  that  they  are  not  without  effect  on  the  lung-tissue.  The  dis- 
eases from  the  inhalation  of  dust  are  usually  purely  professional  diseases,  which 
occur  especially  in  workmen  whose  occupation  brings  with  it  the  continual  inhala- 
tion of  some  kind  of  dust.  Since  we  do  not  have  to  deal  with  a  specific  influence, 
as  in  the  inhalation  of  infectious  substances,  but  usually  only  with  a  mechanical 
effect;  all  diseased  conditions  excited  by  the  different  sorts  of  dust  may  be  treated 
in  common. 

We  must  first  mention,  however,  a  condition  of  the  lungs  which  can  scarcely 
be  regarded  as  pathological,  although  it  has  its  origin  in  the  constant  inhalation 
of  dust,  especially  of  coal-dust — the  ordinary  black  pigmentation  of  the  lungs. 
There  can  now  no  longer  be  any  doubt,  although  there  was  once  a  long  dispute 
about  it,  that  the  black  pigment  in  the  lung  comes,  in  large  part  at  least,  from  the 
inhalation  of  carbon.  The  particles  of  carbon  pass  into  the  lungs  themselves,  and 
thence  into  the  bronchial  glands  by  means  of  the  lymphatics.  Only  a  part  of  the 
coal-dust  inhaled  is  removed  with  the  expectoration,  and  it  may  easily  be  found 
in  it  microscopically,  and  often  by  the  naked  eye,  as  we  see  it  in  the  well-known 
black  expectoration  which  we  often  have  in  the  morning,  if  we  have  spent  the 
previous  evening  in  a  room  filled  with  smoke.  In  Germany,  Traube  was  the  first 
to  discover  the  particles  of  carbon  in  the  expectoration  of  a  charcoal-burner.  In 
the  man's  lungs,  after  death,  the  vegetable  formation  of  these  particles  could  be 
recognized,  and  Traube  gave  the  correct  explanation  of  them.  In  workmen  who 
inhale  large  amounts  of  charcoal-dust,  anthracite  coal-dust,  soot,  or  graphite,  the 
"normal"  pigmentation  of  the  lung  passes  into  a  pathological  condition,  anthra- 
cosis  pulmonum. 

Zenker  first  discussed  comprehensively  the  fact  of  the  entrance  of  the  different 
sorts  of  dust  into  the  lungs  and  the  consequent  results.  Besides  the  anthracosis 
already  mentioned,  the  pulmonary  disease  from  inhaling  the  dust  of  flint  and 
other  stones  is  of  especial  importance,  the  so-called  stone-cutter's  lung — chalicosis 
pulmonum — and  also  that  from  inhaling  metallic  dust,  especially  oxide  of  iron — 
siderosis  pulmonum.  The  "  stone-lungs  "  have  been  observed  in  workmen  in  the 
stamping-rooms  of  glass-factories,  in  mill-stone  cutters,  stone-polishers,  stone- 
hammerers,  plasterers,  workers  in  porcelain,  masons,  slate-quarrymen,  potters, 
etc.  "  Metal-dust  lungs  "  occur  in  file-cutters,  iron- workers,  mirror-polishers,  and 
especially  in  grinders,  who  inhale  a  mixture  of  stone-  and  iron-dust.  The  first  case 
of  a  "red  iron  lung"  was  observed  by  Zenker,  in  a  girl  wbo  had  inhaled  a  thick 
dust  of  iron  for  ten  or  twelve  hours  a  day.     Her  work  was  to  color  blotting-paper 


246  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

with  a  powder  of  red  oxide  of  iron.  Among  the  other  forms  of  dust  which  may 
give  rise  to  pulmonary  disease  we  may  mention  tobacco-dust,  cotton-dust,  saw- 
dust, and  flour-dust. 

The  anatomical  changes  in  the  "  dust-lungs "  consist  of  a  chronic  bronchitis, 
and  especially  a  chronic  interstitial  inflammation,  leading  to  the  formation  of 
connective  tissue,  and  caused  by  the  mechanical  irritation  of  the  foreign  body. 
The  lungs  are  studded  with  nodules,  which  feel  hard  to  the  touch,  and  which 
«rate  on  section  with  a  knife.  All  of  these  nodules  consist  of  firm  connective 
tissue,  in  which  the  particles  of  stone  or  iron  are  encapsuled.  By  the  union  of 
single  nodules  we  may  get  more  extensive  induration  and  cicatricial  formation. 
Chemical  examination  of  such  lungs  gives,  as  might  be  supposed,  a  large  amount 
of  silicic  acid,  iron,  etc. 

In  most  of  the  cases  which  come  to  autopsy  we  find  further  changes  in  the 
lungs,  which  are  not  the  immediate  result  of  the  inhalation  of  dust,  but  consist  of 
sequelae  and  complications.  Chronic  diffuse  bronchitis  in  the  worker  in  dust, 
like  any  other  chronic  bronchitis,  may  give  rise  to  pulmonary  emphysema,  and 
later  to  cardiac  hypertrophy,  etc.  We  very  often  find  in  the  lungs  co-existing 
and  pronounced  tubercular  changes.  It  need  not  be  stated  more  fully  that  these 
changes  are  not  the  direct  result  of  the  inhalation  of  dust,  but  that  the  changes  in 
the  lungs  set  up  by  such  an  inhalation  furnish  merely  a  favorable  soil  for  infec- 
tion with  tuberculosis.  In  most  cases,  the  "  dust-lungs  "  acquire  a  marked  clinical 
significance  chiefly  from  the  sequelae  mentioned— namely,  emphysema  and  tuber- 
culosis. The  circumscribed  nodules  of  interstitial  pneumonia  have  no  very  marked 
symptoms  following  them.  In  all  cases  where  there  is  a  fatal  termination,  with 
pulmonary  symptoms,  we  should  regard  the  immediate  action  of  the  dust  as  much 
less  the  cause  of  death  than  are  the  secondary  diseases. 

The  actual  points  to  be  considered  in  judging  of  the  clinical  symptoms  of  the 
diseases  from  inhaling  dust  are  contained  in  what  has  been  said.  The  symptoms 
are  those  of  common  chronic  bronchitis,  or  pulmonary  emphysema,  or  phthisis, 
and  attention  to  the  injurious  influences  associated  with  the  patient's  calling  is 
the  only  possible  way  of  making  a  diagnosis,  but  in  individual  cases  it  may  always 
be  a  matter  of  doubt  how  far  other  accidental  causes  of  disease  may  come  into  play. 

The  prognosis  depends,  in  the  first  place,  upon  whether  the  patient  can  be 
removed  from  the  action  of  these  injurious  influences  or  not,  but  we  must  also 
mention  the  fact,  which  has  been  often  observed,  that  many  people  get  somewhat 
used  to  the  dust.  After  they  have  once  recovered  from  the  initial  bronchitis,  such 
people  can  live  in  an  atmosphere  of  dust  for  a  long  time  without  any  noticeable 
injury. 

The  prophylaxis  of  diseases  from  inhaling  dust  forms  an  extended  chapter  in 
the  hygiene  of  occupations,  which  we  can  not  dwell  upon  here.  The  workman 
must  be  taught  the  danger  to  which  he  is  exposed,  and  the  danger  itself  must  be 
diminished  as  much  as  possible  by  sufficient  ventilation  of  the  work-rooms,  by 
cleanliness,  and,  under  some  circumstances,  by  a  change  in  the  technicalities  of 
the  business. 

We  need  not  give  any  special  data  regarding  the  treatment  of  diseases  from 
inhaling  dust.  They  are  founded  on  the  same  principles  as  are  given  for  the 
treatment  of  chronic  bronchitis,  emphysema,  and  chronic  pulmonary  tuberculosis. 


EMBOLIC  PROCESSES  IN  THE  LUNGS.  247 

CHAPTER  X. 

EMBOLIC   PROCESSES   IN   THE   LUNGS. 

(Ila-morrhaijic  Infarction  of  the  Lungs.") 

iEtiology. — The  sources  from  which  the  material  for  an  embolic  plugging  of 
branches  of  the  pulmonary  artery  comes  lie  either  in  the  right  side  of  the  heart  or 
in  the  veins  of  the  body.  Pathological  anatomy  teaches  us  how  often  thrombi  are 
formed  in  the  veins,  especially  in  the  veins  of  the  lower  extremities  and  in  the 
pelvic  veins,  and  in  the  right  side  of  the  heart,  in  the  recesses  between  the  tra- 
becule, in  the  auricles,  on  the  valves  and  the  chordae  tendineae,  and  at  the  apex  of 
the  ventricle.  The  particles,  torn  loose  from  thrombi  so  situated,  are  carried  on 
by  the  blood-current,  reach  the  lungs,  plug  a  larger  or  a  smaller  branch  of  the 
pulmonary  artery,  according  to  the  size  of  the  particles,  and  thus  cause  further 
changes  in  the  lung-tissue.  Since  the  branches  of  the  pulmonary  artery  are  "  ter- 
minal arteries,"  and  since  thus  the  vascular  territory  belonging  to  each  branch 
can  not  be  supplied,  or  can  be  supplied  only  to  a  small  amount,  with  blood  by 
collateral  circulation  from  other  vessels,  the  closure  of  a  branch  of  the  artery 
shuts  the  territory  supplied  by  it  out  of  the  circulation.  The  pressure,  in  the  part 
of  the  vessel  lying  peripherally  to  the  point  of  plugging,  becomes  almost  nil,  and, 
as  a  result,  there  is  a  backward  current  into  the  region  shut  off,  flowing  from  the 
capillaries  in  the  vicinity,  and  even  from  the  veins  belonging  to  it.  Thus  we  get 
atypical  "engorgement."  The  walls  of  the  capillaries  and  veins,  in  which  the 
normal  blood-current  has  ceased,  lose  their  natural  consistency  as  a  result  of  this. 
The  vascular  walls  become  abnormally  pervious.  The  fluid  of  the  blood,  the 
white  blood-corpuscles,  and  also  very  many  red  blood-corpuscles,  penetrate  through 
the  walls  of  the  vessels  into  the  surrounding  tissue,  and  change  it  into  the  so-called 
haemorrhagic  infarction. 

Every  embolic  closure  of  a  branch  of  the  pulmonary  artery  does  not  necessarily 
result  in  the  formation  of  an  infarction.  Upon  the  sudden  plugging  of  a  main 
trunk,  or  of  several  large  branches  of  the  pulmonary  artery,  death  may  ensue  at 
once,  so  that  naturally  all  further  changes  in  the  lung-tissue  cease.  We  also  find 
quite  frequently,  especially  in  central  portions  of  the  lung,  embolism  of  single 
branches  of  the  pulmonary  artery,  without  the  formation  of  an  infarction.  In 
such  cases  there  must  necessarily  be  a  little  circulation  in  the  vascular  territory 
which  has  been  shut  off,  either  by  anastomoses  between  the  territory  of  the  pul- 
monary artery  and  that  of  the  bronchial  or  mediastinal  artery,  or  by  the  neigh- 
boring capillaries,  whose  arteries  of  supply  remain  open. 

The  changes  thus  far  described  are  the  result  of  a  purely  mechanical  closure  of 
a  pulmonary  artery.  We  have  noticed  this  especially  where  simple  fibrinous 
plugs  have  given  the  occasion  for  the  embolic  process.  Pulmonary  infarctions 
are  most  frequent  in  chronic  heart  disease,  in  all  forms  of  primary  and  secondary 
dilatation  of  the  heart,  but  especially  in  disease  at  the  mitral  orifice,  and  in  mitral 
stenosis.  Thrombus  formation  is  frequent  in  the  dilated  right  side  of  the  heart, 
and  furnishes  material  for  pulmonary  emboli;  but  these  emboli  are  seen  in  all 
other  possible  conditions  of  disease,  in  which  thrombosis  in  the  right  side  of  the 
heart  or  in  the  veins  may  occur. 

The  changes  in  the  lungs  assume  quite  a  different  appearance  if  the  embolic 
material  is  not  simple  fibrine,  but  if  it  contains  at  the  same  time  some  specific 
infectious  matter.  If  emboli  reach  the  lungs  from  an  aciite  malignant  endocar- 
ditis in  the  right  side  of  the  heart,  or,  as  is  most  frequently  the  case,  from  a  puru- 
lent (septic)  phlebitis  anywhere  in  the  body,  giving  rise  to  a  puriform,  liquefying 
thrombus,  the  specific  factors  in  inflammation — that  is,  bacteria — get  into  the 


2±S  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

luno-s.  Thus  arise  embolic  abscesses  arid  embolic  gangrenous  nodules  in  the  lungs. 
We  have  already  spoken  of  the  latter,  and  the  former  are  among  the  most  constant 
lesions  in  every  typical  pyaemia. 

The  fundamental  facts  as  to  the  occurrence  and  significance  of  embolic  pro- 
cesses in  general,  and  those  located  in  the  lungs  in  particular,  were  discovered  by 
Virchow.  For  the  fuller  understanding  of  the  results  of  embolic  closure  of  the 
vessels  we  must  thank  chiefly  the  labors  of  Cohnheim. 

Pathological  Anatomy. — Haemorrhage  infarctions  may  involve  one  or  more 
lobules,  or  almost  a  whole  lobe  of  the  lung,  according  to  the  situation  of  the 
embolus.  Most  infarctions  are  situated  at  the  periphery  of  the  lung,  and  have 
approximately  a  conical  shape,  corresponding  to  the  extent  of  the  region  of  the 
vessel.  The  base  of  the  cone  lies  against  the  surface  of  the  pleura.  It  generally 
projects  a  little  above  that  surface,  and  its  dark  color  can  usually  be  plainly  rec- 
ognized through  it.  The  pleura  itself  is  the  seat  of  a  fibrinous  inflammation  at 
the  point  to  which  the  infarction  reaches,  and  sometimes  for  a  large  space  around 
it.  The  conical  shape  of  the  infarction  is  plainly  recognized  on  section.  The 
lung-tissue  is  changed  to  a  firm,  fragile,  uniformly  black-red  tissue,  devoid  of  air. 
The  embolus  can  usually  be  readily  found  in  the  branch  of  the  pulmonary  artery 
leading  to  the  infarction.  Under  the  microscope  we  see  a  diffuse  infiltration  of 
tissue,  with  red  blood-corpuscles  in  the  infarcted  portion.  The  alveoli  and  finer 
bronchi  are  also  filled  with  coagulated  blood.  Under  favorable  circumstances,  in 
cases  of  longer  standing,  the  blood  may  be  reabsorbed  in  part.  The  lung  again 
contains  air,  but  it  remains  much  pigmented  in  that  place,  and  more  or  less  in- 
durated from  the  development  of  interstitial  connective  tissue. 

Hasmorrhagic  infarctions  are  usually  situated  in  the  lower  lobes,  and  more 
frequently  on  the  right  side  than  on  the  left. 

The  smaller  embolic  abscesses  are  sometimes  very  numerous,  and  are  dissemi- 
nated over  the  whole  lung.  In  larger  abscesses  the  conical  shape  may  often  be 
plainly  recognized.  Where  an  abscess  extends  to  the  pleura,  a  purulent  pleurisy 
arises  from  direct  infection.  Combinations  and  transitional  forms  between  the 
ordinary  hsemorrhagic  infarction  and  embolic  abscesses  are  occasionally  found  in 
the  lungs. 

Symptoms. — We  often  find  at  the  autopsy  embolism  of  single  branches  of  the 
pulmonary  artery,  with  or  without  infarction,  which  has  caused  no  symptoms  at 
all  during  life. 

Embolism  of  the  main  trunk,  or  of  a  large  branch  of  the  pulmonary  artery, 
may  cause  sudden  death,  as  has  been  repeatedly  observed  in  patients  with  heart 
disease,  or  with  venous  thrombosis.  If  death  be  not  immediate,  sudden  severe 
dyspnoea  and  oppression  arise.  The  diagnosis  may  at  least  be  suspected  in  such  a 
case  if  we  know  of  a  possible  source  for  an  embolus.  In  some  instances,  where  an 
embolus  is  situated  m  a  large  branch  of  the  pulmonary  artery,  but  has  not  com- 
pletely filled  it,  we  can  hear  a  systolic  vascular  murmur  over  the  affected  spot,  as 
has  been  observed  by  Litten.  The  diagnosis,  however,  becomes  certain  if  the 
further  signs  of  infarction  appear  later. 

The  most  characteristic  symptom  of  infarction  in  the  lungs  is  the  bloody 
expectoration.  If  we  see  quite  suddenly  bloody  sputum  in  a  patient  with  mitral 
stenosis,  we  are  usually  right  in  assuming  a  hasmorrhagic  infarction  of  the  lung. 
Either  the  sputum  consists  almost  entirely  of  dark  blood,  or  the  blood  is  mixed 
with  more  or  less  mucus ;  but  there  is  never  much  air  in  it.  The  bloody  expecto- 
ration often  lasts  for  several  days. 

We  try  to  learn  more  of  the  size  and  situation  of  the  lesion  by  a  physical  ex- 
amination of  the  lungs.  Of  course  this  often  gives  a  negative,  or  at  least  a  doubt- 
ful, result.     It  goes  without  saying  that  small  infarctions,  and  also  those  which 


BROWN  INDURATION  OF  THE  LUNGS.  249 

are  central,  can  not  be  made  out  by  physical  examination.  Large  peripheral 
infarctions  may  give  rise  in  many  cases  to  dullness  on  percussion,  crepitant  rales, 
and  harsh  or  bronchial  respiration,  but  it  is  often  hard  to  decide  in  an  individual 
case  whether  the  physical  signs  which  we  meet  with  are  not  due  to  other  patho- 
logical changes  in  the  lungs,  like  bronchitis  or  hydrothorax.  We  sometimes  hear 
a  pleuritic  friction-sound  in  some  part  of  the  chest  a  few  days  after  we  suspect 
that  an  infarction  has  occurred,  by  which  the  diagnosis  gains  additional  certainty. 
We  have  already  mentioned  the  subjective  symptoms  in  embolism  of  a  large  pul- 
monary vessel — sudden  dyspnoea  and  oppression.  Small  nodules  often  cause  no 
special  symptoms,  but  in  other  cases  the  patient  feels  a  severe  pleuritic  pain,  due 
to  irritation  of  the  pleura. 

Fever  may  be  wholly  absent,  though  we  sometimes  see  a  moderate  rise  of  tem- 
perature at  the  onset. 

The  embolic  abscesses  in  the  lungs  hardly  ever  give  rise  directly  to  clinical 
symptoms.  They  form  a  part  of  the  general  picture  of  pyaemia  and  similar  gen- 
eral infectious  processes.  Marked  symptoms  on  the  part  of  the  respiratory  appa- 
ratus are  seen  only  when  the  abscesses  are  present  in  very  large  number.  If  an 
empyema  develops  from  a  focus  which  extends  to  the  pleura,  it  sometimes  gives 
rise  to  definite  physical  signs. 

It  follows  from  all  that  has  been  said  before,  that  in  the  diagnosis  of  embolic 
processes  the  chief  stress  must  always  be  laid  on  the  presence  of  an  aetiological 
factor.  We  must  regard  the  bloody  sputum  as  the  main  direct  symptom  in 
haemorrhagic  infarction.  Embolic  abscesses  in  the  lungs  may  often  be  suspected 
in  pyaamic  diseases,  but  they  can  hardly  ever  be  made  out  absolutely. 

The  prognosis  is  entirely  dependent  upon  the  underlying  disease.  In  heart 
disease  the  occurrence  of  a  haemorrhagic  infarction  is  usually  on  the  whole  an 
unfavorable  sign,  since  it  points  to  weakness  of  the  right  ventricle,  and  hence  to 
the  formation  of  a  thrombus  in  it ;  yet  it  often  happens  that  the  symptoms  of  a 
pulmonary  infarction  may  pass  away  entirely. 

We  need  not  give  special  directions  for  treatment.  It  is  in  part  purely  symp- 
tomatic, and  in  part  coincides  with  the  treatment  of  the  underlying  affection.  As 
regards  prophylaxis,  we  must  bear  in  mind  the  absolute  necessity  of  as  perfect  rest 
as  possible  in  those  patients  in  whom  the  presence  of  venous  thrombi,  as  in  the 
femoral  veins,  suggests  the  possibility  of  pulmonary  embolism. 


CHAPTER  XL 

BROWN  INDURATION  OP  THE  LUNGS. 

{Lungs  of  Heart  Disease.) 

In  heart  disease,  especially  in  mitral  stenosis,  we  often  find  a  peculiar  change 
in  the  lungs,  whose  origin  must  be  sought  in  the  long-persisting  engorgement  of 
the  pulmonary  circulation.  The  lungs  are  hard  and  dense,  and  show  on  a  fresh 
section  an  abnormal  brownish-yellow  color.  In  the  larger  pulmonary  vessels,  the 
arteries  and  veins,  there  is  a  thickening  and  cloudiness  of  the  intima  as  a  result  of 
the  stasis.  We  see  here  and  there  on  the  surface  of  the  section,  and  beneath  the 
pleura,  little  dark  spots  of  pigment  and  fresh  haemorrhages.  We  term  this  condi- 
tion brown  induration  of  the  lungs. 

Microscopic  examination  shows  that  the  capillaries  are  evidently  dilated  and 
twisted  as  a  result  of  the  persistent  stasis.     They  even  extend  a  good  way  into  the 


250  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

alveoli,  whose  lunien  is  thus  actually  diminished.*  The  interstitial  connective  tis- 
sue seems  somewhat  thickened,  and  we  find  in  it  many  pigment  granules,  the 
remains  of  the  extravasated  and  decomposed  red  blood-corpuscles.  According  to 
Rindfleisch,  the  muscular  constituents  of  the  parenchyma  of  the  lung,  the  smooth 
muscular  fibers  at  the  entrance  and  in  the  walls  of  the  alveoli,  show  a  distinct 
hypertrophy.  .  In  the  intima  of  the  larger  vessels  we  often  find  fatty  degeneration 
of  the  endothelium,  and  sometimes  even  fatty  degeneration  of  the  muscular  coat. 

As  regards  the  clinical  significance  of  brown  induration  of  the  lungs,  it  is 
possible  that  the  extensive  diminution  of  the  lumina  of  the  alveoli  throughout 
the  whole  lung  may  contribute  somewhat  to  the  increase  of  the  dyspnoea  in  heart 
disease,  but  in  practice  this  factor  can  not  be  separated  from  the  other  causes 
which  produce  dyspnoea. 

We  have  no  certain  factors  by  which  to  diagnosticate  brown  induration  of  the 
lungs  during  life.  The  anatomical  lesions,  too,  show  a  certain  variation,  not 
always  to  be  explained,  in  that,  under  apparently  the  same  conditions,  the  brown 
induration  is  often  very  marked,  and  often  only  extremely  slight.  In  cases  where 
we  find  this  induration  in  the  cadaver  we  sometimes  hear,  during  the  patient's 
life,  a  very  sharp,  puerile  respiratory  murmur,  Avhich  seems  to  be  characteristic 
of  many  cases  of  the  "heart-disease  lung."  We  might  lay  still  more  stress  upon 
the  presence  of  large,  characteristic  cells  in  the  expectoration,  which  are  thickly 
filled  with  large  and  small  yellow  or  brown  pigment-granules.  These  large  pig- 
mented cells  are  iu  all  probability  white  blood-corpuscles,  which  have  taken  up 
the  pigment  from  the  red  blood-corpuscles  destroyed  within  the  alveoli.  At  the 
autopsy  we  also  find  these  cells  lying  within  the  alveoli.  Besides  these  pigment- 
cells  we  also  frequently  see  the  still  intact  red  blood-corpuscles  in  the  expectora- 
tion of  patients  with  heart  disease. 

The  prognosis  and  treatment  coincide  with  those  of  the  underlying  cardiac 
disease. 


CHAPTER  XII. 

TUMORS  OF  THE  LUNGS.  CANCER  OF  THE  LUNGS.  ECHINOCOCCUS 
OF  THE  LUNGS.  PULMONARY  SYPHILIS. 

1.  New  Growths  in  the  Lungs.  Cancer  of  the  Lungs.— Most  of  the  new 
growths  which  are  met  with  in  the  lungs  are  of  a  secondary  nature.  Secondary 
cancers  are  sometimes  found  in  the  lungs,  with  carcinoma  of  other  organs,  whose 
origin  may  always  be  explained  by  supposing  a  growth  of  the  primary  tumor  into 
a  vein,  and  the  consequent  carriage  of  the  germs  of  the  growth  to  the  lungs. 
These  secondary  nodules  in  the  lungs  usually  cause  no  special  clinical  symptoms, 
unless  they  are  very  numerous  and  extensive,  when  they  give  rise  to  dyspnoea, 
and  physical  signs.  Several  years  ago  there  came  to  the  clinic  in  Leipsic  a  case 
of  secondary,  and  very  extensive,  miliary  carcinosis  of  the  lungs,  which  ran  a 
brief  and  fatal  course,  simulating  acute  miliary  tuberculosis  with  predominant 
pulmonary  symptoms. 

We  must  mention  enchondroma  among  the  other  secondary  new  growths,  but 
it  may  also  occur  primarily  in  the  lungs  in  very  rare  cases.  Secondary  sarcoma 
of  the  lungs  is  also  very  rare.     We  have  seen  a  very  extensive  form  of  it  after 

*  This  view  had  been  universally  accepted,  but  it  has  been  somewhat  shaken  bj'  Basch.  He  be- 
lieves that  the  effect  of  passive  congestion  upon  the  pulmonary  capillaries  is  to  stretch  them,  thus 
tending  to  make  the  lumen  of  the  alveoli  not  smaller,  but  larger  (vide  chapter  on  heart  disease). 


TUMORS  OF  THE  LUNGS.— PULMONARY  SYPHILIS.  251 

primary  sarcoma  of  the  bronchial  glands,  and  also  in  a  case  of  lympho-sarcoma  of 
the  cervical  lymph-glands,  where  the  sarcoma  had  grown  into  the  jugular  vein; 
and,  finally,  we  have  seen  it  repeatedly  in  congenital  primary  sarcoma  of  the 
kidneys  {vide  chapter  on  new  growths  in  the  kidneys). 

Among  the  primary  new  growths  in  the  lung,  cancer  is  the  only  one  which 
has  much  clinical  significance.  In  its  clinical  relations  we  can  also  rank  with  it 
certain  malignant,  metastatic  forms  of  alveolar  sarcoma.  The  typical  cancer  of 
the  lungs  is  always  a  cylindrical-celled  carcinoma,  which  undoubtedly  arises  from 
the  bronchial  epithelium.  It  is  especially  common  in  elderly  people,  over  forty, 
and  seems  to  be  found  somewhat  more  frequently  in  the  right  lung  than  in  the 
left,  and  in  the  upper  lobes  than  in  the  lower.  By  its  diffusion  the  lung-tissue  in 
the  parts  affected  by  cancer  is  changed  to  a  yellowish -gray  and  quite  soft  and 
crumbling  mass,  devoid  of  air.  We  can  usually  scrape  away  from  the  section  the 
characteristic  cancer-juice,  in  which  the  microscope  shows  the  typical  cancerous 
elements.  The  pleura  is  very  often  involved.  The  new  growth  has  either  ex- 
tended directly  into  it,  or  single,  and  more  circumscribed,  secondary  nodules  have 
formed  in  it.  The  lymph-glands  are  almost  invariably  affected,  especially  the 
bronchial  glands,  and  also  the  axillary  and  cervical  glands.  Secondary  carcinoma 
of  other  organs  is  rare,  but  it  is  found  in  some  cases  in  the  other  lung,  the  liver, 
the  brain,  and  elsewhere. 

It  is  almost  always  difficult  to  interpret  correctly  the  clinical  symptoms  of 
cancer  of  the  lungs  at  the  beginning  of  the  disease.  They  are  referred  to  some 
other,  more  frequent  chronic  pulmonary  disease,  such  as  chronic  bronchitis,  phthi- 
sis, or  pleurisy,  but  in  the  further  course  of  the  disease  we  succeed,  at  least  in  a 
number  of  cases,  in  making  a  correct  diagnosis.  In  other  cases,  especially  in  old 
people,  the  disease  may  remain  latent. 

The  general  symptoms  in  the  lungs  have  little  that  is  characteristic.  The 
patient  complains  of  gradually  increasing  difficulty  in  respiration,  and  of  pressure 
and  distress  in  the  chest,  which  may  finally  increase  to  the  most  intense  dyspnoea. 
Most  patients  suffer  very  much  from  the  labored,  frequent,  and  spasmodic  cough. 
The  expectoration  in  some  cases  has  no  peculiarity,  but  it  often  assumes,  at  least 
for  a  time,  a  characteristic  consistency  which  is  extremely  important  for  diagnosis. 
It  contains  blood,  and  also  has  a  peculiar  "currant-jelly-like  "  appearance.  Under 
the  microscope  we  can  sometimes  make  out  the  characteristic  elements  of  the 
tumor  in  it.     Severe  haemoptyses  are  also  seen  in  cancer  of  the  lungs. 

Physical  examination  of  the  lungs  gives  a  positive  result  in  many  cases,  such 
as  dullness,  bronchial  respiration,  diminished  respiration,  rales,  and  sometimes 
pleuritic  friction-sounds,  none  of  which  has  anything  characteristic  in  itself,  but 
they  are  of  distinct  significance  in  making  out  the  seat  and  the  extent  of  the  new 
growth.  Special  mention  must  be  made  of  the  often-noticed  diffuse  projection 
and  swelling  of  the  diseased  side. 

The  occurrence  of  certain  sequelae  is  of  great  diagnostic  significance.  The 
chief  one  is  the  discovery  of  swelling  in  the  lymph-glands  in  the  neck  or  axilla, 
and  also  a  number  of  symptoms  of  compression,  which  either  are  produced  directly 
by  the  new  growth,  or  are  due  to  the  secondary  enlargement  of  the  lymph-glands. 
Pressure  on  the  superior  vena  cava,  or  a  large  branch  of  it,  causes  oedema  in  the 
face,  neck,  over  the  wall  of  the  chest,  or  in  one  arm.  The  subcutaneous  veins  in 
the  regions  named  appear  dilated  and  tortuous.  Pressure  on  the  oesophagus 
causes  difficulty  in  deglutition ;  pressure  on  the  brachial  plexus,  intense  neuralgic 
pains  and  paresis  of  one  arm ;  pressure  on  the  recurrent  nerve,  paralysis  of  the 
vocal  cords  and  hoarseness ;  pressure  on  the  trachea  or  a  primary  bronchus,  the 
symptoms  of  tracheal  or  bronchial  stenosis. 

Besides  the  symptoms  already  mentioned  we  must  consider  the  general  syrup- 


252  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

toms.  As  in  carcinoma  in  general,  so  in  pulmonary  carcinoma,  the  well-known 
cancerous  cachexia  gradually  develops.  The  patient  grows  dull,  loses  his  appetite 
more  and  more,  disturbances  of  digestion  and  sometimes  moderate  elevations  of 
temperature  develop,  until  he  finally  succumbs  to  general  marasmus. 

The  whole  duration  of  the  disease  is  from  six  months  to  two  years.  The  prog- 
nosis is  fatal.  The  treatment  can  be  only  purely  symptomatic,  and  we  employ  the 
same  remedies  as  in  other  pulmonary  affections. 

We  must  still  briefly  consider  a  new  growth  in  the  lungs  which  is  extremely 
interesting  from  a  theoretical  point  of  view.  In  workmen  in  the  cobalt  mines  of 
Schneeberg,  in  the  Saxon  Voigtland,  the  development  of  malignant  lympho- 
sarcomata  in  the  lungs,  with  the  occasional  formation  of  metastases  in  the  glands, 
the  liver,  the  spleen,  etc.,  is  of  frequent  occurrence.  The  disease  runs  its  course 
under  the  type  of  a  chronic  pulmonary  affection,  and  almost  always  ends  fatally. 
The  endemic  occurrence  seems  to  point  to  an  infectious  origin  for  the  tumor. 

2.  Echinococcus  of  the  Lungs. — Primary  echinococcus  in  the  lungs  is  very 
rare.  In  most  cases  the  echinococci  are  brought  to  the  lungs  secondarily  from 
other  organs,  either  by  way  of  the  blood-current,  or,  as  is  far  offener  the  case,  by 
perforation  of  an  echinococcus  of  the  liver  through  the  diaphragm. 

The  symptoms  of  echinococcus  of  the  lungs  are  manifold.  The  parasite  some- 
times remains  entirely  concealed.  In  other  cases  a  more  or  less  severe,  and  often 
febrile,  affection  of  the  lungs,  is  developed,  with  pain  in  the  chest,  cough,  and  some- 
times bloody  expectoration,  and  dyspnoea.  Physical  examination  of  the  lungs 
gives  in  some  cases  dullness,  absence  of  respiratory  murmur,  and  diminished  vocal 
fremitus,  while  after  the  expectoration  of  the  echinococcus  {vide  infra)  symp- 
toms of  a  cavity  may  ensue.  A  correct  interpretation  of  all  these  symptoms  is 
possible  only  when,  as  has  often  been  observed,  the  echinococcus  cysts  are  coughed 
up,  or  at  least  when  parts  of  them,  like  the  membranes  or  the  booklets,  are  found 
in  the  expectoration. 

The  termination  of  the  disease  may  be  favorable  if  the  echinococci  are  expec- 
torated, or  if  we  succeed  in  removing  them  by  operative  means.  We  can  hardly 
hope  to  be  able  to  kill  the  parasite  by  inhalations  of  turpentine  or  benzine.  Some- 
times the  echinococcus  cyst  becomes  gangrenous,  or  suppurates.  Rupture  into  the 
pleura,  into  the  peritoneum,  into  the  pericardium,  and  externally,  has  also  been 
observed.  This  last  termination  is  the  most  favorable,  since  otherwise,  if  the 
affection  progresses,  a  fatal  result  may  be  caused  by  the  sequela?,  or  rarely  by  the 
occurrence  of  suffocation.  The  details  of  the  natural  history  of  the  echinococcus 
are  given  in  the  chapter  on  echinococcus  of  the  liver. 

3.  Pulmonary  Syphilis.— This  would  also  be  the  place  to  speak  of  syphilitic 
new  growths  in  the  lungs,  but,  in  our  opinion,  in  spite  of  the  quite  abundant  litera- 
ture of  this  subject  in  recent  times,  no  definite  statement  as  to  pulmonary  syphilis 
can  be  made.  Those  physicians  who  are  disposed  to  consider  every  pulmonary 
disease  in  a  previously  syphilitic  subject  to  be  of  a  syphilitic  nature,  certainly 
regard  many  things  as  pulmonary  syphilis  which  have  nothing  at  all  to  do  with 
syphilis.  At  least,  we  have  found  that  all  those  cases  which  at  first  suggested  a 
diagnosis  of  pulmonary  syphilis,  finally,  Lipon  more  accurate  examination  and 
after  longer  observation,  have  turned  out  to  be  something  else,  usually  tubercu- 
losis. The  only  form  of  pulmonary  syphilis  that  has  been  established  pathologic- 
ally is  syphilis  of  the  larger  and  medium-sized  bronchi,  which  is  recognized  at 
the  autopsy  by  extensive  radiated  cicatrices  in  the  bronchial  mucous  membrane, 
and  which  sometimes  lead  to  stenosis.  Single  gummatous  nodules  in  the  lungs 
are  of  the  greatest  rarity.  We  sometimes  find  in  the  pleura  peculiar  radiated 
cicatrices,  which  perhaps  are  of  syphilitic  origin.  Practically  we  are  always  justi- 
fied, if  severe  and  otherwise  inexplicable  pulmonary  symptoms  occur  in  a  previ- 


PLEURISY.  253 

ously  syphilitic  subject,  in  trying  specific  treatment ;  but  very  seldom  do  we  get 
any  good  result  from  it.  The  pulmonary  syphilis  of  the  new-born,  which  occurs 
in  the  form  of  single  nodules  or  as  a  diffuse  syphilitic  infiltration,  the  so-called 
pneumonia  alba,  has  only  a  pathological  interest. 


SECTION  V. 

Diseases   of  the  Pleura. 

CHAPTER  I. 


PLEURISY. 

(Pleuritis.) 

iEtiology. — We  make  the  general  distinction  of  a  primary  and  a  secondary 
pleurisy. 

By  primary  pleurisy  we  mean  those  cases  where  previously  healthy  people  are 
attacked  with  an  inflammation  of  the  pleura.  We  have  no  doubt  that  such  cases 
occur,  but  they  are  much  rarer  than  is  generally  believed,  for  many  cases  of 
secondary  pleurisy  give  one  the  impression  of  a  primary  disease,  either  because 
the  primary  affection  has  caused  no  symptoms  up  to  that  time,  or  because  it  can 
not  be  detected.  Taking  cold  is  one  of  the  chief  exciting  causes  of  primary  pleu- 
risy, and  mechanical  injury  may  also  sometimes  act  as  a  cause. 

Secondary  pleurisy  arises,  in  a  great  majority  of  cases,  from  a  direct  invasion 
of  the  pleura  by  an  inflammatory  process  originating  in  some  neighboring  organ. 
We  have  already  had  to  point  out  repeatedly,  in  the  description  of  pulmonary 
diseases,  how  the  different  pathological  changes  in  the  lung  likewise  involve  the 
pleura  if  they  reach  that  organ.  Thus  arises  the  pleurisy  in  croupous  pneumonia, 
in  lobular  catarrhal  pneumonia,  in  pulmonary  gangrene,  in  hemorrhagic  infarc- 
tion, and  in  embolic  abscess.  Since  many  of  these  affections  often  develop  in  the 
course  of  the  most  diverse  diseases,  we  can  easily  understand  that  pleurisy  is  a 
not  infrequent  complication  of  all  possible  severe  diseases. 

By  far  the  most  important  secondary  form  is  tubercular  pleurisy.  The  teach- 
ing of  daily  clinical  and  pathological  experience  is  that  the  ordinary  chronic 
pulmonary  tuberculosis  is  almost  constantly  complicated  with  pleurisy.  The 
latter  is  often  entirely  subordinate  to  the  phthisis,  but  in  many  cases  certain  sub- 
jective symptoms,  like  pain,  and  also  physical  signs,  are  certainly  to  be  referred 
to  the  pleurisy.  Of  much  greater  practical  importance,  however,  are  those  cases 
of  tubercular  pleurisy  which  arise  as  an  apparently  primary  pleurisy.  Among 
these  are  the  larger  part  of  all  ordinary  "pleuritic  effusions."  The  type  of  the 
disease  is  wholly  dominated  by  the  pleurisy.  This  may  improve  decidedly,  as 
often  happens,  or  even  in  many  cases  be  completely  cured  (vide  infra),  but,  if 
we  keep  the  patient  long  enough  under  observation,  marked  signs  of  tuberculosis 
usually  arise  later  on  (see  the  general  course  of  the  disease),  whence  it  follows 
that  the  initial  pleurisy  must  be  regarded,  in  an  etiological  sense,  as  tubercular. 
The  special  origin  of  tuberculosis  in  these  cases  is  not  always  quite  clear.  There 
is  certainly  a  small  tubei'cular  focus  often  present  in  the  lungs,  which  has 
caused  no  symptoms  in  itself,  but  which  became  the  point  of  origin  for  a  pleurisy. 
Not  infrequently  the  pleurisy  seems  to  start  from  a  tuberculous  bronchial  gland 
breaking  into  the  pleural  cavity  and  infecting  the  latter  with  tuberculous  virus. 


254  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

Other  organs  besides  the  lungs  may  be  the  point  of  origin  for  a  pleurisy. 
Thus  pleurisy  arises  from  affections  of  the  ribs  or  vertebras,  such  as  caries,  from 
perforation  of  an  oesophageal  cancer,  etc.  Inflammations  of  other  serous  mem- 
branes are  especially  apt  to  invade  the  pleura.  Thus  it  arises  as  a  result  of  a 
pericarditis  or  peritonitis.  Since  the  pleural  and  peritoneal  cavities  are  in  direct 
communication  with  each  other  by  the  lymphatics  of  the  diaphragm,  we  can  con- 
ceive that  both  a  purulent  and  a  tubercular  peritonitis  may  result  in  a  secondary 
pleurisy. 

Secondary  pleurisy  sometimes  arises  in  the  course  of  certain  diseases  in  another 
way.  In  acute  rheumatism,  in  rare  cases,  a  pleurisy  develops,  which  must  be 
considered  due  to  the  specific  causes  of  the  disease.  In  chronic  nephritis  and  in 
genuine  gout  we  sometimes  see  pleurisy  of  which  the  precise  origin  is  as  yet  not 
certainly  known.  Perhaps  in  these  conditions  the  abnormal  accumulation  of  the 
products  of  tissue-metamorphosis  in  the  blood  and  the  tissues  is  the  cause  of  the 
development  of  inflammation. 

Pathological  Anatomy. — The  inflamed  pleura  is  markedly  injected,  it  bas  lost 
its  normal  luster,  and  instead  has  a  dull  surface.  This  dullness  is  due  to  the 
coagulated  fibrinous  exudation  upon  the  pleura,  the  exudation,  in  mild  cases, 
forming  only  a  thin  layer.  In  more  advanced  cases,  however,  the  surface  of  the 
pleura  is  covered  with  thick,  rough,  and  shaggy  masses  of  fibrine.  As  long  as  the 
fluid  in  the  pleura  is  little  or  not  at  all  increased,  we  speak  of  a  simple  fibrinous 
or  dry  pleurisy  ( pleuritis  fibrinosa  vel  sicca). 

In  other  cases,  however,  besides  the  layer  of  fibrine  there  is  an  abundant  exuda- 
tion of  fluid  from  the  capillaries  of  the  pleura,  forming  a  pleuritic  effusion.  This 
is  ordinarily  of  a  simple  serous  character — serous  and  sero-fibrinous  effusions. 
The  fluid  collects  between  the  surfaces  of  the  pleura,  or,  if  there  is  at  the  same 
time  an  abundant  coating  of  fibrine,  between  the  gaps  and  in  the  meshes  of  the 
fibrinous  exudation.  In  such  cases  there  are  often  many  flakes  of  fibrine  floating 
in  the  fluid. 

In  every  serous  effusion  we  also  find  a  number  of  pus-corpuscles,  which  give 
to  it  a  slight  cloudiness,  but  if  the  number  of  pus-corpuscles  increases  very  much, 
Ave  have  a  fibrino-purulent  or  a  purely  purulent  exudation.  This  is  always  due 
to  the  presence  of  a  specific  organized  poison  which  excites  the  suppuration.  The 
pleurisies  which  come  from  embolic  abscesses,  from  gangrenous  foci  in  the  lungs, 
and  from  carious  ribs,  and  those  which  arise  from  the  rupture  of  tubercular  cavi- 
ties into  the  pleura,  are  almost  always  of  a  suppurative  character.  We  call  the 
purulent  pleuritic  effusion  empyema.  If  putrefactive  agencies  enter  the  pleural 
cavity  at  the  same  time  with  the  pus  poison,  as  in  the  pleurisies  which  develop 
in  pulmonary  gangrene,  the  purulent  exudation  assumes  an  ichorous,  putrid 
character — ichorous  effusion. 

Under  certain  circumstances  the  effusion  assumes  a  hsemorrhagic  character — 
hemorrhagic  effusion — especially  if  haemorrhages  arise  from  the  old  or  newly 
formed  capillaries  dilated  by  the  inflammation.  They  arise  partly  by  diapedesis 
and  partly  from  rupture  of  the  walls  of  the  vessels.  The  exact  cause  of  the  haemor- 
rhages is  usually  unknown.  We  know  by  experience  that  haemorrhagic  effusions 
are  most  frequent  in  tubercular  pleurisy,  a  fact  which  is  of  diagnostic  importance. 
Haemorrhagic  pleurisy  is  also  a  frequent  complication  of  septic — especially  puer- 
peral— diseases,  as  a  result  of  embolic  affections  of  the  lungs.  We  can  often  refer 
the  onset  of  a  haeinorrhagic  pleurisy,  too,  to  a  general  haemorrhagic  diathesis,  as 
in  scurvy. 

The  amount  of  fluid  collected  in  one  pleural  cavity  is,  in  the  majority  of  cases, 
somewhere  between  a  pint  and  a  quart  (500-1,000  c.  c),  but  it  may  reach  three  or 
four  quarts.    Every  large  effusion  must  influence  the  position  of  the  yielding  walls 


PLEURISY.  255 

of  the  pleural  cavity,  the  chest-wall,  the  lungs,  the  mediastinum,  and  the  dia- 
phragm, through  the  consequent  increase  of  pressure  in  the  affected  pleural  cavity; 
and  the  resultant  symptoms  of  pressure  in  the  neighboring  organs  are  of  the 
greatest  clinical  significance.  Attention  is  first  called  to  the  lungs  themslves. 
Since  the  normal  lung  is  expanded  in  the  thorax  beyond  its  elastic  equilibrium,  it 
will  retract  as  soon  as  a  part  of  the  pleural  cavity  is  occupied  with  fluid.  Until 
it  has  reached  its  position  of  elastic  equilibrium  there  can  be  no  question  of  aposi 
tive  pressure  on  the  lung.  The  lung  floats  on  the  effusion,  in  a  certain  way,  if 
there  be  no  adhesions,  but,  as  the  amount  of  the  fluid  further  increases,  com- 
pression of  the  lung  follows.  With  a  very  large  effusion  the  lung  is  pushed 
wholly  up  and  back  against  the  vertebral  column,  and  is  changed  to  an  almost 
bloodless,  airless,  flat  mass.  It  is,  however,  possible  that  the  atelectasis  of  the  lung 
is  not  caused  exclusively  by  compression  from  without,  but  that,  after  the  normal 
respiratory  movements  have  ceased,  a  part  of  the  air  in  the  lung  may  be  absorbed 
by  the  vessels,  or  even  by  the  effusion. 

We  also  see  the  results  of  the  pressure  exerted  by  the  pleuritic  effusion  in  the 
mediastinum  and  diaphragm,  as  well  as  in  the  kings.  Displacements  of  the  heart 
arise  from  the  lateral  pressure  on  the  mediastinum,  which  must  take  place  if  the 
pressure  in  the  diseased  pleural  cavity  is  equal  to  that  of  the  atmosphere,  for  a 
greater  and  positive  pressure  is  unnecessary,  since  a  negative  pressure  prevails  on 
the  healthy  side. 

The  downward  pressure  of  the  diaphragm,  ivhich  usually  affects  both  halves  of 
it,  although  in  unequal  degree,  makes  itself  manifest  on  the  right  by  the  low  posi- 
tion of  the  liver,  and  on  the  left  by  the  downward  displacement  of  the  stomach 
and  large  intestine.  It  must  be  particularly  noticed,  however,  that  adhesions  may 
prevent  all  pressure-displacements  which  we  have  mentioned,  both  of  the  lungs 
and  of  the  neighboring  organs. 

As  regards  the  further  changes  and  terminations  of  the  pleuritic  processes,  they 
depend  upon  the  amount  and  character  of  the  effusion.  Favorable  cases  may 
result  in  complete  recovery  and  absorption  of  the  effusion.  The  fluid  contents 
are  taken  up  directly  by  the  lymphatics  of  the  pleura,  and  the  solid  constituents, 
the  fibrine  and  the  white  blood-corpuscles,  are  decomposed,  dissolved,  and  absorbed. 

In  most  of  the  severe  cases,  however,  an  extensive  new  formation  of  connective 
tissue  and  vessels  takes  place.  The  fluid  effusion  is  mostly  absorbed,  but  the 
pleura  itself  is  thickened  and  changed— the  so-called  pleuritic  thickening.  Very 
commonly  extensive  loose  or  firm  adhesions  form  between  the  two  layers  of  the 
pleura— adhesive  pleurisy.  Spaces  may  be  left  between  the  adhesions,  in  which 
the  remains  of  the  fluid  effusion  may  be  encapsuled— "  sacculated  pleuritic  effu- 
sion." In  protracted  cases,  and  especially  in  relapses  of  inflammation,  as  a  result 
of  phthisis,  the  pleural  membranes  may  finally  reach  a  thickness  of  one  or  two 
centimetres. 

Even  in  cases  with  marked  thickening  final  recovery  is  possible.  This  always 
is  attended  with  great  cicatricial  contraction  of  the  pleura,  in  which  the  whole 
chest- wall  is  involved.  The  normal  expansion  of  the  lungs  and  thorax  is  not 
restored  for  months,  if  at  all. 

It  is  largely  owing  to  the  nature  of  the  primary  disease  that  extensive  pleuritic 
effusions  so  seldom  fully  recover.  Hence  we  often  notice  that,  after  temporary 
improvements,  new  returns  of  the  pleurisy  occur,  or  serious  and  usually  tuber- 
cular diseases  of  the  lungs  and  other  organs. 

In  old  pleural  thickenings  we  sometimes  see  a  deposit  of  lime-salts,  the  so-called 
"pleuritic  ossification." 

In  purulent  effusion,  too,  a  final  absorption  is  also  possible ;  but  this  demands 
much  time,  and  thick,  cheesy  masses  of  pus  are  often  left  hi  the  pleural  sac.     In 


256  DISEASES  OP  THE  RESPIRATORY  ORGANS. 

most  cases  of  empyema,  if  there  is  not  timely  operative  interference,  the  pus  seeks 
an  outlet  for  itself.  It  may  break  through  the  visceral  pleura  into  a  bronchus, 
and  be  emptied  externally,  thus  giving  rise  to  a  pyo-pneumothorax ;  but  in  many 
cases  the  pleura  seems  to  be  destroyed  only  superficially,  and  the  pus  is  pressed 
into  the  alveoli  as  into  a  sponge,  especially  by  the  movements  of  coughing,  and 
thence  reaches  the  bronchi,  without  letting  the  air  enter  the  pleural  cavity 
(Traube).  In  Other  cases  the  empyema  breaks  externally  through  the  chest-wall 
— empyema  necessitatis.  The  point  of  rupture  is  usually  found  in  the  vicinity  of 
the  stern  vim,  where  the  chest  wall  is  thinnest.  In  very  rare  cases  the  empyema 
breaks  into  the  deeper  parts  of  the  body,  or  into  the  abdominal  cavity. 

Course  of  the  Disease. — We  will  speak  in  what  follows  especially  of  the  course 
And  symptoms  of  ordinary,  apparently  primary  {vide  supra),  fibrinous  or  sero- 
fibrinous pleurisy,  the  so-called  simple  pleuritic  effusion.  What  is  said  of  it 
obtains  in  large  measure  in  the  other  forms  of  pleurisy  also.  The  physical  signs, 
of  course,  are  almost  wholly  independent  of  the  character  of  the  effusion.  As  far 
as  the  different  forms  of  pleurisy  differ  clinically,  we  will  mention  their  peculiari- 
ties below. 

Only  rarely  is  the  onset  of  pleurisy  quite  acute  and  sudden,  beginning  with  a 
rigor.  In  such  cases  we  must  guard  against  confusing  it  with  croupous  pneu- 
monia. Pleurisy  usually  begins  slowly  and  gradually.  The  symptoms,  which 
the  patient  himself  feels,  are  in  many  cases  to  be  referred  directly  to  the  disease  of 
the  pleura.  One  of  the  most  constant  is  the  pleuritic  pain,  the  stitch  in  the  side. 
A  more  or  less  severe  pain  comes  on  in  the  side  at  every  deep  breath,  and  hence 
upon  any  physical  exertion;  also  upon  movements  of  the  body,  in  stooping, 
coughing,  or  gaping.  Shortness  of  breath  soon  appears,  and  constantly  increases. 
There  is  often  a  frequent,  dry  cough.  Besides  that,  severe  general  symptoms 
almost  always  develop;  the  patient  feels  dull,  looks  pale,  and  has  no  appetite. 
Patients  who  can  endure  a  good  deal  often  keep  at  work  for  a  long  time,  until, 
after  feeling  miserable  for  three  or  four  weeks,  they  are  forced  to  stay  at  home 
and  summon  a  physician.  It  is  very  important  to  know  that  in  not  a  few  cases 
the  general  symptoms  are  much  more  prominent  at  the  beginning  of  pleurisy 
than  the  local  ones.  The  patient  comes  to  the  physician  complaining  only  of 
weakness,  loss  of  appetite,  or  headache,  and  the  physical  examination  is  the  first 
thing  that  shows  the  presence  of  perhaps  a  large  pleuritic  effusion. 

In  most  of  the  severe  cases  the  further  course  is  slow  like  the  beginning,  but 
sometimes  the  severest  symptoms,  most  intense  dyspnoea,  marked  cyanosis,  etc., 
may  come  on  in  a  short  time,  owing  to  a  sudden  increase  of  the  effusion.  On  the 
other  hand,  in  mild  cases  the  symptoms  may  disappear  again  in  a  few  weeks,  but  the 
objective  signs  in  such  cases  are  generally  to  be  made  out  for  a  longer  time.  The 
disease  ordinarily  lasts  for  at  least  five  or  six  weeks,  and  often  much  longer.  Gradual 
recovery  follows,  or  the  onset  of  some  new  disease,  usually  tubercular  (vide  infra). 

Single  Symptoms.— The  pleuritic  pain,  the  stitch  in  the  side,  is  one  of  the  most 
frequent  subjective  symptoms.  We  have  previously  mentioned  that  in  primary 
diseases  of  the  lungs,  too,  as  in  croupous  pneumonia,  the  stitch  in  the  side  is  due  to 
the  accompanying  pleurisy.  It  is  remarkable  that  the  intensity  of  the  pain  in  no 
way  corresponds  to  the  apparent  intensity  of  the  disease.  There  is  often  the  sever- 
est pain  in  the  side  when  the  physical  examination  shows  almost  nothing.  On 
the  other  hand,  we  often  hear  a  decided  pleuritic  rub  without  the  patient's  com- 
plaining of  any  special  pain.  Pressure  on  the  chest- wall  on  the  affected  side  is 
often  very  painful.  With  severe  pain  we  may  consider  the  possibility  of  an  inva- 
sion of  the  intercostal  nerves  by  the  inflammation.  We  have  never  observed 
cases,  like  those  described  by  some  authors,  of  "  crossed  pleuritic  pain  " — that  is, 
cases  where  the  pain  is  localized  on  the  side  not  affected. 


PLEURISY.  257 

Cough  and  Expectoration. — The  cough  is  probably  directly  excited  by  the  dis- 
ease of  the  pleura.  We  often  find  the  pain  in  the  side,  and  also  the  cough,  brought 
on  by  a  deep  inspiration.  Expectoration  is  entirely  absent  in  uncomplicated  pleu- 
risy, or  it  is  scanty,  and  consists  simply  of  mucus.  Much  expectoration  always 
means  a  pulmonary  complication.  A  large  amount  of  purulent  sputum  is  evacu- 
ated if  a  purulent  effusion  breaks  into  the  lungs  {vide  supra). 

Dyspnoea. — The  respiration  is  usually  shallow,  and  consequently  frequent,  be- 
cause of  the  pleuritic  pain.  In  every  large  effusion  which  prevents  respiration 
in  one  lung  the  dyspnoea  becomes  more  severe,  and  may,  with  very  extensive 
effusions,  reach  the  highest  degree  of  orthopnoea.  The  stronger  the  patient  was 
before  the  disease,  and  the  more  rapidly  the  effusion  develops,  the  more  severe,  as 
a  rule,  is  the  dyspnoea. 

Fever. — Most  severe  pleurisies  are  associated  with  fever,  but  its  height  is  not 
very  great,  so  that  it  quite  rarely  reaches  104°  (40°  C).  The  fever  has  no  typical 
course.  In  cases  with  an  acute  beginning  it  is  sometimes  quite  continuous,  or 
slightly  remitting  at  first.  If  improvement  takes  place,  the  fever  goes  down  in 
about  two  or  three  weeks  by  lysis,  so  that  this  part  of  the  temperature  curve  may 
be  precisely  like  the  period  of  defervescence  in  typhoid. 

In  the  more  protracted  cases  the  fever  gradually  becomes  more  remitting,  vary- 
ing between  100°  and  101°  (380-38-5°  C),  and  it  assumes  more  and  more  the  form 
of  hectic  fever.  The  longer  the  evening  rise  of  temperature  lasts,  the  more  we  are 
justified  in  suspecting  tuberculosis.  In  empyema  we  see  a  higher,  irregular  fever, 
sometimes  associated  with  severe  chills. 

The  pulse  is  constantly  rapid,  up  to  100  and  over.  In  all  severe  cases  the 
strength  and  tension  of  the  pulse  are  much  diminished.  Irregularity  of  the  pulse 
is  not  infrequent.  All  these  changes  are  probably  due  in  great  part  to  the  press- 
ure of  the  effusion  on  the  heart  and  large  vessels.  Lichtheim  has  discovered 
experimentally  that  the  compression  of  the  vessels  in  the  compressed  lung  does 
not  lower  the  arterial  tension. 

General  Symptoms. — Pleurisy  is  almost  always  associated  with  a  pronounced 
general  malaise,  muscular  weakness,  and  dullness.  The  patient  is  pale,  and  often 
markedly  cyanotic  in  cases  with  much  disturbance  of  respiration.  There  is 
great  emaciation  if  the  disease  is  of  long  duration. 

The  appetite  declines  from  the  outset.  There  is  often  occasional  vomiting, 
especially  in  the  first  period  of  the  disease.  The  bowels  are  usually  constipated. 
Many  patients  complain  of  headache. 

The  condition  of  the  urinary  secretion  is  very  important.  In  every  pleuritic 
effusion  the  amount  of  urine  is  decidedly  diminished  so  long  as  the  effusion 
increases  or  remains  at  the  same  height.  The  daily  amount  is  sometimes  only 
eight  or  ten  ounces  (200-400  c.  c).  The  urine  is  also  concentrated,  its  specific  grav- 
ity being  about  1020-1028.  Sediments  of  urates  often  form.  This  diminution  of 
the  excretion  of  water  by  the  kidneys  is  largely  the  result  of  the  diminished  arte- 
rial pressure.  An  increase  of  the  amount  of  urine  is  always  a  favorable  symp- 
tom, often  the  first  sign  of  beginning  absorption  of  the  effusion.  If  a  large  effu- 
sion is  rapidly  absorbed,  the  amount  of  urine  may  increase  to  eighty  or  a  hundred 
ounces  (2500-3000  c.  c.)  daily.  The  urine,  then,  of  course,  is  abnormally  clear  and 
of  low  specific  gravity. 

Physical  Signs. 

1.  Fibrinous  Pleurisy — Pleuritis  Sicca.— Simple  fibrinous  pleurisy  sometimes 
gives  rise  to  no  physical  signs  at  all.  If  it  develops  as  a  result  of  some  pulmonary 
affection,  the  physical  signs  present  are  often  dependent  upon  this  alone. 

In  many  cases,  however,  dry  pleurisy  may  cause  marked  objective  signs.  On 
17 


258  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

inspection,  we  are  struck  by  the  impaired  mobility  of  the  affected  side  on  respira- 
tion, which  is  due  to  the  pain  caused  by  breathing.  Because  of  this  same  tender- 
ness the  patient  at  first  often  lies  on  the  sound  side.  Percussion  gives  no  qualita- 
tive change  of  resonance  as  yet.  With  the  beginning  of  exudation  slight  dullness 
appears,  at  first  almost  always  in  the  lower  posterior  portion  of  the  lungs.  Some- 
times the  resonance  becomes  tympanitic  as  a  result  of  retraction  of  the  lung.  We 
can  almost  constantly  make  out,  especially  in  the  back,  that  the  lower  edge  of  the 
lung  moves  less  than  usual  on  respiration.  Auscultation  gives  a  respiratory  mur- 
mur that  is  either  qualitatively  unchanged  or  indefinite,  but  it  is  always  dimin- 
ished. The  peculiar  pathognomonic  sign  of  dry  pleurisy,  however,  is  the  pleuritic 
friction-rub,  that  characteristic  rubbing,  grating,  creaking  sound,  which  arises 
from  the  sliding  of  the  rough  pleural  surfaces  over  each  other,  and  is  detected 
especially  in  the  lateral  portions  of  the  thorax.  We  can  hear  it  both  on  inspira- 
tion and  on  expiration.  It  is  often  jerky,  one  rub  following  another  after  a  con- 
siderable interval.  If  we  ai*e  sure  we  hear  a  pleuritic  rub,  it  is  direct  evidence  of 
the  existence  of  a  dry  pleurisy,  but  its  absence  will  not  let  us  exclude  pleurisy. 
The  friction-sound  must  be  absent  if  there  are  pleuritic  adhesions.  We  can  often 
feel  a  marked  rub  by  laying  the  hand  on  the  chest.  Sometimes  the  patient  feels 
it  himself,  but  in  other  cases  he  has  no  sensation  of  it.  We  may  confound  a  slight 
rub  with  fine  crepitant  rales.  Repeated  examinations  before  and  after  the  patient 
has  coughed  usually  confirm  the  diagnosis,  since  the  rales  are  often  changed  by 
coughing. 

2.  Pleuritic  Effusion. — Small  amounts  of  fluid  in  one  pleural  cavity  escape  dis- 
covery. Physical  signs  first  appear  when  the  amount  of  effusion  reaches  eight  or 
ten  ounces  (200-300  c.  c). 

Inspection  shows  first  the  more  or  less  marked  impairment  of  motion  on  the 
affected  side  on  respiration.  If  the  amount  of  the  effusion  is  large,  there  is  an 
evident  distention  of  the  affected  side  in  the  lower  posterior  and  lateral  portions 
of  the  thorax.  The  intercostal  spaces  are  flattened  or  even  a  little  convex.  The 
nipples  and  shoulder-blades  are  farther  removed  from  the  median  line  on  the 
affected  side  than  on  the  healthy  side.  The  hypochondrium  on  the  affected  side 
is  more  prominent.  In  an  extraordinarily  large  effusion  on  the  left  side  we  have 
seen  and  felt,  in  the  left  hypochondrium,  the  lower  surface  of  the  diaphragm, 
which  was  actually  arched  downward.  By  direct  measurement  in  severe  cases  we 
can  make  out  accurately  that  the  affected  side  is  expanded  several  centimetres. 

With  every  large  effusion  there  is  marked  dyspnoea  and  accelerated  respiration. 
The  slight  excursions  of  the  affected  side  on  respiration  are  usually  very  striking, 
while  the  sound  side  moves  so  much  the  more.  In  this  stage  of  pleurisy  the 
patient  often  lies  upon  the  affected  side,  in  order  to  breathe  with  the  healthy  lung 
with  as  little  restraint  as  possible.  With  large  effusions  complete  orthopncea  may 
develop. 

The  signs  due  to  displacement  of  the  neighboring  organs,  which  are  noticeable 
on  inspection,  will  be  mentioned  below  in  the  appropriate  connection. 

Everywhere  that  a  layer  of  fluid  comes  between  the  lung  and  the  chest-wall 
there  is  a  loss  of  clearness  in  the  percussion-note.  If  the  thickness  of  the  layer 
of  effusion  is  five  or  six  centimetres,  the  resonance  seems  completely  dull  or  flat. 
The  pleuritic  dullness  is  almost  always  first  made  out  in  the  lower  posterior  por- 
tions of  the  thorax,  more  rarely  in  the  lower  lateral  portions.  With  a  slight 
effusion  the  height  of  the  dullness  is  only  a  few  centimetres,  but,  with  much 
effusion,  it  rises  higher  in  the  back  and  the  lateral  portions  of  the  thorax;  and  on 
the  right,  resonance  gradually  grows  dull  anteriorly  and  inferiorly,  above  the 
liver.  With  very  large  effusions  the  dullness  may  begin  in  front  at  the  second  or 
third  rib,  or  in  rare  cases  even  the  whole  half  of  the  chest,  front  and  back,  may 


PLEURISY.  259 

give  a  totally  flat  percussion-note.  Pleuritic  dullness  is  always  attended  with  a 
marked  feeling-  of  resistance  on  percussion. 

With  medium-sized  effusions,  where  the  dullness  does  not  extend  over  the 
whole  back,  the  upper  boundary  of  the  dullness  usually  forms  an  oblique  line, 
highest  at  the  vertebral  column  and  thence  running  obliquely  downward  to  the 
side  of  the  thorax.  We  can  no  more  confirm  the  opposite  opinion,  which  souk; 
authors  hold,  than  can  Weil  and  others,  yet  of  course  no  one  can  establish  a 
schematic  rule.  The  lower  boundary  of  the  effusion  can  not  be  distinguished  on 
the  right  by  percussion  from  the  liver  dullness.  On  the  left  in  front  and  on  the 
side,  however,  we  can  often  distinguish  the  dullness  of  the  effusion  from  the  tym- 
panitic resonance  of  the  stomach,  and  this  is  of  diagnostic  value  (see  the  dis- 
placement of  organs,  as  given  below). 

[In  moderate  effusion  without  adhesions  or  pneumonic  complications,  the  line 
of  flatness  in  the  back,  the  patient  being  in  the  vertical  position,  is  lowest  near 
the  spinal  column,  and  rises  in  a  curve  like  the  letter  S  as  it  passes  outward  toward 
the  axillary  region.  The  experiments  by  Dr.  Garland,  of  Boston,  with  reference 
to  this  point  are  well  known.  Before  attempting  to  mark  out  this  line  the  patient 
should  be  told  to  take  several  deep  inspirations,  in  order  to  inflate  the  triangular 
portion  of  lung  which  dips  down  near  the  vertebra?.] 

The  percussion-note  above  a  pleuritic  effusion  deserves  attention.  The  begin- 
ning of  pleuritic  dullness  is  almost  always  relative,  gradually  passing  to  an  abso- 
lute flatness.  The  pulmonary  resonance  above  the  beginning  of  dullness  is  usu- 
ally tympanitic,  from  retraction  of  the  lung-tissue.  We  find  the  tympanitic 
resonance  beautifully  distinct  in  large  effusions  in  the  first  and  second  intercostal 
spaces  in  front.  It  is  loud  and  deep,  and  remains  unchanged  with  the  mouth 
open — Skoda's  resonance.  With  very  large  effusions,  which  cause  an  actual  com- 
pression of  the .  lung,  we  sometimes  find,  in  the  second  intercostal  space,  a  dull 
tympanitic  resonance,  which  becomes  higher  on  opening  the  mouth.  This  reso- 
nance arises  from  the  vibrations  of  air  in  a  large  bronchus  surrounded  by  com- 
pressed lung — "Williams's  tracheal  tone."  With  large  effusions  we  sometimes 
hear  over  the  retracted  lung,  in  the  upper  anterior  intercostal  spaces,  a  distinct 
buckram  sound — the  "  cracked-pot  sound." 

Displacement  of  the  neighboring  organs,  which  is  made  out  chiefly  by  percus- 
sion, forms  one  of  the  most  important  physical  signs  in  pleurisy  with  effusion. 

In  right-sided  effusions  the  liver,  especially  the  right  lobe,  is  displaced  down- 
ward. We  find  the  lower  border  of  the  liver  dullness  extending  several  centi- 
metres below  the  ribs.  In  very  large  effusions  the  liver  may  be  pushed  down  to 
the  level  of  the  umbilicus.  The  pushing  of  the  mediastinum  to  the  left  in  large 
effusions  may  be  recognized  upon  percussing  from  the  right  toward-  the  left,  by 
dullness  over  the  upper  part  of  the  sternum,  reaching  to  or  beyond  the  left  border 
of  the  sternum.  The  displacement  of  the  heart  to  the  left  in  the  majority  of  well- 
marked  cases  is  associated  with  a  displacement  of  the  apex  of  the  heart  upward. 
This  is  easily  explained  by  considering  the  position  of  the  heart  and  the  direction 
of  the  pressure,  which  first  acts  from  below.  We  recognize  the  displacement  of  the 
heart  chiefly  by  the  position  of  the  apex-beat,  which  is  seen  and  felt  at  or  outside 
the  left  mammillary  line  in  the  fifth  space,  or  often  higher,  as  we  have  said — in 
the  fourth.  Percussion  gives  a  corresponding  displacement  of  the  left  boundary  of 
the  cardiac  dullness  to  the  left.  § 

In  left-sided  effusions  the  displacement  of  the  heart  to  the  right,  which  can  usu- 
ally be  made  out  even  in  moderate  effusions,  is  especially  noticeable.  Resonance 
over  the  lower  part  of  the  sternum  is  diminished,  the  heart's  dullness  extends  to 
the  right  border  of  the  sternum  or  several  centimetres  beyond  it.  In  the  most 
marked  cases  the  heart  is  pushed  to  the  right  mammillary  line.    The  displacement 


260  DISEASES  OF  THE  EESPIRATOEY  ORGANS. 

of  the  mediastinum  is  also  to  be  made  out  over  the  upper  part  of  the  sternum,  the 
dullness  reaching  to  the  right  border  of  the  sternum  or  beyond.  The  low  position 
of  the  diaphragm  is  made  out  by  a  depression  of  the  left,  and  in  marked  cases  of 
the  right,  lobe  of  the  liver.  It  is  an  especially  important  sign,  however,  that 
dullness  occurs  in  the  zone,  about  a  hand-breadth  wide,  of  normal  tympanitic 
resonance  above  the  left  border  of  the  ribs — the  "  semilunar  space  "  of  Traube. 
The  normal  tympanitic  resonance  here  comes  from  the  stomach  or  lai^ge  intestine. 
As  the  diaphragm  is  pressed  downward  the  pleuritic  effusion  presses  on  these 
organs.  The  semilunar  space  is  therefore  diminished,  and  finally,  with  large  effu- 
sions, there  is  absolute  dullness  down  to  the  edge  of  the  ribs. 

Changes  in  dullness  in  pleuritic  effusions  may  occur  with  a  change  of  the 
patient's  position,  but  they  may  often  be  absent  on  account  of  adhesions.  The 
respiratory  displacement  of  the  lower  border  of  the  lung  is  almost  always  absent. 

Auscultation  always  gives  a  diminished  respiratory  murmur  over  the  pleuritic 
effusion.  With  a  beginning  effusion  it  may  sound  approximately  vesicular,  but 
later  it  becomes  indefinite,  hoarse,  and  finally  bronchial,  if  the  larger  bronchi  re- 
main open  for  the  respiratory  current  of  air.  The  bronchial  respiration  sounds 
distant  and  low,  and  has  the  character  of  the  sharp  German  ch,  but  in  rare  cases 
it  also  assumes  a  distinct  amphoric  tone,  so  that  it  sounds  almost  like  a  cavernous 
respiration.  The  respiratory  murmur  may  finally  disappear  entirely  over  very 
large  effusions.  Above  the  upper  boundary  of  the  effusion  the  respiration  almost 
always  sounds  harsh.  Among  the  adventitious  sounds  we  must  mention  the 
pleuritic  friction  sound,  which  of  course  can  be  heard  only  at  the  upper  boundaiy 
of  the  effusion,  where  the  two  pleural  surfaces  meet.  Moist  rales  and  rhonchi 
signify  a  co-existing  disease  in  the  lungs.  With  slight  effusions  we  often  hear, 
on  deep  breathing,  pure  crepitant  rales  on  inspiration,  as  the  walls  of  the  alve- 
oli and  bronchioles  in  the  atelectatic  lung,  which  were  stuck  together,  are  torn 
apart. 

On  auscultation  of  the  voice  we  sometimes  hear  bronchophony,  and  sometimes 
that  bleating,  nasal  sound  known  as  Eegophony.  Baccelli  advanced  the  theory 
that  auscultation  of  the  whispered  voice  might  be  of  service  in  diagnosticating  the 
character  of  the  effusion.  With  a  sei'ous  effusion  we  can  understand  a  whisper 
distinctly  through  the  thorax,  but  not  with  a  purulent  effusion,  since  theoreti- 
cally the  cell-elements  destroy  the  waves  of  resonance.  This  theory  holds  true  in 
many  cases,  but  by  no  means  in  all. 

On  auscultation  of  the  heart  we  notice,  as  a  result  of  its  displacement,  an  abnor- 
mal extension  of  the  region  over  which  the  heart-sounds  are  audible.  If  the  inflam- 
mation spreads  from  the  pleura  to  the  outer  surface  of  the  pericardium,  we  can 
sometimes  hear  an  extra-pericardial  friction-rub,  accompanying  both  the  respira- 
tion and  the  action  of  the  heart. 

The  vocal  fremitus  is  always  diminished  over  the  pleuritic  effusion,  and  in 
marked  cases  is  entirely  absent. 

3.  Absorption  of  the  Effusion— Pleuritic  Contraction.— The  beginning  absorp- 
tion of  the  effusion  is  usually  first  made  evident  by  the  percussion-note  in  the 
upper  part  of  the  dullness  becoming  clearer  and  sometimes  tympanitic.  The 
respiratory  murmur  is  also  plainer.  Where  it  was  bronchial  it  becomes  in- 
definite and  gradually  vesicular  again.  The  vocal  fremitus  is  again  to  be  felt. 
All  these  improvements  take  place  gradually  but  slowly.  It  is  usually  a  very  long 
time  before  the  percussion-note  resumes  its  normal  clearness. 

The  changes  in  the  form  of  the  thorax  are  especially  striking.  Only  in  pleu- 
risies with  slight  effusion  does  the  somewhat  expanded  thorax  resume  its  old  form 
without  further  change.  After  every  severe  pleurisy  with  large  effusion  there  is, 
during  its  absorption,  a  marked  contraction  of  the  affected  half  of  the  chest.     In 


PLEURISY.  261 

cases  of  moderate  intensity  the  contraction  affects  only  the  lower  lateral  portions 
of  the  thorax,  in  severe  cases  the  upper  and  anterior  portions  as  well.  We  find 
the  most  marked  contractions  in  children  and  young  persons  with  a  yielding 
thorax.  The  circumference  of  the  affected  side  is  much  less  than  that  of  the 
sound  side.  The  ribs  are  pressed  together  and  the  intercostal  spaces  become 
very  narrow.  The  fossae  are  deepened  and  the  nipples  and  shoulder-blades  are 
drawn  nearer  the  vertebral  column,  which  takes  on  an  abnormal  lateral  curva- 
ture, in  which  its  convexity  is  directed  usually  toward  the  affected  side,  but  some- 
times to  the  sound  side.  Dullness  and  diminution  of  the  respiratory  murmur  and 
vocal  fremitus  continue  with  the  contraction  of  the  pleura,  but  they  no  longer 
depend  upon  the  presence  of  a  fluid  effusion,  but  are  due  to  the  jdeuritic  thickening. 

The  process  of  marked  contraction  always  lasts  for  months,  or  even  longer. 
In  favorable  cases  the  contraction  of  the  thorax  may  be  readjusted  very  much 
later,  often  after  years.  The  thickening  is  absorbed,  and  the  lungs  and  thorax 
gradually  expand,  but  in  other  cases  there  are  extensive  adhesions  between  the 
pleural  surfaces,  especially  over  the  lower  lobe,  which  result  in  a  permanent  dis- 
turbance of  respiration.  In  almost  all  cases  of  pleurisy  with  contractions  there 
arises  a  vicarious  emphysema  in  the  lung  on  the  sound  side. 

Complications.  —Peculiar  complications  of  pleurisy  are  rare.  Where  such  occur 
they  are  due  either  to  the  primai'y  disease  which  has  led  to  the  pleurisy,  or  the 
simultaneous  action  of  the  same  cause  of  disease,  such  as  tuberculosis.  Hence  it 
happens  that  we  speak  of  the  frequent  "  complication  "  of  pleurisy  with  chronic 
bronchitis  or  with  tuberculosis  of  the  lungs  or  other  organs.  It  is  important  to 
bear  in  mind  that,  by  a  direct  advance  of  the  inflammation,  the  pleurisy  may  also 
invade  the  pericardium,  and  rarely  the  peritoneum,  through  the  diaphragm ;  but 
we  see  this  extension  of  the  process  almost  solely  in  tubercular  and  purulent  pleu- 
risies. We  must  mention,  finally,  that  we  have  seen  several  cases  with  a  large 
serous  effusion,  in  which  an  acute  haemorrhagic  nephritis  occurred.  For  the 
paralysis  of  the  arm  on  the  corresponding  side  observed  in  some  cases  of  empy- 
ema, compare  page  538. 

DIFFERENT   FORMS  OF  PLEURISY. 

1.  The  Simple  Fibrinous  or  Exudative  Pleurisy,  as  a  result  of  croupous  or 
extensive  lobular  pneumonia,  often  causes  but  few  symptoms  in  comparison  with 
the  primary  disease.  Recovery  is  usually  complete,  but  may  be  much  delayed, 
as  in  croupous  pneumonia. 

The  so-called  primary  simple  fibrinous  or  sero-fibrinous  pleurisy,  which  we 
must  regard  as  a  distinctly  rare  affection,  contrary  to  the  generally  prevailing 
opinion,  has  a  like  favorable  course. 

2.  Tubercular  Pleurisy. — In  an  aatiological  sense  we  must  declare  the  larger 
part  of  the  ordinary  "pleuritic  effusions,"  which  clinically  seem  to  be  primary 
to  be  tubercular.  We  do  not  know  how  far  at  first  the  specific  anatomical  changes 
of  tuberculosis  are  present,  or  whether  there  is  always  some  previous  tubercular 
affection  in  the  lungs  or  bronchial  glands,  but  the  further  course  of  the  cases,  if 
we  can  watch  them  for  years,  almost  always  permits  us  finally  to  recognize  the 
tubercular  nature  of  the  disease ;  yet  we  can  not  say  that  phthisis  is  always  the 
immediate  sequel  of  the  pleurisy. 

In  a  comparatively  small  number  of  cases  do  the  symptoms  of  acute  tubercu- 
losis, or  more  frequently  of  chronic  phthisis,  appear  as  an  immediate  result  of  the 
pleurisy,  which  at  that  time  is  usually  still  present  or  in  the  contracting  stage. 
The  objective  changes  of  phthisis  are  evident  either  in  the  apex  or  in  the  lower 
lobe  of  the  affected  side.     The  fever  continues,  the  pulmonary  affection  advances, 


262  DISEASES  OF  THE  EESPIRATORY  ORGANS. 

the  other  lung  is  also  attacked,  and  the  disease  takes  a  fatal  course  under  the 
t}7pe  of  an  ordinary  phthisis,  now  more  acute  and  now  more  chronic. 

In  other  cases  acute  tubercular  affections  arise  sooner  or  later  as  a  result 
of  the  pleurisy — tubercular  meningitis,  or  general  miliary  tuberculosis.  In  other 
cases  still  the  disease  develops  under  the  form  of  tuberculosis  of  the  serous  mem- 
branes, to  which  we  will  return  again  in  the  description  of  tubercular  pericar- 
ditis and  tubercular  peritonitis.  We  often  have  to  do  with  a  double  pleurisy 
with  no  evident  complication  in  the  lungs.  In  varying  succession  are  added  the 
symptoms  of  chronic  tubercular  peritonitis,  with  pain,  swelling,  and  effusion  of 
fluid  into  the  abdomen,  or  the  symptoms  of  tubercular  pei'icarditis.  Death  finally 
ensues  with  persistent  hectic  fever  and  increasing  general  emaciation  and  weakness. 
The  whole  affection  usually  runs  a  chronic  course,  lasts  for  months,  and  often 
shows  marked  remissions  and  temporary  improvements. 

In  very  many  instances  the  pleuritic  effusion  has  throughout  an  apparently 
favorable  course.  After  some  weeks  the  fever  ceases,  the  effusion  is  absorbed,  the 
patient  gets  up,  and  is  finally  discharged  as  nearly  well.  Of  course,  some  dullness 
and  retarded  motion  often  remain  in  the  affected  side,  but  even  these  may  gradu- 
ally disappear.  These  cases,  too,  very  often  turn  out  in  the  end  to  be  tubercu- 
lar. After  a  longer  or  shorter  period  of  apparent  health,  sometimes  after  the 
lapse  of  years,  a  "new"  disease  appears — that  is,  either  a  return  of  the  pleurisy, 
a  pleurisy  on  the  other  side,  or  some  other  acute  or  chronic  tubercular  affection. 
In  such  cases,  too,  we  must  look  upon  the  former  pleurisy,  in  an  aetiological 
sense,  as  tubercular.  It  is  not  impossible,  however,  for  even  a  tubercular 
pleurisy  to  recover,  and  for  the  recovery  to  be  permanent,  if  no  other  organ  is 
at  the  same  time  affected  by  tuberculosis,  especially  if  the  lungs  remain  un- 
affected. 

Finally  we  must  mention  the  cases  where  a  pleuritic  effusion  develops  second- 
arily to  an  already  pronounced  phthisis.  Here  too  we  almost  always  have  to  do 
with  a  tubercular  pleurisy. 

The  anatomical  changes  in  tubercular  pleurisy  consist  in  the  ordinary  signs 
of  inflammation,  and  also  the  presence  of  the  specific  nodules  of  tubercle.  The 
number  of  tubercles  differs  very  much  in  different  cases.  The  pleura  is  in  some 
cases  completely  studded  with  miliary  nodules,  and  in  others  we  find  the  tuber- 
cles, at  least  with  the  naked  eye,  only  in  single  spots.  The  effusion  is  usually  of 
a  sero-fibrinous  character.  Sometimes  it  is  hasmorrhagic,  as  the  majority  of  cases  of 
apparently  primary  "  hsemorrhagic  pleurisy  "  are  generally  of  a  tubercular  nature. 
The  exudation  is  rarely  purulent,  and  when  this  is  the  case  it  is  apparently  invari- 
ably caused  by  the  simultaneous  infection  of  the  pleura  with  another  sort  of  virus 
which  gives  rise  to  the  suppuration. 

3.  Purulent  Pleurisy— Empyema.— We  have  already  described  the  aetiology  of 
empyema,  and  we  have  seen  that  it  can  be  excited  only  by  infection  of  the  pleura 
with  a  specific  virus  which  can  set  up  suppuration.  The  clinical  symptoms  are 
usually  severe.  The  fever  is  higher  than  in  the  other  forms  of  pleurisy,  but  it  is 
irregularly  intermittent,  and  is  often  associated  with  chills.  There  are  severe 
general  symptoms  besides  the  fever,  such  as  great  dullness,  headache,  and  a  dry 
tongue.  We  sometimes  notice  a  slight  oedema  of  the  chest-wall  on  the  affected 
side.  Otherwise  the  local  symptoms  and  disturbances  are,  of  course,  the  same  as 
in  the  other  forms  of  pleurisy.  If  the  pus  is  not  evacuated  artificially,  the  em- 
pyema may  finally  break  externally  or  into  the  lungs  (vide  supra).  In  the  latter 
case  a  very  large  expectoration  of  pus  suddenly  occurs,  and  is  usually  followed  by 
pneumothorax. 

Diagnosis. — Our  chief  attention  in  regard  to  diagnosis  is  directed  to  the  distinc- 
tion between  pleurisy  and  acute  or  chronic  pneumonia,  which  is  not  very  easy  in 


PLEURISY.  263 

all  cases.     We  will  therefore  briefly  contrast  the  distinctive  features  as  made  out 
on  physical  examination. 

Inspection. — A  marked  distention  of  the  affected  side  points  to  effusion ;  it 
does  not  occur  in  pneumonia. 

Percussion. — The  dullness  in  pleurisy  is  complete,  and  the  feeling  of  resistance 
on  percussion  is  very  marked ;  in  pneumonia,  however,  the  dullness  is  rarely  so 
marked,  and  there  is  often  a  tympanitic  sound.  The  discovery  by  percussion  of 
signs  of  displacement  of  the  neighboring  organs  is  of  especial  weight,  as  the» 
signs  are  always  absent  in  uncomplicated  pneumonia,  while  with  few  exception! 
they  can  easily  be  demonstrated  in  every  case  of  pleurisy  where  the  exudation  is 
at  all  considerable. 

Auscultation. — Diminished  or  suppressed  respiratory  murmur  points  to  pleu- 
risy, loud  bronchial  breathing  and  rales  to  pneumonia;  but  we  must  not  forget 
that  in  pneumonia  auscultation  may  give  the  same  signs  as  in  pleurisy,  if  a 
bronchus  is  plugged. 

Vocal  Fremitus. — Marked  vocal  fremitus  over  dullness  is  direct  evidence  of 
pneumonia,  diminished  or  absent  vocal  fremitus  of  pleurisy ;  but  the  vocal  fremi- 
tus may  also  be  diminished  in  pneumonia  if  a  bronchus  is  plugged. 

Besides  the  physical  signs,  we  must  of  course  consider  the  other  symptoms — the 
manner  of  onset,  the  course  of  the  disease,  the  fever,  the  sputum,  the  occurrence 
of  herpes,  etc. 

If  we  have  diagnosticated  a  pleuritic  effusion,  the  next  question  is  always  as  to 
the  character  of  the  effusion,  because  the  prognosis  and  treatment  are  to  a  large 
degree  dependent  upon  this.  Although  certain  well-known  etiological  circum- 
stances, and  the  severity  of  the  fever  and  the  general  symptoms,  often  permit  us 
to  suspect  the  nature  of  the  effusion,  whether  serous  or  purulent,  the  only  certain 
information  comes  from  an  exploratory  puncture  with  a  hypodermic  syringe. 
There  is  not  the  least  reason,  if  the  syringe  be  carefully  disinfected  and  the  fluid 
be  cautiously  withdrawn,  why  we  should  not  perform  this  perfectly  safe  experi- 
ment in  all  important  cases,  thus  making  the  diagnosis  certain.  Besides  a  macro- 
scopic inspection,  a  careful  microscopic  examination  of  the  fluid  withdrawn  is 
sometimes  of  importance.  Besides  the  ordinary  constituents — red  and  white  blood- 
corpuscles,  endothelial  cells,  and  Cholesterine  crystals — we  may  sometimes  find 
something  of  special  diagnostic  significance,  like  bacteria  in  septic  pleurisy,  car- 
cinoma-cells in  cancerous  pleurisy,  etc. 

We  can  not  always  judge  from  the  beginning  whether  a  pleurisy  is  tuber- 
cular or  not;  but  we  should  never  forget,  as  has  already  been  affirmed,  that  in 
every  case  of  pleurisy,  even  if  it  is  apparently  primary,  there  is  a  strong  sus- 
picion of  tuberculosis.  We  must  observe  in  particular  the  general  habit  and 
the  nutrition  of  the  patient,  and  inquire  into  the  hereditary  predisposition  and 
any  previous  illnesses.  In  the  further  course  of  the  disease  persistent  hectic  fever, 
slowly  increasing  emaciation  and  pallor,  fresh  relapses,  and  the  onset  of  pulmo- 
nary symptoms,  point  to  the  tubercular  character  of  the  pleurisy.  Every  double 
pleurisy,  and  every  pleurisy  associated  with  pericardial  or  peritoneal  symptoms, 
leads  us  most  decidedly  to  suspect  tuberculosis.  A  hemorrhagic  effusion,  as  we 
have  said,  points  strongly  to  tuberculosis.  Tubercle  bacilli  are  usually  not  pres- 
ent in  the  fluid  exuded  in  tubercular  pleurisy,  because  the  tubercular  nodules  on 
the  serous  membrane  hardly  ever  ulcerate. 

Prognosis. — The  prognosis,  as  regards  the  immediate  danger  of  the  disease, 
depends  entirely  upon  the  severity  of  the  symptoms,  and  especially  upon  the 
dyspnoea.  The  prognosis,  as  regards  the  further  course  of  the  disease,  depends 
chiefly  upon  the  nature  of  the  pleurisy.  Many  secondary  and  also  many  appar- 
ently primary  pleurisies,  although  extensive,  recover  completely  and  permanently 


264  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

after  weeks  or  months.  Unfortunately,  we  only  too  frequently  have  to  give  a 
doubtful  or  an  unfavorable  prognosis,  especially  if  the  tubercular  nature  of  the 
pleurisy  be  probable  or  certain.  The  prognosis  of  empyema  depends  partly  upon 
the  underlying  disease,  but  especially  upon  judicious  and  timely  operative  inter- 
ference. The  healing  process  in  empyema  may  occupy  many  months,  but  it  may 
finally  be  complete.  The  possibilities  of  a  spontaneous  rupture  of  empyema,  in- 
ternally or  externally  have  been  mentioned  above.  With  incomplete  healing, 
which  leaves  a  pleural  fistula,  we  must  fear  the  appearance  of  general  amyloid 
disease  in  various  organs. 

In  rare  instances  with  large  effusions  sudden  death  occurs,  an  event  which  can 
not  always  be  explained  with  certainty.  Probably  there  are  different  factors  in 
different  cases,  such  as  pulmonary  embolism,  cerebral  embolism,  sudden  cerebral 
anaemia,  weakness  of  the  heart,  or  the  onset  of  pulmonary  oedema. 

Treatment. — In  the  beginning  of  the  disease  the  treatment  is  purely  symp- 
tomatic. We  try  to  alleviate  the  patient's  symptoms,  the  pain  and  dyspnoea,  by 
local  applications,  especially  by  mustard  plasters,  warm  poultices,  which  are 
usually  more  grateful  than  cold  applications,  sometimes,  too,  by  dry  cups,  also  by 
embrocations  with  chloroform  liniment,  and,  with  severe  symptoms,  by  mor- 
phine internally  or  subcutaneously.  Unfortunately,  we  have  but  few  remedies  to 
check  the  inflammatory  process  in  the  pleura.  If  an  ice-bag  is  well  borne,  it  may 
be  of  service.  The  efficacy  of  the  much-used  painting  with  iodine  is  doubtful,  but 
it  may  always  be  tried  if  there  is  a  severe  pleuritic  pain.  An  iodoform  ointment, 
one  to  fifteen,  or  iodoform  collodion,  perhaps  deserves  more  confidence.  If  a  large 
effusion  has  formed,  we  try  to  hasten  its  absorption  by  diuretics.  Acetate  of  potas- 
sium, squills,  or  boro-tartrate  of  potassium  and  sodium*  [tartarus  boraxatus,  P.  Gr.] 
may  be  prescribed.  When  there  is  weak  action  of  the  heart,  infusion  of  digitalis 
may  be  given,  alone  or  combined  with  diuretics.  The  attempt  has  also  been  made 
to  draw  off  a  large  amount  of  water  from  the  body,  and  thus  to  hasten  the  absorp- 
tion of  the  effusion,  by  prescribing  drastic  purgatives  or  such  diaphoretics  as  pilo- 
carpine, salicylate  of  sodium,  and  hot  packs.  The  so-called  Schroth's  treatment 
serves  the  same  purpose — that  is,  withdrawing  as  much  fluid  as  possible  from  the 
ingesta — but  the  last-named  methods  of  treatment  generally  have  the  result  of 
exhausting  and  weakening  the  patient.  We  therefore  make  use  of  them  only  rarely. 
It  is  very  doubtful  whether  the  internal  exhibition  of  iodide  of  potassium  can  fur- 
ther the  absorption  of  the  effusion,  as  many  physicians  believe.  Besides  the  treat- 
ment by  drugs  we  must  also  take  care  to  give  the  patient  sufficient  food,  in  order 
to  pi'event  the  loss  of  strength. 

In  many  cases  the  operative  treatment  of  pleurisy  (introduced  by  Trousseau) — ■ 
the  evacuation  of  the  effusion  by  puncture — is  of  the  greatest  importance.  Many 
cases  of  pleurisy  with  effusion  run  a  favorable  course  without  it,  and  we  consider 
it  at  least  superfluous  to  puncture  every  effusion  without  sufficient  grounds,  but 
puncture  is  often  one  of  the  most  serviceable  therapeutic  influences  at  our  com- 
mand. The  first  and  most  important  indication  for  puncture  is  present  when  the 
effusion  becomes  so  large  as  to  be  directly  dangerous  to  life.  As  soon  as  the  pa- 
tient's dyspnoea  reaches  a  dangerous  degree,  and  the  cyanosis  becomes  marked  and 
the  pulse  weaker,  a  puncture  must  be  made  as  a  direct  vital  indication.  Where 
the  exudation  is  of  considerable  size  there  may  be  a  very  sudden  aggravation  of 
the  symptoms,  so  that  in  such  cases  one  should  not  wait  too  long.  Trousseau 
urged  that  tapping  should  invariably  be  performed  when  the  dullness  caused  by 
the  exudation  involves  not  only  the  back,  but  also  the  whole  or  nearly  all  of  the 
anterior  wall  of  the  thorax.     The  benefit  of  such  a  puncture  is  often  pronounced. 

[*  Wc  would  use  the  simpler  bitartrate  of  potassium. — Trans.] 


PLEURISY.  205 

The  second  indication  is  a  too  protracted  absorption  of  the  effusion.  Puncture  is 
indicated  if  the  effusion  does  not  disappear  after  an  apparent  remission  of  the 
inflammatory  symptoms,  especially  after  the  fever  has  gone.  We  often  see  the 
further  absorption  stimulated  by  such  a  puncture.  It  has  been  said  tbat,  if  pos- 
sible, tapping  should  be  delayed  until  the  fever  has  ceased,  but  to  us  this  docs 
not  seem  at  all  necessary.  We  have  repeatedly  performed  paracentesis  in  febrile 
cases,  whether  because  of  the  extent  of  the  exudation,  the  dyspnoea  of  the 
patient,  or  the  duration  of  the  disease;  and  we  have  not  infrequently  observed 
a  speedy  abatement  of  the  fever  after  the  withdrawal  of  the  exudation.  In  early 
cases,  of  course,  one  would  not  tap  unless  there  were  some  urgent  reason  for  it. 

[There  is  considerable  danger  in  delaying  interference  with  a  large  effusion. 
especially  if  it  has  come  on  pretty  rapidly,  however  comfortable  the  patient  may 
be.  The  liability  to  sudden  and  fatal  dyspnoea  under  these  circumstances  is  now 
well  recognized.] 

As  regards  the  performance  of  the  puncture,  we  can  not  here  go  into  all  the 
numerous  methods  and  forms  of  apparatus  proposed.  The  distinctions  are  imma- 
terial. The  simpler  the  method,  the  easier  it  is  to  perform,  and  hence  the  better 
it  is. 

Every  puncture  must  be  preceded  by  an  exploratory  puncture  in  order  to  settle 
the  diagnosis  as  to  the  presence  and  chai'acter  of  the  exudation.  A  medium-sized 
trocar  with  a  lateral  opening,  to  which  a  rubber  catheter  can  be  fastened,  serves  to 
evacuate  the  fluid.  Billroth's  and  Fräntzel's  trocars  are  useful.  The  operation 
can  be  done  with  at  least  equal  convenience  by  means  of  a  hollow  needle.  Our 
own  experience  with  the  form  of  needle  proposed  by  Fiedler  leads  us  to  recom- 
mend it  highly,  for  the  point  of  this  needle  can  not  irritate  the  tissues,  and  it  per- 
mits of  the  removal  of  any  clots  of  fibrine  which  may  offer  obstruction  to  the  flow 
of  liquid.  The  instruments  and  the  chest-wall  at  the  point  of  puncture  must  be 
carefully  disinfected.  We  usually  choose  rather  a  low  point  for  puncture,  some- 
where in  the  sixth  intercostal  space,  in  the  middle  or  posterior  axillary  line.  The 
patient  sits  up  in  bed,  but  is  held  and  supported  by  another  person,  when  it  is 
possible.  Before  and  during  the  puncture  he  takes  a  little  strong  wine.  A  small 
cut  of  the  skin  beforehand  sometimes  aids  the  insertion  of  the  trocar.  In  many 
cases,  especially  with  a  large  effusion,  we  can  evacuate  a  large  part  of  the  fluid  by 
simple  puncture  and  siphoning,  since  the  prevailing  pressure  in  pleuritic  effusions 
is,  with  few  exceptions,  positive,  from  ten  to  twenty-five  millimetres  of  mercury. 
The  evacuating  tube  of  the  trocar  must  be  previously  filled  with  carbolized  water 
and  conducted  under  a  layer  of  the  same  into  the  vessel  prepared  to  receive  the 
effusion  The  evacuation  of  the  effusion  should  always  be  slow  and  gradual. 
Many  physicians  advise  to  cease  when  1,500  c.  c.  have  been  removed,  but  if  the  fluid 
is  allowed  to  escape  slowly  and  everything  is  going  well,  this  quantity  may  often 
be  exceeded  with  impunity  in  the  case  of  large  exudations.  While,  as  we  have  said, 
in  most  instances  the  exudation  may  be  satisfactorily  removed  by  simple  puncture 
and  siphonage,  it  will  sometimes  prove  necessary  to  employ  aspiration.  Hence 
some  physicians  invariably  do  so,  and  to  this  there  is  no  objection,  even  if  it  is 
unnecessary.  The  forms  of  apparatus  most  used  for  this  are  those  invented  by 
Dieulafoy,  and  Potain.  In  puncture  with  aspiration  we  proceed  more  slowly  and 
cautiously. 

[The  necessity  for  two  punctures — one  exploratory,  the  other  distinctly  opera- 
tive— -does  not  seem  clear.  The  two  can  be  perfectly  combined,  a  fair-sized  trocar 
or  needle  being  as  easy  of  introduction  and  producing  really  no  more  pain  than  a 
very  fine  one,  and  being  more  sure  to  give  results  on  which  reliance  can  be  placed. 
A  preliminary  incision  through  the  skin  seems  also  useless,  and  has  never  been 
practiced  by  the  editor  in  a  considerable  experience  with  these  cases.      An  ordi- 


266  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

nary  Davidson's  syringe  makes  a  very  satisfactory  pump,  and  can  always  be 
obtained.  The  needle  or  trocar  should  be  withdrawn  immediately  as  soon  as  cough 
comes  on,  or  the  patient  shows  the  slightest  discomfort  due  to  the  removal  of  the 
fluid.] 

Unpleasant  incidents  which  may  cause  a  cessation  of  the  process  are  rare.  If 
the  patient  complains  of  dizziness  and  faintness  we  must  stop.  Sometimes  very 
severe  cough  occurs  on  puncturing,  at  which  we  must  also  stop.  Sometimes  we 
see,  after  the  puncture,  an  abundant  expectoration  of  frothy,  serous  sputum — 
"expectoration  albumi)ieuse"—a,  kind  of  pulmonaiw  oedema,  caused,  perhaps,  by 
a  marked  perviousness  of  the  walls  of  the  vessels,  or  by  weakness  of  the  left 
ventricle. 

When  the  process  is  over,  we  close  the  little  opening  with  a  bit  of  sticking- 
plaster  or  with  iodoform  collodion.  A  regular  surgical  dressing  is  scarcely  ever 
necessary. 

If  the  exploratory  puncture  has  shown  a  purulent  effusion,  we  can  first  evacuate 
the  pus  by  puncture,  if  the  vital  indication  exists.  But  a  permanent  cure  from 
tapping  is  exceptional.  The  pus  almost  always  reappears.  Empyema  is  like  an 
abscess,  which  can  not  be  cured  until  a  permanent,  free  exit  for  the  pus  has  been 
provided ;  hence  drainage  of  the  pleural  cavity  must  be  provided  for  after  the 
empyema  has  been  evacuated.  To  this  end,  therefore,  most  physicians  at  present 
open  the  pleural  cavity  in  empyema  by  an  incision—"  thoracotomy."  We  incise 
it  by  layers  in  the  fifth  or  sixth  intercostal  space,  outside  of  the  mammillary  line. 
The  length  of  the  incision  is  some  two  or  three  centimetres.  After  the  pus  has 
been  removed  we  have  an  artificial  pneumothorax  opening  outward.  The  incision 
may  be  dilated  if  necessary,  and  a  long  drainage-tube  is  then  thrust  through  it 
into  the  pleural  cavity,  the  external  end  being  prevented  from  slipping  into  the 
chest  by  transfixing  it  with  a  safety-pin.  Then  an  antiseptic  bandage  is  applied, 
which  at  first  must  be  changed  frequently,  as  long  as  there  is  much  secretion.  If 
the  pus  has  a  sufficient  exit,  the  fever  will  subside  at  once,  in  an  uncomplicated 
empyema.  A  fresh  rise  of  temperature  almost  always  depends  upon  the  reten- 
tion of  pus.  The  point  of  puncture  is  soon  changed  to  a  good  drainage-canal  by 
granulations.  We  can  then  take  out  the  tube,  clean  it,  and  easily  reinsert  it.  If  all 
goes  well,  we  can  gradually  shorten  the  drainage-tube  more  and  more,  and  finally 
remove  it  altogether.  The  cavity  of  the  empyema  has  filled  with  granulations,  and 
there  follows  a  definite  healing,  almost  always,  of  course,  with  marked  contraction. 
Many  cases  do  not  run  so  undisturbed  a  course.  If  the  exit  is  insufficient,  we 
must  sometimes  dilate  the  opening  with  some  blunt  instrument,  and  insert  a  lai'ger 
tube.  In  simple  empyema,  where  the  pus  does  not  smell  badly,  it  is  unnecessary 
to  wash  out  the  pleural  cavity  with  disinfecting  fluids,  like  salicylic  and  boracic 
acid  solution,  permanganate  of  potassium,  or  dilute  chlorine-water.  Carbolic  acid 
should  not  be  used,  on  account  of  the  danger  of  poisoning  by  it.  If  the  empyema 
is  septic,  or  if  there  is  from  the  first  a  stinking,  sanious  exudation,  it  is  necessary 
to  wash  it  out.  We  must  then  sometimes  make  a  second  counter-opening  in  the 
chest-wall  in  order  to  get  a  completely  free  discharge,  and  to  wash  out  the  pleural 
cavity  well.  The  details  upon  this  and  upon  many  other  special  points  in  the 
treatment  of  empyema,  and  especially  upon  the  resection  of  a  rib,  which  is  some- 
times necessary,  are  to  be  found  in  the  text-books  on  surgery.  It  may  be  added 
that  in  the  surgical  clinic  at  Leipsic  the  pleural  cavity  was  often  punctured  with 
an  ordinary  large-sized  trocar,  through  the  cannula  of  which  a  drainage-tube  was 
introduced  into  the  chest.  The  cannula  was  then  removed,  and  the  further  treat- 
ment was  as  above  described. 

In  treating  the  chronic,  contracted  pleurisies  with  thickening,  but  without  fluid 
effusion,  methodical  respiratory  efforts,  "lung-gymnastics,"  are  of  use.     Besides 


PNEUMOTHORAX.  207 

these  we  should  strengthen  the  general  condition  as  much  as  possible.  We  should 
advise  the  patient  to  breathe  deeply,  and  prescribe  cold  sponging  of  the  chest  daily. 
Inspiration  of  compressed  air  by  means  of  a  pneumatic  apparatus  is  often  accom- 
panied by  good  results.  Well-to-do  patients,  who  have  had  a  severe  pleurisy, 
should  be  sent  to  a  suitable  climatic  health-resort. 


CHAPTER  II. 
PERIPLEURITIS, 

Under  the  name  of  ''  peripleuritis  "  Wunderlich  was  the  first  to  describe  a  rare 
form  of  disease,  which  consists  of  an  inflammation  of  the  connective  tissue 
between  the  costal  pleura  and  the  ribs,  and  which  terminates  in  the  formation  of 
an  abscess.  Similar  cases  have  since  been  repeatedly  observed,  and  all  were  char- 
acterized by  the  lack  of  any  discoverable  aetiology.  There  is  neither  a  previous 
injury,  nor  a  primary  disease  of  the  ribs  or  the  pleura.  Nevertheless  the  cause  must 
be  sought  in  an  invasion  of  micrococci,  which  excite  the  suppuration.  A  knowl- 
edge of  the  particulars,  however,  can  only  be  gained  from  future  investigations. 
They  will  determine  whether  peripleuritis  can  be  regarded  as  an  independent  dis- 
ease or  not. 

The  disease  occurs  chiefly  in  men.  It  usually  begins  suddenly  with  a  chill, 
and  runs  its  course  with  quite  a  high  fever.  In  pronounced  cases  the  local  symp- 
toms have  the  greatest  similarity  to  those  of  an  empyema,  but  the  greater  protru- 
sion of  the  chest-wall  is  striking.  The  ribs  are  crowded  apart  by  the  abscess,  and 
there  is  often  spontaneous  rupture  externally,  scarcely  ever  into  the  pleura.  Per- 
cussion gives  no  symptoms  of  displacement  of  the  neighboring  organs,  a  distin- 
guishing point  from  empyema.  It  is  of  diagnostic  significance  that  we  can  often 
discover  normal  lung-tissue  containing  air  below  the  abscess.  The  mobility  of  the 
lower  border  of  the  lung  is  also  usually  retained,  contrary  to  what  is  the  case  in 
empyema.  Another  important  sign  was  first  brought  to  notice  by  Bartels :  the 
wall  of  the  abscess  relaxes  on  inspiration  and  becomes  tense  on  expiration.  We 
may  also  mention  that  acute  nephritis  has  often  been  observed  among  the  complica- 
tions. 

From  these  points  we  may  be  able  to  make  the  diagnosis  during  life,  at  least  in 
many  cases.  The  prognosis  is  quite  unfavorable,  but  recovery  does  occcur.  The 
treatment  can  be  only  operative,  and  is  quite  analogous  to  that  for  empyema. 


CHAPTER  III. 

PNEUMOTHORAX. 

( Pyo-jo  n  eumothorax.    Sero-pneumotlio  rax. ) 

iEtiology. — Pneumothorax — that  is,  a  collection  of  air  or  gas  in  the  pleural 
cavity — arises,  in  an  overwhelming  majority  of  cases,  from  the  penetration  of  air 
into  the  pleural  cavity  through  an  opening  in  the  pleura.  The  opening  may  be 
in  the  external  chest-wall  from  a  penetrating  wound  of  the  chest  or  an  empyema 
operation,  or  it  may  be  in  the  pulmonary  pleura.  Pneumothorax  is  by  far  most 
frequently  associated  with  phthisis,  when  a  cavity  lying  beneath  the  ptdmonary 
pleura  perforates  into  the  pleural  cavity.     This  is  more  apt  to  happen  in  compara- 


268  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

tively  acute  phthisis  than  in  very  chronic  forms,  because  the  extensive  adhesions 
and  contractions  in  the  latter  hinder  its  development.  It  usually  appears  in  quite 
far  advanced  cases,  but  it  may  sometimes  arise  with  but  slight  changes  in  the 
lung. 

Pulmonary  gangrene  or  abscess,  as  well  as  phthisis,  may  cause  pneumothorax 
by  perforation  into  the  pleural  cavity.  It  may  also  arise  from  the  rupture  of  an 
empyema  into  the  lung.  In  some  cases  a  perforation  of  the  oesophagus  or  stomach 
into  the  pleura,  as  in  gastric  ulcer,  has  been  observed,  with  the  formation  of  pneu- 
mothorax. 

The  development  of  this  condition  from  severe  injuries,  as  from  laceration 
of  the  lung,  without  injury  to  the  chest-wall,  is  rare.  Forced  respiratory  move- 
ments, associated  with  physical  exertion,  seem  especially  capable  of  exciting  such 
a  process.  We  have  ourselves  seen  pneumothorax  develop  suddenly  in  a  pre- 
viously healthy  woman  while  hanging  out  her  washing,  and  another  time  in  a 
young  man  during  very  labored  rowing.  Both  cases  recovered  rapidly  and  com- 
pletely. 

All  the  last-named  causes,  however,  are  far  less  important  than  phthisis.  We 
have  yet  to  mention  that  in  phthisis,  too,  there  is  sometimes  a  definite  exciting 
cause — severe  coughing,  vomiting,  or  muscular  exertion — which  may  favor  the 
development  of  the  pneumothorax. 

Many  authors  maintain  that,  by  decomposition  of  a  putrid  pleuritic  effusion, 
gas  may  be  produced,  and  thus  we  may  have  pneumothorax ;  but  such  an  event  is 
extremely  rare,  if  it  ever  happens. 

Pathological  Anatomy. — On  opening  the  pleural  cavity  a  part  of  the  air  usu- 
ally rushes  out,  sometimes  with  an  audible  noise.  We  then  look  into  a  large 
cavity  filled  with  air,  and  find,  in  total  pneumothorax,  the  lung  completely  re- 
tracted and  lying  compressed  against  the  vertebral  column.  If,  however,  the  air 
fills  only  a  part  of  the  pleural  cavity,  as  a  result  of  extensive  adhesions  of  the 
pleurae,  we  speak  of  a  circumscribed  or  sacculated  pneumothorax.  The  amount  of 
air  contained  in  the  pleural  cavity  may  reach  2,000  cubic  centimetres.  The  pressure 
which  it  is  under  is  almost  always  positive— on  an  average  five  or  ten  centimetres 
of  water. 

In  the  cases  of  pneumothorax  arising  from  perforation  of  the  pulmonary  pleura 
we  can  usually  make  out  the  point  of  perforation  in  the  lungs.  This  is  more  fre- 
quently situated  in  the  upper  lobe  than  in  the  lower.  Sometimes  it  is  already 
grown  over  or  is  covered  by  a  layer  of  fibrine,  and  can  no  longer  be  found.  The 
opening  is  usually  quite  small,  but  it  may  reach  the  size  of  a  ten-cent  piece.  Left- 
sided  pneumothorax  seems  to  be  somewhat  more  frequent  than  right-sided. 

The  pleura  itself  is  only  rarely  normal.  Usually  agents  of  inflammation  have 
entered  it  with  the  air,  and  hence  it  is  found  in  a  state  of  inflammation.  A  part 
of  the  cavity  is  then  filled  with  effusion.  This  is  usually  wholly  purulent — pyo- 
pneumothorax— or  sero-purulent,  but  it  may  even  be  serous  or  sero-fibrinous — 
sero-pneumothorax,  or  hydro-pneumothorax. 

The  neighboring  organs,  especially  the  heart  and  liver,  are  found  pushed  out 
of  their  normal  position,  as  in  large  pleuritic  effusions. 

Symptoms  and  Conrse. — The  onset  of  pneumothorax  (we  speak  in  what 
follows  especially  of  pneumothorax  in  phthisis)  is  quite  often  made  known  by  a 
sudden  pain,  usually  associated  with  an  increase  of  the  dyspnoea  and  of  the  general 
symptoms.  There  is  sometimes  collapse.  The  temperature  sinks  below  normal, 
the  pulse  rises  to  140  and  over.  The  patient  looks  pale  and  cyanotic.  He  usually 
sits  upright  or  is  in  a  half-sitting  position  in  bed,  either  more  on  the  affected  side, 
in  order  to  use  the  normal  lung  as  much  as  possible  for  breathing,  or  more  on  the 
sound  side  on  account  of  the  tenderness.     If  the  pneumothorax  has  come  on  as 


PNEUMOTHORAX.  269 

a  result  of  the  rupture  of  an  empyema  into  the  lungs,  there  is  at  the  same  time  a 
Very  abundant  expectoration  of  pus. 

Although  in  many  cases  the  symptoms  mentioned  lead  to  a  suspicion  of  pneu- 
mothorax, yet  a  certain  diagnosis  can  be  made  only  after  a  physical  examination. 

Inspection  gives  a  very  marked  distention  of  the  affected  side.  The  intercostal 
spaces  are  stretched  out,  or  even  protruded.  In  some  cases,  as  we  have  ourselves 
noticed,  there  is  a  marked  elastic  "  air-cushion  feeling  "  on  palpati  ug  the  intercostal 
spaces.  On  respiration,  the  affected  side  is  almost  entirely  motionless,  while  the 
excursions  of  the  other  side  are  the  more  marked.  The  displacement  of  the  heart 
is  often  evident  from  the  visible  displacement  of  the  apex-beat. 

Percussion  gives  over  the  pneumothorax  a  remarkably  loud,  full,  deep  note, 
but  usually  not  tympanitic,  on  account  of  the  tension  of  the  walls.  It  is  especially 
important  to  note  that  this  resonance  extends  beyond  the  normal  limits  of  the 
lung  on  the  right  down  to  the  seventh  or  eighth  rib,  and  on  the  left  to  the  fifth  or 
sixth  rib,  and  sometimes  even  to  the  edge  of  the  thorax. 

The  displacement  of  the  neighboring  organs  can  also  be  made  out  by  percus- 
sion. With  right-sided  pneumothorax  we  find  the  lower  border  of  the  liver  dull- 
ness abnormally  low,  and  the  left  border  of  the  cardiac  dullness  pushed  over  to 
the  anterior  axillary  line.  In  left-sided  pneumothorax  the  cardiac  dullness  is 
usually  entirely  absent  from  its  normal  place,  and  is  found  instead  to  the  right  of 
the  sternum.  The  left  lobe  of  the  liver  is  pushed  downward,  and  we  do  not  find 
tympanitic  resonance  in  the  semilunar  space. 

Upon  auscultation  we  are  struck  by  the  entire  absence  of  respiratory  murmur. 
This  is  in  special  contrast  to  the  clear  resonance  on  percussion.  In  other  cases, 
however,  we  hear  a  number  of  metallic  sounds,  at  least  in  many  places  and  at 
many  times,  which  are  very  characteristic  of  pneumothorax.  First  among  these 
is  amphoric,  metallic  respiration.  This  arises  in  open  pneumothorax  {vide  infra) 
from  the  direct  passage  of  the  air  in  and  out,  but  in  all  other  cases  it  is  the  ordi- 
nary respiratory  murmur  of  the  larynx,  trachea,  and  lungs,  which  has  acquired  a 
metallic  timbre  from  resonance  in  the  pneumothorax.  In  an  analogous  way  arise 
the  metallic-sounding  rales  ["  metallic  tinkling  "],  and  the  metallic  resonance  of 
the  cough  and  voice.  Heubner  has  devised  a  particularly  beautiful  and  practi- 
cally important  method  for  demonstrating  the  metallic  sound  in  pneumothorax. 
If  we  strike  lightly  on  a  pleximeter  with  a  little  rod,  usually  the  handle  of  a  per- 
cussion hammer,  while  we  auscult  near  it — "  rod  percussion  " — we  very  often  hear 
quite  a  distinct  high  metallic  sound. 

The  vocal  fremitus  over  a  pneumothorax  is  usually  diminished,  but  it  may  be 
felt  in  spite  of  quite  a  large  collection  of  air. 

A  number  of  special  physical  signs  are  found  if  a  purulent  or  serous  effusion 
be  added  to  the  pneumothorax.  In  the  first  place,  the  resonance  is  thereby  ren- 
dered dull,  to  a  greater  or  less  extent,  in  the  lower  parts  of  the  chest.  The  bound- 
aries of  the  fluid  by  percussion  show  a  very  evident  change  with  the  patient's 
change  of  position,  because  the  fluid  in  pneumothorax  can  move  easily  in  all 
directions.  Since  the  form  of  the  airspace  left  must  therefore  change,  the  pitch 
of  all  the  metallic  sounds  manifest  anywhere  must  change  too,  when  the  patient 
sits  up  or  lies  down — Biermer's  change  of  note.  In  many  cases  at  every  motion  of 
the  fluid,  excited  for  example  by  slightly  shaking  the  patient,  there  arises  a  metal- 
lic splashing  sound,  the  so-called  succussion  of  Hippocrates. 

Forms  of  Pneumothorax. — According  to  the  condition  of  the  perf  oration  during 
life,  we  distinguish  three  kinds  of  pneumothorax  (Weil).  We  speak  of  an  "open 
pneumothorax,"  if  the  point  of  perforation  remains  open,  so  that  the  air  on  respi- 
ration constantly  passes  in  and  out  of  the  pleural  cavity.  If  the  perforation  is 
completely  closed,  we  have  a  "closed  pneumothorax."    The  third  and  most  fre- 


270  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

quent  form  is  the  "  valvular  pneumothorax,"  in  which  air  enters  the  pleural  cavity 
at  each  inspiration,  but  on  expiration  there  is  a  valve-like  closure  of  the  perfora- 
tion, and  thus  the  air  can  not  escape  again ;  but  as  soon  as  the  pressure  in  the 
pleural  cavity  increases  so  that  no  more  air  can  enter  it  on  inspiration,  the  valvu- 
lar pneumothorax  becomes  closed.  In  open  pneumothorax  the  pressure  in  the 
pleural  cavity  must  be  the  same  as  the  atmospheric  pressure.  A  positive  pressure 
in  the  pleural  cavity  can  exist  only  in  a  closed  or  a  valvular  pneumothorax. 

The  clinical  diagnosis  of  the  form  of  pneumothorax  is  not  always  possible,  and 
has  usually  no  great  practical  importance.  The  very  loud,  metallic,  amphoric 
respiratory  murmur,  which  may  be  heard  in  open  pneumothorax,  must  be  men- 
tioned, and  Wintrich's  change  of  pitch  (see  page  223)  can  sometimes  be  heard 
in  this  form.  It  is  worthy  of  mention  that  symptoms  of  displacement  of  the 
neighboring  organs  must  also  arise  in  open  pneumothorax.  The  predominant 
atmospheric  pressure  here  is  positive  in  contrast  to  the  negative  pressui'e  in  the 
other  pleural  cavity,  and  to  the  normal  negative  pressure  which  previously 
acted  on  the  upper  surface  of  the  diaphragm.  A  very  marked  protrusion  of  the 
affected  side,  and  great  displacement  of  the  heart  and  liver,  however,  speak  most 
strongly  against  an  open  pneumothorax.  Some  authors  have  tried  to  find  a  point 
of  distinction  for  the  different  forms  of  pneumothorax  in  the  composition  of  the 
gas  in  the  pleural  cavity,  but  the  results  of  chemical  analysis  are  still  contradic- 
tory. According  to  Ewald,  we  find  in  open  pneumothorax  not  over  five  per  cent, 
of  carbonic  acid  and  about  twelve  to  eighteen  per  cent,  of  oxygen ;  in  closed  pneu- 
mothorax, however,  fifteen  to  twenty  per  cent,  of  carbonic  acid  and  ten  per  cent. 
at  most  of  oxygen.  If  in  an  open  pyo-pneumothorax  or  sero-pneumothorax  the 
point  of  perforation  lies  below  the  level  of  the  fluid,  there  sometimes  arise  on 
every  inspiration  metallic  sounds,  since  the  bubbles  of  air  drawn  in  rise  and  come 
up  through  the  fluid — "the  water-pipe  sound,"  "metallic  tinkling."  A  peculiar 
sipping  and  short  snapping  sound  on  inspiration,  heard  by  us  in  one  case,  seems  to 
point  directly  to  the  existence  of  a  valvular  pneumothorax.  Upon  change  of  po- 
sition of  the  patient  we  can  often  make  out  Biermer's  change  of  note. 

Course  of  the  Disease. — In  many  cases  the  occurrence  of  pneumothorax  causes 
such  a  high  degree  of  respiratory  disturbance  that  death  ensues  in  a  few  hours  or 
days.  In  other  cases  the  patient  improves,  and  may  feel  quite  well  for  a  long  time 
hi  spite  of  the  condition.  Usually,  of  course,  the  underlying  disease,  commonly 
phthisis,  leads  to  death  after  a  longer  or  shorter  period.  Pneumothorax  may  some- 
times heal.  The  healing  takes  place  in  this  way,  that  the  air  is  first  replaced  by 
a  fluid  effusion,  and  then  the  latter  is  gradually  absorbed,  but  the  air  may  also  be 
wholly  or  partly  absorbed.  It  depends  upon  the  origin  of  the  lesion,  then,  and 
lipon  the  intensity  of  the  underlying  disease,  whether  the  recovery  is  permanent 
or  not. 

Diagnosis. — The  diagnosis  of  pneumothorax  is  usually  easy  with  careful  exami- 
nation, but  the  symptoms  may  sometimes  be  of  so  little  prominence  as  to  excuse 
overlooking  it.  It  is  very  difficult  and  often  quite  impossible  to  make  a  differen- 
tial diagnosis  between  very  large  cavities  and  a  saccular  pneumothorax,  since  both 
conditions  must  have  in  part  precisely  the  same  symptoms.  We  may  mention  as 
the  chief  points  in  distinction :  A  cavity  is  apt  to  be  situated  in  the  apex,  pneumo- 
thorax in  the  lower  part  of  the  thorax;  over  a  cavity  the  chest- wall  is  often 
sunken  in,  over  pneumothorax  it  is  prominent;  the  vocal  fremitus  is  usually 
marked  over  a  cavity,  weak  over  pneumothorax ;  symptoms  of  displacement,  and 
also  evident  succussion,  point  to  pneumothorax. 

Treatment. — The  only  remedy  which  can  alleviate  the  often  severe  symptoms 
is  morphine.  In  hopeless  cases  we  may  confine  ourselves  to  prescribing  this 
exclusively,  both  internally  and  subcutaneously ;  but  in  cases  where  the  patient's 


HYDROTHORAX.     HJSMATOTHORAX.  271 

previous  strength  was  fairly  good,  wo  may  try  to  obtain,  by  operative  inter- 
ference, an  improvement  of  the  symptoms,  and  finally  a  complete  healing  of  the 
pneumothorax.  If  there  is  simple  pneumothorax  without  a  fluid  effusion,  we  try 
to  remove  as  much  air  as  possible  by  aspiration.  With  a  large  serous  effusion  re- 
moval of  the  effusion  is  indicated,  and  with  purulent  effusion  either  a  simple  punct- 
itre,  or,  better,  puncture  or  incision  with  subsequent  drainage.  The  method  then  is 
just  the  same  as  in  the  treatment  of  empyema.  "We  must  also  state  that  the  above- 
mentioned  improvement  or  healing  in  pneumothorax  has  been  repeatedly  observed 
independently  of  any  operative  interference. 


CHAPTER  IV. 
HYDROTHORAX.     H2EMATOTHORAX. 

1.  Hydrothorax. — We  term  the  occurrence  of  a  serous  transudation  into  the 
pleural  cavity,  independent  of  an  inflammation  of  the  pleura,  hydrothorax,  or 
thoracic  dropsy.  The  cause  of  hydrothorax  is  in  rare  cases  a  local  hindrance  to 
the  outflow  of  venous  blood  or  lymph  from  the  thorax,  as  in  compression  of  the 
veins  or  of  the  thoracic  duct  by  tumors;  but  in  the  great  majority  of  cases  the 
hydrothorax  is  part  of  a  general  dropsy,  occurring  especially  in  pulmonary 
emphysema  and  in  cardiac  or  renal  disease.  Hydrothorax  is  often  first  developed 
after  marked  oedema  of  the  subcutaneous  cellular  tissue  and  ascites,  but  it  may 
sometimes  be  one  of  the  first  symptoms  of  dropsy.  It  is  usually  bilateral,  but  it  is 
often  unilateral,  or  at  least  much  larger  on  one  side  than  on  the  other.  The 
pleura  itself  is  normal  or  else  cedematous.  We  often  find  it  traversed  with  a  net- 
work of  dilated  lymphatics.  The  serous  fluid  in  hydrothorax  is  distinguished 
from  an  inflammatory  serous  effusion  by  the  smaller  amount  of  albumen  in  it,  by 
the  scanty  number  of  cell-elements,  and  by  the  absence  of  or  the  slight  tendency 
to  spontaneous  coagulation. 

The  clinical  importance  of  hydrothorax  lies  in  the  hindrance  to  respiration 
which  it  causes.  As  a  result  of  this  the  hydrothorax  may  be  regarded  in  many 
cases,  especially  in  renal  disease,  as  the  chief  cause  of  death.  The  objective  evi- 
dence of  it  comes  from  the  physical  examination,  which  must,  in  general,  give 
the  same  signs  as  in  pleuritic  effusion.  We  can  note  only  the  bronchial  respira- 
tion from  compression  in  hydrothorax,  which  is  often  very  loud,  and  which  may 
even  give  rise  to  a  confusion  with  pneumonic  infiltration  in  the  lungs. 
This  frequent  and  very  loud  respiratory  murmur,  contrasting  with  that  of  pleu- 
ritic effusion,  is  explained  by  the  normal  condition  of  the  lungs  and  the  absence 
of  all  adhesions.  For  the  same  reason,  too,  the  change  in  the  boundary  of  the 
dullness,  as  a  result  of  the  patient's  change  of  position,  is  usually  more  marked  in 
hydrothorax  than  in  pleuritic  effusion.  We  often  hear  crepitant  rales  over  the 
hydrothorax,  which  arise  in  the  retracted  and  partly  atelectatic  lung.  The  chief 
factor,  however,  in  distinguishing  hydrothorax  from  a  pleuritic  effusion  is  the 
character  of  the  primary  disease  if  any  exists. 

The  treatment  is  directed  especially  to  the  underlying  disease.  If  we  succeed 
in  regulating  the  heart's  action,  or  in  restoring  the  secretion  of  urine,  the  hydro- 
thorax often  disappears  with  the  other  dropsical  symptoms.  If  the  dyspnoea 
caused  by  it  reaches  a  dangerous  degree,  we  often  see  great  relief  from  aspirating 
the  fluid.  The  nature  of  the  underlying  condition,  of  course,  renders  the  benefit 
in  many  cases  only  transitory. 

2.  Haematothorax. — Effusions  of  blood  into  the  pleural  cavity  (hsematothorax) 


272  DISEASES  OF  THE  RESPIRATORY  ORGANS. 

arise  most  frequently  from  traumatic  lacerations  of  blood-vessels,  rarely  from  the 
bursting  of  an  aneurism  of  the  aorta  into  the  pleural  cavity,  from  erosion  of  an 
intercostal  artery  in  caries  of  the  ribs,  from  the  rupture  of  a  cavity  into  the  pleura 
in  phthisis,  if  it  simultaneously  opens  a  blood-vessel,  etc.  In  many  such  cases  a 
typical  exudative  pleurisy  follows  the  effusion  of  blood.  The  physical  signs  are 
the  same  as  in  other  pleural  effusions.  Severe  dyspnoea  may  demand  the  removal 
of  the  blood  by  puncture,  or  even  by  an  incision. 


CHAPTER  V. 
NEW   GROWTHS   OF   THE   PLEURA. 

The  majority  of  new  growths  occurring  in  the  pleura  are  of  a  secondary  nature. 
We  sometimes  find  single  metastatic  nodules  of  cancer  in  the  pleura  after  primary 
carcinoma  of  other  organs,  especially  of  the  mammary  gland  and  the  lungs,  but 
most  carcinomata  of  the  pleura  arise  from  primary  carcinoma ta  of  the  lungs 
owing  to  a  direct  invasion  of  the  pleura  by  the  new  growth. 

Of  the  primary  new  growths  in  the  pleura,  only  one  is  of  great  importance — 
the  endothelial  carcinoma,  first  described  by  E.  Wagner.  This  develops  de  novo, 
in  a  diffuse  manner,  from  a  proliferation  of  the  endothelial  cells  of  the  lymphatics 
and  the  connective  tissue.  Metastases  occur  in  the  lungs,  in  the  lymph-glands,  in 
the  liver,  in  the  muscles,  etc. 

Single  secondary  nodules  of  cancer  in  the  pleura  cause  no  special  clinical  symp- 
toms, but  the  cases  of  diffuse  cancer  of  the  pleura  as  a  result  of  primary  cancer  of 
the  lungs  are  important,  inasmuch  as  the  symptoms  of  disease  of  the  pleura  often 
quite  predominate  over  the  pulmonary  disease.  The  dullness  is  intense,  the  re- 
spiratory murmur  and  the  vocal  fremitus  diminished.  In  one  such  case  we  saw 
a  proliferation  of  the  cancer  upon  the  ribs  in  front  so  that  thei*e  was  externally  a 
very  marked  circumscribed  swelling.  The  character  of  the  sputum  is  the  only 
thing  that  can  give  us  definite  information  as  to  the  origin  of  the  new  growth 
in  the  lungs  (see  the  chapter  on  cancer  of  the  lungs). 

Primary  endothelial  carcinoma  of  the  pleura  runs  a  course  similar  to  chronic 
pleurisy.  As  we  sometimes  find  a  co-existing  fluid  effusion  in  the  pleural  cavity, 
displacement  of  the  neighboring  oi'gans  may  occur.  The  affection  goes  on  for  a 
long  time  without  fever,  or  with  slight  and  irregular  elevations  of  temperature. 
Most  cancers  of  the  pleura  are  associated  with  severe  pain. 

The  diagnosis  of  new  growths  in  the  pleura  can  usually  be  made  only,  if  at  all, 
in  the  more  advanced  stages  of  the  disease.  At  first  almost  all  the  cases  are 
regarded  as  simple  or  tubercular  chronic  pleurisy.  The  diagnosis  is  founded  less 
upon  the  physical  signs  than  upon  the  general  course  of  the  disease,  the  habit  of 
the  patient,  and  the  evidence  of  some  metastases  in  the  glands  and  other  organs. 
In  some  cases  characteristic  elements  of  the  new  growth  can  be  found  by  the 
microscope  in  the  cloudy  fluid  obtained  by  an  exploratory  puncture. 

The  prognosis  is  absolutely  unfavorable,  the  treatment  purely  symptomatic.  In 
endothelial  carcinoma  we  might  perhaps  try  arsenic  internally. 


MEDIASTINAL  TUMORS.  273 

CHAPTER  VI. 
MEDIASTINAL   TUMORS. 

In  the  anterior  mediastinum,  in  quite  rare  cases,  extensive  new  growths  occur, 
which  are  of  importance  on  account  of  their  severe  clinical  symptoms.  The 
point  of  origin  for  the  tumor  is  either  the  mediastinal  lymph-glands,  or  the 
connective  tissue,  or  sometimes  the  remains  of  the  thymus  gland.  In  their 
anatomical  character  the  tumors  are  almost  always  sarcomata,  usually  lympho- 
sarcoma, rarely  alveolar  sarcoma.  They  usually  occur  in  youth  or  middle  age, 
and  are  somewhat  more  frequent  in  men  than  in  women.  The  special  «etiological 
factors  are  unknown.  In  some  cases  an  injury  is  stated  to  be  the  cause  of  'their 
origin. 

The  clinical  symptoms  are  usually  of  a  very  indefinite  nature  at  first.  The 
patient  complains  of  general  languor,  headache,  pain  in  the  chest,  and  slight  diffi- 
culty in  breathing,  and  only  gradually  do  severe  subjective  and  objective  symp- 
toms develop  in  the  chest. 

The  symptoms  are  in  part  directly  due  to  the  tumor,  but  in  larger  part  they  are 
symptoms  of  compression  from  the  gradually  increasing  pressure  of  the  tumor 
on  a  number  of  neighboring  organs. 

The  pain  in  the  chest,  which  is  located  chiefly  in  the  sternal  region,  and  is 
associated  with  a  marked  feeling  of  oppression,  may  be  very  severe.  It  sometimes 
shoots  into  the  lateral  portions  of  the  chest  and  into  the  arms,  showing  pressure 
on  the  brachial  plexus. 

The  dyspnoea  may  finally  increase  to  an  extreme  degree.  A  patient  with 
lympho-sarcoma  under  our  observation  could,  in  the  last  days  of  her  life,  breathe 
only  while  standing.  The  dyspnoea  is  due  to  a  compression  of  the  heart  and 
lungs,  and  sometimes  to  actual  stenosis  of  the  trachea  or  a  primary  bronchus. 
Paralysis  of  the  dilators  of  the  glottis  may  also  occur  from  a  pressure  paralysis 
of  the  recurrent  nerves.  Paralysis  of  one  vocal  cord  has  been  repeatedly  observed. 
In  the  case  mentioned  above  a  marked  goitre  developed,  as  a  result  of  vascular 
stasis,  which  further  increased  the  dyspnoea  by  pressure  on  the  trachea.  A  hydro- 
thorax  from  local  venous  stasis  may  also  aid  in  increasing  the  dyspnoea. 

Pressure  on  the  oesophagus,  and  disturbances  of  deglutition  due  to  it,  are  rare. 
Pressure  on  the  vagus  nerve  and  the  sympathetic  sometimes  causes  anomalies  in 
the  rate  of  the  pulse — either  marked  acceleration  or  slowing  of  the  pulse..  If 
the  sympathetic  is  involved  there  is  inequality  of  the  pupils.  In  some  cases,  by 
pressure  on  the  tumor,  an  artificial  dilatation  of  the  pupil  can  be  excited  at  will. 
By  pressure  on  the  vessels,  especially  on  the  superior  vena  cava,  the  subclavian 
vein,  etc.,  oedema  and  cyanosis  may  arise  in  the  corresponding  parts  of  the  body. 

Objective  examination  of  the  chest  gives  a  marked  diffuse  prominence  of  the 
sternal  region  in  a  part  of  the  advanced  cases;  in  other  cases  this  swelling  is 
absent.  The  discovery  of  an  abnormal  dullness  in  the  anterior  part  of  the  chest 
is  of  diagnostic  importance ;  this  usually  joins  the  cardiac  dullness  on  the  left, 
and  on  the  right  it  extends  a  varying  distance  beyond  the  right  border  of  the 
sternum.  The  heart  is  often  pushed  somewhat  to  the  left.  We  heard  over  the 
pulmonary  artery  in  our  case  a  marked  systolic  murmur,  caused  by  compression 
of  the  vessel.     A  dissimilarity  of  the  pulse  on  the  two  sides  is  not  infrequent. 

The  diagnosis  of  a  mediastinal  tumor  is  usually  possible  in  cases  with  well- 
marked  symptoms,  but  in  other  cases  it  is  difficult  and  uncertain.  The  differential 
diagnosis  between  mediastinal  tumors  and  aneurism  of  the  aorta  (q.  v.)  causes 
especially  great  difficulty.  Tumors  may  also  be  confounded  with  abscesses  in  the 
anterior  mediastinum. 
18 


274 


DISEASES  OF  THE  RESPIRATORY  ORGANS. 


The  prognosis  is  in  all  cases  absolutely  unfavorable.  The  disease  terminates 
fatally,  sometimes  after  a  duration  of  six  months  or  a  year. 

The  treatment  can  be  only  symptomatic.  Internally  we  may  try  iodide  of  po- 
tassium or  arsenic,  and  externally  iodoform  ointment.  In  the  last  stages  of  the 
disease  we  must  try  to  alleviate  the  patient's  great  distress  by  narcotics. 


CHAPTER  VII. 

ACTINOMYCOSIS   OF   THE   THORACIC   CAVITY. 

Bollinger  and  others  have  described  a  peculiar  tumor  affecting  the  jaw-bones 
of  cattle,  and  occasioned  by  the  presence  of  a  special  form  of  fungus,  known  as  the 
actinomyces  or  ray-fungus.  More  recently  a  class  of  diseases  has  been  studied 
in  human  beings,  occasioned  by  the  same  fungus  (Ponfick,  Israel,  and  others). 
These  diseases  may,  as  in  cattle,  affect  the  jaws,  the  floor  of  the  mouth,  and  the 
neck ;  but  in  these  cases  they  are  mainly  of  surgical  interest.  The  actinomycotic 
diseases  of  the  internal  organs,  however,  possess  a  great  clinical  importance ;  and, 
inasmuch  as  the  lungs  and  pleura  are  the  most  frequently  affected  organs,  it  will 
be  well  to  present  briefly  here  the  most  important  facts  which  have  as  yet  been 
learned  with  regard  to  actinomycosis.  The  botanical  position  of  actinomyces  has 
not  yet  been  definitively  settled.  Cohn  and  O.  Israel  regard  it  as  a  mold  fungus. 
Boström.  on  the  other  hand,  classes  it  with  the  algae,  and  namely  with  the  variety 

cladothrix.  In  its  growth,  the  fungus  forms 
small  or  moderate-sized  gray  or  sulphur- 
yellow  nodules  which  may  be  distinguished 
with  the  naked  eye  in  the  pus  of  the  dis- 
eased tissue  (see  below),  and  which  upon 
microscopic  examination  resolve  them- 
selves into  a  tangle  of  mycelium.  It  is  an 
especial  characteristic  that  many  of  these 
mycelia  bear  on  their  ends  a  club-shaped 
swelling.  These  are  placed  for  the  most 
part  like  radii  on  the  periphery  of  a  nod- 
ule, and  so  surround  the  entire  mass  like 
a  circlet  of  rays  (see  Fig.  28).  In  nature 
actinomyces  seems  to  appear  especially 
upon  plants,  for  example  upon  the  beard 
of  spikes  of  wheat.  Thus  is  explained  the 
frequency  of  infection  in  the  plant-eating 
cattle,  and  a  similar  direct  infection  seems 
occasionally  to  be  possible  in  man.  It  is 
worthy  of  note  that  the  fungus  seems  to 
locate  itself  often  in  carious  teeth.  Thus 
apparently  arises  the  above-mentioned  dis- 
ease in  the  buccal  cavity;  while  on  the 
other  hand,  the  fungus  may  be  carried  further  by  inspiration  into  the  respiratory 
tract,  or  by  swallowing  into  the  primce  vice.  Of  course  it  may  also  be  directly 
swallowed  or  inhaled. 

Wherever  the  fungus  fastens  itself  in  the  body  it  occasions  first  a  new  growth 
of  granulation-tissue,  which  has  a  tendency  to  break  down  into  a  whitish  or 
brownish  pasty  mass.     The  brown  color  is  occasioned  by  the  haemorrhage  which 


^ 


Fig.  28. — Masses  of  actinomyces,  from  Johne. 


ACTINOMYCOSIS  OF  THE  THORACIC   CAVITY.  275 

frequently  occurs.  Very  often  actinomycosis  goes  on  to  suppuration;  still,  this 
probably  depends  upon  the  influence  of  pathogenic  germs  which  have  secondarily 
infected  the  part.  Of  especial  importance  is  the  tendency  of  the  disease  to  extend 
from  the  lungs  to  the  pleura  and  from  the  pleura  to  the  peripleuritic  connective 
tissue,  and  still  further  to  the  wall  of  the  thorax.  Thus  arise  not  only  extensive 
abscesses  and  wide-branching  fistulous  tracts,  but  also  a  very  characteristic, 
extremely  tough  infiltration  of  interstitial  tissue  in  the  affected  part.  Not  infre- 
quently there  is  at  last  a  perforation  reaching  the  outer  surface  of  the  body. 

The  entire  process,  as  a  rule,  is  slow  and  insidious,  but  constantly  progressive. 
The  symptoms  consist  at  first  in  slight  thoracic  discomfort,  pain,  cough,  and  expec- 
toration. Physical  examination  will  often  detect  changes  in  the  lungs,  but  the 
correct  interpretation  of  the  signs  found  is  of  course  at  first  difficult,  if  not  impos- 
sible. The  more  the  disease  spreads  the  greater  is  the  distress.  Usually  there  is 
hectic  fever,  which  may  assume  a  pyaemic  character  if  there  is  extensive  suppura- 
tion. The  patient  gradually  loses  flesh,  and  in  repeated  instances  amyloid  degen- 
eration of  the  liver,  spleen,  and  kidneys  has  been  observed.  If  a  focus  breaks  into 
a  pulmonary  vein,  the  disease  may  be  developed  by  metastasis  in  other  internal 
viscera.  Moreover,  there  may  be  a  direct  extension  of  the  disease  to  the  pericar- 
dium, or  through  the  diaphragm  into  the  peritoneal  cavity. 

The  diagnosis  of  actinomycosis  is  at  first  difficult.  It  is  established  when  the 
characteristic  fungus  is  found  in  the  sputum,  but  this  has  occurred  in  only  a  few 
cases  as  yet.  If  very  extensive  peripleuritic  and  pericostal  suppuration  has  taken 
place,  and  the  process  has  spontaneously  broken  outward  or  been  laid  open  by 
surgical  means,  the  demonstration  above  described  in  reference  to  the  fungus  is 
easy. 

The  treatment  can  only  be  symptomatic,  unless  the  diseased  spot  can  be  reached 
by  operation,  and  then  the  treatment  becomes  surgical.  Permanent  cure  has  so 
far  been  attained  in  but  rare  instances. 


DISEASES   OF   THE   CIRCULATORY   ORGANS. 


SECTION  I. 
Diseases  of  the  Heart. 

CHAPTER   I. 

ACUTE    ENDOCARDITIS. 

{Endocarditis  verrucosa.    Endocarditis  ulcerosa.) 

JEtiology. — Excitants  of  inflammation  of  different  sorts,  which  circulate  in  the 
blood,  may  settle  on  the  endocardium,  especially  on  the  valves  of  the  heart,  and 
there  give  rise  to  an  acute  endocarditis.  Endocarditis,  therefore,  in  its  etiological 
relations,  is  not  to  he  regarded  as  a  single  disease ;  infectious  agents  of  inflamma- 
tion seem  to  be  its  chief,  if  not  exclusive,  cause.  Lately,  pathogenic  micro-organ- 
isms have  been  injected  into  the  blood  (the  streptococcus  pyogenes,  staphylococcus 
aureus,  and  others),  and  in  this  way  an  artificial  endocarditis  has  been  set  up  in 
animals.  The  experiments  are  more  apt  to  succeed  if  the  valves  or  tbe  inner  coat 
of  the  vessels  have  been  subjected  to  some  slight  injury  before  the  injection, 
thus  promoting  the  settling  of  the  germs  upon  them  (Orth  and  Wyssokowitsch, 
Ribbert). 

Of  the  infectious  diseases  to  which  man  is  liable,  it  is  predominantly  acute 
articular  rheumatism  in  which  acute  endocarditis  is  a  frequent  and  important 
complication.  Endocarditis  also  occurs  in  certain  diseases  which  are  probably 
allied  astiologically  to  articular  rheumatism,  in  certain  forms  of  "  hemorrhagic 
disease,"  such  as  peliosis  rbeumatica,  and  in  chorea.  The  appearance  of  endocar- 
ditis as  a  result  of  gonorrhoea  or  of  gonorrhceal  rheumatism  is  rare,  but  it  has  cer- 
tainly occurred.  In  the  course  of  the  acute  exanthemata,  too,  like  scarlet  fever 
and  measles,  as  well  as  in  acute  and  chronic  nephritis,  we  sometimes  notice  the 
appearance  of  an  acute  endocarditis. 

While  endocarditis  in  the  diseases  previously  named  often  takes  a  severe 
course,  in  many  other  infectious  diseases — like  typhoid,  small-pox,  and  quite  fre- 
quently chronic  phthisis — slight  inflammations  of  the  endocardium  are  often 
found  in  the  cadaver,  which  have  an  anatomical  but  not  a  clinical  interest.  These 
probably  are  not  directly  connected  with  the  primary  disease,  but  are  a  complica- 
tion due  to  the  absorption  of  septic  material,  the  occurrence  of  this  state  of  things 
being  easily  explained  by  the  ulcerative  processes  of  phthisis,  the  intestinal  ulcers 
of  typhoid,  etc.  We  can  probably  explain  in  an  analogous  fashion  the  origin  of 
the  limited  endocarditic  aggregations  which  we  sometimes  find  in  persons  who 
have  died  of  ulcerative  carcinomata,  and  similar  diseases. 

Acute  endocarditis  plays  ä  very  important  role  as  a  complication  of  severe 
septic  and  pyaemic  diseases.  Beyond  a  doubt  the  same  pathogenic  bacteria  are 
here  the  cause  both  of  the  general  sepsis  and  of  the  special  acute  endocarditis; 
but  the  latter  at  times  stands  so  prominently  in  the  central  point  of  the  picture 

(276) 


ACUTE  ENDOCARDITIS.  277 

that  we  may  very  well  give  its  name  to  the  whole  disease,  on  the  principle  "a 
potiori  fit  denominatio." 

Finally,  we  have  still  to  mention  the  important  fact  that  acute  endocarditis 
quite  frequently  develops  on  the  soil  of  an  already  existing  chronic  endocarditis — 
the  so-called  acute  recurring  endocarditis.  In  women,  pregnancy  and  the  puer- 
peral state  sometimes  seem  to  give  the  occasion  for  a  recrudescence  of  the  endo- 
carditis; but  possibly  the  old  endocarditis  merely  furnishes  a  favorable  soil  for  a 
new  infection. 

Pathological  Anatomy. — We  usually  distinguish  an  endocarditis  verrucosa, 
with  the  formation  of  large  or  small  papillary  nodules  on  the  endocardium,  and 
an  endocarditis  ulcerosa  (endocarditis  diphtheritica),  with  ulcerations  as  a  result 
of  the  destruction  and  wasting  away  of  the  superficially  necrosed  tissue.  The 
malignant,  invariably  fatal  form  of  severe  septic  endocarditis  is  chiefly  ulcerative 
endocarditis.  Endocarditis  verrucosa  is  the  milder  form,  which  is  seen  especially 
in  acute  rheumatism,  but  we  can  not  draw  either  a  sharp  anatomical  or  a  sharp 
clinical  distinction  between  the  two,  since  malignant  cases  of  endocarditis  verru- 
cosa are  also  observed.  It  is  ajt  present  still  impossible  to  give  a  positive  aotiolog- 
ical  classification  of  the  different  forms  of  endocarditis. 

The  endocardial  growths  are  usually  situated  on  the  valves,  especially  on  their 
edges  of  closure.  More  rarely  we  find  them  on  the  chordae  tendinese  and  on  the 
endocardium  of  the  ventricle  and  auricle.  In  the  mildest  cases  they  are  scarcely 
as  large  as  the  head  of  a  pin,  but  in  severe  cases  they  may  increase  to  quite  large 
warty  and  glandular  masses.  Microscopically,  the  base  of  the  nodule  consists  of 
a  newly  formed  vascular  tissue,  infiltrated  with  small  cells,  which  on  its  surface 
changes  to  a  granular,  coagulated  mass.  This  last  is  formed  partly  of  coagulated 
albumen,  dead  cells,  and  fibrine  deposited  from  the  blood,  and  partly  of  micrococci. 
The  micrococci  are  found  without  exception  in  all  cases  of  ulcerative  endocarditis 
— having  been  first  discovered  by  Eberth.  In  the  milder  forms  of  endocarditis 
verrucosa  micrococci  have  also  been  found  by  Eberth,  Klebs,  and  others,  but  their 
invariable  presence  has  not  yet  been  established.  The  endocardial  ulcers  arise 
from  the  destruction  of  the  superficially  necrosed  nodules.  If  the  thin  valve  in 
any  place  yields  to  the  blood-pressure,  we  have  the  so-called  acute  valvular  aneu- 
rism. Complete  perforation  of  a  valve,  and  tearing  off  of  fragments  of  a  valve 
and  of  the  chordae  tendineae,  are  also  seen. 

The  great  majority  of  cases  of  acute  endocarditis  are  confined  to  the  valves  of 
the  left  side  of  the  heart — the  mitral  and  aortic  valves.  Endocarditis  on  the  tricus- 
pid valve  is  seldom  seen  except  as  a  secondary  affection  in  old  cases  of  heart  dis- 
ease. In  a  case  of  acute  ulcerative  endocarditis  in  a  grown  man  seen  by  us,  the 
process  was  confined  exclusively  to  the  tricuspid  valve,  and  there  were  very  many 
embolic  abscesses  in  the  lungs.  This  may  be  considered  a  great  rarity.  In  con- 
trast to  the  ordinary  localization  of  endocarditis  we  find  fcetal  endocarditis  most 
frequently  in  the  right  side  of  the  heart. 

Many  other  organs  may  be  affected  by  the  endocarditis,  through  embolism.  In 
the  benign  endocarditis  verrucosa  the  masses  of  fibrine  deposited  on  the  irregulari- 
ties of  the  valve  furnish  the  embolic  material.  They  cause  large  or  small  infarc- 
tions in  the  kidneys  and  spleen,  embolic  softening  of  the  brain,  etc.  In  the  malig- 
nant, ulcerative  forms,  however,  large  numbers  of  bacteria  get  into  the  circulation 
at  the  same  time  with  the  necrotic  masses  of  tissue  which  have  been  torn  off. 
Here,  then,  we  have  to  do  not  merely  with  simple  mechanical  obstruction  but 
with  infectious  emboli.  The  emboli  in  ulcerative  endocarditis,  therefore,  either 
give  rise  to  embolic  abscesses  in  the  cardiac  muscles,  the  kidneys,  the  spleen,  the 
lungs,  the  retina,  etc.,  or  they  result  in  haemorrhages,  especially  into  the  skin,  but 
also  into  the  kidneys,  the  brain,  the  retina,  and  the  serous  membranes.     It  is  not 


278  DISEASES  OE  THE  CIRCULATORY  ORGANS. 

yet  known  why  in  some  cases  abscesses  are  more  frequent  and  in  others  hemor- 
rhages. The  two,  however,  may  he  combined.  In  general,  we  may  suppose  that 
the  development  of  abscesses  is  everywhere  connected  with  the  presence  of  bac- 
teria, while  haemorrhages  may  also  arise  from  toxic  influences,  for  example,  fibrine 
ferment;  but  changes  in  the  vascular  walls  caused  by  bacteria  might  also  give 
rise  to  haemorrhages.  Embolic  abscesses  belong  almost  exclusively  to  the  severe 
form  of  septic  endocarditis.  Haemorrhages  are  seen  in  this  form,  and  also — with- 
out co-existing  abscesses — in  certain  severe  forms  of  endocarditis  occurring  in  the 
course  of  acute  rheumatism  and  allied  diseases. 

Clinical  History. — Since  acute  endocarditis  is  not  serologically  a  distinct  dis- 
ease, and  since  its  clinical  course  is  very  different  in  different  cases,  it  seems  ad- 
visable to  us  to  describe,  in  what  follows,  the  most  important  varieties  separately; 
but  it  must  be  expressly  noted  that  the  separate  classes  can  by  no  means  be  sharply 
defined,  and  that  there  are  many  intermediate  forms. 

1.  Slight  endocarditis  verrucosa  is  quite  frequently  found  in  the  cadaver, 
without  the  slightest  signs  of  any  affection  of  the  heart  during  life.  The  little 
papillary  excrescences  on  the  valves  of  the  heart  in  phthisis,  and  carcinoma,  whose 
aetiology  has  been  explained  above,  are  to  be  classed  under  this  head. 

2.  The  typical  form  of  benign  acute  endocarditis  is  most  frequent,  clinically, 
in  the  course  of  acute  articular  rheumatism.  It  is  much  rarer  in  other  infectious 
diseases  (vide  supra).  In  rare  cases  its  appearance  has  been  noticed  as  an  appar- 
ently primary  disease. 

It  is  only  rarely  associated  from  the  outset  with  subjective  symptoms,  like  pain 
in  the  cardiac  region,  palpitation,  and  dyspnoea.  It  is  usually  first  discovered  on 
physical  examination  of  the  heart.  The  impulse  of  the  heart  in  many  cases  is 
abnormally  strong  and  diffuse,  the  pulse  is  accelerated,  but  strong,  often  some- 
what jerky  [pulsus  celer),  and  usually  regular,  but  sometimes  a  little  irregular. 
Percussion  at  first  shows  no  deviations  from  the  limits  of  normal  dullness.  On 
auscultation,  we  hear  at  the  apex,  more  rarely  at  the  base,  a  loud  blowing,  systolic 
souffle.  Diastolic  murmurs  are  rare  in  acute  endocarditis.  The  pulmonic  second 
sound  is  often  accentuated.  But  the  physical  signs  in  the  heart  are  only  slightly 
marked  in  many  cases  of  acute  endocarditis.  This  is  understood  if  we  remember 
that  the  occurrence  of  a  heart-murmur  depends  wholly  on  the  localization  of  the 
endocarditis,  on  the  development  of  some  valvular  insufficiency,  etc. 

Besides  the  direct  symptoms  pointing  to  the  cardiac  affection,  the  onset  of  an 
acute  endocarditis  is  often,  but  not  always,  associated  with  fever,  or,  if  fever  be 
already  present,  with  an  increase  of  it,  and  of  the  general  disturbance.  Embolic 
processes  may  occur  in  the  brain,  the  spleen,  the  kidneys,  and  the  extremities,  but 
they  are  comparatively  rare.  Sometimes  a  pericarditis  develops  as  a  result  of  the 
endocarditis  {vide  infra). 

It  is  hard  to  make  any  accurate  statements  as  to  the  duration  of  this  form  of 
endocarditis.  The  physical  signs  may  last  for  days,  or  for  several  weeks.  Com- 
plete recovery  is  possible,  but  in  the  majority  of  cases  this  variety  passes  into 
chronic  valvular  disease  of  the  heart. 

3.  Malignant,  non-septic  form,  of  acute  endocarditis  ("  rheumatoid  endocar- 
ditis "  of  Litten).  In  many  cases  this  form  is  perhaps  only  a  quantitative  increase 
of  the  preceding  form,  but  in  other  cases  it  is  probably  distinct  from  it  setiologic- 
ally.  The  severe  general  infection  is  usually  quite  prominent  here,  and  the  dis- 
ease resembles  in  many  particulars  grave  septic  endocarditis.  The  objective  signs 
in  the  heart  are  the  same  as  in  the  preceding  form,  but  more  intense  and  exten- 
sive. The  subjective  symptoms  in  the  heart,  like  palpitation  and  distress,  may  be 
quite  pronounced,  but  they  may  also  be  almost  wholly  absent  in  this  form.  The 
general  condition,  however,  is  usually  bad.     There  is  sometimes  high  fever  with 


ACUTE   ENDOCARDITIS.  279 

an  irregular  or  intermitting  course,  but  in  many  cases  the  fever  is  remarkably 
low  in  spite  of  quite  severe  constitutional  symptoms. 

The  constitutional  infection  is  very  often  manifested  in  these  cases  by  the 
appearance  of  small  or  large  haemorrhages  in  the  skin,  sometimes  in  the  mucous 
membranes,  as  in  the  conjunctiva  and  the  soft  palate,  and  rarely  in  the  retina. 
Secondary  articular  swellings  often  develop;  they  are  alwaj's  of  a  serous  charac- 
ter, and  never  purulent.  Renal  haemorrhages  and  acute  hemorrhagic  nephritis 
are  quite  frequent.  Large  emboli  may  also  occur  in  the  different  organs  in  this 
as  in  every  other  form  of  endocarditis. 

The  duration  of  the  disease  extends  over  many  weeks.  In  severe  cases  death 
ensues  with  a  gradual  aggravation  of  the  general  condition,  and  often  with  severe 
cerebral  symptoms,  like  stupor  and  delirium.  In  milder  cases,  however,  the  patient 
may  finally  get  well. 

Regarding  the  occurrence  of  this  form,  we  see  it  most  frequently  in  acute 
articular  rheumatism;  also,  in  rare  cases,  in  gonorrhoea,  where  it  comes  on  some 
three  or  four  weeks  after  the  beginning  of  the  urethral  affection ;  also  in  nephritis, 
chorea,  peliosis  rheumatica,  etc.  The  apparently  primary  cases  of  this  sort  usu- 
ally belong  to  the  recurrent  form  of  acute  endocarditis. 

4.  The  recurrent  form  of  acute  endocarditis  consists  of  an  acute  increase  of  the 
endocardial  process,  brought  on  by  some  exciting  cause,  in  a  patient  already  suf- 
fering from  chronic  endocarditis.  The  acute  disease  may  show  all  the  gradations 
from  the  mildest  to  the  severest.  The  mild  cases  often  run  their  course  wüthout 
any  special  symptoms.  To  this  form  we  must  probably  often  refer  the  more  or 
less  temporary  elevations  of  temperature  which  we  often  see  in  patients  with 
chronic  valvular  disease  of  the  heart.  In  rarer  cases  the  recurrent  endocarditis 
comes  on  quite  suddenly  in  the  form  of  a  severe  acute  attack.  This  sometimes 
seems  to  be  clinically  a  primary,  independent  disease,  especially  if  the  previous 
chronic  heart  disease  has  up  to  that  time  caused  no  special  symptoms.  The  patient 
has  general  malaise,  headache,  chills,  and  fever.  The  last  may  be  quite  high — 
104°  (40°  C.)  and  over— or  moderate,  varying  between  100°  and  102°  (38°-39°  C), 
or  it  may  be  entrrely  absent.  In  many  cases  it  is  intermittent,  when  the  return  of 
fever  is  often  associated  with  a  chill.  The  symptoms  in  the  heart  may  be  quite 
pronounced,  but  in  this  form,  too,  they  may  be  obscure  and  indefinite.  In  the 
further  course  of  the  disease  we  meet  with  cutaneous  haemorrhages,  retinal 
haemorrhages,  articular  swellings,  large  renal  haemorrhages,  or  typical  haemor- 
rhagic  nephritis — in  short,  just  the  same  general  type  of  disease  as  in  the  other 
malignant  forms  of  acute  endocarditis.  The  course  is  rarely  rapid,  and  often  lasts 
for  weeks.     Severe  cases  almost  always  end  fatally. 

5.  The  severe  septic  ulcerative  endocarditis  has  already  been  described  as  a 
complication  of  a  general  septic  disease.  We  therefore  refer  to  the  appropriate 
chapter  (see  p.  108)  for  all  particulars.  Septic  endocarditis  is  probably  entirely 
distinct  aetiologically  from  the  forms  so  far  described,  and  is  manifested  by  quite 
a  rapid  fatal  course,  with  severe  typhoid  or  pyaemic  symptoms.  It  is  characterized 
anatomically,  apart  from  the  cardiac  affection,  by  the  appearance  of  metastatic 
abscesses  in  the  various  organs,  but  in  many  cases,  as  we  have  said,  abscesses  and 
haemorrhages  are  combined. 

Diagnosis. — The  diagnosis  of  an  endocarditis,  coming  on  secondarily  in  the 
course  of  articular  rheumatism  and  other  diseases,  can  be  made  only  by  a  physical 
examination  of  the  heart.  We  must  therefore  give  constant  attention  to  the  con- 
dition of  the  heart  in  diseases  which  we  know  may  give  rise  to  endocarditis. 

The  diagnosis  of  the  malignant  form  of  endocarditis  often  causes  great  diffi- 
culty, especially  if  the  patient  is  not  seen  until  the  later  stages.  It  is  confused 
with  typhoid,  meningitis,  or  acute  miliary  tuberculosis.     Examination  of  the  heart 


280  DISEASES  OF  THE  CIRCULATORY  ORGANS. 

may  furnish  evident  signs,  but,  as  we  have  said,  not  invariably.  Of  the  other 
symptoms  the  cutaneous  and  retinal  haemorrhages  are  of  special  diagnostic  im- 
portance, since  they  are  very  much  rarer  in  the  other  diseases  just  named.  The 
acute  hemorrhagic  nephritis,  too,  in  connection  with  the  other  symptoms,  is,  at 
least  to  a  certain  degree,  characteristic  of  malignant  endocarditis.  The  course  of 
the  fever  is  of  diagnostic  value  only  when  it  is  decidedly  intermittent.  A  careful 
search  for  some  etiological  factor  is  very  important  for  diagnosis  in  all  cases. 

Prognosis. — In  the  description  of  the  course  of  the  disease  we  have  already 
mentioned  the  prognosis  of  the  different  forms.  The  severe  cases  of  acute  endo- 
carditis, some  of  which  are  complicated  by  the  presence  of  an  underlying  affection, 
usually,  and  the  cases  of  severe  septic  endocarditis  always,  end  fatally.  In  mild 
cases  recovery  is  possible,  but  the  process  of  repair  is  often  so  incomplete  that 
chronic  valvular  disease  of  the  heart  develops  from  the  acute  endocarditis. 

Treatment. — The  chief  requisite  in  the  treatment  of  every  endocarditis  is  as 
complete  rest  as  possible  for  the  patient.  If  ice  is  well  borne,  the  continuous 
application  of  an  ice-bag  to  the  cardiac  region  is  of  service.  Digitalis  may  be 
indicated  under  some  circumstances  with  a  weak  and  irregular  action  of  the  heart, 
but  on  the  whole  this  remedy  is  not  often  used  in  acute  endocarditis.  With  severe 
local  symptoms,  like  oppression  and  dyspnoea,  we  prescribe  mustard  plasters  and 
small  doses  of  morphine,  and  in  some  cases  local  blood-letting.  Weakness  of  the 
heart  is  to  be  combated  by  stimulants — wine,  camphor,  and  ether. 

The  treatment  is  also  to  be  directed  against  the  primary  disease,  although  we 
can  rarely  succeed  in  influencing  the  endocarditis  in  this  way.  In  articular  rheu- 
matism especially,  which  is  the  most  frequent  cause  of  acute  endocarditis,  salicylic 
acid  is  unfortunately  almost  wholly  powerless  against  the  endocarditis. 

In  the  severe  forms  of  endocarditis  the  treatment  can  be  only  purely  symptom- 
atic, and  we  try  to  keep  up  the  patient's  strength  as  much  as  possible.  The  exhi- 
bition of  large  doses  of  salicylic  acid  or  quinine  has  usually  no  result,  or  only  a 
temporary  one.  In  many  cases  the  use  of  arsenic,  kept  up  for  a  long  time,  seems 
to  us  to  be  of  service. 

[For  remarks  upon  the  alkaline  treatment  of  rheumatism,  see  page  909.] 


CHAPTER  II. 

VALVULAR   DISEASE   OF   THE    HEART. 

( Chronic  Endocarditis.) 

Etiology. — A  large  number  of  cases  of  chronic  valvular  disease  of  the  heart 
proceed  from  acute  endocarditis.  Hence  the  frequent  statement  in  the  history 
of  heart  disease  that  the  patient  has  had  articular  rheumatism,  once  or  many 
times.  As  a  result  of  the  endocarditis,  which  has  its  chief  seat  on  the  cardiac 
valves,  there  is  considerable  thickening  of  the  valvular  connective  tissue.  Pro- 
cesses of  contraction  also  take  place,  and  also  adhesions,  and  finally  in  many 
cases  quite  marked  calcification.  All  these  processes  have  the  necessary  result, 
that  such  deformed  valves  can  no  longer  fulfill  their  well-known  physiological 
functions  in  regulating  the  circulation.  There  follows  a  disturbance  in  the  circu- 
lation of  the  heart  itself,  and,  as  an  immediate  result  of  it,  a  disturbance  of  the 
general  circulation,  the  pernicious  effects  of  which  must  finally  be  manifested  in 
the  whole  system. 

In  quite  a  large  number  of  cases  of  heart  disease,  however,  we  can  not  obtain 
a  history  of  acute  endocarditis.     We  have  to  do  here  with  an  endocarditis  which 


VALVULAR  DISEASE  OF  THE  HEART.  281 

is  chronic  from  the  start,  which  also  leads  gradually  to  thickening,  contraction, 
adhesion,  and  calcification  of  the  valves.  The  aetiology  of  this  chronic  sclerotic 
endocarditis  is  still  obscure  in  many  of  its  relations.  The  same  injurious  influ- 
ences which  cause  acute  articular  rheumatism,  probably,  act  on  the  patient  in  a 
chronic  manner  from  the  beginning;  at  least,  we  not  infrequently  learn  from 
patients  with  chronic  heart  disease,  without  previous  acute  articular  rheumatism, 
that  in  former  years  they  suffered  repeatedly  from  slight  rheumatic  symptoms, 
to  which  they  paid  but  little  attention.  In  typical  chronic  arthritis  defor- 
mans, too,  heart  disease  occurs,  though  not  very  often.  In  other  cases,  however, 
we  must  consider  the  possibility  of  other  injurious  influences,  partly  infectious, 
and  partly,  perhaps,  of  a  chemical  or  mechanical  nature.  Chronic  alcoholism, 
and  also  constitutional  syphilis,  true  gout,  and  immoderate  muscular  exertion, 
are  the  exciting  causes  which  chiefly  come  to  our  notice.  The  chronic  heart  dis- 
ease in  such  cases  often  develops  at  the  same  time  with,  and  from  the  same  causes 
as,  general  endarteritis,  or  atheroma  of  the  vessels.  To  this  we  may  ascribe  the 
origin  of  many  cases  of  heart  disease  in  advanced  age.  The  influence  of  chronic 
nephritis  is  not  to  be  disputed  in  the  development  of  chronic  valvular  disease.  A 
hereditary  predisposition  to  heart  disease  is  not  very  frequent,  but  yet  it  can  be 
made  out  with  certainty  in  many  cases.  We  have  ourselves  seen  five  members  of 
the  same  family  who  have  suffered  from  chronic  heart  disease,  some  from  pure 
valvular  disease  and  some  from  severe  so-called  idiopathic  hypertrophy.  Perhaps 
the  very  frequent  occurrence  of  heart  disease  in  many  families  is  also  connected 
with  a  special  family  predisposition  to  rheumatic  affections,  the  occurrence  of 
which  predisposition  can  not,  in  our  opinion,  be  denied.  Finally,  a  small  number 
of  cases  of  heart  disease,  especially  in  the  right  side  of  the  heart,  depend  upon 
anomalies  of  development  of  the  heart— congenital  heart  disease. 

Of  163  cases  of  undoubted  chronic  valvular  disease  which  we  have  collected, 
86  cases  might  with  great  probability  be  ascribed  to  articular  rheumatism,  while  in 
77  cases  the  patients  had  never  suffered  from  rheumatic  symptoms.  In  part  of 
the  last-named  cases  no  definite  cause  could  be  ascertained,  and  in  the  rest  perhaps 
some  one  of  the  factors  mentioned  above  was  to  be  found.  A  number  of  women 
referred  their  symptoms  to  previous  pregnancies  and  parturitions.  As  has  also 
been  noted  by  others,  the  cases  without  previous  articular  rheumatism  were  more 
often  aortic  disease  than  mitral.  Particularly  in  cases  where  syphilis  was  to  be 
looked  upon  as  a  probable  cause  have  we  almost  invariably  found  the  chief  changes 
in  the  aortic  valves. 

Valvular  disease  of  the  heart  occurs  at  every  age  of  life.  The  time  of  origin 
of  most  cases,  corresponding  in  part  to  the  occurrence  of  acute  articular  rheuma- 
tism, falls  in  youth  and  middle  age,  somewhere  between  eighteen  and  forty.  In 
the  female  sex  heart  disease  is  somewhat  more  frequent  than  in  the  male. 

General  Pathology  of  Valvular  Disease  of  the  Heart.— Every  valve  of  the  heart, 
in  order  to  fulfill  its  physiological  task,  must,  on  the  one  hand,  open  perfectly  at 
the  right  time  in  order  to  furnish  a  free  passage  to  the  blood-current  through 
the  appropriate  orifice,  and  must,  on  the  other  hand,  close  firmly  and  perfectly  at 
the  right  time  in  order  to  make  any  abnormal  backward  flow  of  blood  impossible. 
In  both  relations  the  function  of  the  valves  may  be  disturbed  by  chronic  endo- 
carditis, the  disturbance  being  the  result  of  their  anatomical  changes.  If  the  tips 
of  the  valves  are  shortened  on  their  free  edges  by  contraction,  or  if  the  complete 
unfolding  of  the  auriculo-ventricular  valves  is  hindered  by  a  shortening  of  their 
chordae  tendinese,  the  closure  of  the  valve  can  not  be  complete.  At  the  moment 
when  the  closure  of  the  valve  is  necessary  a  fissure  remains  open  between  its 
apices.  We  call  this  condition  an  insufficiency  of  the  valve.  On  the  other  hand, 
the  valves  may  lose  their  capability  of  free  and  sufficient  separation  from  one 


282  DISEASES  OF  THE  CIRCULATORY  ORGANS. 

another,  as  a  result  of  thickening  and  calcification  of  the  connective  tissue,  and 
also  as  a  result  of  adhesions  of  the  points  of  the  valves  with  one  another.  At 
the  moment  when  the  blood-current  should  pass  freely  through  the  open  orifice, 
the  valve  remains  a  stiff,  narrow  ring,  through  which  the  blood  must  force  its 
wav — stenosis  of  the  orifice.  The  changes  in  the  valves  are  often  of  such  a  sort 
that  they  cause  at  the  same  time  both  an  insufficiency  of  the  valve  and  a  stenosis 
of  the  orifice.  The  thickening  and  calcification  of  the  valves  in  stenosis  cause, 
as  a  rule,  a  valvular  insufficiency  at  the  same  time ;  but  an  insufficiency,  set  up  by 
a  contraction  of  the  edges  of  the  valves,  may  occur  without  a  coincident  stenosis 
of  the  orifice. 

Every  valvular  disease  affects  the  blood-current  first  in  this  way :  that  a  stasis 
of  the  blood  ensues,  beginning  at  the  diseased  valve  and  extending  backward 
against  the  current.  The  flow  of  blood  through  the  pulmonary  veins,  and  also 
through  the  veins  of  the  body,  is  impeded,  and  the  filling  of  the  arterial  system 
is  thus  diminished.  To  avoid  repetition,  we  will  describe  more  particularly, 
in  the  pathology  of  the  disease  of  individual  valves,  the  precise  circumstances 
under  which  this  disturbance  of  the  circulation  occurs.  Every  such  abnormal 
distribution  of  the  blood,  and  the  necessary  slowing  of  the  circulation,  from  the 
increased  tension  in  the  venous  system  on  the  one  hand,  and  the  diminished  ten- 
sion in  the  aortic  system  on  the  other,  would  soon  exert  a  most  pernicious  influ- 
ence on  the  whole  body,  if  a  number  of  compensatory  processes  did  not  develop 
in  the  heart  itself.  We  shall  see  how  the  disturbance  of  circulation  in  disease  of 
each  individual  valve  can  be  overcome  by  the  increased  work  of  certain  definite 
portions  of  the  heart,  and  how  the  heart  does  in  fact  respond  to  these  increased 
demands  put  upon  its  working  strength.  It  is  one  of  the  wisest  contrivances  in 
our  organism,  that  the  heart  has  control  of  a  reserve  fund  of  strength,  which 
comes  into  action,  if  need  be,  in  a  way  to  compensate  as  far  as  possible  for  any 
disturbance  of  the  circulation.  This  explains  why  a  man  with  valvular  disease 
of  the  heart  may  be  almost  perfectly  well  for  a  long  time,  while  the  increased 
work  of  certain  portions  of  his  heart  is  able  to  keep  up  an  approximately  normal 
circulation  in  spite  of  the  existing  valvular  disease.  We  call  a  heart  disease,  in 
which  there  is  at  least  no  marked  disturbance  of  circulation,  a  compensated  heart 
disease. 

The  abnormally  increased  work,  which  single  portions  of  the  heart  must  per- 
form in  every  case  of  disease  in  order  to  keep  up  the  normal  circulation,  leads  to 
hypertrophy  of  that  portion,  just  as  in  any  other  muscle.  This  hypertrophy  does 
not  consist  in  an  increase  in  thickness  of  the  individual  muscular  fibers,  but  chiefly 
in  an  increase  in  number.  The  whole  diameter  of  the  cardiac  muscle  increases, 
and  thus  its  capacity  for  work  naturally  becomes  greater.  It  goes  without  saying 
that  increased  nutritive  processes  and  a  large  supply  of  nourishment  for  the  heart 
are  necessary  to  bring  about  such  a  hypertrophy,  by  which  alone  a  compensation 
of  the  heart  disease  is  possible  for  any  length  of  time.  Hence  we  find  the  second- 
ary hypertrophy  of  the  heart  absent,  or  at  least  only  imperfectly  developed,  in 
weak  people,  especially  in  such  as  have  suffered  from  some  other  chronic  wasting 
disease  besides  the  heart  disease,  like  phthisis  or  carcinoma. 

Although  the  compensatory  processes  in  the  heart  can  prevent  for  a  long  time 
any  marked  disturbance  of  the  circulation,  the  already  overburdened  heart  can  no 
longer  completely  satisfy  any  additional  demands  upon  it,  even  in  a  compensated 
heart  disease.  Hence  patients  with  a  compensated  heart  disease  are  free  from  sub- 
jective disturbance  from  their  trouble  only  when  they  take  complete  bodily  rest, 
while  the  signs  of  a  disturbed  circulation  usually  become  quite  apparent  on  slight 
physical  exertion. 

The  hypertrophied  cardiac  muscle  can  seldom  supply  permanently  the  abnor- 


VALVULAR  DISEASE  OF  THE  HEART.  283 

mally  great  drafts  made  upon  its  strength.  There  finally  comes  a  condition  of 
"fatigue,"  of  "cardiac  insufficiency."  The  cause  lies  either  in  the  increase  of  the 
valvular  disease,  so  that  the  hindrance  to  the  blood-current  caused  by  it  can  no 
longer  be  completely  overcome,  or  in  the  fact  that  the  nervous  and  muscular  ele- 
ments in  the  heart  have  their  function  gradually  impaired  by  a  disturbance  of 
circulation  in  the  heart  itself.  In  short,  in  every  heart  disease  the  moment  may 
finally  come  when  the  capacity  of  the  heart  has  reached  its  limit,  and  hence  the 
compensation  of  the  heart  disease  ceases.  The  results  of  stasis  now  apj)ear  with 
increasing  severity  in  the  different  organs,  as  we  shall  learn  to  recognize  later  on, 
and  the  patient  finally  succumbs  to  them,  unless  some  intercurrent  event  puts  an 
end  to  life. 

After  these  general  remarks,  which  will  be  understood  better  from  what  fol- 
lows, we  will  pass  on  to  the  special  description  of  the  different  forms  of  heart  dis- 
ease and  their  physical  signs. 

1.  Insufficiency  of  the  Mitral  Valve. 

Mitral  insufficiency  is  one  of  the  most  frequent  forms  of  heart  disease.  It 
develops  in  acute  or  chronic  endocarditis  of  the  mitral  valve,  from  contraction  of 
the  free  edges  of  the  valve  or  from  shortening  of  the  chordae  tendineae.  In  rare 
cases  it  comes  on  from  partial  adhesion  of  the  valves  with  the  walls  of  the 
ventricle. 

The  closure  of  the  mitral  valve  occurs  normally  at  each  systole  of  the  left  ven- 
tricle. It  prevents  the  return  of  blood  from  the  left  ventricle  to  the  left  auricle. 
If  the  mitral  valve  is  insufficient  and  its  closure  is  incomplete,  at  every  systole  of 
the  left  ventricle  a  part  of  the  blood  is  thrown  back  from  it  into  the  left  auricle 
through  the  open  space  of  the  ostium  venosum.  This  abnormal  backward  wave 
encounters  the  blood-current  coming  in  an  opposite  direction  into  the  left  auri- 
cle from  the  pulmonary  veins.  Since  these  two  opposing  currents  rebound 
on  each  other,  and  since  the  backward  wave  of  blood  presses  through  the  open 
space  in  the  mitral  orifice,  decided  vertiginous  movements  arise  in  the  blood, 
which  are  the  cause  of  a  loud  blowing,  systolic  murmur  in  the  heart.  We  hear 
this  murmur  loudest  at  the  apex  of  the  heart,  corresponding  to  the  laws  of  con- 
duction in  the  thorax ;  yet  it  usually  is  propagated  so  far  that  it  may  often  be 
heard  at  the  other  cardiac  orifices,  although  weaker.  A  loud  systolic  mitral  mur- 
mur can  also  be  heard  sometimes  in  the  back,  on  the  left  and  occasionally  on  the 
right.  Only  in  a  few  cases  do  we  find  the  murmur  louder  nearer  the  base  of  the 
heart  than  at  the  apex,  corresponding  more  to  the  anatomical  position  of  the 
mitral  valve.  We  often  hear  the  first  sound  of  the  heart  at  the  apex  besides  the 
murmur,  but  sometimes  we  do  not.  The  second  sound  is  often  not  to  be  heard  at 
the  apex,  probably  because  it  is  obscured  by  the  relatively  protracted  murmur. 

Since  the  left  auricle,  at  each  systole  of  the  ventricle,  receives  blood  from  two 
sides — its  normal  quantity  from  the  pulmonary  veins,  and  besides  that  the  abnor- 
mal blood-wave  from  the  left  ventricle— it  becomes  much  dilated.  At  the  next 
diastole  of  the  left  ventricle  the  whole  amount  of  blood  collected  hi  the  auricle 
under  increased  pressure  pours  into  the  left  ventricle  through  the  mitral  valve, 
which  is  now  wide  open  (supposing  a  pure  insufficiency  of  the  valve  without  any 
stenosis).  We  see,  then,  that  in  pure  mitral  insufficiency  the  left  ventricle  must 
be  overfilled  during  the  diastole.  The  left  ventricle  must  also  expel  in  the  follow- 
ing systole  an  abnormally  large  amount  of  blood.  Although  by  this  contraction 
only  a  part  of  the  blood  reaches  the  aorta  in  the  direction  of  the  normal  blood- 
current  while  a  part  pours  back  into  the  auricle,  the  work  of  the  left  ventricle  is 
of  course  excessive.     This  is  the  explanation,  then,  why,  in  pure  mitral  insuffi- 


284  DISEASES  OF  THE  CIRCULATORY  ORGANS. 

ciency,  the  left  ventricle  is  dilated  as  a  result  of  its  increased  filling  in  diastole,  and 
is  hypertropkied  as  a  result  of  its  increased  labor.  The  general  arterial  tension 
thus  remains  approximately  normal.  It  is  not  increased,  since  a  part  of  the  ab- 
normal amount  of  blood,  which  pours  out  of  the  left  venfc-icle  at  every  systole, 
flows  backward  into  the  auricle.  About  the  normal  amount  of  blood  reaches  the 
aorta,  and  hence  the  radial  pulse,  in  pure  mitral  insufficiency,  remains  of  about 
normal  strength  and  tension. 

The  anomalies  in  the  movements  of  the  blood  in  mitral  insufficiency  produce 
still  other  effects.  We  have  already  seen  that  the  left  auricle  is  dilated  from  its 
overfilling.  It  also  becomes  hypertrophied,  so  far  as  its  weak  muscular  structure 
permits,  but  it  is  not  in  itself  capable  of  compensating  for  the  disturbance  which 
the  pulmonary  circulation  suffers  from  the  mitral  insufficiency,  for  the  back  cur- 
rent from  the  left  ventricle,  and  the  consequent  high  pressure  in  the  left  auricle, 
must  plainly  offer  an  abnormal  hindrance  to  the  flow  of  blood  from  the  pulmo- 
nary veins.  This  stasis  sets  back  through  the  pulmonary  capillaries  and  arteries 
into  the  right  ventricle.  This  may  be  recognized,  on  physical  examination,  by 
the  change  in  the  pulmonic  second  sound,  which  is  louder,  more  valvular,  and 
"  accentuated,1'  since  the  closure  of  the  semilunar  valves  in  the  pulmonary  artery 
now  takes  place  under  the  abnormally  high  pressure  which  prevails  in  the  arteries 
of  the  lungs.  The  inght  ventricle  has  the  task  of  overcoming  this  abnormal  stasis 
in  the  pulmonary  circulation.  It  can  overcome  the  abnormal  resistance  in  the 
pulmonary  circulation  by  increased  work,  and  as  a  result  it  becomes  hypertrophied. 
So  long  as  the  hypertrophy  of  the  l'ight  ventricle  suffices  to  maintain  the  normal 
pulmonary  circulation,  the  stasis  extends  no  farther  backward,  but  in  the  later 
stages  of  heart  disease  we  see  the  right  ventricle  becoming  paralyzed,  and  more 
and  more  dilated  as  a  result  of  stasis.  The  flow  of  venous  blood  from  the  body 
into  the  right  auricle  and  ventricle  is  now  rendered  more  difficult.  The  signs  of 
venous  stasis  become  manifest ;  the  patient  has  a  cyanotic  hue,  congestive  oedema 
appears  in  the  face  and  the  extremities,  symptoms  of  passive  congestion  of  the 
liver,  spleen,  and  kidneys  appear,  and,  in  short,  there  is  developed  the  picture  of 
an  uncompensated  heart  disease. 

If  we  now  sum  up  the  physical  signs  of  mitral  insufficiency,  the  different 
methods  of  investigation  give  the  following  results: 

Inspection. — The  cardiac  region  often  seems  rather  prominent,  as  a  result  of 
the  hypertrophy  of  the  heart.  This  protrusion  is  most  marked  in  young  persons 
with  a  yielding  thorax.  The  apex-beat  is  somewhat  displaced  toward  the  left  as  a 
result  of  the  hypertrophy  and  dilatation  of  the  left  ventricle,  and  it  is  quite  marked. 
Besides  that,  we  often  see  and  feel  a  diffuse  pulsation  in  the  whole  cardiac  region. 
In  the  epigastrium  we  sometimes  see  or  feel  an  epigastric  pulsation  proceeding 
from  the  hypertrophied  right  ventricle.  In  cases  which  are  no  longer  perfectly 
compensated  the  stasis  in  the  veins  of  the  body  is  rendered  apparent  by  the  general 
cyanotic  appearance  of  the  patient  and  the  marked  filling  of  the  jugular  veins  in 
the  neck.  Undulatory  or  pulsating  movements  often  occur  in  the  latter  (see  tri- 
cuspid insufficiency,  below). 

Palpation. — This  confirms  the  abnormal  strength  of  the  apex-beat,  and  its 
displacement  to  the  left.  We  often  feel  a  systolic  thrill  at  the  apex  of  the  heart 
— a  "cat's  purr" — by  laying  the  hand  flat  on  the  chest.  This  whirl  of  blood, 
which  is  audible  as  a  murmur,  may  be  perceived  as  a  fine  tremor  of  the  chest- 
wall. 

The  radial  pulse  is  quite  strong  and  usually  regular.  The  sphygmographic 
tracing  of  it  gives  nothing  characteristic  in  mitral  insufficiency. 

Percussion. — This  usually  gives  at  first  only  a  moderate  increase  of  the  heart's 
dullness  to  the  left,  and  a  little  upward,  but  in  the  later  stages  there  is  at  the  same 


VALVULAR  DISEASE  OF  THE  HEART.  285 

time  an  increase  of  the  heart's  dullness  to  the  right,  caused  hy  hypertrophy  and 
dilatation  of  the  right  ventricle.  The  whole  area  of  cardiac  dullness  may  finally 
extend  two  fingers'  breadth  beyond  the  right  edge  of  the  sternum,  and  to  the  left 
it  may  reach  the  mammillary  line,  or  even  pass  beyond  it. 

Auscultation. — At  the  apex  of  the  heart  we  hear  a  loud,  quite  long,  pure  sys- 
tolic blowing  murmur,  limited  to  the  systole,  cither  replacing  the  first  sound  or 
accompanying  it.  The  second  sound  is  often  obscure  or  inaudible  at  the  apex,  but 
the  pulmonic  second  sound  is  increased  and  accentuated.  Auscultation  of  the 
vessels  gives  nothing  characteristic. 

2.  Stenosis  of  the  Mitral  Orifice  (Mitral  Stenosis). 

Mitral  stenosis  often  develops  in  chronic  endocarditis  of  the  mitral  valve,  as  a 
sequel  to  a  previous  insufficiency.  The  valve  constantly  grows  stift'er  and  more 
rigid,  and  the  signs  of  stenosis  gradually  predominate  over  those  of  insufficiency. 
Hence  we  very  often  find  stenosis  and  insufficiency  of  the  mitral  valve  combined, 
but  often  the  signs  of  stenosis  are  so  much  more  prominent  that  we  can  properly 
speak  of  a  pure  mitral  stenosis. 

The  disturbance  which  the  circulation  suffers  in  mitral  stenosis  is  much  greater 
than  in  mitral  insufficiency.  In  mitral  stenosis  the  orifice  may  finally  become  so 
narrow  that  it  scarcely  admits  an  ordinary  lead-pencil.  The  influx  of  blood  into 
the  left  ventricle  is  accordingly  much  impeded.  During  the  diastole  of  the  left 
ventricle  the  blood  must  force  its  way  through  the  stiff  and  narrow  ring  of  the 
mitral  valve.  Thus  irregular  vertiginous  movements  develop  in  the  blood,  which, 
in  the  majority  of  cases,  give  rise  to  an  audible  diastolic  murmur.  In  mitral 
stenosis  the  left  ventricle  receives  a  very  small  amount  of  blood.  Hence,  in 
mitral  stenosis,  the  left  ventricle  is  usually  small,  its  cavity  contracted,  and  the 
amount  of  blood  thrown  into  the  arteries  with  the  systole  is  less  than  normal. 
In  high  degrees  of  mitral  stenosis  the  radial  pulse  is  weak  and  small,  and,  besides 
that,  we  often  find  it  irregular  (see  Fig.  29).     If  we  find  a  hypertrophy  of  the  left 


Fig.  29. — Pulse  curve  in  marked  mitral  stenosis. 

ventricle  in  marked  mitral  stenosis,  as  sometimes  happens,  for  which  there  is  no 
other  special  explanation,  it  is  probably  always  to  be  referred  to  a  previous  insuffi- 
ciency of  the  mitral  valve. 

The  hindrance  to  the  flow  into  the  left  ventricle  in  mitral  stenosis  soon  leads 
to  a  marked  stasis,  which  extends  to  the  right  side  of  the  heart  through  the  left 
auricle,  and  the  pulmonary  veins,  capillaries,  and  arteries.  The  left  auricle  is 
dilated  first,  and  its  walls  are  hypertrophied,  but  it  can  overcome  only  a  very  small 
part  of  the  resistance  at  the  mitral  orifice.  The  right  ventricle  can,  by  more  work, 
so  increase  the  pressure  in  the  pulmonary  vessels  that,  in  spite  of  the  narrowed 
orifice,  an  approximately  sufficient  quantity  of  blood  may  pour  into  the  left  ven- 
tricle. Hence  we  find  in  mitral  stenosis  a  very  marked  hypertrophy  and  dilata- 
tion of  the  right  ventricle.  The  stasis  in  the  pulmonary  circulation,  manifest 
objectively  by  the  accentuation  of  the  pulmonic  second  sound,  has  as  a  result  a 
gradually  developing  ectasis  of  the  pulmonary  capillaries.  Thickening  of  the 
intima  of  the  pulmonary  arteries  and  veins  also  usually  develops.  (See  the  chap- 
ter on  brown  induration  of  the  lungs.) 


2S6  DISEASES  OF  THE  CIRCULATORY   ORGANS. 

The  results  of  physical  examination  are  as  follows : 

Inspection. — The  whole  cardiac  region  may  seem  slightly  prominent,  as  a  result 
of  the  hypertrophy  of  the  heart.  The  heart's  action  is  usually  extended  over  a 
larger  area,  but  in  pure  mitral  stenosis  the  apex-beat  is  no  stronger  than  usual, 
though  often  displaced  to  the  left.  We  have  frequently  noticed  a  marked  pulsa- 
tion in  the  epigastrium,  produced  by  the  right  side  of  the  heart.  The  jugular  veins 
are  apt  to  be  prominent,  and  show  the  different  forms  of  undulatory  and  pulsating 
movement. 

Palpation. — This  also  gives  signs  corresponding  to  the  more  extended  action 
of  the  heart.  We  sometimes  feel  the  piilsation  of  the  dilated  right  ventricle  even 
to  the  right  of  the  sternum.  In  some  cases  we  feel  a  diastolic  thrill  at  the  apex 
of  the  heart,  which  alone  may  almost  establish  the  diagnosis  of  mitral  stenosis. 
This  thrill  arises  from  the  same  vertiginous  currents  in  the  blood  which  form  the 
basis  of  the  diastolic  murmur  (vide  infra).  The  radial  pulse  is  small  in  every 
severe  mitral  stenosis,  and  is  very  often  irregular. 

Percussion. — Percussion  gives  especially  an  increase  of  the  heart's  dullness  to 
the  right,  reaching  to  the  right  border  of  the  sternum  or  beyond  it.  The  dull- 
ness also  often  extends  farther  to  the  left  than  normal.  This  may  have  its  origin 
in  a  co-existing  hypertrophy  of  the  left  ventricle  (vide  supra),  otherwise  it  depends 
on  a  dilatation  of  the  right  side  of  the  heart  so  great  that  the  left  ventricle  is  pushed 
farther  to  the  left  and  backward  by  it. 

Auscultation. — The  characteristic  auscultatory  sign  of  mitral  stenosis  is  the 
diastolic  [pre-systolic]  murmur  at  the  apex.  This  is  never  so  loud  and  blowing  as 
the  systolic  murmur  of  insufficiency,  but  it  usually  sounds  more  rolling  or  rippling. 
It  is  loudest  at  the  apex,  and  it  is  transmitted  only  slightly  toward  the  base.  Since, 
as  has  been  said,  the  left  ventricle  in  mitral  stenosis  is  sometimes  pushed  to  the  left 
and  backward  by  the  very  much  enlarged  right  ventricle,  in  looking  for  the  mur- 
mur we  must  often  go  far  to  the  left,  in  order  not  to  auscult  the  right  ventricle 
only. 

The  origin  of  the  murmur  is  easily  explained.  In  the  diastole  of  the  left 
ventricle  the  blood-current  must  foi'ce  its  way  through  the  narrow  mitral  orifice, 
whence  vertiginous  movements  arise  in  the  blood,  and  produce  the  murmur. 
Since  the  blood  flowing  through  the  narrow  orifice  has  a  current  of  relatively 
slight  intensity,  the  murmur  produced  by  it  can  not  be  very  loud.  Even  in  the 
highest  degrees  of  mitral  stenosis  the  murmur  is  often  quite  low.  Not  infre- 
quently the  murmur  comes  on  in  the  second  half  of  the  diastole — namely,  when, 
by  the  contraction  of  the  left  auricle,  the  blood-current  is  hurried  through  the 
narrow  orifice.  We  call  such  a  murmur,  audible  at  the  end  of  the  diastole  only, 
a  presystolic  murmur,  since  it  usually  passes  immediately  into  the  first  sound. 

It  is  by  no  means  very  rare  that  the  murmur  is  absent  in  marked  mitral 
stenosis.  If  such  cases  do  not  come  under  observation  until  the  last  stages  of  the 
disease,  the  mitral  stenosis  can  readily  escape  recognition.  We  have  ourselves 
often  known  the  previously  distinct  diastolic  or  presystolic  murmur  in  mitral  ste- 
nosis gradually  to  disappear  with  the  increase  of  the  heart  disease.  In  these  cases 
the  intensity  of  the  blood-current  through  the  narrow  orifice  becomes  so  slight 
that  an  audible  murmur  is  no  longer  produced.  The  sounds  that  are  heard  arise 
probably  from  the  right  ventricle. 

The  first  sound  at  the  apex  is  retained  in  pure  mitral  stenosis,  and  often  it  is 
even  remarkably  loud  and  valvular,  a  condition  which  we  usually  try  to  explain 
by  the  theory  that  the  difference  (the  "  difference  in  tension  ")  between  the  abnor- 
mally slight  tension  of  the  valve  in  diastole,  in  mitral  stenosis,  and  its  high  tension 
in  systole  is  relatively  great.  If  insufficiency  of  the  valve  co-exists,  we  may  hear 
a  systolic  murmur  with  the  first  sound  or  instead  of  it. 


VALVULAR  DISEASE  OF  THE  HEART.  287 

The  very  marked  accentuation  of  the  pulmonic  second  sound,  the  result  of 
the  abnormally  high  tension  in  the  pulmonary  artery,  is  almost  constant.  It 
fails  only  in  very  anaemic,  weak  people,  or  in  co-existing  insufficiency  of  the 
tricuspid  valve  (vide  infra).  The  second  sound  at  the  base  is  very  often  "  divided  " 
or  reduplicated.  The  closure  of  the  semilunar  valves  in  diastole  does  not  happen 
at  the  same  time  in  the  pulmonary  artery  and  in  the  aorta,  on  account  of  the 
unequal  tension  in  the  two  vessels,  so  that  consequently  the  two  sounds  are  heard, 
one  shortly  after  the  other.  Although  this  division  of  the  second  sound  is  par- 
ticularly frequent  in  mitral  stenosis,  it  is  by  no  means  a  pathognomonic  sign  of  it. 

Mitral  stenosis  is  one  of  the  severest  forms  of  heart  disease.  It  almost  always 
causes  greater  subjective  disturbance  than  mitral  insufficiency.  Hypertrophy  of 
the  right  ventricle  can,  indeed,  maintain  for  a  time  an  approximately  complete 
compensation,  but  the  signs  of  marked  stasis  in  the  pulmonary  circulation,  and 
further  in  the  veins  of  the  body,  are  apt  to  appear  quite  early.  The  dyspnoea 
becomes  more  marked,  and  dropsical  symptoms  gradually  arise  and  cause  a  fatal 
termination. 

3.  Insufficiency  of  the  Semilunar  Valves  of  the  Aorta. 

Insufficiency  of  the  aortic  valves  is  most  frequently  due  to  contraction  of  the 
free  edges  of  the  valves.  Tears,  perforations,  or  adhesions  of  the  valve  to  the 
wall  of  the  vessel  more  rarely  lead  to  insufficiency.  The  cause  of  all  these  changes 
is  either  an  endocarditis  affecting  the  valves,  or  a  general  atheroma  of  the  arteries, 
which  gradually  invades  the  valves  from  the  intima  of  the  aorta. 

The  function  of  the  aortic  valves  is  to  close  tightly  at  the  time  of  diastole  of 
the  left  ventricle,  in  order  to  prevent  any  return  of  blood  from  the  aorta  into  the 
ventricle.  If  these  valves  are  insufficient — that  is,  if  they  do  not  close  perfectly 
at  each  diastole — there  is  a  return  current  of  blood  from  the  aorta  into  the  left 
ventricle.  The  left  ventricle  then  receives  blood  during  its  diastole  from  two  sides : 
the  normal  flow  from  the  left  auricle,  and  the  blood  which  comes  back  from  the 
aorta.  These  two  currents  of  blood,  directed  against  each  other,  meet  in  the  left 
ventricle  during  its  diastole,  give  rise  to  a  marked  vertiginous  movement  of  the 
blood  there,  and  thus  cause  a  characteristic  diastolic  murmur. 

As  a  result  of  the  excessive  expansion  of  the  left  ventricle  at  every  diastole,  it 
finally  becomes  permanently  dilated.  Dilatation  of  the  left  ventricle  therefore 
forms  a  constant  anatomical  lesion  in  every  aortic  insufficiency,  and  is  shown  not 
only  in  the  dilatation  of  the  whole  ventricular  cavity,  but  also  in  the  very  char- 
acteristic flattening  of  the  trabeculae  and  of  the  papillary  muscles.  The  abnor- 
mally great  filling  of  the  ventricle  during  diastole,  moreover,  gives  rise  to  increased 
labor;  for  the  left  ventricle  must  expel  an  abnormally  large  amount  of  blood  at 
each  systole,  which  is  of  course  a  sort  of  task  of  Sisyphus,  since  a  part  of  the  blood 
thrown  out  constantly  rolls  back  into  it.  The  increased  labor  must  always  lead 
at  last  to  a  hypertrophy  of  the  left  ventricle,  which  may  attain  the  highest  degree 
seen  in  any  form  of  valvular  disease. 

From  the  facts  enumerated  we  can  easily  understand  the  physical  signs  of 
insufficiency  of  the  aortic  valves. 

Inspection.  —Great  hypertrophy  of  the  left  ventricle  often  causes  a  marked 
protrusion  of  the  whole  cardiac  region.  The  very  strong  apex-beat,  displaced 
downward  and  to  the  left,  is  especially  striking.  It  may  usually  be  seen  in  the 
sixth  intercostal  space,  outside  the  left  mammillary  line,  and  sometimes  even  at 
the  anterior  axillary  line.  Besides  that,  we  often  see  a  marked  diffuse  tremor  of 
the  whole  cardiac  region. 

Palpation. — We  can  appreciate  the  heart's  action  to  a  still  greater  extent  by 


288  DISEASES  OF  THE  CIRCULATORY   ORGANS. 

palpation  than  by  inspection.  The  apex-beat  is  very  resistant,  massive,  and 
plainly  heaving' — that  is,  the  finger  or  stethoscope  applied  to  the  apex  is  lifted  by 
the  beat  at  every  systole.  In  rare  cases  a  diastolic  thrill,  corresponding  to  the 
diastolic  murmur,  can  be  felt  over  the  base  of  the  heart.  In  two  such  cases 
observed  by  us  the  murmur  had  a  marked  musical  character  {vide  infra).  The 
appearances  in  the  arteries  are  given  below. 

Percussion. — Percussion  gives  an  extension  of  the  cardiac  dullness  to  the  left, 
beyond  the  left  mammillary  line  and  even  to  the  anterior  axillary  line,  caused  by 
the  hypertrophy  and  dilatation  of  the  left  ventricle.  The  upper  boundary  of 
the  cardiac  dullness  is  normal,  or  it  may  extend  up  to  the  third  rib.  The  right 
boundary  is  in  its  normal  place  at  the  left  border  of  the  sternum,  but  it  may  also 
be  pushed  farther  to  the  right,  either  because  the  large  left  ventricle  of  itself  causes 
an  extension  of  the  whole  heart  to  the  right,  or  because  the  right  ventricle  is  also 
hypertrophied.  The  latter  change  occurs  in  pure  aortic  insufficiency  when  the 
compensation  is  no  longer  complete,  and  the  stasis  extends  backward  from  the 
left  ventricle,  through  the  pulmonary  circulation,  into  the  right  side  of  the  heart. 

It  may  also  be  remarked  here  that,  in  insufficiency  of  the  aortic  valves,  the 
ascending  aorta  is  often  considerably  dilated  by  the  marked  impulse  from  the 
amount  of  blood  pouring  into  it.  A  moderate  degree  of  dullness  is  found  over 
the  dilated  aorta,  which  may  sometimes  be  made  out  at  the  sternal  end  of  the 
second  right  intercostal  space. 

Auscultation. — Insufficiency  of  the  aortic  valves  is  characterized  by  a  long- 
drawn,  loud,  blowing  diastolic  murmur,  the  origin  of  which  has  been  explained 
above.  The  place  in  which  the  murmur  is  heard  loudest  is  not  the  sternal  end 
of  the  second  right  intercostal  space,  the  ordinary  point  for  auscultation  of  the 
aorta,  but  it  almost  always  lies  farther  to  the  left,  Corresponding  to  the  back- 
ward current  of  blood  toward  the  left  ventricle,  which  begets  the  murmur,  we 
hear  the  latter  loudest  over  the  upper  part  of  the  sternum  or  even  at  its  left  bor- 
der. In  some  cases  the  murmur  assumes  a  marked  "  musical  character  " — that 
is,  there  is  a  definite  high  musical  tone,  which  is  due  to  a  tendinous  fiber  arising 
from  a  wearing  away  of  the  valve,  and  set  in  vibration  by  the  diastole,  or  to  some 
similar  cause.  The  diastolic  murmur  is  often  audible  at  the  apex,  but  it  is  faint 
there.  Only  in  rare  cases,  and  especially  when  the  aortic  insufficiency  results 
from  acute  endocarditis,  is  the  diastolic  murmur  absent.  During  the  systole 
there  is  usually  a  short  systolic  murmur  heard  over  the  aorta.  This  may,  of 
course,  depend  upon  a  co-existent  aortic  stenosis,  but  it  is  also  frequently  present  in 
cases  of  uncomplicated  insufficiency  of  the  valves.  The  explanation  is,  that  at  the 
time  of  the  beginning  of  the  contraction  of  the  left  ventricle  the  reflux  of  blood 
in  the  aorta  has  not  wholly  ceased,  so  that  the  outgoing  blood-current  has  first  to 
overcome  this  obstacle.  It  is  easy  to  see  why  this  should  give  rise  to  an  audible 
systolic  sound,  and  also  why  it  should  have  some  influence  upon  the  development 
of  a  hypertrophy  of  the  left  ventricle  (O.  Rosenbach).  It  is  very  remarkable 
that,  as  Traube  first  pointed  out,  we  often  hear  the  first  sound  at  the  apex  very 
obscure  and  dull,  or  else  a  short  systolic  murmur  instead  of  it.  This  obscurity  of 
the  first  sound  at  the  apex  is  of  theoretical  interest,  because  it  contradicts  the 
hypothesis  that  the  first  mitral  sound  is  a  muscular  sound.  It  would  be  especially 
inexplicable,  on  this  theory,  why  the  first  sound  is  so  obscure  in  insufficiency  of 
the  aortic  valves,  in  spite  of  the  hypertrophied  and  toiling  left  ventricle ;  but  if 
we  regard  the  first  ventricular  sound  as  originating  in  the  mitral  valve,  then, 
according  to  Traube,  its  absence  in  aortic  insufficiency  may  be  explained  by  the 
fact  that  the  mitral  valve  during  the  ventricular  diastole  is  put  in  a  certain 
degree  of  tension  by  the  backward  current  of  blood.  The  greater  tension,  which 
develops  during  the  ventricular  systole,  does  not  suffice  to  produce  a  sound  in 


VALVULAE  DISEASE  OF  THE  HEART. 


2*9 


the  valves,  since  the  origin  of  a  valvular  sound  does  not  depend  upon  the  absolute 
tension,  but  upon  the  amount  of  its  sudden  increase.  The  systolic  murmur,  often 
heard  at  the  apex  in  aortic  insufficiency,  may  depend  upon  a  co-existing  true 
mitral  insufficiency,  but  it  is  probably  often  due  to  a  relative  insufficiency  of 
the  mitral,  since  the  valves,  which  are  normal  in  themselves,  can  no  longer  cause 
a  perfect  closure  of  the  left  mitral  orifice  now  that  the  left  ventricle  is  dilated. 

Symptoms  in  the  Peripheral  Arteries.— Such  remarkable  symptoms  are 
found  in  the  peripheral  arteries  in  aortic  insufficiency  that  they  demand  a  brief 
special  description.  The  first  striking  symptom  is  the  strong  pulsation  not  only 
of  the  larger  but  also  of  the  smaller  arteries,  even  those  the  pulsation  of  which  is 
not  generally  visible.  We  see  and  feel  not  only  a  strong  pulsation  in  the  carotids, 
but  also  in  the  tortuous  brachial  artery,  in  the  radial,  ulnar,  temporal,  dorsalis 
pedis,  etc.  We  sometimes  feel  an  arterial  pulse  in  the  liver  through  the  ab- 
dominal walls. 

The  rapid  decline  of  the  pulse— the  pulsus  celer  [Corrigan  pulse] — is  most  charac- 
teristic of  aortic  insufficiency,  and  is  to  be  felt  especially  in  the  radial  artery,  but 
also  in  the  femoral,  dorsalis  pedis,  and  other  vessels.  An  abnormally  large  quan- 
tity of  blood  is  thrown  into  the  arteries  from  the  hypertrophied  and  dilated  left 
ventricle ;  hence  the  high  ascent  of  the  pulse ;  but  since  at  the  next  diastole  of  the 
ventricle  the  blood  escapes  in  two  directions,  into  the  capillaries  and  back  into 
the  ventricle,  an  abnormally  rapid  and  deep  decline  of  the  pulse  follows  the 
high  ascent  of  its  wave — a  condition  which  explains  the  ''jumping,"  "springing" 
pulse  (pulsus  celer)  in  aortic  insufficiency.  The  quality  of  the  pulse  may  be 
plainly  recognized  also 
in  the  sphygmographic 
tracing  (see  Fig.  30). 
The  abnormal  back- 
ward wave  may  even 
be  detected  in  the  cap- 
illaries. We  often  see 
a  marked  pallor  of  the 
finger  -  nails  at  every 
diastole  of  the  heart  in 
patients  with  aortic  in- 
sufficiency —  Quincke's 
capillary  pulse. 

The       auscultatory 

phenomena  over  the  arteries  are  partly  connected  with  the  changing  conditions 
of  tension  of  the  arterial  walls.  We  very  often  hear  a  short,  rough,  systolic 
murmur  in  the  carotid.  The  second  sound,  which  is  well  known  to  be  the  trans- 
mitted aortic  second  sound,  is  absent.  Instead  of  it  we  sometimes  hear  faintly 
transmitted  the  aortic  diastolic  murmur.  The  sound  of  the  medium-sized  and 
smaller  arteries  is  very  characteristic.  By  applying  the  stethoscope  lightly  we 
hear  over  the  femoral,  the  brachial,  and  often  over  the  radial,  the  ulnar,  the  pal- 
mar arch,  and  the  dorsalis  pedis,  a  marked  valvular  sound,  which  is  changed 
by  pressure  on  the  artery,  especially  in  the  larger  arteries,  to  a  loud  stenotic 
murmur.  The  quicker  the  pulse,  the  more  certain  are  we  to  hear  these  sounds 
in  the  arteries.  The  double  sound  in  the  femoral  (Traube's  double  sound)  is 
quite  a  frequent  phenomenon,  about  the  origin  and  significance  of  which  there 
has  been  much  discussion  of  late  years.  The  double  sounds  either  follow  each 
other  shortly,  so  that  the  first  seems  something  like  a  preparatory  blow  for  the 
second,  or  they  are  separated  from  each  other  by  a  longer  interval,  like  the  two 
sounds  of  the  heart.  Traube  explained  the  origin  of  the  first  sound  by  the  sudden 
19 


Fig.  30.— Pulse  curve  in  aortic  insufficiency. 


290  DISEASES  OF  THE  CIRCULATORY  ORGANS. 

tension  of  the  vessel-wall,  as  in  the  simple  femoral  sound,  and  the  second  sound 
by  the  sudden  relaxation  of  it.  Friedreich  has  pointed  out  in  regard  to  this  that, 
in  co-existing  tricuspid  insufficiency,  a  sound  may  also  be  produced  in  the  femoral 
vein  by  tension  of  the  venous  valves.  The  double  sound  in  the  femoral  may 
probably  have  different  causes  of  origin.  It  is,  of  course,  by  far  the  most  fre- 
quent in  aortic  insufficiency,  but  it  has  also  been  repeatedly  observed  in  other 
forms  of  heart  disease,  as  in  mitral  stenosis.  The  so-called  Duroziez's  double 
murmur  in  the  femoral  is  more  rare,  and  it  is  noticed  almost  exclusively  in  aortic 
insufficiency.  This  is  when  we  hear,  by  pressing  the  stethoscope  on  the  femoral, 
two  murmurs  jDlainly  distinct  from  each  other,  of  which  the  first  comes  from  the 
passage  of  the  systolic  blood-wave,  and  the  second  from  the  passage  of  the  abnor- 
mal backward  wave  coming  from  the  periphery  of  the  vascular  system  through 
the  artificially  contracted  vessel. 

Aortic  insufficiency  is  in  so  far  a  comparatively  favorable  form  of  heart  disease 
for  the  patient,  that  it  may  be  almost  perfectly  compensated  for  years  by  hyper- 
trophy of  the  left  ventricle.  Many  patients  with  moderate  aortic  insufficiency 
feel  perfectly  well,  and  are  even  capable  of  quite  hard  work.  They  have  not  the 
slightly  cyanotic  hue  which  almost  all  patients  with  mitral  disease  have,  but  they 
have  a  normal  or  even  a  pale  complexion.  If,  however,  the  signs  of  disturbed 
compensation  once  appear,  the  severest  sequelae  may  develop  quite  rapidly  in 
aortic  insufficiency.  The  left  side  of  the  heart  can  no  longer  satisfy  the  abnor- 
mally great  demands  upon  it.  Hence  the  stasis  of  the  blood  sets  backward  through 
the  pulmonary  circulation  and  into  the  veins  of  the  body.  The  difficulty  in 
breathing  becomes  marked,  oedema  appears,  and  the  patient  dies  with  the  symp- 
toms of  general  dropsy.  We  will  speak  more  fully  below  of  certain  intercurrent 
events  in  aortic  insufficiency,  such  as  cerebral  haemorrhage  and  pericarditis. 

4.  Stenosis  of  the  Aortic  Orifice. 

Except  for  the  mild  forms  of  aortic  stenosis,  which  often  come  on  with  aortic 
insufficiency,  aortic  stenosis  is  a  rare  disease.  It  arises  from  marked  thick- 
enings and  calcifications,  and  especially  from  adhesions  of  the  aortic  valves  to 
one  another.  The  stenosis  may  become  so  considerable  that  the  orifice  is  finally 
reduced  to  a  mere  fissure,  through  which  the  left  ventricle  must  force  the  blood 
at  its  systole.  The  vertiginous  movements  thus  arising  in  the  blood  produce  a 
loud  systolic  murmur.  The  left  ventricle  is  compelled  to  do  greater  work  in 
consequence  of  the  increased  resistance  of  the  aortic  orifice,  and  hence  becomes 
hypertrophied.  Since  it  demands  more  time  to  drive  its  contents  through  the 
narrow  orifice  than  it  does  under  nonnal  conditions,  we  often  find  in  aortic 
stenosis  a  marked  slowing  of  the  pulse,  but  the  pulse,  as  we  can  conceive,  is 
small,  and  the  artery  feels  contracted  and  hard. 

Inspection  and  Palpation.— 0\\  physical  examination  of  the  heart  we  find 
the  apex-beat  displaced  outward,  corresponding  to  the  hypertrophy  of  the  left 
ventricle ,  but  nevertheless  it  is  by  no  means  very  strong ;  it  is  even  sometimes 
remarkably  weak,  which  condition  is  explained  in  part  by  the  slower  contraction 
of  the  ventricle,  and  in  part  by  the  absence  of  the  backward  impulse  (compare 
the  Gutbrod-Skoda  theory  of  the  heart-beat). 

Percussion. — Percussion  gives  an  extension  of  the  heart's  dullness  to  the  left. 
The  right  ventricle  is  also  dilated  and  hypertrophied  to  a  moderate  degree  in  the 
later  stages,  if  the  stasis  extends  backward  through  the  pulmonary  circulation. 

Auscultation. — On  auscultation,  we  hear  over  the  aorta  a  very  loud  "  sawing," 
long-drawn,  systolic  murmur,  which  is  usually  transmitted  to  the  right,  corre- 
sponding to  the  course  of  the  aorta,  in  distinction  from  the  diastolic  murmur  of 


VALVULAR  DISEASE  OF  THE   HEART.  291 

aortic  insufficiency.  It  is  usually  to  be  heard  loudest  at  the  sternal  end  of  the 
second  right  intercostal  space,  but  it  is  audible  to  a  lesser  extent  over  almost  the 
whole  heart.  It  is  usually  quite  loud  over  the  carotids.  The  aortic  second  sound 
is  feeble,  or  not  to  be  heard  at  all.  With  co-existing  insufficiency  of  the  valve 
it  is  replaced  by  a  diastolic  murmur. 

The  character  of  the  pulse  has  already  been  mentioned.  The  pulse  is  small, 
and  is  sometimes  in  noticeable  contrast  with  the  strength  of  the  apex-beat ;  in 
compensated  cases  it  is  regular  and  often  slow,  to  a  slight  or  sometimes  to  a  great 
degree.  The  sphygmographic  tracing  (see  Fig.  31)  gives  a  low  wave,  and  a  com- 
paratively slow  rise  and  fall  of  the  curve. 

An  aortic  stenosis  of  a  mild  degree  may  be  quite  well  borne  by  the  patient  for 
a  long  time.  In  stenosis  of  a  higher  degree  we  sometimes  notice  peculiar  symp- 
toms, which  probably  must  be  referred  to  anaemia  of  the  brain,  especially  attacks 
of  dizziness  and  faintness.  Epileptic  attacks  have  even  been  observed.  In  other 
respects  the  same  disturbances  of  compensation  finally  appear,  as  in  all  other 


Fig.  31. — Pulse  curve  in  stenosis  of  the  aortic  orifice. 

forms  of  valvular  disease.  The  course  of  the  disease  is  more  unfavorable  than 
that  of  aortic  insufficiency,  but,  on  the  other  hand,  it  is  more  favorable  than  that 
of  mitral  stenosis. 

5.  Insufficiency  of  the  Tricuspid  Valve. 

Insufficiency  of  the  tricuspid  valve  is  extremely  rare  as  an  independent 
disease  of  the  heart,  but  a  secondary  insufficiency  of  the  tricuspid  is  quite  fre- 
quent, and  is  therefore  of  practical  interest,  as  it  complicates  other  already-existing 
valvular  diseases  in  the  left  side  of  the  heart.  It  arises  either  from  a  secondary 
endocarditis  affecting  the  tricuspid,  in  quite  an  analogous  manner  with  mitral 
insufficiency,  or  it  is  a  so-called  relative  insufficiency.  This  name  we  give  to  that 
form  of  insufficiency  which  develops  when  the  edges  of  the  tricuspid  valve, 
normal  in  themselves,  at  last  fail  to  meet  one  another,  from  the  increasing  dilata- 
tion of  the  right  ventricle. 

The  necessary  result  of  tricuspid  insufficiency  is,  that  in  every  systole  of  the 
right  ventricle  a  backward  current  passes  through  the  open  tricuspid  orifice  into 
the  right  auricle,  and  thence  into  the  veins  of  the  body.  The  tricuspid  insuffi- 
ciency ensuing  in  other  forms  of  heart  disease  must  therefore  increase  the  stasis 
in  the  veins  of  the  body,  and  is  thus  far  an  unfavorable  complication.  It  has  a 
compensatory  significance  only  as  it  affords  relief  to  the  pulmonary  circulation. 
Since  a  part  of  the  blood  passes  back  from  the  right  ventricle  into  the  veins, 
less  blood  than  usual  must  reach  the  pulmonary  arteries.  The  decrease  in  ten- 
sion thus  produced  in  these  arteries  makes  itself  apparent  on  auscultation,  since 
the  accentuation  of  the  pulmonic  second  sound  in  valvular  disease  of  the  mitral 
orifice  diminishes  when  tricuspid  insufficiency  takes  place. 

That  tricuspid  insufficiency  must  result  in  a  hypertrophy  of  the  right  ven- 
tricle is  explained  in  just  the  same  way  as  the  hypertrophy  of  the  left  ventricle 
in  mitral  insufficiency,  from  the  increased  influx  of  blood  at  increased  tension 
into  the  right  ventricle  during  diastole;  but  this  effect  of  tricuspid  insufficiency 
can  rarely  be  made  out  in  any  individual  case,  since  the  right  ventricle  is  usually 
already  hypertrophied  as  a  result  of  the  disease  in  the  left  side  of  the  heart. 


292  DISEASES  OF  THE  CIECULATOEY  ORGANS. 

The  most  important  symptom  from  which  we  can  diagnosticate  tricuspid  in- 
sufficiency is  the  venous  pulse.  The  cause  of  this  is  the  backward  wave  of  blood 
produced  at  each  systole  of  the  right  ventricle.  So  long  as  the  venous  valve 
above  the  bulbus  jugularis  is  closed,  we  usually  see  only  a  "  bulbar  pulse,"  but 
very  soon  this  valve  also  yields  to  the  continued  impulse  of  the  blood,  and  then 
a  strong,  purely  venous  pulse  is  visible  along  the  whole  course  of  the  jugular 
vein  up  to  the  vicinity  of  the  mastoid  process.  The  contraction  of  the  right 
auricle  very  often  causes  a  decidedly  weaker  elevation  of  the  vein,  which  just 
precedes  the  marked  pulsation  caused  by  the  ventricular  systole  (anadicrotic 
venous  pulse).  On  account  of  the  straighter  course  of  the  right  innominate  vein, 
the  jugular  venous  pulse  is  often  stronger  on  the  right  side  than  on  the  left.  We 
must  state,  however,  that  the  jugular  venous  pulse  is  not  an  absolutely  certain 
sign  of  tricuspid  insufficiency,  since  it  may  arise  in  hypertrophy  of  the  right  side 
of  the  heart  without  any  insufficiency  of  the  tricuspid,  from  the  closure  of  the 
valves. 

If  there  is  pulsation  in  the  bulb  of  the  jugular  vein  and  the  jugular  valve  is 
still  capable  of  closing,  a  low,  audible,  venous,  valvular  sound  may  be  produced  by 
its  closure.  A  sound  may  also  arise  in  tricuspid  insufficiency,  as  has  been  already 
said,  from  the  tension  of  the  valves  in  the  femoral  vein.  A  visible  pulsation  in 
the  larger  veins  of  the  extremities  is  very  rare,  but  in  tricuspid  insufficiency  we 
quite  frequently  feel  a  venous  pulsation  of  the  liver.  This  may  be  quite  apparent 
even  in  many  cases  where  the  jugular  venous  pulse  is  absent,  because  the  veins 
in  the  liver  are  without  valves. 

Auscultation  over  the  right  side  of  the  heart  gives  a  systolic  murmur  in  insuffi- 
ciency of  the  tricuspid,  arising  from  the  regurgitating  blood-current.  This  may 
be  heard  loudest  over  the  lower  part  of  the  sternum,  or  at  the  sternal  end  of  the 
right  fifth  rib.  The  significance  of  this  murmur  in  diagnosis,  however,  is  impaired 
by  the  fact  that  it  can  not  always  be  separated  from  the  systolic  mitral  murmur 
that  often  co-exists. 

6.  Stenosis  of  the  Tricuspid  Orifice. 

Stenosis  of  the  tricuspid  orifice  is  an  uncommonly  rare  disease,  and  hence  it  is 
without  practical  significance.  It  has  usually  been  observed,  up  to  the  present 
time,  as  a  congenital  form  of  heart  disease,  almost  always  combined  with  other 
anomalies  of  development  in  the  heart. 

The  physical  signs  of  tricuspid  stenosis  can  easily  be  constructed  theoretically. 
The  first  result  must  be  a  marked  dilatation  of  the  right  auricle,  and  the  occur- 
rence of  a  diastolic  or  presystolic  murmur  over  the  right  side  of  the  heart.  From 
the  rarity  and  complex  character  of  the  cases,  however,  we  have  so  far  seldom 
had  an  opportunity  to  confirm  these  theories  at  the  bedside. 

The  prognosis  of  this  form  of  heart  disease  is  very  unfavorable,  since  a  long- 
continued  compensation  by  increased  labor  on  the  part  of  the  right  auricle  is 
scarcely  conceivable. 

[Seventy  cases  of  tricuspid  stenosis  have  been  collected  by  Bedford  Fenwick, 
whose  analysis  affords  good  grounds  for  thinking  that  the  lesion  is  often  acquired. 
In  fifty  per  cent,  of  the  cases  there  was  a  clear  history  of  rheumatism,  and  nearly 
all  of  the  patients  were  more  than  twenty  yeai*s  of  age  at  the  time  of  death. 

This  lesion  is  never  found  alone,  but  invariably  combined  with  mitral  stenosis; 
all  but  eight  of  the  cases  were  in  women.  Fenwick  thinks  that  the  influence  of 
sex  lies  in  the  less  onerous  nature  of  the  work  of  women  than  of  men,  the  granu- 
lating edges  of  the  valves  being  kept  more  in  apposition,  thus  healing  with 
adhesion  and  causing  obstructions  at  the  orifice.] 


VALVULAR  DISEASE  OF  THE  HEART.  293 

7.  Insufficiency  of  the  Pulmonary  Valve. 

Insufficiency  of  the  pulmonary  valve  is  also  a  very  rare  form  of  heart  disease. 
It  occurs  as  a  congenital  anomaly,  of  ton  combined  with  other  failures  of  develop- 
ment, or  as  a  disease  acquired  after  birth.  The  anatomical  changes  in  tbe  valve, 
which  lead  to  insufficiency,  are  precisely  analogous  to  those  which  cause  insuffi- 
ciency of  the  aortic  valve. 

The  physical  signs  of  this  form  of  valvular  disease  consist  chiefly  of  a  marked 
dilatation  and  hypertrophy  of  tbe  right  ventricle,  to  be  made  out  by  percussion, 
and  of  a  loud  diastolic  murmur  over  the  pulmonary  valve.  These  signs  are 
explained  in  just  the  same  way  as  the  precisely  analogous  signs  in  the  left  ven- 
tricle in  aortic  insufficiency. 

In  general,  pulmonary  insufficiency,  like  aortic  insufficiency,  seems  to  be  com- 
pensated quite  well  for  a  long  time  by  hypertrophy  of  the  right  ventricle.  In 
many  cases  a  co-existing  patency  of  the  foramen  ovale  also  seems  to  be  of  favor- 
able influence,  so  far  as  it  lessens  the  stasis  in  the  right  auricle  and  the  veins  of 
the  body,  while  it  renders  easier  the  filling  of  the  left  ventricle. 

8.  Stenosis  of  the  Pulmonary  Orifice  (Pulmonary  Stenosis)  and  the  other  Con- 
genital Diseases  of  the  Heart. 

1.  Congenital  Pulmonary  Stenosis.— While  the  stenosis  of  the  pulmonary 
orifice  acquired  in  later  life  is  so  rare  that  it  has  only  a  slight  practical  sig- 
nificance, the  congenital  pulmonaiy  stenosis  is  of  far  greater  importance.  It  is, 
on  the  whole,  the  most  frequent  of  the  congenital  forms  of  heart  disease.  Its 
origin  is  to  be  referred  either  to  an  endocarditis  of  the  pulmonary  valves  during 
foetal  life,  or  to  anomalies  in  the  development  of  the  heart.  The  stenosis  is  often 
situated  not  merely  at  the  pulmonary  orifice  itself,  but  farther  back  in  the  conus 
arteriosus,  which  seems  to  be  narrowed  by  the  formation  of  myocardial  cicatrices. 
The  pulmonary  artery  is  often  also  narrowed  as  a  whole.  In  the  majority  of 
cases  we  find,  in  addition,  other  anomalies  of  development  in  the  heart,  espe- 
cially patency  of  the  foramen  ovale,  great  defects  in  the  ventricular  septum,  and, 
in  about  half  the  cases,  patency  of  the  ductus  Botalli,  etc. 

The  symptoms  of  congenital  pulmonary  stenosis  sometimes  appear  soon  after 
the  birth  of  the  child.  The  first  thing  that  strikes  us  is  the  marked  cyanosis, 
which  is  constant,  or  else  comes  on  with  crying,  or  with  movements  of  the  body. 
Many  children,  however,  reach  a  fair  age,  five  or  ten  years,  but  rarely  more.  In 
some  cases  the  heart  disease  may  be  so  perfectly  compensated  that  the  child  may 
be  comparatively  well  for  a  time,  and  severe  disturbances  may  not  appear  for 
several  years. 

As  a  rule,  children  with  congenital  pulmonary  stenosis  present  a  very  strik- 
ing appearance.  The  cyanosis  is  especially  noticeable  in  the  face,  the  lips,  the 
nose,  and  the  hands  and  nails.  The  parts  mentioned  feel  cool.  The  eyes  are 
often  somewhat  prominent,  and  there  is  a  slight  cedematous  swelling  about  them. 
The  peculiar  club-like  thickening  of  the  terminal  phalanges  of  the  fingers  and 
toes,  a  result  of  stasis,  as  seen  also  in  many  cases  of  bronchiectasis,  is  very  char- 
acteristic.    The  nails  also  present  a  characteristic  claw-like  curvature. 

The  whole  development  of  the  child  is  remarkably  retarded.  The  muscles 
and  fatty  layer  are  slight.  The  gums  are  sometimes  very  spongy  and  disposed  to 
bleed.     In  severe  cases  the  child  suffers  from  faintness,  vertigo,  etc. 

On  physical  examination  of  the  heart,  we  usually  find  the  cardiac  region  rather 
prominent.  Percussion  gives  an  increase  of  tbe  heart's  dullness,  especially  toward 
the  right.     This  extension  of  the  dullness  is  due  to  the  hypertrophy  of  the  right 


294  DISEASES  OF  THE  CIRCULATORY  ORGANS. 

ventricle,  which  must  arise  in  the  same  way  as  hypertrophy  of  the  left  ventricle 
in  aortic  stenosis.  On  auscultation,  we  hear  a  loud  systolic  murmur,  which  is  per- 
ceptible over  the  whole  heart,  but  which  has  its  greatest  intensity  at  the  sternal 
end  of  the  second  left  intercostal  space.  The  eddies  of  blood,  which  produce  the 
murmur,  may  also  often  be  felt  by  the  hand  as  a  systolic  thrill.  In  some  cases,  how- 
ever, we  miss  the  murmur  in  pulmonary  stenosis,  just  as  in  mitral  stenosis.  The 
pulmonic  second  sound  is  weak  or  inaudible,  or  it  is  replaced  by  a  murmur  if  there 
is  also  insufficiency  of  the  valve. 

The  course  of  congenital  pulmonary  stenosis  is  always  unfavorable.  As  has 
been  stated  above,  only  a  few  children  get  beyond  the  age  of  fifteen  years,  Death 
ensues,  either  with  general  disturbances  of  compensation  evidenced  by  dyspnoea 
and  dropsy,  as  in  every  other  form  of  heart  disease,  or  from  complications.  Among 
the  latter,  we  may  mention  especially  the  very  frequent  development  of  phthisis. 

2.  The  Remaining  Congenital  Lesions  of  the  Heart.— Inasmuch  as  other  con- 
genital lesions  than  pulmonary  stenosis  have  but  slight  clinical  importance,  we 
will  limit  ourselves  here  to  a  brief  review  of  the  same.* 

(a)  Patency  of  the  foramen  ovale  is  a  comparatively  frequent  lesion,  whether 
alone  or  combined  with  others.  Physical  signs  are  mostly  absent.  In  a  few 
cases  a  presystolic  murmur  has  been  heard.  When  mitral  insufficiency  co-exists 
with  a  patent  foramen  ovale,  venous  pulsation  may  be  caused. 

(&)  Defects  in  the  septum  between  the  ventricles.  These  are  most  frequently 
situated  in  the  posterior  section  of  the  anterior  septum,  and  they  likewise  are 
associated  with  other  anomalies,  such  as  abnormal  distribution  of  the  arteries, 
pulmonary  stenosis,  or  defects  in  the  septum  between  the  auricles.  Sometimes  the 
patency  of  the  septum  gives  rise  to  a  systolic  murmur,  but  a  diagnosis  of  the  con- 
dition during  life  is  scarcely  ever  possible. 

(c)  Persistence  of  the  ductus  Botalli.  Inasmuch  as  this  contributes  blood 
from  the  aorta  to  the  pulmonary  circulation  the  pressure  in  the  latter  is  raised, 
hence  there  is  to  be  observed  accentuation  of  the  second  pulmonic  sound  and 
hypertrophy  of  the  right  ventricle.  There  is  sometimes  also  a  loud  systolic 
murmur. 

(d)  We  have  already  spoken  of  congenital  stenosis  of  the  tricuspid  valve. 
Congenital  narrowing  of  the  mitral  valve  and  of  the  aortic  valves  may  also  occur, 
but  they  are  extremely  rare. 

9.  Combined  Valvular  Diseases  of  the  Heart. 

Although  in  what  has  preceded  we  have  dealt  with  the  several  forms  of  valvu- 
lar disease  of  the  heart  separately,  in  order  to  present  them  in  a  general  way, 
yet  in  reality  combinations  of  them  often  occur  in  great  variety.  We  find 
especially,  as  has  already  been  mentioned,  stenosis  of  an  orifice  co-existing  with 
insufficiency  of  the  accompanying  valve;  but  diseases  of  two  or  more  different 
valves  are  not  infrequent,  combined  in  the  most  diverse  manners.  The  physical 
signs  of  these  "  combined  forms  of  heart  disease  "  may,  of  course,  be  inferred  from 
the  signs  of  anomalies  of  single  valves,  but  the  phenomena  are  often  so  compli- 
cated that  the  diagnosis  of  combined  heart  disease  is  generally  much  harder  than 
that  of  the  simple  forms.  Sometimes  the  single  forms  neuti'alize  one  another  in 
their  action.  For  example,  the  left  ventricle  is  usually  small  in  pure  mitral  ste- 
nosis, but,  if  aortic  insufficiency  be  also  present,  it  is  nevertheless  found  dilated,  at 

*  A  more  extensive  presentation  of  the  subject  can  be  found  in  Gerhardt's  "  Handbuch  der  Kinder- 
krankheiten," Band  iv,  written  by  Rauchfuss,  and  in  text-books  on  pathological  anatomy — for  ex- 
ample, Orth's. 


VALVULAR  DISEASE  OF  THE  HEART. 


205 


least  to  a  certain  degree.  The  influence  of  an  absolute  or  relative  tricuspid  insuf- 
ficiency on  the  action  of  mitral  disease,  especially  the  decrease  in  tension  in.  the 
pulmonary  vessels  caused  by  it,  and  also  the  diminished  accentuation  of  the  pul- 
monic sound,  have  been  mentioned  above. 

In  reference  to  the  clinical  symptoms  of  combined  heart  disease  we  may  say, 
on  the  whole,  that,  in  a  large  number  of  cases,  the  disease  of  one  valve  stands  out 
as  predominant  in  the  whole  picture  of  the  disease.  The  other  anomalies  are  only 
slightly  noticeable,  and  often  of  later  date.  Hence,  we  may  find  at  the  autopsies 
of  patients,  who  during  life  have  shown  the  symptoms  of  disease  of  only  one 
particular  valve,  unimportant  changes,  like  fresh  endocarditis,  on  the  other  valves, 
which  have  been  without  clinical  significance. 


General  Comparison  of  the  most  Important  Physical  Signs  in  Valvular 

Disease  of  the  Heart. 


Form  of 
Heart  Disease. 


1.  Mitral  in- 
sufficiency, 


2.  Mitral 
stenosis. 


3.  Aortic  in- 
sufficiency, 


4.  Aortic 
stenosis. 


Inspection. 


Strong  apex-beat, 
often  somewhat 
displaced  out 
ward. 

Area  of  cardiac  im 
pulse     enlarged, 
epigastric  pulsa- 
tion. 


Apex  -  beat  very 
strong,  displaced 
downward  and  to 
the  left.  Visible 
pulsation  of  the 
medium  -  sized 
and  smaller  ar- 
teries. 


Apex  -  beat  dis- 
placed to  the 
left. 


Palpation. 


Systolic  thrill  at 
the  apex.  Quite 
strong  radial 
pulse. 

Diastolic  thrill  at 
the  apex.  Small 
and  often  irregu- 
lar pulse. 


Very  strong,  heav- 
ing apex  -  beat, 
Pulsus  celer. 


Heart's  action  not 
very  strong. 

Pulse  small, 

sometimes  slow. 


Percussion. 


Hypertrophy  of 
the  left,  later  of 
the  right  ven- 
tricle. 

Hypertrophy  of 
the  right  ven- 
tricle. 


Marked  hyper- 
trophy of  the 
left  ventricle. 


Hypertrophy  of 
the  left  ven- 
tricle. 


Auscultation. 


Loud  systolic  murmur 
at  the  apex.  Pul- 
monic second  sound 
accentuated. 

Diastolic  or  presys- 
tolic murmur  at  the 
apex.  First  sound 
sometimes  loud. 
Pulmonic  second 
sound  accentuated, 
and  sometimes 

double. 

Loud  diastolic  aortic 
murmur,  especially 
over  the  upper  part 
of  the  sternum. 
Sounds  in  the  ar- 
teries (femoral  and 
brachial  sounds, 
etc.).  Sometimes 
a  double  sound  or 
double  murmur  in 
the  femoral. 

Loud  systolic  aortic 
murmur,  transmit- 
ted to  the  right. 


[Bramwell  reports  that  of  131  cases  with  macroscopic  valvular  lesion,  the  tri- 
cuspid was  implicated  in  33  "58  per  cent. ;  in  all  but  12  per  cent,  of  these  the 
changes  were  recent.  Hence  he  thinks  that  tricuspid  endocarditis  is  generally 
recovered  from,  and  this  he  attributes  to  the  relatively  small  strain  to  which  that 
valve  is  subjected.  The  obvious  therapeutic  deductiou  is  the  importance  of  rest 
in  mitral  endocarditis.] 


General  Sequelje  and  Complications  of  Valvular  Disease  of  the  Heart. 

After  having  discussed,  in  what  precedes,  the  mechanism  of  the  single  forms  of 
valvular  disease,  and  the  physical  signs  derived  from  it,  we  must  now  describe  a 
number  of  symptoms  and  sequelae  which  may  be  present  to  a  greater  or  less  degree 
in  all  forms  of  valvular  disease.  With  them  we  must  also  mention  certain  pecul- 
iarities of  the  individual  forms. 


296  DISEASES  OF  THE  CIRCULATOEY  OEGANS. 

1.  Subjective  Symptoms. — Fully  compensated  heart  disease  may  exist,  at  least 
for  a  long  time,  without  any  subjective  symptoms.  This  is  especially  the  case  in 
aortic  insufficiency,  more  rarely  in  mitral  insufficiency.  Stenosis  of  the  mitral 
or  of  the  aortic  valves  almost  always  causes  subjective  symptoms.  These  symp- 
toms often  do  not  exist  so  long  as  the  patient  keeps  perfectly  quiet  physically  and 
mentally,  but  they  develop  under  appropriate  circumstances. 

The  existing  subjective  symptoms  in  heart  disease  are  by  no  means  always 
referred,  in  the  first  place,  to  the  heart  itself.  It  sometimes  happens  that  the 
patient  comes  to  the  physician  complaining  of  various  digestive  disturbances,  or 
in  other  cases  of  headache,  vertigo,  etc.  The  physical  examination  alone  leads  us 
to  recognize  the  heart  disease.  As  a  rule,  the  patient's  first  and  chief  complaint 
is  directed  toward  his  difficulty  in  breathing.  The  shortness  of  breath,  which 
increases  on  any  physical  exertion,  comes  on  quite  early  in  many  cases.  In  the 
later  stages  it  is  almost  always  the  most  distressing  symptom.  It  arises  as  a  result 
of  the  overfilling  of  the  pulmonary  vessels  with  blood,  and  the  consequent  delay 
in  the  pulmonary  circulation,  and  impairment  of  the  transfer  of  gases  in  the  lung. 
In  the  later  stages  the  anatomical  changes  in  the  lung  tend  to  increase  the  dyspnoea. 
Until  lately  it  was  usually  assumed  that  the  distended  capillaries  encroached 
upon  the  lumen  of  the  alveoli,  and  thus  diminished  their  capacity  for  air.  Basch, 
however,  claims  that  the  alveoli  become  distended  by  the  passive  congestion  in 
the  pulmonary  circulation,  because  the  capillaries  are  stretched  (swelling  of  the 
lungs).  One  element  in  the  development  of  the  dyspnoea  is  the  "pulmonary 
rigidity."  The  diminished  expansibility  of  the  lungs  thus  occasioned  offers  the 
same  hindrance  to  respiration  as  is  seen  in  pulmonary  emphysema.  Further 
investigations  are  necessary  in  order  to  determine  the  clinical  importance  of  these 
conditions. 

The  secondary  bronchitis  of  heart  disease  is  a  very  great  factor  in  the  dyspnoea. 
This  bronchitis  is  a  frequent  result  of  the  pulmonary  stasis.  Often  the  respiratory 
distress  increases  and  decreases  simultaneously  with  corresponding  variations  in 
the  bronchitis.  A  purely  mechanical  cause  of  dyspnoea  is  the  compression  of  the 
lower  portion  of  the  left  lung  by  great  cardiac  hypertrophy.  The  highest  grade 
of  dyspnoea  is  reached  when  finally  hydrothorax  and  pulmonary  oedema  are  devel- 
oped. From  what  has  already  been  stated,  it  is  easy  to  see  why  lesions  of  the 
mitral  valve  which  directly  impair  the  pulmonary  circulation  lead  sooner  to 
shortness  of  breath  than  do  lesions  of  the  aortic  valves.  Sometimes  the  dyspnoea 
in  heart  disease  occurs  in  paroxysms  (cardiac  asthma).  This  is  probably  in  most 
cases  dependent  upon  a  sudden  cardiac  failure,  especially  involving  the  left  ven- 
tricle. 

Palpitation  is  the  first  subjective  symptom  to  be  mentioned  of  those  which 
are  referred  directly  to  the  heart.  It  is  not  yet  accurately  determined  under 
what  circumstances  the  action  of  the  heart  is  perceived  by  the  patient  himself. 
We  sometimes  see  an  uncommonly  strong  action  of  the  heart,  as  in  aortic  insuffi- 
ciency, which  is  not  perceived  at  all  subjectively.  In  other  cases,  where  objec- 
tively the  heart  is  not  especially  active,  palpitation  forms  the  patient's  chief 
complaint.  It  usually  first  appears  when  the  heart  disease  ceases  to  be  fully 
compensated.  It  is  increased  or  first  excited  by  physical  exertion  or  mental 
excitement.  In  many  patients  attacks  of  palpitation  occur  without  any  discover- 
able external  cause,  due  apparently  to  nervous  disturbance.  They  are  sometimes 
associated  with  a  striking  acceleration  of  the  pulse,  the  so-called  tachycardia. 

Pain  in  the  cardiac  region  is  only  rarely  present  in  heart  disease.  The  patients 
more  frequently  complain  of  an  indefinite  feeling  of  pressure  and  oppression  in 
the  chest,  but  attacks  of  severe  pain  in  the  cardiac  region  do  occur,  especially  in 
patients  with  aortic  insufficiency — pain  shooting  into  the  shoulders  and  arms,  the 


VALVULAR  DISEASE  OF  THE   HEART.  297 

so-called  angina  pectoris,  vide  infra,.  Pains  in  the  epigastrium  and  abdomen, 
which  sometimes  form  the  chief  annoyance  of  the  patient,  usually  depend  upon 
passive  congestion  of  the  liver  (vide  infra),  or  upon  the  tension  of  the  abdominal 
walls  from  ascites,  oedema,  etc. 

We  must  finally  mention  here  the  rheumatoid  pains  in  the  joints  and  muscles, 
from,  which  many  patients  with  heart  disease  suffer. 

The  greatest  subjective  distress  occurs  in  the  last  stages  of  heart  disease,  when 
general  dropsy  develops.  The  patient's  helplessness  usually  culminates.  All 
motions  of  the  body  are  difficult,  the  dyspnoea  and  oppression  in  the  chest  con- 
stantly increase,  until  death  finally  releases  the  patient  from  his  mournful 
condition. 

2.  Sequelae  in  the  Heart  Itself. — We  have  already  discussed  the  most  impor- 
tant sequela?  of  valvular  disease  in  the  heart  itself,  its  hypertrophies  and  dilata- 
tions. It  remains  for  us  to  describe  the  influence  of  the  cardiac  disease  on  the 
frequency  and  regularity  of  the  heart's  action,  and  also  to  discuss  some  secondai  y 
diseases  of  the  cardiac  muscle  and  of  the  pericardium. 

In  every  well-compensated  heart  disease  the  heart's  action  may  for  a  long  time 
be  of  approximately  normal  frequency  and  regularity.  We  often  find  a  constant 
and  moderate  acceleration  of  the  pulse,  which  is  easily  increased  from  temporary 
causes.  Permanent  slowing  of  the  pulse  is  rare  in  valvular  disease  of  the  heart. 
It  is  most  frequent  in  aortic  stenosis,  where  it  is  in  part  of  compensatory  signifi- 
cance. Marked  changes  in  the  frequency  of  the  pulse  depend  upon  severe  dis- 
turbances of  the  nervous  apparatus  in  the  heart.  Hence  they  are,  as  a  rule,  as- 
sociated with  irregular  action  of  the  heart.  The  frequency  of  the  pulse  may  then 
reach  120  or  140  a  minute.  Diminution  of  the  frequency  to  50  or  30  are  much 
rarer.  We  may  mention  as  an  unusual  but  interesting  symptom  the  sudden  at- 
tacks of  enormous  acceleration  of  the  pulse  to  200  or  more — tachycardia — which 
seem  to  be  especially  frequent  in  mitral  disease.  In  the  interval  there  is  usually 
a  quiet  action  of  the  heart  and  a  complete  compensation  of  the  heart  disease.  The 
increase  in  the  pulse  comes  on  quite  suddenly,  and  is  frequently  associated  with 
subjective  feelings  of  palpitation  and  distress.  It  may  last  for  several  hours  and 
then  disappear  again,  also  quite  suddenly.  The  precise  cause  of  these  attacks  is 
unknown.  We  may  probably  regard  it  as  a  temporary  paralysis  of  the  inhibitory 
apparatus  of  the  heart. 

Arhythmia  of  the  heart  is  of  still  greater  importance  than  anomalies  of  the 
pulse-frequency.  It  always  points  to  a  severe  distui'bance  of  the  nervous  appa- 
ratus of  the  heart.  The  general  circulatory  disturbance  which  follows  every  valv- 
ular disease  must  of  course  make  itself  felt  in  the  heart  itself,  and  the  nerves  and 
ganglia  of  the  heart  can  not  remain  undisturbed  by  it.  Hence  we  generally  see 
marked  variations  in  the  frequency  and  rhythm  of  the  heart's  action  along  with 
the  other  signs  of  beginning  disturbance  of  compensation;  but  daily  clinical 
experience  teaches  us  that  there  is  not  a  perfect  parallelism  between  the  two  symp- 
toms. We  find  often  enough  in  heart  disease  quite  a  considerable  irregularity  of 
the  pulse  without  any  of  the  other  signs  of  marked  disturbance  of  compensation, 
and,  on  the  other  hand,  we  see  in  many  patients  an  almost  perfect  regularity  of 
the  pulse  up  to  death.  In  mitral  disease,  especially  in  mitral  stenosis,  arhythmia 
of  the  heart  is  much  more  frequent  than  in  aortic  disease. 

We  can  not  here  discuss  in  detail  the  different  forms  and  symptoms  of  cardiac 
irregularity.  An  inequality  in  the  intensity  of  the  single  beats  is  very  often  asso- 
ciated with  the  irregularity :  the  irregular  pulse  is  also  an.  unequal  pulse.  The 
weaker  heart-beats  sometimes  cause  a  pulse  which  is  no  longer  perceptible  in  the 
radial  artery,  so  that  we  can  determine  the  true  frequency  of  the  heart-beat,  not 
by  counting  the  radial  pulse,  but  only  by  auscultation  of  the  heart.     The  occur- 


Fig.  32.— Pulsus  bigeminus. 


29S  DISEASES  OF  THE  CIRCULATORY  ORGANS. 

rence  of  the  so-called  pulsus  bigeminus  is  of  interest  (see  Fig.  32).     A  second 
weaker  contraction  follows  the  first  strong  systole,  even  before  the  ventricular 

diastole  has  fully  ended,  and  then  comes  a  longer 
pause.  We  feel  alternately  a  strong  and  quite  weak 
pulse.  The  latter  may  be  imperceptible,  so  that  it 
can  be  made  out  only  by  the  sphygmograph.  In 
such  cases,  with  co-existing  tricuspid  insufficiency, 
we  sometimes  find  the  number  of  the  venous  pul- 
sations twice  as  great  as  the  number  of  the  radial 
pulsations,  because  the  second  weaker  contraction 
of  the  heart  produces  a  visible  venous  pulse,  but  not  an  appreciable  radial  pulse. 
On  the  whole,  the  pulsus  bigeminus  is  a  bad  sign,  since  it  always  points  to  a 
marked  disturbance  of  the  cardiac  innervation ;  but  it  may  also  pass  away  again 
and  give  place  to  a  regular  action  of  the  heart. 

Chronic  valvular  disease  of  the  heart  is  often  combined  with  anatomical 
changes  in  the  cardiac  muscle,  and  sometimes  in  the  pericardium. 

Among  the  changes  in  the  cardiac  muscle,  cloudy  swelling,  and  especially  fatty 
degeneration  of  the  muscular  fibers,  are  the  most  frequent.  The  fatty  degenera- 
tion of  the  muscle  occurs  either  in  a  diffuse  form,  or  in  little  yellowish  spots, 
which  are  plainly  visible  on  the  papillary  muscles  and  trabecule.  The  opinion 
has  often  been  expressed  that  fatty  degeneration  of  the  muscles  is  the  cause  of 
the  disturbance  of  compensation;  that  the  cardiac  muscle  performs  its  increased 
work  until  fatty  degeneration  ensues  and  reduces  its  strength.  This  theory  does 
not  entirely  correspond  to  the  facts.  We  have  often  seen  the  greatest  disturbance 
of  compensation  in  valvular  disease  when  section  of  the  cardiac  muscle  showed 
no  fatty  degeneration ;  and,  on  the  other  hand,  we  have  seen  great  fatty  degenera- 
tion of  the  heart,  as  in  pernicious  anaemia,  when  there  were  no  signs  of  cardiac 
weakness  during  life.  Anatomically,  with  our  present  aids  to  research,  we  can 
hardly  ever  decide  with  certainty  whether  the  cardiac  muscle  was  still  capable 
of  performing  its  normal  functions  or  not.  The  usual  state  of  the  case  is  probably 
this,  that  fatty  degeneration  of  the  cardiac  muscle  is  a  result  of  the  disturbance 
of  compensation,  and  especially  of  the  deficient  supply  of  arterial  oxygenated 
blood  to  the  muscle  (see  the  chapter  on  anaemia). 

A  frequent  affection  of  the  cardiac  muscle  in  valvular  disease  is  the  presence 
of  cicatricial  changes  and  so-called  myocarditic  nodules  in  the  substance  of  the 
heart.  Chronic  endocarditis  may  directly  invade  the  subjacent  parts  of  the 
cardiac  muscles  and  set  up  a  chronic  inflammation  there,  but  the  cardiac  cicatrices 
usually  have  another  origin.  The  connective-tissue  thickening  beneath  the  endo- 
cardium is  the  result  of  a  simple  atrophy  of  the  superficial  muscular  fibers  due  to 
the  increased  internal  pressure  of  the  blood,  as  in  mitral  or  aortic  insufficiency. 
The  connective-tissue  nodules  within  the  cardiac  muscle,  however,  depend  upon 
a  deficiency  in  the  local  supply  of  arterial  blood.  Simple  sclerotic  thickening  of 
the  coronary  arteries,  or  complete  embolism,  or  thrombosis  of  a  small  branch  of 
one  of  them,  is  the  evident  cause  of  these  circumscribed  cicatrices.  It  is  certain 
that  the  latter  may  reduce  the  capacity  of  the  cardiac  muscle  for  work,  but,  on 
the  other  hand,  we  often  find  cicatrices  of  myocarditis  without  any  signs  of  a 
previous  disturbance  in  the  compensation  of  the  heart.  A  fuller  discussion  of 
this  subject  will  be  found  in  the  next  chapter. 

Pericarditis  is  not  very  rare  as  a  result  of  chronic  valvular  disease.  It  is 
always  a  dangerous  complication,  and  may  cause  death.  Regarding  its  origin, 
we  have  found  that  almost  all  the  cases  of  heart  disease  complicated  with  peri- 
carditis show  changes  in  the  aortic  valves.  Hence  it  does  not  seem  improbable  to 
us  that  the  origin  of  the  secondary  pericarditis  in  such  cases  is  due  to  a  direct 


VALVULAR  DISEASE  OF  THE  HEART.  299 

invasion  of  the  pericardium  by  the  excitants  of  inflammation  passing  from  the 
aortic  valves  through  the  walls  of  the  blood-vessel. 

3.  Symptoms  of  Stasis  in  the  Different  Organs  of  the  Body.— As  has  frequently 
been  mentioned  in  what  precedes,  the  results  of  stasis  of  the  blood  make  them- 
selves manifest  in^heart  disease  in  various  organs.  We  have  already  spoken  of 
the  important  results  of  blood  stasis  in  the  lungs.  It  remains  for  us  to  discuss 
the  symptoms  of  stasis  in  the  systemic  veins. 

As  soon  as  the  flow  of  venous  blood  into  the  right  side  of  the  heart  is  hindered, 
the  venous  stasis  is  shown  by  the  cyanotic  appearance  of  the  patient.  This 
cyanosis  may  exhibit  any  degree.  In  heart  disease  which  is,  on  the  whole,  still 
well  compensated,  it  is  recognized  only  by  the  practiced  eye  of  the  physician  as 
a  slight  bluish  tinge  of  the  lips,  the  alae  of  the  nose,  the  cheeks,  or  the  nails. 
With  the  increase  of  the  disturbance  of  compensation  the  cyanosis  increases,  if 
it  be  not  modified  by  the  co-existence  of  general  anaemia.  In  mitral  disease, 
especially  in  mitral  stenosis,  the  cyanosis  is  usually  more  marked  than  in  aortic 
disease.  The  large  veins  also  become  plainly  visible  as  a  result  of  their  complete 
filling,  especially  the  large  external  jugulars. 

A  further  important  symptom  which  follows  the  venous  stasis  is  the  oedema, 
the  dropsy  of  heart  disease.  As  we  know  from  general  pathology,  every  venous 
stasis,  if  it  reaches  a  certain  grade,  leads  to  a  transudation  of  the  fluid  of  the  blood 
from  the  capillaries.  If  the  lymphatics  can  no  longer  carry  this  transudation 
away,  it  collects  in  the  meshes  of  the  tissues  and  leads  to  oedema.  The  oedema  of 
heart  disease,  therefore,  does  not  appear  until  the  venous  stasis  has  reached  a  certain 
degree,  and  the  compensation  of  the  heart  disease  has  become  impaired.  It  first 
appears  in  those  parts  where  there  is  a  particularly  loose  tissue,  as  in  the  eyelids 
and  the  scrotum,  or  where  mechanical  conditions  favor  its  development.  The  legs 
usually  swell  first,  especially  about  the  ankles,  because  here  the  stasis  of  the  venous 
blood  is  increased  by  gravity.  At  first,  slight  oedema  appears  only  temporarily 
and  by  day,  and  disappears  again  while  the  body  is  in  bed  at  night ;  but,  as  the  dis- 
turbance of  compensation  increases,  the  oedema  also  constantly  grows  worse,  espe- 
cially in  the  dependent  parts  of  the  body,  until  finally  it  may  reach  the  highest 
degree  of  dropsy.  Besides  the  oedema  of  the  skin,  transudations  into  the  internal 
cavities  occur,  especially  into  the  abdomen  and  the  pleural  cavity. 

The  patient's  distress  is  decidedly  increased  by  marked  oedema,  as  has  already 
been  said.  All  the  motions  of  the  swollen  extremities  are  considerably  impeded. 
Hydrothorax  and  ascites  increase  the  dyspnoea,  the  former  by  compression  of  the 
lungs,  the  latter  by  upward  pressure  on  the  diaphragm.  The  passage  of  urine 
may  be  rendered  very  difficult  by  oedema  of  the  prepuce.  Besides  that,  we  must 
mention  that  the  skin,  when  very  ©edematous,  is  quite  apt  to  become  the  seat  of 
furuncular  and  erysipelatous  inflammations. 

The  results  of  stasis  in  the  internal  organs  may  be  best  seen  in  the  liver,  spleen, 
and  kidneys. 

Passive  congestion  of  the  liver  is  manifested  by  quite  a  considerable  increase 
in  the  size  of  the  organ.  The  lower  boundary  of  the  liver  dullness  extends 
several  fingers'  breadth  beyond  the  edge  of  the  ribs,  and  the  lower  border  of  the 
liver  may  often  be  plainly  felt.  The  liver  may  also  be  enlarged  in  cases  where 
there  are  no  other  marked  signs  of  passive  congestion,  such  as  dropsy.  Quite 
severe  pain  in  the  hepatic  region  sometimes  arises  from  the  tension  of  the  capsule 
of  the  liver.  In  the  later  stages  the  liver  may  grow  smaller  again  from  the  par- 
tial atrophy  of  its  cells. 

Jaundice  often  develops  in  heart  disease,  as  a  result  of  passive  congestion  of 
the  liver,  or  perhaps  sometimes  from  a  secondary  duodenal  catarrh.  The  peculiar 
mixture  of  a  cyanotic  and  slightly  jaundiced  hue  of  the  skin  is  very  characteristic 


300  DISEASES  OF  THE  CIRCULATORY  ORGANS. 

in  many  cases,  especially  in  mitral  disease.  It  should  be  added  that  the  yellowish 
discoloration  of  the  skin  in  heart  disease  is  probably  not  always  a  genuine  icterus, 
but  may  be  occasioned  by  the  deposit  of  other  pigments  in  the  skin. 

Passive  congestion  of  the  spleen  arises  if  the  stasis  of  the  blood  extends  to  the 
splenic  vein.  The  spleen  increases  in  size  and  becomes  firm  and  dense.  It  is 
often  hard  to  make  out  the  congestion  from  the  increase  of  the  splenic  dullness, 
because  percussion  of  the  spleen  is  uncertain  if  there  be  also  ascites,  hydrothorax, 
etc.  We  can  often,  however,  plainly  feel  the  enlarged  spleen  under  the  edge  of 
the  ribs  on  the  left. 

We  recognize  passive  congestion  of  the  kidneys  by  the  changes  in  the  urine. 
The  amount  diminishes ;  the  urine  becomes  darker,  more  concentrated,  of  a  higher 
specific  gravity,  and  of  greater  acidity.  A  sediment  of  uric  acid  or  of  sodic  urate 
very  commonly  forms  in  it.  In  marked  degrees  of  stasis  there  is  albumen  in  the 
urine.  The  amount  of  albumen  is  usually  slight,  but  it  may  equal  one  third 
or  one  fourth  of  its  volume.  Under  the  microscope  we  find,  in  the  urine  of  simple 
passive  congestion,  only  an  occasional  hyaline  cast,  and  a  few  red  and  white  blood- 
corpuscles.  Genuine  acute  or  chronic  nephritis,  however,  may  also  develop  as  a 
complication  in  heart  disease. 

We  may  refer  the  numerous  gastric  and  digestive  disturbances,  like  loss  of 
appetite,  vomiting,  constipation,  and  diarrhoea,  from  which  such  patients  often 
suffer,  to  the  stasis  in  the  blood-vessels  of  the  stomach  and  intestines. 

4.  Embolic  Processes. — The  slowing  of  the  circulation,  and  the  disturbances  in 
the  nutrition  of  the  walls  of  the  vessels,  which  result  from  it,  often  give  rise  in 
heart  disease  to  the  formation  of  thrombi.  These  are  situated  in  the  heart  itself, 
on  the  diseased  valves,  in  the  recesses  between  the  trabecular,  in  the  auricles, 
etc.,  or  else  they  form  in  the  veins,  especially  in  those  of  the  lower  extremity. 
Prom  these  thrombi  fibrinous  plugs  may  easily  be  set  loose  and  enter  the  circu- 
lation, and  thus  give  rise  to  embolic  processes  in  distant  organs.  Some  of  the 
embolisms,  whose  clinical  relations  are  especially  important,  have  been  more  fully 
described  elsewhere,  and  will  be  mentioned  only  briefly  here. 

Embolism  of  the  pulmonary  arteries,  proceeding  from  venous  thrombi  or  from 
thrombi  in  the  right  side  of  the  heart,  gives  rise  to  haemorrhagic  infarction  of 
the  lungs.  Its  pathogenesis  and  symptoms  have  already  been  discussed  in  a  pre- 
vious section  (see  page  247). 

Embolism  of  the  cerebral  arteries  is  a  common  cause  of  apoplectic  attacks, 
which  are  not  infrequent  in  heart  disease,  and  which  usually  lead  to  hemiplegia. 
The  anatomical  cause  of  the  hemiplegia  in  these  cases  is  the  embolic  softening  of 
the  brain  which  develops.  The  details  of  this  are  given  in  the  section  on  cerebral 
diseases  (see  page  737). 

Embolism  of  the  larger  arteries  of  the  extremities,  like  the  femoral  and  the 
brachial,  is  much  rarer  than  the  forms  mentioned.  It  leads  to  embolic  gangrene 
of  the  extremities,  unless  an  adequate  collateral  circulation  can  be  established. 
The  skin  of  the  peripheral  parts,  the  fingers  or  toes,  first  becomes  cool,  bluish, 
and  at  last,  if  the  circulation  be  wholly  checked,  almost  black.  The  gangrene 
advances  slowly,  usually  occupying  weeks.  Ulcerations  develop  as  the  necrotic 
portions  are  thrown  off.  The  affection  is  extremely  painful.  The  patient  soon 
becomes  very  miserable  from  the  pain  and  the  septic  fever  that  usually  attend 
the  ulcerations,  and  extensive  gangrene  almost  always  ends  fatally. 

Embolism  of  the  renal  artery,  with  the  formation  of  an  ensuing  haemorrhagic 
infarction,  may  run  its  course  without  symptoms,  but  sometimes  it  may  be  recog- 
nized by  the  sudden  appearance  of  blood  in  the  urine. 

Embolic  infarction  of  the  spleen  is  often  marked  by  swelling  of  the  spleen 
and  by  severe  perisplenitic  pains.     In  other  cases  it  is  wholly  without  symptoms. 


VALVULAR  DISEASE  OF  THE  HEART.  301 

Embolism  of  a  mesenteric  artery  is  a  very  rare  event.  Its  symptoms  consist 
in  a  sudden  intestinal  haemorrhage,  in  severe  colicky  pains,  general  collapse,  and 
peritonitis. 

5.  Complications  on  the  Part  of  the  Nervous  System.— The  most  important 

complication  on  the  part  of  the  nervous  system— embolic  softening  of  the  brain 

has  already  been  mentioned.  We  must  also  state  that  cerebral  haemorrhage  may 
occur  in  heart  disease.  It  is  especially  frequent  in  aortic  insufficiency  either 
as  a  result  of  co-existing  atheroma  of  the  cerebral  arteries,  or  perhaps  of  the  ab- 
normally high  tension  of  the  walls  of  the  vessels  during  systole. 

Mental  disorders  have  been  repeatedly  observed  in  chronic  valvular  disease. 
They  are  the  result  of  the  disturbance  of  the  circulation,  and  the  consequent  im- 
pairment of  nutrition  in  the  brain.  Hence  they  usually  make  their  first  appear- 
ance mthe  last  stages  of  heart  disease,  at  the  same  time  with  the  other  disturbances 
of  compensation.  The  psychoses  in  heart  disease  most  frequently  have  the  char- 
acter of  melancholia,  but  conditions  of  excitement  also  occur. 

6.  Secondary  Affections  of  the  Joints  are  not  rare  in  heart  disease.  As  acute 
endocarditis  develops  in  the  course  of  acute  articular  rheumatism,  so,  on  the  other 
hand,  rheumatic  pains  in  the  muscles  and  joints,  and  even  acute  swelling  of  the 
joints,  associated  with  fever,  appear  in  the  course  of  chronic  heart  disease.  Both 
affections — that  of  the  heart  and  that  of  the  joints— arise  from  the  same  specific 
cause  of  disease,  and  hence  they  may  occur  in  varying  succession. 

7.  General  Symptoms— Fever.— In  congenital  heart  disease,  as  we  have  said, 
the  child's  general  nutrition  is  very  backward.  In  heart  disease  in  adults,  how- 
ever, we  by  no  means  always  see  an  injurious  influence  on  the  general  condition 
of  nutrition.  In  many  patients  we  even  find  a  remarkably  good  development  of 
fat.  A  marked  general  disturbance  of  nutrition,  such  as  great  anaemia  and  gen- 
eral emaciation,  often  develops  in  the  later  stages,  especially  in  aortic  insuffi- 
ciency.    The  wasting  is  of  course  often  hidden  by  the  oedema. 

In  general,  chronic  heart  disease  runs  its  course  without  fever,  but  periods  often 
occur  in  the  course  of  the  disease  when  there  is  a  moderate  and  usually  irregular 
fever.  Marked  disturbances  of  the  general  condition  may  or  may  not  be  associated 
with  it.  The  basis  of  the  fever  is  probably  an  acute  exacerbation  of  the  endo- 
carditis, except,  of  course,  in  accidental  complications.  All  variations  occur,  from 
a  mild  febrile  movement  without  further  symptoms  to  a  severe  acute  recurring 
endocarditis  (q.  v.).  In  other  cases  the  fever  is  connected  with  secondary  swelling 
of  the  joints,  or  with  embolic  processes. 

General  Course  and  Prognosis  of  Valvular  Disease  of  the  Heart. 

The  course  of  valvular  disease  of  the  heart  is  in  most  cases  very  chronic.  It 
may  last  for  years.  So  long  as  there  is  a  complete  compensation,  the  patient  feels 
almost  perfectly  well;  sometimes  he  even  has  no  misgivings  as  to  his  trouble. 
The  slight  difficulty  in  respiration  and  the  incapacity  for  physical  exertion  are 
noticed,  but  little  attention  is  paid  to  them,  because  the  patient  is  used  to  them. 
In  other  cases  there  is  a  moderate  disturbance  for  a  long  time,  but  it  may  be  borne 
quite  easily  if  the  patient  is  rational  and  prudent  in  his  conduct. 

We  can  not  make  any  general  statement  as  to  the  length  of  the  stage  of  com- 
pensation, because  cases  differ  very  greatly  in  this  respect.  It  depends  in  part 
upon  the  intensity  of  the  heart  disease,  in  part  upon  the  external  conditions 
under  which  the  patient  lives,  and  in  part,  certainly,  upon  the  different  indi- 
vidual capacity  for  work  and  power  of  resistance  of  the  heart.  Thus  it  happens 
that  many  cases  last  for  decades,  while  in  others  severe  sequela?  appear  within  a 
few  months.     External  injurious  agencies,  acting  on  the  patient,  are  of  great 


302  DISEASES  OF  THE  CIRCULATORY  ORGANS. 

influence  on  the  course  of  heart  disease.  Severe  physical  exertion,  an  injudicious 
manner  of  living,  intercurrent  febrile  disease,  nieutal  disturbances,  care,  and 
auxiety  are  often  followed  by  unhappy  consequences. 

If  the  first  signs  of  disturbed  compensation  appear,  if  severe  dyspnoea,  slight 
oedema  of  the  ankles,  etc.,  develop  for  the  first  time,  these  symptoms  may  disap- 
pear again  completely  under  proper  treatment.  Severe  disturbances  of  compen- 
sation even,  great  general  dropsy,  associated  with  very  weak  and  irregular  action 
of  the  heart,  may  abate,  after  a  few  weeks'  duration,  and  the  patient  may  feel 
quite  well  again.  Exacerbations  of  the  disease  may  come  on  several  times  and 
as  often  improve.  Finally,  of  course,  the  improvement  is  incomplete.  Persistent 
oedema  and  the  other  results  of  venous  stasis  ensue,  the  symptoms  constantly 
increase  in  severity,  especially  the  dyspnoea,  until  the  patient  dies  after  a  long 
and  distressing  illness.  Immediately  before  death  in  heart  disease,  certain  ir- 
regularities in  the  innervation  of  the  heart  and  in  the  respiration  sometimes 
develop.  Among  these  the  so-called  Cheyne-Stokes  phenomenon  deserves  especial 
mention.  It  consists  in  a  peculiar  periodical  variation  in  the  respiratory  move- 
ments. There  will  be,  first,  a  complete  pause  in  the  respiration  (apncea),  and  this 
will  be  succeeded  by  feeble  breathing  gradually  becoming  stronger,  then  gradually 
abating,  and  finally  ending  in  another  complete  cessation  of  the  respiration.  The 
patient  usually  becomes  more  comatose  during  the  cessation  of  respiration ;  his 
pupils  contract.  During  the  hard  breathing  the  patient  recovers  somewhat,  and 
his  pupils  dilate  again.  The  chief  cause  of  this  rhythmical  breathing  is  proba- 
bly to  be  sought  in  the  decided  lowering  of  the  excitability  of  the  respiratory 
centre.  During  the  apncea  a  considerable  amount  of  carbonic  acid  collects  in 
the  blood  before  the  respiratory  centre  is  sufficiently  stimulated  to  resume  its 
activity. 

In  regard  to  the  single  forms  of  valvular  disease,  aortic  insufficiency  generally 
gives  the  best  prognosis,  inasmuch  as  it  may  be  very  perfectly  compensated  for 
many  years,  but  if  severe  disturbance  of  compensation  once  occurs  in  this  form  of 
heart  disease,  it  gives  a  very  unfavorable  prognosis,  since,  as  a  rule,  we  can  not 
re-invigorate  the  heart.  Mitral  insufficiency  is  also  quite  a  favorable  form  of 
heart  disease,  which  may  be  compensated  for  a  long  time.  Mitral  stenosis  is 
decidedly  more  unfavorable  in  its  prognosis,  and  is  associated  with  more  disturb- 
ance; but  in  all  mitral  diseases  very  severe  conditions  may  improve  once  or  even 
repeatedly.  Aortic  stenosis  is  also  capable  of  quite  good  compensation,  and  in  this 
respect  it  is  even  more  favorable  for  the  patient  than  mitral  stenosis,  but  it  often 
causes  persistent  cerebral  symptoms,  such  as  headache  and  vertigo,  depending  on 
anaemia  of  the  brain. 

Whether  established  valvular  disease  of  the  heart  is  curable  is  a  question  which 
can  not  be  answered  unconditionally  in  the  negative.  Of  course  in  the  great 
majority  of  cases  it  is  in  itself  incurable;  only  its  sequelae  can  be  prevented  or 
removed  to  a  certain  degree.  In  children  and  young  people,  however,  cases  some- 
times do  occur,  as  we  ourselves  have  seen,  in  which  there  are  all  the  signs  of  a 
pronounced  heart  disease,  but  after  a  long  time  recovery  is  complete.  Of  course 
it  is  very  hard  to  decide  whether  we  really  have  to  do  with  a  valvular  disease  that 
has  been  cured,  because  simple  dilatation  of  the  heart,  relative  insufficiency  of 
the  valves,  anaemic  cardiac  murmurs,  etc.,  may  easily  be  confounded  with  pure 
valvular  disease  of  the  heart. 

Among  the  dangerous  intercurrent  accidents  in  valvular  disease  we  must  make 
especial  mention  of  embolic  processes,  which  may  occur  suddenly  and  without 
warning.  The  different  forms  of  embolism  have  been  mentioned  above,  and  also 
the  occurrence  of  cerebral  haemorrhage  in  heart  disease.  Intercurrent  acute  dis- 
eases, like  typhoid  and  pneumonia,  often  take  a  very  severe  and  dangerous  course 


VALVULAR  DISEASE  OF  THE  HEART.  303 

in  patients  with  heart  disease,  because  they  make  increased  demands  upon  the 
heart's  capacity  for  work. 

Treatment  of  Valvular  Heart  Disease.* 

1.  Prophylaxis. — Our  remedies  to  prevent  the  development  of  heart  disease 
are  very  limited.  To  avert  endocarditis  in  articular  rheumatism  by  the  present 
method  of  treating  acute  rheumatism  with  salicylic  acid  is  impossible.  The  prob- 
ability of  the  onset  of  endocarditis  may  be  lessened  only  so  far  as  the  whole 
duration  of  the  disease  is  often  considerably  shortened  by  salicylic  acid. 

We  can  also  do  little  in  the  way  of  prophylaxis  against  the  development  of  heart 
disease  that  is  chronic  from  the  start,  since  the  cause  of  the  disease  is  in  many 
cases  wholly  unknown  to  us.  Those  injurious  influences  deserve  the  most  atten- 
tion which  may  favor  the  development  of  arterial  atheroma  and  its  consequent 
chronic  valvular  disease.  Undue  indulgence  in  alcohol,  too  much  smoking,  and 
injudicious  and  luxurious  ways  of  living,  are  especially  to  be  avoided.  The  part 
which  these  factors  play,  however,  in  the  development  of  a  pure  valvular  disease, 
is  certainly  much  less  than  their  influence  upon  the  development  of  certain  func- 
tional and  nervous  disturbances  of  the  heart  (see  a  later  chapter). 

[There  is  evidence  that  the  alkaline  treatment  of  acute  rheumatism  lessens  the 
danger  of  cardiac  complications  (see  page  909).] 

2.  Treatment  of  Compensated  Heart  Disease. — If  we  have  to  treat  a  heart 
disease  which  already  exists,  but  which  is  at  the  same  time  fully  compensated,  our 
treatment  must  be  chiefly  hygienic.  The  patient  must  be  made  aware  of  his  heart 
disease  without  making  him  needlessly  anxious.  He  must  be  told  that  his  further 
good  health  depends  in  great  part  upon  his  own  conduct,  his  discretion,  and  his 
perseverance.  The  patient  must  avoid  everything  which  makes  great  demands 
upon  the  heart,  or  which  may  have  a  directly  injurious  influence  on  it.  All 
violent  bodily  exertion,  too  intense  mental  work,  and  also  all  excesses  in  eating, 
drinking,  smoking,  etc.,  must  be  avoided.  That  the  physician's  directions  will 
often  collide  with  the  demands  of  the  patient's  occupation,  as  well  as  with  his 
favorite  amusements  and  his  habits,  should  not  deter  the  physician  from  demand- 
ing the  fulfillment  of  his  prescriptions,  at  least  so  far  as  possible. 

Treatment  by  drugs  is  usually  unnecessary  in  compensated  heart  disease.  We 
do  not  know  a  remedy  which  has  a  directly  favorable  action  on  heart  disease. 
The  protracted  use  of  iodide  of  potassium,  Fowler's  solution,  arsenite  of  antimony 
("granules  of  antimony"),  nitrate  of  silver,  etc.,  has  been  recommended.  The 
efficacy  of  these  remedies  is  not  proven.  We  can  always  try  them,  if  a  mild  dis- 
turbance makes  a  prescription  desirable  and  other  remedies  are  not  especially 
indicated.  Beyond  this,  the  physician  is  usually  contented  with  an  endeavor  to 
improve  the  appetite  and  nutrition  of  the  patient  by  means  of  iron,  quinine,  and 
bitters.  If  there  is  a  suspicion  that  the  heart  disease  may  be  due  to  syphilis,  a 
trial  of  iodide  of  potash  may  be  made,  but  a  brilliant  result  from  the  employment 
of  anti-syphilitic  measures  is  hardly  to  be  expected. 

The  employment  of  baths  in  heart  disease  deserves  special  consideration. 
Numerous  experiences  go  to  prove  that  they  are  not  only  well  borne  by  cardiac 
patients,  but  that  they  exercise  a  peculiarly  beneficial  and  invigorating  influence 
upon  the  action  of  the  heart.  In  this  regard,  the  greatest  reputation  is  possessed 
by  the  warm  mud  baths,  which  are  rich  in  carbonic  dioxide,  particularly  those  at 
Nauheim.     Even  where  there  is  incipient  failure  of  compensation,  there  will  be 

*  A  brief  critical  sketch  of  the  mechanical  treatment  of  circulatory  disturbances,  the  so-called 
Oertel  method,  will  be  found  in  the  appendix  to  the  fifth  chapter  of  this  section. 


304  DISEASES  OF  THE   CIRCULATORY  ORGANS. 

marked  improvement  upon  the  use  of  these  or  similar  baths.  Patients  may  also 
employ  at  home  either  simple,  or,  still  better,  salt  baths,  at  a  temperature  of  90"5°- 
93°  (26°-27°  R. ) .  That  a  change  of  climate  may  prove  beneficial  is  self-evident.  It 
is  particularly  appropriate  that  patients  with  a  tendency  to  bronchitis  or  rheuma- 
tism should  spend  the  winter  South. 

3.  Treatment  of  Disturbances  of  Compensation. — As  soon  as  the  compensa- 
tory activity  of  the  heart  begins  to  be  impaired  in  valvular  disease,  as  soon  as 
dyspnoea  and  oedema  ensue,  we  must,  almost  always,  resort  to  digitalis.  Digitalis 
in  small  doses  has  the  property  of  reducing  the  frequency  of  the  pulse,  and  also 
of  strengthening  the  individual  heart-beats,  and  thus  increasing  the  blood-pressure. 
Digitalis  is  indicated  in  every  case  of  heart  disease  if  disturbances  of  compensation 
appear,  and  if  the  pulse  also  is  abnormally  small,  of  abnormally  low  tension,  of 
increased  frequency,  and  irregular.  The  desired  action  of  digitalis,  then,  is  to 
make  the  pulse  slower,  more  regular,  and  of  higher  tension.  Under  the  influence 
of  an  increase  of  the  arterial  pressure  thus  produced,  the  disturbances  of  compen- 
sation disappear  in  a  way  that  is  often  surprising ;  the  urine  especially  bceomes 
more  abundant,  the  scanty,  dark,  concentrated  urine  of  passive  congestion  disap- 
pears, the  daily  amount  increases,  and  the  urine  therefore  becomes  clear  and  of  a 
low  specific  gravity.  The  oedema  also  disappears,  the  dyspnoea  ceases,  the  head 
is  clear,  the  general  condition  is  better — in  short,  a  complete  compensation  of  the 
heart  disease  may  be  re-established.  This  change  is  sometimes  accomplished  in 
a  comparatively  short  time— in  a  few  days  or  weeks. 

The  dose  in  which  digitalis  is  to  be  prescribed  can  not  be  given  absolutely, 
because  the  amount  of  the  active  principle  which  the  plant  contains  does  not 
seem  to  be  quite  alike  in  different  places.  This  is  the  explanation  of  the  some- 
what different  statements  as  to  the  dose  to  be  employed.  In  general,  we  should 
begin  with  small  doses.  We  usually  prescribe  an  infusion  of  the  leaves  of  a 
strength  of  1  or  1'5  parts  of  digitalis  to  150  parts  of  distilled  water  —  a  tea- 
spoonful  every  one  or  two  hours.  The  addition  of  syrup  causes  the  medicine  to 
decompose  more  easily,  and  is  quite  useless.  The  favorite  addition  of  diuretics, 
liquor  potassii  acetatis,  30  parts,  or  boro-tartrate  of  potassium  and  sodium,  four 
to  eight  parts  added  to  the  infusion,  diminishes  the  strength  of  the  remedy.  It  is 
advisable  to  give  digitalis  in  powder,  because  we  can  thus  define  the  dose  more 
accurately.  We  prescribe  powders  of  one  or  two  grains  of  digitalis  leaves  (grm. 
0-05-0"1)  with  seven  or  eight  grains  of  sugar  (grm.  0"4),  and  give  that  amount 
every  two  or  three  hours.  The  drug  may  also  be  given  in  capsules  or  suspended 
in  water.  It  is  often  a  good  plan  to  inclose  the  powder  in  capsules.  The  other 
preparations  of  digitalis,  the  vinegar  and  the  tincture,  are  less  active.  We  usually 
prescribe  the  latter  when  a  patient  with  a  moderately  persistent  disturbance  of 
compensation  is  to  use  digitalis  in  small  doses  for  a  long  time.  We  have  not  yet 
succeeded  in  isolating  the  active  principle  of  digitalis  in  a  durable  form.  The 
"digitaline"  preparations  brought  into  the  market  up  to  the  present  time  are 
uncertain  in  their  action,  and  hence  are  properly  but  little  prescribed. 

Digitalis  is  a  remedy  which  is  not  free  from  danger,  because  there  is  a  stage  in 
its  action,  which  often  appears,  when  it  is  injurious.  The  pulse  then  sinks  below 
the  normal,  becomes  weaker  and  also  irregular  and  intermittent,  if  it  was  previously 
regular.  The  patient's  general  condition  becomes  bad,  nausea  and  vomiting  set 
in,  and  a  state  resembling  collapse  may  arise.  Therefore  it  is  a  very  important  rule, 
never  to  prescribe  digitalis  in  large  doses  unless  the  patient  can  be  observed  con- 
stantly and  carefully.  As  soon  as  the  first  signs  of  the  unfavorable  action  of  digi- 
talis occur,  the  remedy  must  be  at  once  omitted.  Then  we  give  some  strong  wine, 
or  strong  cafe  noir,  to  prevent  the  patient's  further  collapse.  Since  digitalis 
is  one  of  the  remedies  which  have  a  so-called  cumulative  action,  the  occurrence 


VALVULAR  DISEASE  OF  THE  HEART.  ;j(,5 

of  symptoms  of  poisoning  may  be  quite  rapid  and  unexpected.  We  do  well 
therefore,  if  the  desired  favorable  action  follows  the  exhibition  of  digitalis,  if  the 
pulse  has  become  quieter  and  more  regular,  and  diuresis  has  been  established,  to 
omit  the  digitalis.  We  usually  let  the  patient  take  the  remedy  for  two  to  four 
days,  and  then  omit  it.  The  action  of  the  digitalis  continues  for  several  days 
afterward.  Sometimes,  however,  nausea  and  vomiting  are  occasioned  by  the 
ingestion  of  no  more  than  fifteen  to  twenty  grains  (grm.  1  to  1'5)  of  digitalis. 
The  drug  must  then  be  stopped,  although  a  decided  beneficial  effect  may  be 
observed  even  on  the  day  after  the  nausea.  After  leaving  off  the  digitalis  we 
usually  prescribe  a  diuretic,  like  acetate  of  potassium,  squills,  boro-tartrate  of 
potassium  and  sodium,  or  diuretic  herbs.  If  the  pulse  again  becomes  rapid  and 
irregular,  we  at  once  resume  the  digitalis.  In  such  cases,  where  the  patient  has 
used  digitalis  repeatedly,  we  must  gradually  increase  the  dose.  The  patient  gets 
accustomed  to  the  remedy,  as  happens  with  so  many  other  drugs.  There  is  no 
maximum  dose,  and  in  individual  cases  we  must  find  out  the  requisite  amount  by 
trial.  Many  patients  finally  become  genuine  "  digitalis  eaters,"  and  can  not  exist 
without  large  doses — seventy-five  grains  (grm.  5)  or  more  of  the  powder  a  day. 
In  very  many  cases,  unfortunately,  the  favorable  action  of  the  digitalis  finally 
ceases  entirely  with  large  doses.  The  remedy  is  then  no  longer  "  borne,"  and  we 
must  omit  it  entirely.  By  that  time  the  last  stage  of  the  disease  has  also  usually 
been  reached. 

If  we  have  to  treat  a  patient  with  symptoms  of  stasis,  and  the  pulse  seems 
neither  especially  small  nor  frequent,  nor  irregular,  we  may  nevertheless  try 
the  effect  of  digitalis,  but  we  must  be  very  cautious  in  the  size  of  our  dose.  The 
question  is  often  hard  to  decide  whether  to  give  a  patient  with  aortic  insufficiency 
digitalis  or  not.  In  this  form  of  heart  disease  there  is  often  a  very  strong  and 
regular,  though  of  course  abnormally  frequent  pulse,  in  spite  of  the  most  pro- 
nounced disturbance  of  compensation.  With  this  we  must  not  forget  that,  in 
spite  of  the  high  pulse,  the  mean  pressure  in  the  arteries  is  low,  and  hence  in  most 
patients  with  aortic  insufficiency  we  can  very  well  make  a  trial  with  digitalis. 
This  is  often  crowned  with  success;  but  still  the  drug  seems  to  be  less  often 
efficient  in  aortic  than  in  mitral  disease. 

In  some,  but  fortunately  not  many,  cases,  the  digitalis  is  ill-borne  from  the 
start,  because  it  excites  severe  nausea  and  vomiting.  In  general  the  incidental 
action  of  digitalis  on  the  stomach  is  one  of  its  troublesome  properties.  If  the 
digitalis  is  not  borne  in  one  form,  we  try  another.  We  give  the  powder  instead 
of  the  infusion,  or  vice  versa,  or  we  employ  the  tincture.  In  such  cases  we  some- 
times succeed  if  we  give  the  digitalis  as  an  enema,  using  a  one-per-cent.  infusion. 

Caffeine  deserves  the  first  mention  among  the  substances  having  a  similar 
action,  which  have  of  late  been  recommended  as  substitutes  for  digitalis  by  Lepine, 
Riegel,  and  others.  Given  in  repeated  small  doses,  a  total  of  fifteen  to  twenty 
grains  a  day  (grm.  1*0  to  1*5),  it  often  slows,  regulates,  and  strengthens  the  activity 
of  the  heart,  and  also  increases  the  arterial  pressure.  The  salicylate  of  caffeine 
and  sodium  is  chiefly  used,  three  to  five  grains  (grm.  0-2  to  0#3)  of  the  powder, 
and  also  the  benzo-citrate  of  caffeine  in  the  same  or  smaller  doses.  The  latter  is 
also  given  subcutaneously.  Besides  caffeine,  we  may  also  mention  here  adonis 
vernalis  and  convallaria  majalis;  but  none  of  these  drugs  are  as  reliable  as  digi- 
talis. In  conditions  of  cardiac  weakness,  tincture  of  strophanthus  (ten  drops 
several  times  a  day)  is  sometimes  decidedly  beneficial. 

[Digitalis  is  used  more  commonly  in  this  country  in  the  form  of  the  tincture. 
The  urine  affords  a  good  guide  as  to  the  safety  of  the  continuance  of  the  drug;  as 
long  as  the  renal  secretion  is  sufficient  in  qiiantity,  and  increasing  rather  than  di- 
minishing, there  is  no  danger  of  the  toxic  effects.  It  is,  consequently,  a  good  plan 
20 


306  DISEASES  OF  THE  CIRCULATORY  ORGANS. 

to  follow  carefully  the  twenty-four-hour  quantity  of  urine  when  this  can  be 
done. 

There  are  cases  iu  which  digitalis  must  be  taken  for  long  periods,  hut  it  should 
then  be  given  only  twice  a  day,  with  twelve  hours'  iuterval  between  the  doses, 
unless  the  patient  has  ready  access  to  his  physician ;  there  is  then  less  risk  of 
toxic  symptoms.  To  the  list  of  drugs  the  action  of  which  is  similar  to  that  of 
digitalis  and  which  may  be  substituted  for  it,  if  it  disagrees  or  is  without  effect, 
may  be  added  helleborein  and  spartein  sulphate  (gr.  j-ij).  Fräser  reports  well  of 
strophanthein ;  but  a  more  extended  use  is  desirable. 

In  mitral  cases,  with  or  without  secondary  tricuspid  regurgitation,  where  the 
cyanosis  and  other  symptoms  show  that  the  right  heart  is  engorged  with  blood 
which  it  can  not  propel  onward,  the  relief  afforded  by  venesection,  or  by  a  dozen 
leeches  in  the  hepatic  region,  may  be  very  great.  Until  the  veins  are  relieved 
either  in  this  way  or  by  free  purgation,  digitalis  and  stimulants  are  useless,  and  a 
resort  to  them  results  merely  in  a  loss  of  time,  and  perhaps  in  a  loss  of  -life  which 
might  be  saved.] 

4.  Symptomatic  Treatment. — Some  symptoms  which  often  occur  in  heart  dis- 
ease demand  a  special  description. 

Dropsy  is  a  symptom  of  venous  stasis,  and  disappears  if  compensation  be 
restored,  spontaneously  or  by  the  use  of  digitalis.  Complete  rest  in  bed  and  eleva- 
tion of  the  swollen  parts  serve  as  the  chief  aid  in  removing  the  dropsy.  Dropsical 
patients  ought  also  to  change  their  position  in  bed  frequently,  if  possible,  that  there 
may  not  be  too  much  oedema  collected  in  the  dependent  portions  of  the  body.  It 
is  a  good  plan  to  wrap  up  the  swollen  arms  and  legs  with  flannel  bandages  under 
gentle  pressure.  Mild  massage  of  the  cedematous  parts  may  sometimes  be  of 
advantage.  The  amount  of  liquid  ingested  is  to  be  limited,  if  possible.  Of  inter- 
nal remedies,  besides  digitalis  and  similar  drugs,  the  true  diuretics,  such  as  acetate 
of  potash,  are  to  be  considered.  They  are  sometimes  ordered  in  combination  with 
digitalis  and  sometimes  alone,  particularly  when  digitalis  can  not  be  borne  or  is 
not  indicated.  Calomel  is  sometimes  especially  efficient  in  cardiac  dropsy.  Its 
diuretic  influence  has  lately  been  emphasized  by  Jendrassik  and  others.  It  is  pre- 
scribed in  powders  of  three  grains  (0-2  grm.)  three  to  five  times  a  day.  Often  a 
very  marked  diuresis  will  be  caused  after  one  or  two  days,  with  rapid  abatement 
of  the  dropsy.  The  administration  of  the  remedy  is  stopped  as  soon  as  the  diuresis 
begins.     It  is  also  omitted,  of  course,  if  stomatitis  develops. 

In  the  last  stages  of  heart  disease  the  patient's  condition  may  be  particularly 
distressing  from  the  severe  general  oedema.  It  is  then  justifiable  to  remove  the 
ascites  or  hydrothorax  by  puncture,  and  to  let  the  oedema  drain  out  by  scarifica- 
tion of  the  skin— little  pricks  with  the  point  of  a  knife— in  order  to  procure  relief 
for  the  patient.  The  scarification  of  the  skin,  however,  is  dangerous,  and  is  not  to 
be  employed  without  urgent  indications,  because  erysipelatous  inflammation,  etc., 
it  apt  to  ensue  at  the  point  of  incision.  We  can  recommend  little  silver  capil- 
lary trocars  (the  so-called  Southey's  trocars),  to  which  a  thin  rubber  tube  is 
attached.  By  the  aid  of  these  trocars  we  can  drain  off  large  amounts  of  serum. 
We  must  always  use  great  cleanliness,  however,  and  the  utmost  disinfection  of  the 
skin,  wrapping  the  parts  in  carbolized  jute  or  salicylated  cotton.  In  patients  with 
heart  disease  it  is  not,  as  a  rule,  advisable  to  attack  the  dropsy  by  sweating,  by  hot 
packs,  or  pilocarpine. 

The  dyspnoea  of  heart  disease  is  usually  the  most  distressing  symptom  of  all. 
Here,  too,  our  chief  task  is  of  course  to  restore  the  compensation ;  but  this  failing, 
we  must  try  to  relieve  the  dyspnoea  symptom atically.  Morphine  is  most  efficient 
in  this  respect.  In  general,  morphine  is,  next  to  digitalis,  the  most  indispensable 
remedy  in  the  treatment  of  severe  heart  disease.     It  is  usually  well  borne,  and 


MYOCARDITIS.  307 

procures  great  relief,  especially  if  given  subcutaneous! y.  If  we  have  to  do  with 
the  last  stage  of  the  disease,  we  need  not  spare  large  doses.  Otherwise,  of  course, 
caution  is  necessary.  In  practice  we  must  often  prescribe  external  applications  to 
the  chest,  mustard  plasters,  hot  poultices,  and  also  hot  foot-baths  with  mustard, 
ashes,  etc.  In  severe  cases  their  action  is  slight.  Acetate  of  lead  in  large  doses 
sometimeo  seems  to  have  a  favorable  influence  in  severe  dyspnoea,  especially  with 
threatening  pulmonary  oedema.  We  give  the  powder,  up  to  a  grain  and  a  half 
(grm.  0*1),  every  two  or  three  hours,  and  it  is  often  a  good  plan  to  add  half  a 
grain  or  a  grain  (grm.  0"03  to  0-05)  of  opium.  We  can  also  frequently  obtain 
distinct  relief  for  the  patient  by  a  vigorous  drastic  purge,  with  compound  infusion 
of  senna  or  gamboge.  Inhalations  of  nitrite  of  amyl  seldom  have  a  beneficial 
effect. 

Palpitation,  constant  or  paroxysmal,  is  met  by  applying  ice  to  the  cardiac 
region;  sometimes  the  "heart-flasks,"  made  of  tin,  act  very  well.  In  patients 
with  aortic  insufficiency  and  very  excited  action  of  the  heart,  we  may  recommend 
the  protracted  use  of  ice.  The  narcotics  are  the  most  efficient  internal  remedies, 
especially  morphine,  which,  of  course,  we  should  reserve  for  severe  cases.  If  the 
palpitation  is  of  a  lesser  degree,  we  may  try  bromide  of  potassium,  or  cherry -laurel 
water,  eventually  with  equal  parts  of  tincture  of  digitalis,  twenty  to  thirty  drops 
of  the  mixture  two  or  three  times  a  day. 

The  subcutaneous  use  of  morphine  is  again  by  far  the  most  potent  remedy  in 
the  anginose  attacks,  associated  with  pain  and  a  feeling  of  distress.  We  may 
also  use  cutaneous  irritation,  mustard-plasters,  etc.,  ice,  and  perhaps  strophanthus 
or  nitrite  of  amyl. 

We  may  prescribe  bitter  remedies — tinctura  amara  (P.  G.),  or  compound  tinct- 
ure of  cinchona— and  muriatic  acid  for  the  loss  of  appetite,  in  case  this  is  not 
improved  by  regulating  the  activity  of  the  heart.  Besides  that,  we  must  always 
endeavor  to  get  a  regular  evacuation  of  the  bowels. 

For  the  attacks  of  faintness  and  vertigo,  occurring  especially  in  aortic  stenosis, 
as  a  result  of  cerebral  anaemia,  we  may  prescribe  a  horizontal  position,  and  stimu- 
lants—wine, ether,  and  Hoffmann's  anodyne.  If  the  cerebral  symptoms  depend 
upon  venous  stasis,  we  try  to  remove  it  by  ice,  mustard-plasters  to  the  neck,  and 
thorough  derivation  to  the  intestines. 

Especial  accidents  and  complications,  like  pulmonary  oedema,  infarctions,  or 
apoplexy,  are  to  be  treated  according  to  the  usual  rules. 


CHAPTER  III. 

MYOCARDITIS. 

{Indurated  Degeneration,  Myodegeneration  of  the  Heart.     Infarction  of  the  Heart.     Sclerosis  of  the 

Coronary  Arteries.) 

^Etiology  and  Pathological  Anatomy.— We  have  of  late  learned  about  a  num- 
ber of  affections  of  the  heart  in  which  all  the  results  of  disturbance  of  the  cir- 
culation may  finally  appear,  without  any  evidence  of  anatomical  disease  of  the 
valves,  either  during  the  patient's  life  or  at  the  autopsy.  We  have  to  do  here  with 
a  lesion  of  the  cardiac  muscle  itself,  or  of  its  nervous  apparatus,  wdiich  reduces 
the  functional  capacity  of  the  heart,  and  thus  excites  precisely  the  same  disturb- 
ances of  the  circulation  as  are  produced  in  valvular  disease  of  the  heart  by  purely 
mechanical  conditions. 

In  a  number  of  cases— but  by  no  means  in  all,  as  we  shall  see  in  the  next  chap- 


308  DISEASES  OF  THE  CIRCULATORY  ORGANS. 

ter — we  succeed  in  detecting  striking  anatomical  changes  in  the  cardiac  muscle. 
The  heart  is  on  the  whole  enlarged,  chiefly  dilated,  though  its  walls  are  usually 
somewhat  hypertrophied  {vide  infra).  In  pure,  uncomplicated  cases  the  valves 
prove  entirely  normal.  If,  however,  we  examine  the  cardiac  muscle  closely,  we 
find  it  studded  with  whitish,  lustrous,  indurated  spots,  arranged  irregularly  and 
often  very  abundant.  They  consist  microscopically  of  cicatricial  connective 
tissue,  while  the  muscular  fibers  have  wholly  or  in  large  part  been  destroyed. 
The  seat  of  this  induration  is  chiefly  in  the  left  ventricle,  especially  at  the  apex 
and  in  the  anterior  wall,  but  we  may  also  find  indurations  in  other  portions  of  the 
heart.  "We  often  see  them  appearing  through  the  endocardial  or  pericardial  sur- 
face of  the  heart  as  dull,  slightly  sunken  places.  The  papillary  muscles  may  also 
undergo  marked  cicatricial  degeneration. 

The  changes  in  the  heart  just  depicted  were  formerly  considered  to  be  of  an 
inflammatory  nature,  and  hence  were  given  the  name  of  myocarditis ;  but  their 
development  is  connected,  in  the  great  majority  of  cases,  as  Weigert,  Ziegler, 
Huber,  and  others  have  shown,  with  changes  in  the  coronary  arteries  and  their 
branches.  In  most  of  the  uncomplicated  cases  of  so-called  myocarditis  we  find 
marked  atheromatous  changes  in  the  coronary  arteries,  usually  coincident  with  a 
more  or  less  extensive,  general  arterio-sclerosis  {vide  infra).  These  changes  may 
lead  in  circumscribed  places  to  a  complete  closure  of  a  branch  of  the  coronary 
artery  by  thrombosis,  and  thus  give  rise  to  the  formation  of  a  true  infarction  of 
the  heart  by  cutting  off  the  further  blood-supply.  These  infarctions  show,  in 
fresh  cases,  a  decided  brownish-yellow,  haemorrhagic  color.  The  finer  histological 
changes  consist  in  a  loss  of  their  nuclei  by  the  muscular  fibers,  and  their  degen- 
eration into  a  crumbling,  cheesy  detritus.  By  the  new  formation  of  connective 
tissue  the  peculiar  cardiac  indurations  finally  arise,  which  are  therefore  to  be 
regarded  as  true  infarction  cicatrices. 

In  many  cases  of  indurated  degeneration  we  can  not  discover  any  complete 
closure  of  the  branches  of  the  coronary  artery  by  thrombosis.  Here  we  have  to 
do  only  with  changes  in  the  caliber  of  the  vessel  by  the  arteriosclerotic  process, 
and  a  consequent  diminution  of  the  arterial  blood-supply  of  the  cardiac  muscle. 
In  all  places  where  this  diminution  of  the  blood-supply  becomes  extreme,  we  also 
find  a  gradual  deterioration  of  the  muscular  fibers,  and  their  replacement  by  con- 
nective tissue.  Where  the  arterial  blood-supply  is  adequate,  either  directly  or 
from  the  collateral  circulation,  the  muscles  remain  intact.  This  is  the  reason  why 
we  often  find  sclerosis  of  the  coronary  arteries  unaccompanied  by  indurated  myo- 
carditis. 

Besides  the  cases  of  uncomplicated  myocarditis  just  described,  we  often  see  the 
same  cicatricial  changes  in  the  cardiac  muscle  combined  with  valvular  affections. 
The  cardiac  indurations,  then,  are  either  due  to  a  co-existing  sclerosis  of  the  coro- 
nary arteries,  or  they  stand  in  a  closer  relation  to  the  endocardial  process.  The 
endocarditis  may  invade  the  cardiac  muscle  immediately.  This  method  of  origin 
of  the  myocarditis  may  be  easily  recognized  by  the  localization  and  extent  of  the 
diseased  parts.  In  other  cases  the  endocarditis  may  give  rise  to  embolic  processes 
in  the  cardiac  muscle.  Thus  the  embolic  infarctions  of  the  heart  arise  in  just  the 
same  way  as  do  the  thrombotic  infarctions  above  described. 

It  remains  for  us  to  describe  a  number  of  sequela?  and  combinations  of  indu- 
rated myocarditis.  As  a  result  of  the  extensive  cicatricial  formation,  it  may  hap- 
pen that  a  circumscribed  portion  of  the  wall  of  the  heart,  usually  of  the  left  ven- 
tricle, becomes  thin  and  yields  to  the  blood-pressure  acting  upon  it  from  within. 
Thus  arises  a  partial  protrusion  of  the  wall  of  the  heart,  a  so-called  cardiac  aneu- 
rism. Such  an  aneurism,  and  also  an  extensive,  fresh  infarction  in  the  heart,  may 
in  very  rare  cases  lead  to  a  rupture  of  the  heart,  with  effusion  of  blood  into  the 


MYOCARDITIS.  309 

pericardium  and  sudden  death.  A  more  common  occurrence  is  that  sometimes  in 
places  where  the  cardiac  cicatrices  reach  the  endocardium,  parietal  thromboses 
form  in  the  heart,  and  give  rise  to  embolic  processes  in  distant  organs. 

Dilatation  of  single  portions  of  the  heart,  especially  of  the  ventricles,  de- 
pends upon  a  general  yielding  of  the  walls  of  the  heart.  If  at  the  same  time 
there  is  a  hypertrophy  of  the  cardiac  muscle,  we  must  look  for  special  causes  for 
it.  Hypertrophy  of  the  left  ventricle  usually  depends  upon  co-existing  general 
arterio-sclerosis,  upon  co-existing  contracted  kidneys,  and  the  like.  Again,  it  is 
probably  often  the  case  that  the  same  causes  give  rise  simultaneously  to  the 
atheroma  and  to  the  hypertrophy  of  the  left  ventricle  (see  the  following  chapter). 
Hypertrophy  of  the  right  ventricle  may  have  its  origin  in  co-existing  chronic 
pulmonary  affections,  like  emphysema.  In  some  cases  the  hypertrophy  of  the 
right  ventricle  is  due  to  the  inadequate  action  of  the  left  ventricle.  If  the  left 
ventricle  begins  to  grow  weak,  the  stasis  backward  from  it  must  extend  through 
the  pulmonary  vessels  into  the  right  side  of  the  heart.  In  consequence  of  the 
increased  demands  upon  the  right  ventricle  this  becomes  hypertrophied.  In 
cases  of  indurated  myocarditis  combined  with  valvular  disease,  the  hypertrophy 
of  single  portions  of  the  heart  depends,  of  course,  in  part  upon  the  valvular  dis- 
ease. 

Regarding  the  special  serological  factors  which  lead  to  sclerosis  of  the  coro- 
nary arteries,  and  thus  to  indurated  myocarditis,  they  are  in  many  cases  as  little 
known  as  the  causes  of  arterio-sclerosis  in  general  (vide  infra).  Chronic  alco- 
holism and  luxurious  habits  of  life  are  very  often  the  predisposing  causes  which 
are  to  be  put  in  the  first  rank.  Perhaps  constitutional  syphilis  plays  a  not  unim- 
portant part,  since  it  may  lead  to  changes  in  the  coronary  arteries,  as  it  has  long 
been  known  to  do  in  the  cerebral  vessels.  Constant  mental  excitement  is  also 
regarded  as  a  factor ;  but  this  must  be  regarded  as  much  more  a  cause  of  the  con- 
ditions to  be  described  in  a  following  chapter.  Heredity,  however,  is  of  greater 
influence,  as  it  seems  to  play  a  certain  part  in  the  development  of  arterio-sclerosis. 
Finally,  we  must  remember  that  the  atheromatous  process  occurs  much  more  fre- 
quently in  advanced  life  than  in  young  people ;  hence  indurated  myocarditis  is  a 
disease  chiefly  to  be  observed  in  the  aged.  Men  are  more  frequently  attacked  by 
it  than  women. 

Although  we  have  so  far  spoken  exclusively  of  chronic  indurated  degeneration 
of  the  cardiac  muscle,  which,  as  we  have  said,  is  not  of  a  peculiarly  inflammatory 
nature,  we  must  also  add  that  there  is  a  true  purulent  inflammation  of  the  car- 
diac muscle.  This  is  one  of  the  symptoms  of  a  general,  infectious,  and  especially 
a  pysemic  process,  or  of  malignant  acute  endocarditis,  so  that  we  may  refer  to  the 
description  of  these  diseases  in  regard  to  abscess  of  the  heart. 

Clinical  History. — We  must  first  mention  that  sometimes  quite  extensive  cica- 
tricial formation  may  be  found  in  the  cardiac  muscle  post-mortem,  without  the 
occurrence  of  any  manifest  symptoms  referable  to  the  heart  during  life.  We  see, 
then,  that  the  heart  may,  under  some  circumstances,  undergo  quite  a  considerable 
loss  in  its  contractile  substance  without  injury. 

In  many  cases,  however,  the  heart's  capacity  for  work  suffers  so  much  that 
the  same  symptoms  arise  as  in  valvular  disease.  The  course  of  such  cases  may  be 
very  chronic.  The  symptoms  begin  quite  gradually.  The  patient  first  has  a 
slight  dyspnoea  or  palpitation,  and  a  feeling  of  distress  in  the  chest,  but  only  from 
external  causes,  like  slight  physical  exertion.  He  sometimes  suffers  from  a  strik- 
ing general  weakness.  He  gets  tired  easily  and  feels  heavy,  and  more  or  less  in- 
capable of  any  mental  activity.  The  symptoms  gradually  increase,  and  just  the 
same  results  of  disturbance  of  the  circulation  appear  as  in  all  the  other  forms  of 
heart  disease.     The  difficulty  in  breathing  becomes  more  marked,  oedema  occurs, 


310  DISEASES  OF  THE  CIRCULATOKY  ORGANS. 

signs  of  stasis  in  the  liver,  intestines,  and  kidneys  appear — in  short,  the  well- 
known  type  of  every  uncompensated  heart  disease  develops. 

Physical  examination  of  the  heart  shows  marked  anomalies  of  the  heart's 
action  in  all  severe  cases.  The  pulse  is  often  irregular  in  regard  to  its  rhythm 
and  the  intensity  of  its  single  beats,  but  the  arhythmia  may  also  be  wholly  absent 
in  spite  of  the  degeneration  of  the  myocardium,  as  we  have  often  convinced  our- 
selves. The  pulse  is  at  first  quite  strong  and  full,  later  it  becomes  weaker,  of 
lower  tension,  and  at  last  sometimes  very  small  and  scarcely  perceptible.  It  may 
be  increased  in  frequency,  but  we  quite  often  notice  in  chronic  myocarditis,  espe- 
cially in  the  early  stages,  a  persistent  slowing  of  the  pulse  to  60,  50,  or  even  less, 
in  a  minute.  With  this  slowness  of  the  pulse  there  is  also  frequently  irregularity 
of  the  heart's  action,  especially  the  appearance  of  occasional  double  beats  (pulsus 
bigeminus).  Percussion  usually  shows  an  increase  of  the  heart's  dullness,  due 
to  dilatation  or  hypertrophy  of  the  heart,  the  increase  being  either  general  or 
chiefly  on  one  side.  Auscultation  shows  the  absence  of  any  murmur,  and  hence 
the  absence  of  valvular  disease.  The  heart-sounds  are  distinctly  audible,  and 
sometimes  quite  loud  and  valvular,  but  in  the  later  stages  often  low  and  obscure. 
The  pulmonic  second  sound  is  accentuated,  when  there  is  stasis  of  the  pulmonary 
circulation.  In  several  cases  we  found  the  second  sound  for  a  long  time  very 
plainly  divided— reduplicated.  We  must  also  mention  that  sometimes  in  pure 
myocarditis  a  systolic  murmur  is  heard  at  the  apex  which  is  due  either  to  a  rela- 
tive insufficiency  of  the  mitral  valve,  or  to  its  incomplete  closure,  as  a  result  of 
defective  muscular  action  of  the  left  ventricle. 

The  whole  course  of  chronic  myocarditis  is  in  most  of  its  relations  precisely 
analogous  to  that  of  chronic  valvular  disease,  so  that  we  need  not  describe  its 
peculiarities  in  detail.  The  patient  is  alternately  better  and  worse.  Severe 
symptoms  of  general  stasis  and  manifest  weakness  of  the  heart  may  appear,  and, 
under  favorable  circumstances,  may  disappear  again.  The  picture  of  the  disease 
may  be  complicated  by  embolic  processes  in  the  brain,  the  lungs,  etc.,  which  usu- 
ally arise  from  thrombi  in  the  heart  {vide  supra).  Finally,  perhaps  after  the 
disease  has  lasted  for  years,  the  patient  dies  from  general  dropsy  or  from  some 
intercurrent  disease. 

We  must  mention  one  symptom  which  has  often  been  brought  into  special 
relation  with  sclerosis  of  the  coronary  arteries  and  with  chronic  myocarditis. 
We  mean  the  attacks  of  so-called  angina  pectoris,  the  stenocardiac  paroxysms. 
These  attacks  consist  in  a  sudden,  intense  pain  in  the  cardiac  region,  which  shoots 
into  the  back,  the  left  shoulder,  and  the  left  arm.  This  pain  is  associated  with  a 
marked  feeling  of  constraint  and  distress.  There  is  no  particular  dyspnoea  in 
pure  angina  pectoris.  The  attacks  last  from  a  few  minutes  to  half  an  hour,  and 
may  be  interrupted  by  entirely  free  intervals. 

We  can  not  deny  that  such  attacks  occur  in  indurated  myocarditis,  due  to 
sclerosis  of  the  coronary  arteries,  but,  on  the  other  hand,  many  cases  run  their 
course  without  angina  pectoris,  and  angina  pectoris  may  also  occur  both  in  other 
forms  of  heart  disease  and  as  a  pure  neurosis.  Hence  we  must  not  overestimate 
the  significance  of  angina  pectoris  in  the  diagnosis  of  sclerosis  of  the  coronary 
arteries.  Besides  angina  pectoris,  attacks  of  dyspnoea  (cardiac  asthma)  and  of 
faintness  also  occur  in  chronic  myocarditis,  the  faintness  being  especially  fre- 
quent in  cases  associated  with  a  slow  pulse.  The  dyspnoea  is  usually  due  to  a 
sudden  weakness  of  the  left  ventricle,  while  the  origin  of  the  faintness  is  not  yet 
fully  explained  (cerebral  anaemia  ?). 

It  is  a  very  important  clinical  fact  that,  in  not  very  rare  cases,  indurated  myo- 
carditis is  the  sole  apparent  cause  of  sudden,  apoplectiform  death.  It  usually 
happens  in  elderly  people  in  comfortable  circumstances  and  good  livers,  who  up 


MYOCARDITIS.  311 

to  that  time  have  not  regarded  themselves  as  really  ill;  hut  they  have  repeatedly 
had  slight  attacks  of  vertigo,  of  oppression,  etc.  Suddenly  a  sort  of  apoplectic 
attack  comes  on,  often  after  some  definite  cause,  after  dinner,  or  after  some  physical 
exertion  or  mental  excitement.  Death  follows  in  a  few  moments,  or  after  a  deep 
coma  that  lasts  for  several  hours  or  even  days.  The  diagnosis  often  remains 
in  doubt  in  such  cases,  especially  if  we  have  not  known  the  patient  previously. 
The  autopsy  shows,  as  the  sole  pathological  lesion,  a  sclerosis  of  the  coronary  arte- 
ries, with  a  more  or  less  extensive  cicatricial  formation  in  the  heart.  Apparently 
in  these  cases  the  moment  must  suddenly  arise  when  the  supply  of  blood  to  the 
heart  is  insufficient,  and  thus  death  is  caused.  Experiments  upon  artificial  closure 
of  the  coronary  arteries,  by  Cohnheim  and  others,  agree  perf ectly  with  the  clinical 
facts  above  mentioned.  Artificial  narrowing  of  the  coronary  arteries  may  also 
be  well  borne  for  a  long  time,  until  suddenly  both  halves  of  the  heart  stand  still 
in  a  condition  of  diastole.  In  rare  cases  sudden  death  may  also  be  due  to  embo- 
lism of  the  main  trunk  of  the  coronary  artery,  or,  as  we  ourselves  have  seen  in 
one  case,  to  the  bursting  of  a  focus  of  myocarditis  with  haemorrhage  into  the 
pericardial  cavity. 

Diagnosis. — The  diagnosis  of  chronic  myocarditis  is  by  no  means  always  easy 
and  certain.  "We  must  first  determine  that  there  is  a  cardiac  lesion  of  some  kind. 
This  is  usually  easy  to  do  from  the  secondary  symptoms  of  stasis,  the  condition 
of  the  pulse,  the  heart's  dullness,  etc.  Then  the  question  arises  whether  we  have 
to  do  with  a  valvular  disease  or  with  a  myopathic  disease  of  the  heart.  Here  aus- 
cultation must  chiefly  decide.  The  absence  of  a  heart  murmur,  in  spite  of  other 
definite  signs  of  heart  disease,  speaks  against  valvular  disease,  but  not  with  com- 
plete certainty.  All  murmurs  may  be  absent  in  the  last  stages,  especially  with 
a  high  degree  of  mitral  stenosis,  and  hence  we  may  easily  confuse  mitral  stenosis 
with  myocarditis,  particularly  when  there  is  marked  arhythmia  of  the  heart.  On 
the  other  hand,  we  have  already  stated  that,  in  pure  myocarditis,  with  the  valves 
intact,  functional  murmurs  may  be  present,  which  may  lead  to  an  erroneous 
opinion  as  to  valvular  disease.  If  by  long  observation  we  have  excluded  a  valvu- 
lar disease,  we  still  have  left  the  distinction  between  myocarditis  and  pure  idio- 
pathic hypertrophy  of  the  heart,  or  fatty  heart  (see  the  following  chapters).  We 
hold  it  impossible  to  make  this  distinction  with  certainty.  The  conditions  of 
disease  mentioned  all  furnish  the  same  clinical  picture  of  cardiac  insufficiency, 
but  during  life  we  can  only  suspect  what  finer  anatomical  relations  are  the  ones 
which  cause  this  insufficiency,  and  we  can  never  diagnosticate  them  with  cer- 
tainty. Irregularity  of  the  pulse  occurs  both  in  indurated  myocarditis  and  in 
pure  hypertrophy  and  dilatation,  without  discoverable  cicatricial  nodules  in  the 
substance  of  the  heart.  A  persistently  slow  pulse,  attacks  of  angina  pectoris  or 
cardiac  asthma,  the  evidence  of  co-existing  sclerosis  of  the  arteries  of  the  body, 
such  as  the  radial,  temporal,  or  femoral,  in  connection  with  other  symptoms,  make 
the  diagnosis  of  indurated  myocarditis  probable,  but  never  completely  certain. 
In  cases,  too,  with  a  sudden  apoplectic  attack—"  heai't  apoplexy  "—it  is  often  im- 
possible to  make  a  certain  distinction  between  it  and  cerebral  embolism,  or  cere- 
bral haemorrhage. 

Prognosis. — The  prognosis  is  as  serious  as  in  any  valvular  disease.  Recovery 
is  impossible,  but  even  extensive  cicatricial  formation  in  the  heart  may  probably 
last  for  years  without  causing  much  disturbance.  "We  must  always  be  prepared 
for  the  occurrence  of  disturbances  of  compensation,  and  the  manifold  sudden  acci- 
dents to  which  patients  with  myocarditis  are  exposed,  but  we  can  not  foretell  the 
time  of  their  occurrence. 

Treatment. — The  treatment  of  chronic  myocarditis  must  be  directed  first  to 
the  dietetic  and  hygienic  care  of  the  patient.     This  is  of  the  greatest  importance. 


312  DISEASES  OF  THE  CIRCULATORY  ORGANS. 

For  obese  persons  accustomed  to  high  living,  a  moderate,  simple  diet  must  be 
accurately  prescribed.  Alcoholic  beverages  must  be  greatly  limited  or  wholly 
forbidden,  and  not  more  than  two  or  three  cigars  allowed  per  diem.  Moderate 
bodily  exercise  is  beneficial,  and  indeed  necessary,  for  the  promotion  of  the  cir- 
culation and  the  more  rapid  diminution  of  the  obesity,  but  the  patient  must  be 
warned  against  too  violent  exertion,  nor  can  great  mental  effort  be  permitted. 
In  summer,  a  quiet  life  in  the  country  or  some  mountain  region  is  to  be  advised, 
or,  under  suitable  circumstances,  the  cautious  use  of  the  waters  of  Carlsbad,  Kis- 
singen, Marienbad,  or  Nauheim.  Frequent  tepid  baths  or  mud  baths  may  usu- 
ally be  employed  even  at  home  with  advantage.  With  disturbance  of  compen- 
sation, and  with  abnormally  frequent,  weak,  and  irregular  action  of  the  heart, 
digitalis  and  similar  remedies  are  indicated,  just  as  in  valvular  disease.  In  cases 
with  an  abnormally  slow  pulse,  we  may  use  them,  provided  great  caution  is 
exercised,  but  we  must  also  be  governed  by  the  other  prevailing  symptoms.  In 
attacks  of  angina  pectoris  the  subcutaneous  injection  of  morphine  is  by  far  the 
most  efficient  and  often  an  indispensable  remedy.  We  may  also  try  nitrite  of 
sodium,  1  or  2  parts  to  120  of  water,  two  or  three  teaspoonf  ills  daily.  The  inhala- 
tion of  a  few  drops  of  nitrite  of  amyl  is  also  sometimes  beneficial,  but  more  often 
it  has  no  effect.  In  cardiac  asthma,  stimulants  like  strong  black  coffee,  ether  and 
camphor,  and  often  narcotics,  are  indicated.  Mustard-plasters,  cold  and  warm 
poultices,  hot  foot-baths,  etc.,  are  also  employed.  Iodide  of  potassium  and  arsenic 
are  especially  recommended  for  continued  use  in  myocarditis.  The  first  remedy 
£  sometimes  seems  to  be  of  service,  and  is  especially  to  be  recommended  where 
there  is  a  suspicion  of  former  syphilis.  With  regard  to  all  further  details  we 
must  refer  to  the  preceding  chapter. 


CHAPTER  IV. 

IDIOPATHIC   HYPERTROPHY  AND   DILATATION   OF  THE   HEART. 

( Over-exertion  of  the  Heart.      Weakened  Heart.) 

iEtiology  and  General  Pathology.— Besides  the  forms  of  heart  disease  already 
described,  cases  not  infrequently  occur  which  present  all  the  signs  of  an  uncom- 
pensated heart  disease  during  life,  and  which  show  at  the  autopsy  a  hypertrophy 
of  the  heart  or  a  dilatation  of  its  cavities,  but  no  other  abnormity,  either  in  the 
valves,  in  the  coronary  arteries,  or  in  the  cardiac  muscle.  The  cardiac  hypertro- 
phy, which  involves  the  left  ventricle  chiefly,  but  often  both  ventricles,  can  not  be 
regarded  as  secondary  in  the  ordinary  sense  of  the  word,  for  in  the  heart  itself  and 
in  the  other  organs  we  find  nothing  which  can  call  forth  a  secondary  hypertrophy 
of  the  cardiac  muscle — no  valvular  disease,  no  chronic  nephritis,  no  general 
arterio-clerosis,  and  no  pulmonary  emphysema.  Hence  we  term  these  cases 
"primary  idiopathic*'  cardiac  hypertrophy,  in  the  sense  that  we  can  not  discover 
any  other  primary  disease  in  them.  Nevertheless,  we  must  also  look  in  such  cases 
for  factors  which  during  life  result  in  increased  work  for  the  heart,  because  only 
thus  can  we  understand  the  development  of  this  form  of  cardiac  hypertrophy. 

Such  factors  may  in  fact  often  be  discovered.  In  a  few  rare  cases  a  congenital 
narrowness  of  the  aortic  system  plays  a  part,  since  by  this  the  heart's  work  is 
manifestly  increased.  The  observations  upon  this  point,  however,  are  very 
scanty,  so  that  we  can  not  yet  estimate  with  certainty  the  practical  significance 
of  this  arterial  anomaly. 

Excessive  physical  exertion  is  of  much  greater  eetiological  importance.     We 


IDIOPATHIC  HYPERTROPHY  AND  DILATATION  OF  THE  HEART.  313 

not  infrequently  see  idiopathic  cardiac  hypertrophy  develop  in  the  hard- working' 
classes — in  blacksmiths,  locksmiths,  pack-carriers,  and  vine-dressers  ("'Tübinger 
heart").  The  increased  work  of  the  heart  upon  every  physical  exertion  is  here 
repeated  almost  every  day  in  the  year,  and  must  finally  lead  to  a,  marked  degree 
of  hypertrophy  from  labor.  This  is  the  chief  form  which  has  been  termed  "car- 
diac over-strain." 

Numerous  cases  of  idiopathic  hypertrophy  of  the  heart  may  often  be  regarded 
as  the  result  of  long-continued  gourmandizing,  hence  the  frequent  appearance  of 
hypertrophy  in  the  obese,  and  particularly  in  great  beer-drinkers.  The  constant 
excessive  ingestion  of  liquid  undoubtedly  gives  rise  to  an  increase  in  the  amount 
of  blood,  and  so  overburdens  the  heart.  Likewise  the  abundant  ingestion  of  food 
occasions  a  constant  slight  increase  of  the  blood  pressure,  and  so,  again,  an  in- 
crease of  the  work  demanded  of  the  heart.  These  influences  are  finally  re-in- 
forced  by  all  the  consequences  of  increasing  obesity,  in  its  relations  to  the  circu- 
lation, which  we  shall  consider  more  minutely  in  the  chapter  upon  obesity.  Ex- 
cessive indulgence  in  beer  has  certainly  the  worst  effect  upon  the  heart.  There  is 
both  a  large  amount  of  fluid,  four  and  sometimes  even  eight  or  ten  quarts  a  day,  and 
a  large  amount  of  nourishment.  Four  quarts  (litres)  of  beer  contain  about  eight 
ounces  (250  grm.)  of  hydrocarbons,  in  solution,  and  therefore  capable  of  complete 
absorption  into  the  circulation.  This  explains  the  great  frequency  of  cardiac 
hypertrophy  which  Bollinger  has  shown  to  exist  at  Munich  ;  but  the  "  Munich 
beer-heart "  is  seen  with  unfortunate  frequency  in  other  towns  than  Munich. 
The  alcohol  is  probably  not  a  factor  in  the  development  of  the  hypertrophy  of 
the  heart,  but  we  may  well  suppose  that  it  promotes,  or  at  least  hastens,  the 
degenerative  changes  in  the  cardiac  muscle,  and  particularly  in  the  cardiac  nerves, 
which  at  last  render  the  heart's  action  inadequate  and  the  circulation  imperfect. 

Finally,  however,  there  are  always  a  number  of  cases  in  which  none  of  the 
causes  so  far  mentioned  can  be  discovered.  In  these  cases  we  are  inclined  to  con- 
jecture that  there  is  an  abnormal  nervous  irritation  of  the  heart,  which  excites  it 
to  increased  activity,  and  hence  causes  its  hypertrophy.  The  cases  which  seem  to 
be  connected  with  continued  mental  excitement  in  business  men,  etc.,  probably 
belong  to  this  group.  We  may  also  recall  the  cardiac  hypertrophy  in  exophthal- 
mic goitre  (vide  infra). 

Since  the  exciting  causes  above  mentioned  to  explain  the  origin  of  the  so- 
called  idiopathic  cardiac  hypertrophy  do  not  by  any  means  constantly  result  in 
this  condition,  we  must  also  assume  a  special  individual,  and  sometimes  appar- 
ently a  hereditary  predisposition,  a  congenital  or  acquired  weakness  of  the  cardiac 
muscle.  Up  to  a  certain  degree  a  healthy,  strong  heart  can  respond  to  the  increased 
demands  made  upon  its  activity.  We  are  even  justified  in  considering  a  certain 
amount  of  hypertrophy  in  such  cases  as  by  no  means  pathological,  just  as  there  is 
nothing  pathological  in  the  hypertrophied  muscles  of  a  gymnast  ;  but  experience 
shows  that  the  relations  of  the  cardiac  muscle  are  different  from  those  of  the 
muscles  of  the  body,  for  the  hypertrophied  heart  does  not  permanently  fulfill  the 
increased  demands  put  upon  it,  but  it  gradually  begins  to  be  paralyzed,  and 
becomes  insufficient.  Hence  the  English  physicians,  since  Stokes's  time,  term 
the  cases  of  cardiac  insufficiency,  without  any  apparent  coarse  anatomical  lesions 
of  the  valves  or  muscle,  "weakened  heart."  This  term  does  very  well  for  those 
cases  where  the  symptoms  of  cardiac  insufficiency  have  appeared  before  much 
hypertrophy  has  developed.  There  are  pure  cases  of  weakened  heart  in  which 
the  heart  seems  merely  dilated  and  its  walls  flabby,  and  not  at  all  or  only  slightly 
hypertrophied.  Such  a  condition  shows  all  the  clinical  symptoms  of  a  chronic 
heart  disease  with  disturbed  compensation. 

It  may  be  mentioned  here  that  dilatation  of  the  heart  may  be  very  acute  in 


314  DISEASES  OF  THE  CIRCULATORY  ORGANS. 

its  development  under  certain  circumstances,  if  great  demands  are  temporarily 
made  upon  a  heart  which  is  not  capable  of  very  much  exertion.  Acute  dilata- 
tion of  the  heart  has  been  seen  in  soldiers  after  a  few  forced  marches.  We  once 
saw  a  case  in  a  previously  healthy  man  who  fell  into  the  water  and  could  only 
with  difficulty  be  saved  from  drowning-.  Acute  dilatation  also  occurs  in  the 
course  of  severe  febrile  diseases,  like  typhoid,  intermittent,  or  pneumonia,  which 
are  sometimes  associated  with  manifest  weakness  of  the  heart.  In  previously 
diseased  hearts,  too,  acute  dilatation  may  develop  after  some  special  cause.  These 
acute  dilatations  may  in  many  cases  be  restored  to  normal  dimensions,  but  they 
always  point  to  a  certain  degree  of  permanent  weakness  of  the  heart. 

Clinical  History.— Idiopathic  dilatations  and  hypertrophies  of  the  heart  may 
certainly  exist  for  a  long  time  without  causing  the  patient  any  subjective  dis- 
turbance. The  symptoms  begin  when  the  heart  can  no  longer  respond  to  the 
demands  made  upon  it,  and  when  it  begins  to  be  paralyzed.  Then  all  the  symp- 
toms of  cardiac  insufficiency  arise,  in  just  the  same  way  as  in  valvular  disease 
and  in  the  severe  muscular  diseases  of  the  heart.  Hence  we  need  not  go  into  the 
details  of  the  disturbances  of  compensation  again.  The  whole  series  of  symptoms 
of  stasis,  as  well  as  the  attacks  of  angina  pectoris  and  cardiac  asthma,  described 
in  the  preceding  chapter,  also  occur  in  idiopathic  hypertrophies  and  dilatations  of 

the  heart. 

The  general  course  of  the  disease  differs  considerably  in  individual  cases. 
Sometimes  there  is  moderate  difficulty  in  breathing  for  a  long  time,  especially 
on  any  physical  exertion.  The  patient  often  complains  of  great  languor,  of 
nervous  irritability,  and  sometimes  of  attacks  of  vertigo  and  faintness,  and  a 
tendency  to  perspiration.  The  appetite  is  poor,  and  there  is  very  apt  to  be  con- 
stipation. The  condition  may  become  quite  suddenly  worse  after  any  marked 
injurious  influence,  especially  after  great  physical  exertion  or  mental  excitement. 
The  pulse  is  small,  weak,  and  irregular,  the  heart-sounds  grow  feeble,  the  dysp- 
noea and  oppression  in  the  chest  increase,  the  amount  of  urine  diminishes,  and 
oedema  appears  in  the  legs.  We  now  have  the  complete  picture  of  an  uncom- 
pensated heart  disease.  With  proper  treatment  the  symptoms  may  disappear 
again ;  but,  sooner  or  later,  they  return.  Death  finally  ensues  from  general  dropsy 
or  from  some  complications  or  intercurrent  attacks,  among  which  we  may  men- 
tion embolic  processes. 

If  the  patient  avoids  all  injurious  influences  by  a  discreet  and  prudent  way  of 
living,  the  course  of  the  disease  may  be  quite  favorable  for  years.  It  is  not  im- 
probable that  a  number  of  mild  cases  may  be  restored  to  health,  or  at  least  re- 
main stationary. 

Diagnosis. — The  diagnosis  is  based  on  the  presence  of  the  aetiological  factors, 
and  on  the  same  symptoms  as  generally  point  to  a  disturbance  in  the  heart — 
namely,  palpitation,  shortness  of  breath,  acceleration  and  arhythmia  of  the  pulse, 
etc.  Physical  examination  in  the  later  stages  of  the  disease  gives  an  increase  of 
the  heart's  dullness  in  both  directions,  usually  chiefly  to  the  right.  Auscultation 
permits  us  to  exclude  valvular  disease  by  finding  the  heart-sounds  everywhere 
distinct.  We  have  left,  then,  only  the  hypothesis  of  an  idiopathic  hypertrophy  of 
the  heart  or  a  chronic  myocarditis.  As  we  have  already  said,  we  consider  it 
impossible  to  make  a  clinical  distinction  between  these  two  diseases,  although 
they  are  aBtiologically  and  anatomically  distinct.  We  can  diagnosticate  the 
enlargement  of  the  heart,  its  functional  disturbance,  and  the  intactness  of  its 
valves,  but  whether  the  substance  of  the  heart  is  simply  hypertrophied  or  is 
studded  with  the  indurations  of  myocarditis,  can  only  be  suspected ;  it  never  can 
be  decided  with  certainty.  Arhythmia  of  the  pulse  may  exist,  in  spite  of  the  lack 
of  all  indurations,  and  it  may  be  absent  in  spite  of  extensive  cicatricial  formation. 


FATTY  HEART.  :H5 

We  may  often  enough  find  that  the  autopsy  confirms  our  hypothesis  of  myocar- 
ditis, made  from  the  serological  factors,  from  the  evidence  of  atheroma  in  the 
external  arteries,  from  the  existing  cardiac  insufficiency,  and  from  certain  charac- 
teristic symptoms  like  stenocardiac  attacks  and  sudden  death;  but  just  as  often, 
even  with  extensive  clinical  and  pathological  experience,  we  shall  have  to  admit 
diagnostic  errors  and  confusion  between  chronic  myocarditis  and  simple  cardiac 
hypertrophy. 

Treatment. — The  principles  of  the  treatment  of  idiopathic  cardiac  hypertrophy 
are  precisely  the  same  as  for  valvular  disease  and  myocarditis.  We  may  therefore 
refer  for  all  particulars  to  the  two  preceding  chapters,  and  to  the  remarks  upon 
the  mechanical  treatment  of  circulatory  disturbances  given  at  the  close  of  the  next 
chapter. 


CHAPTER  V. 


FATTY  HEART. 

{Cor  adiposum.     Fatty  Degeneration  of  the  Heart.) 

iEtiology  and  Pathological  Anatomy.— By  the  name  of  "  fatty  heart "  we  often 
mean,  at  present,  two  quite  distinct  conditions  of  the  heart — the  one  an  abnormal 
deposit  of  fat  in  the  heart,  and  the  other  a  fatty  degeneration  of  the  muscular 
fibers  of  the  heart.  The  first  is  usually  one  symptom  of  great  general  corpulency. 
At  the  autopsy  of  very  fat  people  we  sometimes  find  the  heart  entirely  inclosed  in 
a  thick  capsule  of  fat.  The  fat  is  situated  chiefly  in  the  external  pericardium  and 
beneath  the  visceral  pericardium.  It  is  usually  very  marked  along  the  course  of 
the  larger  vessels  within  the  grooves  of  the  heart,  but  in  marked  cases  the  fat  also 
involves  the  muscular  substance.  The  heart  itself  is  otherwise  quite  normal  or 
somewhat  hypertrophied  or  dilated.  There  are  sometimes  also  present  sclerosis 
of  the  coronary  arteries  and  indurations  of  myocarditis. 

We  have  already  mentioned  fatty  degeneration  of  the  muscular  substance  of  the 
heart  as  a  frequent  result  of  valvular  disease.  In  myocarditis  and  idiopathic 
cardiac  hypertrophy,  and  in  the  secondary  hypertrophy  after  chronic  nephritis 
and  pulmonary  emphysema,  we  also  meet  with  fatty  degeneration.  We  often  find 
it,  as  well  as  fatty  degeneration  of  other  organs,  in  severe  acute  infectious  diseases, 
in  phosphorus  poisoning,  and  in  all  marked  primary  and  secondary  anaemias. 
Under  the  microscope  we  find  the  muscular  fibrillae  studded  with  little  drops 
of  fat,  which  may  be  so  numerous  that  the  nuclei  and  the  transverse  striatum  of 
the  fibers  are  quite  concealed  by  them.  We  often  find,  besides  the  fatty  gran- 
ules, albuminous  granules,  which  disappear  on  the  addition  of  acetic  acid  ("  cloudy- 
swelling  "  of  the  cardiac  muscle).  If  the  fatty  degeneration  is  of  high  degree,  we 
can  easily  recognize  it  with  the  naked  eye.  Beneath  the  endocardium,  especially 
on  the  trabecular  and  papillary  muscles,  we  see  very  fine  and  delicate  yellow  points 
and  striae.  With  great  fatty  degeneration,  as  in  phosphorus  poisoning  and  per- 
nicious anaemia,  the  whole  cardiac  muscle  is  manifestly  yellow,  and  also  soft  and 
flabby.  It  is  claimed  that  rupture  of  the  heart  may  occur  as  a  result  of  marked 
fatty  degeneration. 

In  fatty  degeneration  of  the  heart  the  fat  comes  from  the  decomposition  of 
albumen  in  the  muscular  cells.  The  occasion  of  it  is  probably  a  defective  supply 
of  oxygen,  which  has  either  a  general  cause,  as  in  anaemia  and  phosphorus  poison- 
ing, or  a  local  cause,  as  disturbed  circulation  in  the  heart  in  heart  disease.  The 
details  of  this  are  given  in  the  chapter  on  anaemia  (page  928). 

Clinical  Symptoms.— Fatty  degeneration  of  the  heart  has  no  special  clinical 


316  DISEASES  OF  THE  CIRCULATORY  ORGANS. 

symptoms.  In  the  conditions  under  which  we  know  it  is  apt  to  occur  we  can 
usually  suspect  it  during  the  lifetime  of  the  patient,  but  we  can  not  diagnosticate 
it.  We  must  also  mention  that  the  frequently  expressed  opinion,  that  fatty  degen- 
eration of  the  heart  is  the  cause  of  general  cardiac  weakness,  is  very  often  in  cor- 
rect. In  pernicious  anaemia  there  may  be  quite  a  strong  and  a  perfectly  regular 
pulse  up  to  death  in  spite  of  the  most  marked  fatty  degeneration. 

We  can  not  say  much  that  is  certain  in  regard  to  the  clinical  symptoms  of  a 
deposit  of  fat  in  the  heart.  "  Fatty  degeneration  of  the  heart "  always  plays  a  far 
larger  part  in  popular  speech  than  it  does  in  reality.  It  is  certainly  a  fact  that  diffi- 
culty with  the  heart  and  respiration  is  very  often  observed  in  fat  people.  Exam- 
ination of  the  heart,  which,  however,  is  decidedly  impeded  by  the  thick  pannicu- 
lus  adiposus,  often  shows  in  such  cases  an  increase  of  the  cardiac  dullness,  a  small 
and  sometimes  irregular  pulse,  and  faint  but  clear  heart-sounds.  The  disturbance 
may  be  very  considerable,  attacks  of  angina  pectoris  and  cardiac  asthma  may 
come  on,  and  death  may  follow  with  increasing  dyspnoea  and  general  oedema. 

If  one  has  opportunity  to  make  an  autopsy  in  such  cases,  there  will  be  found  no 
constant,  single  anatomical  change  as  the  cause  of  the  cardiac  disturbance,  but  either 
idiopathic  cardiac  hypertrophy  (see  the  preceding  chapter),  or  so-called  myocarditic 
changes  with  sclerosis  of  the  coronary  arteries  and  the  like.  Very  often  there  is, 
of  course,  a  marked  deposit  of  fat  upon  the  heart  itself,  but  the  question  arises 
whether  this  can  directly  and  seriously  embarrass  the  cardiac  activity.  The  fact 
is  that  we  often  have  seen  similar  well-marked  cases  of  fatty  heart  which  during 
life  presented  no  special  cardiac  symptoms.  There  would  be  more  reason  in 
ascribing  an  unfavorable  influence  to  the  fatty  infiltration  of  the  cardiac  muscle- 
but  here  there  is  probably  in  most  cases  a  simultaneous  atrophy  of  the  muscular 
tissue. 

Therefore  we  can  not  associate  with  the  term  "  fatty  heart1'  any  uniform  clin- 
ical conception.  It  would  be  better  to  speak  of  the  "  heart  of  obesity,"  that  is,  of 
all  the  manifold  injuries  to  which  the  heart  of  obese  persons  is  exposed. 

Treatment. — A  great  part  of  the  disturbance  in  respiration  in  fat  people  de- 
pends not  upon  the  cardiac  weakness,  but  on  the  corpulency  itself.  The  great 
bulk  of  the  body,  and  the  hindrance  to  the  activity  of  the  respiratory  muscles,  are 
very  important  factors.  Treatment  directed  against  the  respiratory  disturbance 
must  hence  chiefly  attack  the  obesity,  and  thus  in  many  cases  we  also  assist  the 
action  of  the  heart.  The  detailed  description  of  the  hygienic  methods  of  cure  to 
be  employed  here  is  to  be  found  in  the  chapter  on  obesity  (page  996). 

In  regard  to  the  special  treatment  of  the  cardiac  symptoms,  this  does  not  differ 
from  the  rules  that  obtain  in  other  forms  of  heart  disease. 


APPENDIX. 

REMARKS  UPON  THE  SO-CALLED   MECHANICAL  TREATMENT   OF  CIRCULATORY 

DERANGEMENTS. 

Of  late  years,  particularly  since  the  publication  of  Oertel's  views,  so  much  has 
been  written  and  spoken  about  the  mechanical  treatment  of  circulatory  derange- 
ments in  heart  disease,  obesity,  and  changes  in  the  pulmonary  circulation  (such 
as  those  caused  by  emphysema,  kyphoscoliosis,  and  the  like),  that  it  seems  neces- 
sary to  consider  briefly  here  the  chief  points  of  this  mode  of  treatment.  There 
can  be  no  doubt  that  in  all  the  diseased  conditions  just  named  the  disturbance  of 
the  circulation  is  one  of  the  main  causes  of  the  clinical  symptoms.  The  symptoms 
dependent  upon  the  venous  stasis  are  repeated  in  all  the  diseases  which  belong  in 
this  group,  in  almost  the  same  way  in  every  case  (see  their  description  on  pages 


FATTY   HEART.  3! 7 

295  et  seq.).  Inasmuch,  however,  as  the  disturbance  may  be  essentially  referred  to 
mechanical  influences,  above  all  to  the  diminution  of  the  difference  between  the 
arterial  and  the  venous  pressure,  and  the  consequent  slowing  of  the  current  and 
abnormal  distribution  of  the  blood,  it  is  eminently  proper  to  endeavor  by  mechan- 
ical means,  so  far  as  practicable,  to  improve  the  circulation.  The  possible  points 
of  attack  are  as  follows : 

1.  Diminution  of  the  Body  Weight  ivhen  this  has  become  Excessive  from  the 
Deposit  of  Fat.— We  shall,  in  a  later  chapter  (page  992),  study  carefully  the  in- 
jurious influence  of  obesity  upon  the  circulation.  All  the  measures  which  lead 
to  the  diminution  of  corpulence,  and  which  are  to  be  carefully  discussed  later  on, 
may  therefore  be  of  the  greatest  benefit  in  tbc  treatment  of  circulatory  disturb- 
ances in  suitable  cases. 

2.  Diminution  of  the  Amount  of  Liquid  in  the  Body— ■"  Desiccation."— This 
is  the  point  upon  which  Oertel  lays  the  greatest  stress.  He  believes  that  he  can 
dimmish  the  amount  of  blood  in  the  body  by  withdrawing  liquids,  and  thus  lighten 
the  task  of  the  heart  and  restore  the  normal  circulation.  On  this  view  rest  the 
proscription  of  excessive  drinking  and  the  limitation  of  liquid  nourishment,  such 
as  soup.  We  must  confess  that  it  is  difficult  for  us  to  decide  upon  this  point. 
Numerous  well-known  physiological  experiments  prove  that  the  body  maintains 
its  amount  of  blood  with  great  tenacity  at  a  certain  constant  ratio.  Inasmuch  as 
the  body  is  able  by  means  of  numerous  ways  (secretion  and  diffusion  of  liquids) 
to  make  speedy  compensation  for  variations  arising  through  changes  in  the 
amount  of  water  ingested,  it  is  by  no  means  proved  that  the  total  amount  of  blood 
in  patients  with  circulatory  derangements  is  increased ;  and  if  actually  there  is  a 
retention  of  fluid  in  the  body  (as  indeed  is  certainly  the  case  where  oedema  has 
developed),  yet  the  liquid  does  not  collect  in  the  vessels,  but  in  the  lymph-spaces 
of  the  interstitial  tissue,  or  possibly  in  the  cells  of  the  parenchyma  itself.  That 
the  total  amount  of  water  in  the  system  may  be  subjected  to  great  variations  must 
certainly  be  admitted;  but  that  there  should  be  any  increase  of  the  labor  demanded 
of  the  heart,  requires  that  a  large  amount  of  fluid  should  be  added  to  the  blood  in 
a  relatively  short  space  of  time,  so  that  an  actual,  although  extremely  temporary, 
hydraamic  plethora  should  exist.  If  this  process  is  very  frequently  repeated,  it 
will  surely  result  in  a  permanent  hindrance  to  the  circulation.  However,  it  is 
probable  that  this  is  the  case  only  in  habitual  beer-drinkers,  and  that  in  such  per- 
sons the  proscription  of  liquid  ingesta  is  of  great  value,  because  the  patient  is  thus 
kept  not  merely  from  water,  but  also  from  the  injurious  and  excessive  use  of  beer 
and  wine.  Another  way  in  which  this  limitation  of  drinking  is  of  still  wider 
practical  importance  is  that  a  patient  who  is  not  allowed  to  drink  while  he  is  eat- 
ing consequently  eats  less,  and  because  he  is  not  allowed  to  drink  until  after  he 
has  finished  eating  is  furthermore,  for  that  veiy  reason,  likely  to  drink  less  than 
he  otherwise  would.  What  might  be  called  the  "  psychological  importance  "  of 
the  much-discussed  prescription  to  abstain  from  liquids  ought  not  therefore  to  be 
contested ;  but  in  our  opinion  this  is  its  main  value.  Iu  lean  patients  who  live 
temperately  the  amount  of  liquids  taken  does  not  demand  any  special  attention 
from  the  physician. 

3.  Strengthening  of  the  Cardiac  Muscle  and  Promotion  of  Compensatory 
Hypertrophy. — That  the  fulfilling  of  this  indication  may  be  of  great  importance 
is  certain,  and  Oertel  lays  the  greatest  stress  upon  inciting  the  heart  to  more  vig- 
orous contractions  by  means  of  suitable  bodily  exertion,  and  especially  by  method- 
ical mountain-climbing,  in  order  by  these  means  to  promote  as  much  as  possible 
the  development  of  cardiac  hypertrophy.  This  view  is  probably  fully  justified 
and  of  obvious  utility  in  many  cases  of  simple  cardiac  weakness,  as  seen  in 
anaemia,  iu  convalescence  from  severe  disease,  and  sometimes  peirhaps  as  a  con- 


318  DISEASES  OF  THE  CIRCULATORY  ORGANS. 

genital  condition.  This  may  also  be  true,  in  many  cases,  of  purely  muscular  dis- 
ease of  the  heart;  hut  as  soon  as  one  considers  it  in  relation  to  those  cases  of 
circulatory  disturbance  where  there  is  actual  mechanical  hindrance  to  the  circu- 
lation, as  from  valvular  lesions,  the  case  seems  wholly  different.  To  be  sure,  one 
might  have  an  idea  that,  by  increasing  the  activity  of  the  heart,  the  hindrance 
would  be  more  easily  overcome.  An  important  consideration,  however,  seems  to 
us  to  be  that  we  can  scarcely  transfer  our  conceptions  with  regard  to  exercise  and 
invigoration  from  the  voluntary  muscles  to  the  cardiac  muscle.  The  mechanic- 
ally dilated  heart  is  minutely  regulated  by  means  of  an  especial  reflex  apparatus, 
independently  of  our  volition.  We  know  that  every  increased  demand  upon  the 
heart's  activity  is  in  most  cases  directly  fulfilled  by  an  increased  cardiac  effort. 
Under  proper  conditions  the  most  marked  cardiac  hypertrophy  may  develop  in  a 
completely  bedridden  patient.  We  must  therefore  consider  carefully  whether,  in 
cases  of  this  sort,  the  further  increase  of  the  demands  upon  tbe  heart  is  judicious; 
whether  it  may  not,  on  the  contrary,  contribute  to  a  premature  exhaustion  of  the 
myocardium.  It  certainly  seems  to  us,  aüd  our  opinion  is  fortified  by  practical 
experience,  that  the  prescription  of  increased  bodily  exertion,  such  as  mountain- 
climbing,  should  always  be  given  with  great  caution,  and  with  consideration  of  the 
individual  circumstances,  if  the  physician  desires  to  avoid  unhappy  consequences. 
We  share  the  belief  that  a  certain  measure  of  bodily  exercise  is  very  suitable  for 
patients  with  valvular  and  other  similar  cardiac  lesions,  but  we  hold  that  the 
benefit  lies  less  in  the  resultant  "  invigoration  of  the  cardiac  muscle  "  than  in  the 
promotion  of  the  venous  circulation  occasioned  by  the  motion  of  the  extremities 
and  the  deeper  inspirations  (see  page  998).  Long  mountain  trips  have  a  great  and 
unique  value  for  those  circulatory  disturbances  alone  which  are  occasioned  by 
obesity,  or  associated  with  simple  weakness  and  slight  dilatation  of  the  heart. 

4.  Promotion  of  the  Circulation  by  Massage,  Passive  Movements,  and  Gym- 
nastics.— It  can  not  be  doubted  that  these  are  suitable  means  for  the  promotion  of 
the  circulation,  especially  in  the  veins.  We  ought  not  to  overestimate  their  value, 
but  we  are  fully  justified  in  the  assertion  that  they  may  sometimes  be  employed 
with  decided  benefit  in  circulatory  derangements.  For  particulars  as  to  the  carry- 
ing out  of  this  method  of  treatment,  we  must  refer  to  appropriate  monographs. 


CHAPTER  VI. 
NEUROSES  OF  THE  HEART. 

1.  Angina  Pectoris  (Stenocardia), — Angina  pectoris  is  a  group  of  symptoms 
which  we  have  already  had  to  mention  repeatedly  as  a  frequent  complication  in 
different  cardiac  affections,  such  as  indurated  myocarditis,  aortic  insufficiency,  etc. 
The  same  symptoms  are  also  seen  as  a  pure  neurosis,  especially  in  anaemic  persons, 
or  in  connection  with  other  nervous  diseases,  like  hysteria,  epilepsy,  and  the  psy- 
choses. We  know  almost  nothing  as  to  the  exact  aetiology  of  the  disease.  In 
quite  a  large  number  of  published  cases  excessive  smoking  has  been  advanced  as 
an  etiological  factor. 

The  most  essential  symptom  of  the  paroxysm  consists  in  a  severe  pain  in  the 
cardiac  region,  shooting  up  into  the  left,  or,  more  rarely,  into  the  right  shoulder. 
There  is  also  a  general  feeling  of  constraint  and  anxiety — "precordial  anxiety." 
The  action  of  the  heart  is  usually  somewhat  accelerated,  either  weak  and  perhaps 
intermittent,  or  strong.  Respiration  is  unimpeded.  Exceptionally,  however,  and 
probably  as  a  result  of  the  pain,  it  becomes  irregular,  now  hurried  and  now  slow. 


NEUROSES  OF  THE  HEART.  319 

The  skin  during  the  paroxysm  is  often  pale  and  cool,  while  at  the  end  of  it  there 
may  be  profuse  sweating.      The  individual  attack  lasts  sometimes  only  a 
minutes,  and  sometimes  half  an  hour  or  more.     In  many  cases  the  paroxysms 
return  very  frequently,  almost  daily,  but  in  others  there  may  be  intervals  of 
weeks  or  months. 

Many  theories  have  been  advanced  as  to  the  nature  of  angina  pectoris,  but 
none  of  them  have  any  certain  foundation.  Since  the  sensory  fibers  of  the  heart 
rise  from  the  vagus  (but  partly,  perhaps,  from  the  sympathetic  also),  we  usually 
term  angina  pectoris  a  neurosis  of  the  vagus. 

The  prognosis  of  tbe  disease  is  not  very  favorable.  Although  life  itself  is  very 
rarely  endangered  by  the  paroxysms,  we  seldom  succeed  in  permanently  prevent- 
ing their  return. 

The  treatment  of  the  paroxysm  is  purely  symptomatic.  Cutaneous  irritant:;, 
like  mustard-plasters  to  the  chest,  and  foot-baths,  are  almost  always  used,  but 
they  have  but  little  effect.  A  subcutaneous  injection  of  one  sixth  to  one  third  of 
a  grain  of  morphine  (grin.  0'01-0-02)  is  the  best  palliative.  All  the  other  reme- 
dies, like  nitrite  of  amyl,  inhalations  of  chloroform,  atropine,  coniine,  etc.,  are 
less  reliable.     Nitrite  of  sodium  has  been  especially  recommended. 

Many  remedies  have  also  been  used  to  prevent  the  return  of  the  paroxysms : 
arsenic,  sulphate  of  zinc,  nitrate  of  silver,  bromide  of  potassium,  quinine,  etc. 
"We  usually  try  one  of  these  remedies,  but  without  promising  any  certain  benefit 
from  them.  Favorable  results  are  often  obtained  from  electrical  treatment — either 
the  application  of  the  faradic  brush  to  the  cardiac  region,  or  cautious  galvaniza- 
tion of  the  vagus  and  sympathetic  in  the  neck,  or  in  the  cardiac  region.  Method- 
ical cold-water  cures  have  also  resulted  in  improvement  in  some  cases  of  angina 
pectoris. 

Finally,  of  course,  we  must  pay  attention  to  any  underlying  diseases,  like 
anaemia  and  epilepsy,  and  to  the  removal  of  injurious  influences  which  may 
affect  the  disease  (smoking!). 

[In  well-marked  angina  sudden  death  during  a  paroxysm  is  not  very  rare.  In 
Dr.  Arnold,  of  Rugby,  the  first  attack  proved  fatal.  The  patient  may,  however, 
live  for  years — cases  of  survival  for  upward  of  twenty,  and  one  even  of  thirty, 
years  being  recorded.  Flint  has  known  recovery  to  occur.  The  prognosis  depends 
somewhat  on  the  condition  of  the  cardiac  valves  and  walls;  but  changes,  espe- 
cially in  the  latter,  may  escape  detection  by  any  save  a  very  skillful  observer. 
Walshe  states  that  in  every  one  of  twenty -four  cases  he  examined  during  life  he 
found  physical  signs  of  changes  either  in  the  heart,  the  aorta,  or  both.  The 
experience  of  Balfour  and  Latham  is  similar. 

With  regard  to  treatment,  it  is  true  that  morphine,  subcutaneously,  brings 
relief;  but  the  duration  of  the  attack  is  short,  the  physician  is  not  always  at  hand, 
and  there  are  scarcely  any  circumstances  under  which  it  is  right  to  arm  a  patient 
with  a  hypodermic  syringe  in  this  any  more  than  in  other  diseases. 

Nitro-glycerine  is  not  only  a  palliative  in  most,  but  also  a  prophylactic  in 
many  cases.  To  cut  short  an  attack,  it  can  be  carried  in  the  pocket ;  to  prevent 
recurrence,  it  can  be  taken  twice  or  thrice  daily-  The  nitrite  of  sodium  seems  to 
act  equally  well,  but  has  not  been  so  long  in  use.  The  nitrite  of  amyl  is  service- 
able chiefly  at  the  moment  of  attack.  It  is  put  up  in  glass  capsules,  one  of  which 
can  be  crushed  in  a  handkerchief  and  the  contents  inhaled ;  it  is  so  volatile  that 
it  can  be  preserved  ready  for  use  in  scarcely  any  other  way. 

The  value  of  the  nitrites  is  greater  than  the  author  would  seem  to  allow.] 

2.  Nervous  Palpitation.— By  "palpitation"  we  understand  the  subjective  sen- 
sation of  the  movements  of  the  heart.  It  is  usually  excited  by  increased  action  of 
the  heart,  but  there  is  no  constant  relation  between  the  intensity  of  the  cardiac 


320  DISEASES  OF  THE  CIRCULATORY  ORGANS. 

pulsations  and  the  subjective  feeling  of  them.  We  sometimes  observe  that 
patients  with  aortic  insufficiency  do  not  perceive  the  very  strong  action  of  their 
hypertrophied  hearts,  while  in  other  cases  a  patient  complains  of  a  troublesome 
feeling  of  palpitation,  although  the  action  of  the  heart  does  not  appear  objectively 
to  be  especially  increased. 

We  term  cases  "nervous  palpitation"  where  the  patient  complains  of  palpita- 
tion when  a  physical  examination  of  the  heart  shows  no  anatomical  change  in  it. 
As  a  rule,  in  these  cases  we  really  have  to  do  with  a  heart  whose  action  is  increased 
by  abnormal  nervous  influences.  In  many  cases  the  palpitation  arises  from  slight 
external  causes,  which  may  give  rise  to  little  or  no  palpitation  in  a  healthy  per- 
son, as,  for  example,  after  the  slightest  mental  excitement,  after  any  slight  phys- 
ical exertion,  after  taking  food,  after  indulging  in  certain  drinks,  like  tea,  coffee, 
wine,  or  beer,  or  in  certain  positions  of  the  body,  as  in  lying  on  the  left  side.  Here, 
then,  we  have  to  do  with  an  abnormal  sensitiveness  of  the  heart  to  external  irrita- 
tion, but  in  other  cases  there  is  probably  a  kind  of  hyperesthesia  of  the  patient 
to  the  movements  of  the  heart,  so  that  the  movements  that  are  of  normal  strength 
are  felt  in  a  troublesome  manner. 

The  patient  rarely  complains  of  continuous  palpitation;  it  usually  occurs  in 
more  or  less  sharply  defined  paroxysms.  Very  commonly  in  pure  nervous  palpi- 
tation we  have  to  do  with  people  who,  in  general,  suffer  from  other  nervous,  hys- 
terical, and  neurasthenic  symptoms,  or  they  are  anaemic  persons,  chlorotic  girls, 
etc. ;  but,  on  the  other  hand,  nervous  palpitation  may  occur  in  very  full-blooded, 
"  plethoric  "  people. 

The  diagnosis  of  nervous  palpitation  can  be  made  only  when  repeated  careful 
examination  shows  no  objective  abnormity  in  the  heart.  In  many  cases,  as  when 
there  are  anaemic  murmurs,  the  decision  may  be  quite  difficult.  We  must  always 
pay  particular  attention  to  the  whole  constitution  and  the  general  impression 
which  the  patient  makes. 

The  prognosis  is  so  far  favorable  in  that  the  disease  is  not  dangerous.  In  many 
cases  improvement  and  final  recovery  may  be  effected,  but  ether  cases,  of  course, 
resist  all  therapeutic  efforts  very  obstinately. 

The  treatment  must  first  be  directed  to  improving  the  patient's  general  con- 
stitution. Anaemic  persons  are  to  be  given  iron,  quinine,  and  strengthening  diet. 
We  put  full-blooded  people,  however,  on  scanty  fare,  and  prescribe  for  them  bitter 
waters,  or  a  bath  cure  at  Marienbad  or  Kissingen.  Where  there  is  hysteria  or 
neurasthenia,  it  requires  special  treatment.  We  should  avoid  all  the  influences 
which  seem  to  excite  palpitation.  As  a  symptomatic  indication  during  an  attack 
we  should  recommend  the  patient  especially  to  keep  quiet.  The  use  of  cold  to 
the  cardiac  region — cold  compresses  and  ice-bags— often  acts  beneficially.  On 
the  other  hand,  however,  it  is  to  be  noted  that  a  tendency  to  palpitation  asso- 
ciated with  cardiac  weakness  may  often  be  allayed  by  methodical  exercise  and 
the  invigoration  of  the  cardiac  muscle  consequent  thereupon  (see  the  appendix  to 
the  preceding  chapter).  Among  internal  remedies  we  must  employ  nervines,  and 
in  severer  cases  even  narcotics.  Among  the  former  we  would  mention  especially 
ethereal  tincture  of  valerian  and  bromide  of  potassium,  which  have  repeatedly 
done  us  good  service.  Digitalis  is  usually  of  little  value  in  pure  neuroses  of  the 
heart,  but  we  may  give  it  as  an  experiment,  say  fifteen  to  twenty  drops  of  the 
tincture  with  the  same  amount  of  cherry -laurel  water. 

3.  Tachycardia.— A  peculiar  and  quite  rare  neurosis  of  the  heart,  tachycardia, 
consists  of  an  enormous  frequency  of  the  pulse,  coming  on  in  paroxysms,  up  to 
200  beats  and  more  a  minute.  We  have  already  mentioned  these  paroxysms  as  a 
rare  symptom  in  mitral  and  also  in  aortic  disease,  but  precisely  similar  attacks 
may  occur  as  a  pure  neurosis  without  any  discoverable  lesion  of  the  heart.     They 


PERICARDITIS.  321 

have  been  observed  in  anaemic  and  nervous,  and  also  in  corpulent  persons.  In 
young  people  the  same  condition  sometimes  occurs  after  diphtheria  and  other 
acute  infectious  diseases  (vide  supra).  In  men  we  must  consider  the  possibility 
of  the  action  of  injurious  dietetic  influences,  like  drinking  and  smoking.  The 
individual  attack  usually  begins  quite  suddenly,  by  day  or  by  night,  sometimes 
without  any  cause,  but  often  it  is  apparently  produced  by  certain  exciting  causes, 
especially  at  times  by  overdistention  of  the  stomach.  The  patient  feels  that  the 
attack  is  coming,  he  becomes  anxious  and  restless,  and  looks  pale ;  but  there  are 
not,  as  a  rule,  at  least  according  to  our  experience,  any  symptoms  like  precordial 
anxiety,  dyspnoea,  or  attacks  of  faintness.  We  notice  in  the  heart  itself,  during 
the  attack,  chiefly  a  great  acceleration  of  the  heart-sounds.  We  sometimes  hear 
indefinite,  adventitious  murmurs.  The  action  of  the  heart  is  often  quite  regular, 
but  there  is  not  infrequently  manifest  arhythmia  during  the  attack.  Increase 
of  the  heart's  dullness  has  been  repeatedly  observed.  In  a  case  of  paroxysmal 
tachycardia,  in  a  patient  who  had  cirrhosis  of  the  liver,  we  could  certainly  detect 
a  considerable  acute  dilatation  of  the  heart  in  every  attack,  which  disappeared 
again  soon  after. 

We  know  little  that  is  definite  as  to  the  nature  of  the  attacks.  The  affection  is 
usually  regarded  as  a  temporary  paralysis  of  the  vagus. 

We  may  also  state  here  that  paroxysmal  and  constant  tachycardia  have  also 
been  repeatedly  observed  in  anatomical  lesions  of  the  cardiac  nerves  and  their 
centers,  in  tumors  and  other  affections  in  the  vicinity  of  the  medulla  oblongata, 
and  in  compression  of  the  vagus  in  the  neck  from  new-growths,  and  aneurisms. 

The  prognosis  of  tachycardia  depends  first  upon  the  nature  of  the  underlying 
disease.  We  do  not  know  whether  a  permanent  recovery  is  possible  in  idiopathic 
cases,  but  we  can  always  succeed  in  improving  the  condition.  The  treatment  dur- 
ing the  attack  consists  in  enjoining  complete  bodily  rest,  and  in  applying  ice  to 
the  heart.  With  marked  subjective  disturbance  we  should  give  bromide  of  potas- 
sium, or  even,  under  some  circumstances,  a  small  injection  of  morphine.  The 
best  way  to  guard  against  the  return  of  the  attacks  is  to  give  precise  hygienic 
directions,  suited  to  the  patient's  constitution  and  manner  of  life.  The  continued 
use  of  iodide  of  potassium  has  sometimes  seemed  to  us  to  be  of  service. 


SECTION    II. 
Diseases  of  the  Pericardium. 

CHAPTER  I. 

PERICARDITIS. 

{Inflammation  of  the  Pericardium.) 

JEtiology.— Pericarditis  seldom  appears  as  a  primary  idiopathic  disease.  It  is 
usually  merely  a  sequel  or  a  complication  of  other  diseases.  Thus,  it  is  observed 
with  particular  frequency  in  the  course  of  acute  articular  rheumatism,  where  it 
appears  sometimes  alone,  sometimes  in  combination  with  acute  endocarditis.  It 
is  not  impossible  that  certain  rare  cases  of  apparently  primary  acute  pericarditis 
belong,  from  an  aatiological  standpoint,  to  acute  articular  rheumatism — that  is, 
they  are  excited  by  the  same  pathogenic  factors  which  exceptionally  attack  the 
pericardium  alone,  without  simultaneous  participation  of  the  joints  in  the  disease. 
21 


322  DISEASES  OF  THE  CIRCULATORY  ORGANS. 

It  must  be  confessed  that  this  view  is  not  actually  proved  to  be  correct,  although 
a  similar  one  is  also  held  in  regard  to  many  cases  of  primary  acute  endocarditis. 
Cases  of  secondary  pericarditis,  unassociated  with  articular  rheumatism,  occur, 
although  much  less  often,  in  other  acute  infectious  diseases,  among  which  scarlet 
fever,  measles,  and  pyiemic  processes,  as  well  as  scurvy  and  purpura  hemorrhagica, 
deserve  especial  mention.  In  pyaemia  the  pericarditis  is  purulent,  and  in  purpura, 
hsemorrhagic.  Among  the  chronic  diseases  in  the  course  of  which  pericarditis 
sometimes  appears,  we  must  mention  especially  chronic  nephritis.  Pericarditis 
has  also  been  observed  in  a  few  cases  in  patients  with  carcinoma. 

A  large  number  of  cases  arise  from  an  extension  of  the  inflammation  from  the 
vicinity.  Thus  we  not  infrequently  see  pericarditis  as  a  result  of  pleurisy,  espe- 
cially on  the  left  side,  and  in  pneumonia  complicated  with  pleurisy.  New  growths 
and  ulcerative  processes  in  the  cesophagus,  in  the  vertebra?,  in  the  bronchial 
glands,  or  in  the  lungs,  also  lead  at  times  to  perforation  into  the  pericardium  and 
a  consequent  inflammation.  The  pericarditis,  too,  which  not  very  rarely  comes 
on  in  the  course  of  chronic  valvular  disease,  is  probably  usually  to  be  regarded 
as  an  extension  of  the  inflammation.  As  has  already  been  mentioned,  it  is  most 
frequent,  according  to  our  experience,  in  aortic  disease,  so  that  we  may  suspect 
a  direct  conduction  of  the  agents  of  inflammation  through  the  aortic  walls  into 
the  pericardium.  Pericarditis  may  also  develop  as  a  result  of  myocarditis,  abscess 
of  the  heart,  etc. 

Tuberculosis  plays  a  very  important  part  in  the  aetiology  of  pericarditis.  No 
small  number  of  apparently  primary  cases  of  pericarditis  turn  out  at  the  autopsy 
to  be  tubercular.  This  apparently  comes  on  in  quite  an  isolated  way,  or  as  one 
symptom  of  a  special  localized  form  of  tuberculosis,  which  we  term  tuberculosis  of 
the  serous  membranes.  In  many  cases  we  can  discover  the  origin  of  a  tubercu- 
lar pericarditis  in  the  direct  extension  of  a  tubercular  pleurisy.  In  apparently 
primary  cases  the  occurrence  of  the  infection  may  sometimes  be  explained  by  the 
discovery  of  a  tubercular  lymph-gland,  which  has  broken  through  into  the  peri- 
cardium. 

Pericarditis  is  usually  a  disease  of  youth  and  middle  life,  but  it  may  also  occur 
in  advanced  age. 

Pathological  Anatomy. — Ordinary  pericarditis  involves  the  two  surfaces  of  the 
internal  pericardium  in  either  a  circumscribed  or  diffuse  manner.  Inflammations 
of  the  outer  surface  of  the  pericardial  sac  are  distinguished  as  external  pericar- 
ditis (vide  infra).  The  anatomical  processes  in  pericarditis  are  precisely  analogous 
to  those  in  inflammations  of  the  serous  membranes  in  general,  especially  of  the 
pleura. 

We  usually  divide  pericarditis  into  fibrinous,  sero-fibrinous,  haemorrhagic,  and 
purulent  (or  ichorous)  forms,  according  to  the  character  of  the  exudation.  The 
fibrinous  and  sero-fibrinous  forms,  with  an  abundant  fluid  effusion  into  the  peri- 
cardial cavity,  are  the  most  frequent,  occurring  in  articular  rheumatism,  in  valvu- 
lar disease  of  the  heart,  etc.  Both  layers  of  the  pericardium  are  covered  with 
masses  of  fibrin e,  which  often  show  a  reticular  or  villous  arrangement  (cor 
villosum).  Besides  that,  we  find  more  or  less  of  a  fluid  effusion  which  distends 
the  pericardium.  The  fluid  is  of  a  serous  nature,  and  contains  more  or  less  numer- 
ous flakes  of  fibrine,  and  is  turbid  from  the  admixture  of  cells — pus-corpuscles, 
and,  in  part,  desquamated  endothelium.  A  purulent  pericarditis  is  always  the 
expression  of  a  specific  infection  of  the  pericardium.  It  is  seen  in  pysemic  dis- 
eases, as  a  result  of  empyema,  and  in  perforation  of  abscesses,  cancers  of  the  cesoph- 
agus, etc.,  into  the  pericardium.  A  haemorrhagic  effusion  is  seen  chiefly  in  tuber- 
cular pericarditis.  In  this  we  find  miliary  tubercles,  and  little  cheesy  nodules  in 
the  inflammatory  new  growths,  besides  all  the  signs  of  inflammation.     The  specific 


PERICARDITIS.  323 

tubercular  changes  are  sometimes  recognizable  with  the  naked  eye,  but  at  other 
times  we  have  to  use  the  microscope  to  find  them.  Hemorrhagic  pericarditis- also 
occurs  in  general  hsemorrhagic  diseases,  such  as  scurvy,  and  in  weak  and  debili- 
tated people,  like  drunkards. 

In  long-continued  pericarditis  the  cardiac  muscle  almost  invariably  undergoes 
changes.  The  heart  is  usually  flabby  and  dilated,  and  the  muscle  often  shows 
fatty  degeneration.  After  the  pericarditis  has  lasted  a  long  time  there  is  often 
quite  a  considerable  atrophy  of  the  cardiac  muscle,  which  is  partly  replaced  by 
fat  tissue.  We  have  already  mentioned  the  occurrence  of  pericarditis  in  connec- 
tion with  valvular  disease  and  degenerations  of  the  myocardium. 

In  favorable  cases  of  pericarditis  we  may  have  a  perfect  recoveiy.  The 
so-called  maculce  tendinece  sometimes  remain  in  the  pericardium  as  residua  of  a 
past  circumscribed  pericarditis.  In  some  cases  the  pericarditis  leads  to  an  adhe- 
sion of  the  two  layers  of  the  pericardium  to  each  other,  and  obliteration  of  the 
pericardial  cavity  (vide  infra).  In  many  cases  a  chronic  pericarditis  finally 
develops  from  the  acute  form,  or  the  whole  affection  takes  a  more  chronic  course 
from  the  outset.  In  this  way  chronic  adhesions  of  connective  tissue  arise,  and 
great  thickening  of  the  pericardium,  but  the  amount  of  fluid  is  usually  small. 
Sometimes  the  chronic  pericarditis  is  interrupted  by  an  acute  exacerbation  of  the 
disease. 

Clinical  Symptoms. — 1.  Subjective  Symptoms,  General  Symptoms,  and  Fever. — 
Mild  forms  of  pericarditis  may  develop,  as  in  the  course  of  an  acute  articular  rheu- 
matism, without  causing  any  subjective  symptoms.  They  are'  discovered  only  by 
a  careful  physical  examination  of  the  heart.  In  severe  cases,  however,  the  peri- 
carditis causes  violent  subjective  symptoms,  which  of  course  have  in  themselves 
little  that  is  characteristic. 

Pain  may  be  felt  in  the  cardiac  region,  and  often  in  the  epigastrium,  but  it 
is  absent  in  very  many  cases.  A  general  feeling  of  constraint  and  distress  is 
almost  constant  in  all  acute  cases  of  any  severity,  and  so  is  a  feeling  of  dyspnoea, 
which  may  increase  to  the  highest  degree  of  orthopneea.  The  patients  often  com- 
plain of  headache.     In  severe  cases  they  become  stupid  and  comatose. 

These  general  symptoms  are  the  direct  result  of  the  disturbance  of  the  circu- 
lation. Blood  pours  into  the  heart  slowly,  and  the  diastole  is  incomplete,  because 
of  the  increased  pressure  in  the  pericardium.  Although  stasis  occurs  in  the  veins, 
there  is  less  blood  in  the  right  ventricle  than  normal.  As  a  result  of  this  the 
pressure  falls,  and  the  rapidity  of  the  current  in  the  pulmonary  circulation  dimin- 
ishes. The  left  ventricle,  also,  contains  too  little  blood,  and  the  tension  in  the 
medium-sized  arteries  is  considerably  lowered.  This  is  the  explanation  of  the 
patient's  dyspnoea  and  cerebral  anaemia.  The  former  is  also  increased  ha  large 
pericardial  effusions  by  the  mechanical  pressure  of  the  distended  pericardium  on 
the  left  lung. 

Acute  pericarditis  is  usually  associated  with  fever.  This  has  no  special  type, 
and  usually  keeps  at  a  moderate  height — 102°  to  lOß^ö0  (390-39-80  C.) — but  it  often 
exhibits  considerable  variations.  In  cases  of  recovery  the  fever  declines  by  lysis. 
Chronic  pericarditis  may  run  its  whole  course  without  fever. 

2.  Physical  Signs — Inspection. — The  general  hue  of  a  patient  with  severe 
pericarditis  is  pale,  but  also  more  or  less  cyanotic.  He  has  an  anxious  expression. 
He  lies  with  the  upper  part  of  the  body  raised,  or  he  sits  up  in  bed.  The  breath- 
ing is  usually  rapid,  labored,  and  somewhat  irregular.  The  veins  in  the  neck  are 
swollen  and  prominent.  We  very  often  see  marked  undulating  or  pulsating 
movements  in  the  jugular  veins,  as  a  result  of  stasis.  The  cardiac  region  seems 
unusually  prominent  in  all  cases  with  much  effusion,  and  the  intercostal  spaces 
there  are  flattened  out.     We  sometimes  detect  a  slight  cedematous  swelling  of  the 


324  DISEASES  OF   THE  CIRCULATORY  ORGANS. 

chest- wall  itself.  When  there  is  a  large  effusion,  the  action  of  the  heart  is  only 
faintly  visible,  and.  is  sometimes  remarkably  diffused. 

Palpation  in  the  milder  cases  shows  the  apex-beat  in  its  normal  position  and 
of  about  normal  strength;  but  if  the  amount  of  the  pericardial  effusion  increases, 
the  heart  is  pushed  away  from  the  chest-Avail  by  it,  and  hence  the  heart-beat 
grows  weaker  until  it  disappears  entirely.  In  such  cases  it  is  sometimes  to  be  felt 
again  if  the  patient  bends  forward  or  lies  on  his  left  side.  In  the  rest  of  the  car- 
diac region  we  sometimes  feel  the  movements  feebly,  but  they  entirely  disappear 
as  the  effusion  increases.  In  some  cases,  by  laying  the  hand  flat  on  the  chest,  we 
can  feel  the  rub  of  the  rough  pericardial  surfaces  against  each  other. 

The  pulse  is  usually  accelerated,  and  in  severe  cases  it  becomes  irregular.  In 
every  large  effusion,  as  we  have  already  said,  the  tension  and  height  of  the  pulse 
are  diminished.  In  severe  cases  the  pulse  sometimes  becomes  very  small  and  weak, 
but,  when  the  heart  is  otherwise  normal  and  strong,  it  may  also  remain  quite 
strong — and  indeed  this  condition  of  the  pulse,  in  contrast  to  the  great  weakening 
of  the  heart-beat,  is  sometimes  of  diagnostic  significance.  In  some  cases  with  a 
large  pericardial  effusion  we  have  seen  a  manifest  pulsus  paradoxus — that  is,  a 
diminution  or  a  complete  disappearance  of  the  radial  pulse  on  every  inspiration. 

Percussion  shows  very  characteristic  changes  if  the  pericardium  is  distended 
by  the  effusion.  The  cardiac  dullness  is  then  increased,  and  usually  assumes  a 
triangular  form  peculiar  to  pericarditis.  The  obtuse  angle  of  the  triangle  is  found 
above  in  the  third  or  second  left  intercostal  space  near  the  left  border  of  the  ster- 
num. The  lateral  boundaries  run  obliquely  to  the  right  and  downward  to  about 
the  right  parasternal  line,  and  to  the  left  and  downward  to  the  left  mammillary 
line,  or  beyond.  The  broad  base  of  the  triangle  which  lies  below  is  usually  not  to 
be  defined  by  percussion  on  account  of  the  adjacent  left  lobe  of  the  liver.  On  the 
border  of  the  dullness  we  often  find  a  tympanitic  resonance  due  to  the  retraction 
of  the  adjacent  lung.  The  area  of  the  dullness  depends,  of  course,  in  the  first  place, 
upon  the  amount  of  the  effusion,  but  we  must  take  special  notice  that  in  regard  to 
this  the  relation  is  not  constant.  In  old  cases  of  pericarditis  especially  we  some- 
times find  the  cardiac  dullness  very  extensive,  while  the  autopsy  detects  only  a 
little  fluid  in  the  pericardium.  This  is  explained  partly  by  a  secondary  dilatation 
of  the  heart,  and  partly  by  a  persistent  retraction  of  the  lung. 

It  is  an  important  diagnostic  sign  of  pericarditis  that  in  many  cases  the  still 
perceptible  apex-beat  lies  within  the  cardiac  dullness,  since  the  pericardial  effusion 
extends  farther  to  the  left  than  the  heart  itself.  It  is  also  worthy  of  note  that  the 
dullness  in  pericarditis  often  shows  very  great  changes  when  the  patient  changes 
his  position.  The  dullness  is  more  extensive  when  the  body  is  erect  than  when 
lying  down,  and  when  the  patient  lies  on  his  side  it  sometimes  shows  a  lateral 
displacement  of  several  centimetres.  The  same  changes,  however,  though  rarely 
so  marked,  also  occur  in  a  hypertrophied  heart. 

The  characteristic  pathognomonic  auscultatory  sign  of  pericarditis  is  the  peri- 
cardial friction-rub.  This  arises  during  the  movements  of  the  heart  from  the 
rubbing  of  the  rough  and  inflamed  pericardial  surfaces  against  each  other.  The 
friction-rub  is  absent  in  pericarditis  if  the  rough  surfaces  of  the  two  layers  of  the 
pericardium  are  separated  from  each  other  by  a  fluid  effusion,  or  if  they  can  no 
longer  rub  against  each  other  from  an  adhesion  of  the  layers  of  the  pericardium. 
We  usually  hear  the  friction-rub  loudest  in  the  neighborhood  of  the  base  of  the 
heart,  but  it  may  also  be  heard  at  other  parts  of  the  heart.  The  quality  of  the 
sound  is  described  as  scraping,  grating,  or  creaking.  The  friction-rub  may  be 
heard  chiefly  either  during  the  systole  or  during  the  diastole  of  the  heart,  but  it  is 
in  general  not  often  closely  associated  with  the  phases  of  the  heart's  action.  We 
sometimes  find  it  intermitting  frequently,  and  jerky.     The  intensity  of  the  fric- 


PERICABDITIS.  325 

tion-rub  sometimes  varies  with  the  phases  of  the  respiration.  It  is  usually  louder 
on  inspiration,  but  sometimes  on  expiration.  If  the  patient  changes  his  position, 
it  sometimes  alters  the  intensity  of  the  sound.  It  is  louder  when  sitting  up  than 
lying  down,  etc.  The  friction-rub  often  sounds  louder  if  the  stethoscope  is  pressed 
firmly  against  the  chest,  since  in  this  way  the  layers  of  the  pericardium  are 
approximated  to  each  other. 

The  heart-sounds,  when  the  valves  are  intact,  may  sometimes  be  heard  as  well 
as  the  friction-rub,  or  they  may  be  completely  drowned  by  the  loud  rub,  at  least 
in  some  parts  of  the  heart.  In  general,  they  are  weak  in  every  case  of  pericardial 
effusion,  since  their  conduction  to  the  ear  is  impaired.  In  large  effusions  where 
no  friction-rub  is  to  be  heard,  we  hear  the  heart-sounds,  especially  the  first,  but 
only  very  faintly  and  obscurely.  This  condition  in  connection  with  the  increase  of 
the  cardiac  dullness  is  of  diagnostic  importance.  If  there  is  also  valvular  disease 
with  the  pericarditis,  the  pericardial  and  endocardial  murmurs  are  sometimes  hard 
to  distinguish  from  each  other,  but  usually  the  former  greatly  preponderate. 

3.  Sequelce  of  Pericarditis. — A  large  pericardial  effusion  may  excite  special 
symptoms  from  pressure  on  the  neighboring  organs.  Thus  we  have  already  said 
that  compression  of  the  left  lung  must  increase  the  dyspnoea.  In  many  cases  we 
also  notice  a  moderate  dullness  over  the  left  lower  back,  from  compression  of  the 
left  lower  lobe.  In  rare  cases  difficulty  in  deglutition  has  been  observed  as  a 
result  of  pressure  on  the  oesophagus,  and  paralysis  of  the  vocal  cords  from  press- 
ure on  the  recurrent  nerve. 

In  cases  of  long-continued  pericarditis  the  same  sequelae  may  develop  as  in  any 
chronic  disease  of  the  heart.  The  amount  of  urine  diminishes  as  a  result  of  the 
low  arterial  pressure.  The  venous  stasis  finally  leads  to  general  dropsy  and  to 
symptoms  of  passive  congestion  in  the  liver,  spleen,  and  kidneys.  We  would  also 
state  that  we  have  repeatedly  met  with  large  effusions  in  the  cavities  of  the  body, 
especially  hydrothorax,  without  any  oedema  of  the  skin.  All  the  symptoms  of 
stasis  mentioned,  however,  are  often  much  less  due  to  the  pericarditis  itself  than 
to  the  atrophy  and  dilatation  of  the  heart  which  frequently  follow  it  (vide 
supra). 

Special  Forms  of  Pericarditis. 

1.  Pericarditis  externa  and  Mediastino-pericarditis  (Pleuro-pericarditis). — 
By  pericarditis  externa  we  mean  an  inflammation  of  the  external  surface  of  the 
pericardial  sac,  which  is  usually  combined  with  an  inflammation  of  the  mediasti- 
nal connective  tissue  and  the  neighboring  pleura,  especially  over  the  lingula  of 
the  left  lung.  This  form  of  pericarditis  may  exist  by  itself,  or  combined  with 
internal  pericarditis.  It  is  a  rare  disease,  and  is  most  frequently  seen  as  a  result 
of  tubercular  pleurisy. 

The  physical  signs  must  differ  so  much,  according  to  the  localization  and  extent 
of  the  process,  that  we  can  give  few  general  data  in  regard  to  them.  There  are  only 
a  few  peculiar  signs,  which  must  be  noted  as  characteristic  of  many  cases.  In  the 
vicinity  of  the  apex -beat,  or  at  the  left  border  of  the  cardiac  dullness,  we  some- 
times hear  a  so-called  extra-pericardial  (pleuro-pericardial)  friction-rub.  This 
depends  both  upon  the  cardiac  movements  and  upon  the  respiratory  movements. 
On  holding  the  breath  we  hear  only  the  murmur  due  to  the  pulsations  of  the 
heart,  wrbile  on  deep  breathing  the  pleuritic  friction-sound  is  chiefly  to  be  heard. 
In  individual  cases  there  are  many  modifications,  which  can  not  all  be  mentioned. 
Another  interesting  sign,  first  found  by  Griesinger  and  Kussmaul  in  a  cicatricial 
mediastino-pericarditis,  is  the  so-called  pidsus  paradoxus.  This  consists  of  a 
diminution  of  the  pulse  at  each  inspiration.  This  condition  arises,  in  part  of  the 
cases  at  least,  from  the  fact  that  the  bands  and  adhesions  of  connective  tissue  at  the 


326  DISEASES  OF  THE  CIRCULATORY  ORGANS. 

origin  of  the  aorta  mechanically  nick  into  and  contract  its  lumen  at  every  inspi- 
ratory movement  of  the  thorax.  This  explanation,  of  course,  does  not  suffice  for 
all  cases,  since  the  pulsus  paradoxus  also  occurs  under  other  conditions,  as  with 
large  pericardial  effusions.  In  some  cases  there  may  he  seen  a  marked  swelling 
of  the  jugular  veins  in  the  neck  at  each  inspiration,  at  the  same  time  with  the  pulsus 
paradoxus,  since  the  large  venous  trunks  also  undergo  a  mechanical  nicking 
and  constriction  at  each  inspiration.  We  have  ourselves  seen  a  very  pronounced 
slowing  of  the  pulse  at  every  inspiration,  in  a  complicated  case  of  extra-pericardial 
adhesions  (vagus  irritation?).  We  must  also  mention  that  Riegel  observed  a  dis- 
appearance of  the  apex-beat  on  expiration  in  some  cases  where  tbere  were  bands 
of  connective  tissue  between  the  lungs  and  the  outer  surface  of  the  heart.  At 
every  expiration  the  bands  were  stretched  more  tightly,  and  hence  checked  the 
movements  of  the  heart. 

2.  Obliteration  of  the  Pericardial  Cavity  {Adhesive  Pericarditis ;  Adhesions 
of  the  Layers  of  the  Pericardium  ;  Concretio  seu  Synechia  pericardii). — We  may 
have  a  more  or  less  complete  adhesion  of  the  two  layers  of  the  pericardium  with 
each  other  as  a  result  of  pericarditis.  We  can  sometimes  observe  the  occurrence 
of  this  condition  duiing  the  course  of  a  pericarditis.  Quite  frequently,  however, 
we  meet  with  extensive  adhesions  of  the  two  layers  of  the  pericardium  on  the 
living  subject,  or  at  autopsies,  without  being  able  to  gather  any  history  of  a  pre- 
vious acute  pericarditis.  The  pericarditis  must  have  occurred  here  in  a  chronic 
way,  and  without  symptoms  from  the  outset. 

Even  extensive  adhesions  of  the  pericardial  surfaces  may  develop  and  remain 
entirely  without  symptoms,  and  be  met  with  accidentally  at  the  autopsy.  In 
other  cases,  however,  the  obliteration  of  the  pericardial  sac  causes  special  physical 
signs  and  severe  clinical  sequelae.  Among  the  first  and  more  important  is  the  sys- 
tolic retraction  of  the  chest,  either  limited  to  the  apex  or  involving  a  larger  area. 
This  is  most  comprehensible  if  there  is  an  adhesion  of  the  pericardium  with  the 
heart,  and  also  with  the  chest- wall  (Skoda) ;  but  we  certainly  find  this  retraction 
at  the  systole  without  co-existing  extra-pericardial  adhesions.  It  is  not,  however, 
an  absolutely  certain  sign  of  an  intra-pericardial  adhesion,  especially  if  we  have  to 
do  with  a  systolic  retraction  at  the  apex  alone,  since  systolic  retractions  may  some- 
times occur  hi  other  disturbances  of  the  heart's  motions;  but  systolic  retractions 
of  the  whole  cardiac  region  are,  in  the  majority  of  cases,  a  certain  sign  of  peri- 
cardial adhesions.  The  amount  of  this  retraction  is  often  dependent  upon  the 
respiration,  it  being  usually  more  marked  on  inspiration. 

The  other  symptoms  of  obliteration  of  the  pericardial  cavity  are  more  rare  and 
in  their  diagnostic  significance  still  more  uncertain.  Friedreich  observed  a  sud- 
den collapse  of  the  jugular  veins  at  each  diastole — the  "diastolic  collapse" — while 
they  became  well  filled  again  at  the  next  systole.  He  explained  this  phenome- 
non by  supposing  that  the  conditions  for  emptying  the  veins,  at  the  moment 
of  the  diastole  of  the  ventricle,  were  especially  favorable,  since  the  chest-wall, 
which  had  previously  been  drawn  in  by  the  systole,  went  back  again  quickly. 
Riess  described  some  cases  of  pericardial  adhesions  where  the  heart-sounds  had  a 
metallic  character  from  the  resonance  of  the  stomach,  which  had  been  drawn  up. 
All  things  considered,  we  must  say  that  although  the  diagnosis  of  pericardial  adhe- 
sions can  be  correctly  made  in  many  cases,  yet  the  signs  given  for  it  are  more  or  less 
uncertain,  since  they  may  be  absent  in  obliteration  of  the  pericardial  sac,  and 
they  may  also  be  caused  by  other  conditions  without  such  an  obliteration. 

In  the  cases  of  pericardial  adhesions  which  give  rise  to  severe  disturbances 
of  the  circulation,  these  are  usually  not  the  direct  result  of  the  pericardial  adhe- 
sions, but  are  due  to  the  secondary  changes  which  develop  in  the  cardiac  muscle. 
Only  when  extensive  extra-pericardial  adhesions  are  also  present  can  there  be 


PERICARDITIS.  327 

such  a  restraint  upon  the  systole  of  the  heart,  in  a  purely  mechanical  way,  as  to 
cause  a  diminished  filling1  of  the  arteries,  and  stasis  in  the  veins.  It  is  usually, 
however,  the  secondary  atrophy,  with  fatty  degeneration  and  dilatation  of  the 
cardiac  muscle,  that  causes  the  severe  disturbances  of  the  circulation.  Such  cases 
give  throughout  the  general  impression  of  valvular  disease.  Dyspnoea,  general 
oedema,  and  signs  of  passive  congestion  in  the  liver  and  kidneys,  are  the  chief 
symptoms  of  the  disease.  It  is  a  striking  observation,  which  other  physicians  and 
we  ourselves  have  made  a  few  times,  that  as  a  result  of  obliteration  of  the  pericar- 
dial sac,  great  ascites,  sometimes  associated  with  hydrothorax,  may  develop  without 
any  simultaneous  oedema  of  the  extremities.  In  all  such  cases  the  diagnosis  is 
usually  far  from  easy.  We  can  sometimes  scarcely  avoid  confounding  it  with 
chronic  myocarditis,  in  the  absence  of  all  heart-murmurs.  If  the  cardiac  muscle 
remains  intact,  extensive  pericardial  adhesions  may  exist  for  years  without  causing 
the  patient  the  slightest  disturbance. 

3.  Tubercular  Pericarditis.— Tubercular  pericarditis  is  an  important  disease 
clinically,  since  in  many  cases  it  is  apparently  primary.  It  may  be  either  quite 
acute  or  chronic.  The  patient  falls  ill  suddenly,  or  more  gradually  with  indefi- 
nite thoracic  symptoms,  dyspnoea,  general  weakness,  moderate  fever,  etc.  If  it 
is  of  long  duration,  there  is  more  or  less  oedema.  When  we  find  on  physical 
examination,  in  such  cases,  the  signs  of  a  pericarditis,  the  diagnosis  of  tubercular 
pericarditis  is  probable,  if  we  discover  a  general  "phthisical  habit,"  hereditary 
predisposition,  and  also  co-existing  disease  of  other  serous  membranes,  especially 
pleurisy,  or  more  rarely  chronic  peritonitis.  In  the  latter  case  the  tubercular 
pericarditis  forms  one  symptom  of  the  so-called  tuberculosis  of  the  serous  mem- 
branes, but,  as  has  been  said  before,  apparently  isolated  primary  tubercular  peri- 
carditis does  occur  (vide  supra).  We  have  seen  such  cases  repeatedly,  especially 
in  old  people.  In  these  cases  the  disease  is  not  easy  to  diagnosticate.  The  patient 
gives  one  the  impression  of  having  heart  disease,  but  the  physical  signs  in  the 
heart  are  sometimes  of  a  very  indefinite  nature.  Friction-rubs  may  be  entirely 
absent,  on  account  of  adhesions  or  of  large  effusions.  This  leads  to  confusion 
with  myocarditis,  or  mitral  stenosis.  In  other  cases,  of  course,  all  the  physical 
signs  of  pericarditis  mentioned  above  may  be  manifest,  and  a  correct  diagnosis 
can  be  made. 

Diagnosis. — From  what  precedes,  it  follows  that  the  diagnosis  of  pericarditis  is 
very  easy  in  many  cases,  but  is  very  difficult  or  impossible  in  others.  The  most 
unequivocal  sign  is  the  characteristic  friction-rub.  The  practiced  ear  can  often 
distinguish  it  from  an  endocardial  sound  by  its  quality.  The  pericardial  sound 
is  a  rubbing,  grating  noise,  near  the  ear;  the  endocardial  is  blowing,  distant 
from  the  ear.  The  following  features  may  serve  as  marks  of  distinction  in 
doubtful  cases:  1.  We  hear  the  pericardial  sounds  at  first,  and  also  later,  over 
the  base  of  the  heart  in  the  vicinity  of  the  pulmonary  valve ;  the  endocardial  are 
often  loudest  at  the  apex.  2.  The  pericardial  murmurs  are  not  so  closely  associ- 
ated with  the  phases  of  the  heart's  action,  with  systole  and  diastole,  as  the  endo- 
cardial. 3.  We  find  that  the  pericardial  sounds  are  not  transmitted  far.  A  loud 
rub  may  be  audible  at  one  spot  which  can  not  be  heard  a  few  centimetres 
away.  Loud  endocardial  murmurs,  however,  are  audible  over  almost  the  whole 
heart.  4.  Sometimes  the  peculiarity  of  the  pericardial  murmur — that  it  becomes 
louder  when  the  patient  sits  up,  on  pressure  with  the  stethoscope,  etc. — may  be  of 
diagnostic  value.  In  many  cases,  too,  the  loud,  functional,  so-called  anaemic  mur- 
murs over  the  base  of  the  heart  may  give  rise  to  confusion  with  pericarditis. 

In  the  cases  where  pericardial  sounds  are  absent  the  diagnosis  is  rendered  pos- 
sible by  the  characteristic  triangular  shape  of  the  cardiac  dullness,  in  connection 
with  the  character  of  the  apex-beat,  the  pulse,  and  the  heart-sounds.     We  have 


328  DISEASES  OF  THE  CIRCULATORY  ORGANS. 

already  called  attention  to  the  ease  with  which  pericarditis  may  he  confounded 
with  myodegeneration  of  the  heart  and  mitral  stenosis  without  auy  murmur.  We 
can  not  lay  down  general  rules  for  differentiating  these  conditions.  The  more 
careful  the  examination,  and  the  greater  the  personal  experience,  the  more  easily 
can  we  avoid  a  false  diagnosis. 

We  have  already  mentioned  the  determining  factors  for  the  diagnosis  of  the 
different  forms  of  pericarditis  and  their  significance. 

Course  and  Prognosis. — Many  cases  of  pericarditis  in  articular  rheumatism, 
pneumonia,  or  heart  disease,  and  also  many  of  the  rare  aud  apparently  primary 
forms,  may  recover  completely.  The  disease  lasts,  in  the  mild  cases,  only  about 
a  week,  in  severe  cases  much  longer. 

Mauy  cases  of  pericarditis,  however,  terminate  fatally.  The  unfavorable  issue 
depends  either  upon  the  severity  of  the  primary  disease,  or  upon  the  intensity 
of  the  pericarditis  itself.  In  extensive  croupous  pneumonia,  in  valvular  disease 
of  the  heart,  or  in  severe  chronic  nephritis,  an  attack  of  pericarditis  is  often  the 
terminal  affection — the  immediate  cause  of  death.  In  otherwise  healthy  people, 
however,  a  severe  pericarditis  with  a  large  effusion  may  he  the  direct  cause  of 
death,  as  a  result  of  the  impairment  of  the  movements  of  the  heart.  The  prog- 
nosis of  every  tubercular  pericarditis  is  absolutely  unfavorable.  The  latter  can, 
indeed,  run  quite  a  chronic  course,  but  it  is  hardly  ever  capable  of  definite  recov- 
ery.    The  prognosis  of  pysemic  pericarditis  is  also  unfavorable. 

In  one  class  of  cases  pericarditis  takes  a  chronic  course  from  the  start,  or 
chronic  pericarditis  develops  from  an  acute  attack.  The  ultimate  prognosis  of 
these  cases  is  usually  unfavorable,  since  the  secondary  atrophy  and  dilatation  of 
the  heart  gradually  lead  to  severe  disturbances  of  the  circulation.  We  have 
spoken  above  of  the  termination  of  pericarditis  in  obliteration  of  the  pericar- 
dial sac. 

Treatment. — Since  pericarditis  is  a  severe  affection  under  all  circumstances,  we 
must  especially  see  that  the  patient  has  perfect  rest  and  care.  Extreme  caution 
must  be  enjoined  upon  him,  especially  in  the  cases  where  at  first  the  subjective 
symptoms  are  slight.  We  must  keep  the  patient  strictly  confined  to  the  bed,  and 
not  let  him  leave  it  even  temporarily. 

The  remedies  which  are  used  against  pericarditis  aim  partly  at  keeping  the 
inflammation  in  check,  and  partly  at  aiding  the  action  of  the  heart.  For  the  first, 
the  continued  application  of  ice  to  the  cardiac  region  deserves  especially  to  be 
recommended.  Local  blood-letting,  ten  or  twelve  leeches  to  the  cardiac  region — 
formerly  very  often  but  now  more  rarely  used — may,  in  otherwise  strong  and 
healthy  persons,  afford  great  relief  in  cases  with  marked  subjective  symptoms. 
Painting  with  tincture  of  iodine  and  vesicatories,  however,  deserve  little  confi- 
dence. Digitalis  is  our  chief  means  to  bring  down  an  accelerated  pulse,  and  to 
strengthen  the  heart's  action.  It  is  a  drug  which  is  most  active  and  most  fre- 
quently used  in  pericarditis,  and  is  always  indicated  when  the  pulse  is  rapid  and 
of  diminished  tension.  Of  course,  the  action  of  the  remedy  must  be  carefully 
watched,  as  in  all  cases  where  digitalis  is  prescribed.  .Tincture  of  strophanthus  is 
also  useful.  As  a  palliative,  morphine  often  does  indispensable  service  where  the 
subjective  symptoms  are  marked  and  the  patient  is  very  restless. 

If  the  symptoms  are  threatening,  the  question  arises  whether  a  large  fluid  peri- 
cardial effusion  is  the  cause  of  the  severe  symptoms.  In  this  case  the  evacuation 
of  the  exudation  is  of  course  imperatively  indicated.  The  difficulty  of  forming  a 
correct  opinion,  however,  is  very  great,  because  in  any  individual  case  it  is  rarely 
possible  to  determine  the  amount  of  fluid  that  may  be  present.  In  the  first  place, 
we  must  consider  the  size  of  the  cardiac  dullness  and  the  weakening  of  the  move- 
ments of  the  heart,  but  both  factors  may  give  rise  to  deception.    Hence  we  always 


HYDRO-PERICARDIUM.  320 

first  make  an  exploratory  puncture  with  a  Pravaz's  hypodermic  syringe.  The  best 
point  for  insertion  is,  in  general,  the  sternal  end  of  the  fourth  or  fifth  [leftj  inter- 
costal space  when  the  patient  is  lying  on  his  back.  If  the  exploratory  puncture 
gives  a  positive  result,  we  make  a  puncture  with  Billroth's,  Fraentzel's,  or  some 
similar  trocar.  With  regard  to  the  details,  we  will  refer  to  the  description  of 
puncture  of  the  pleura.  Puncture  of  the  pericardium  is  always  performed  by  the 
aid  of  aspiration.  It  is  less  dangerous  than  might  be  feared.  Even  injuries  If) 
the  heart  during  the  operation  have  scarcely  ever  had  grave  results.  The  tempo- 
rary relief  to  the  patient,  in  cases  of  successful  puncture,  is  usually  very  striking) 
but  the  permanent  results  of  pericardial  puncture  are,  of  course,  much  less  favor- 
able than  those  of  puncture  of  the  pleura,  which  is  chiefly  due  to  the  character  of 
the  underlying  disease.  In  some  cases  of  purulent  pericarditis,  drainage  of  the 
pericardium  has  also  been  practiced  after  the  analogy  of  the  treatment  of  em- 
pyema, but  experience  on  this  point  is  not  yet  very  extensive. 

[The  experiments  of  Rotch  show  that  pericardial  effusion  causes  dullness  in  the 
fifth  right  interspace,  a  sign  which  he  thinks  is  not  produced  in  cardiac  enlarge- 
ment. So  far  as  is  known  to  the  editor,  he  is  the  only  person  who  has  acted  on 
this  observation,  and  punctured  on  the  right  of  the  sternum  for  pericardial  effu- 
sion. In  the  case  referred  to,  the  signs  pointed  to  a  very  large  acute  effusion  of 
rheumatic  origin.  The  first  puncture  was  made  in  the  fifth  left  interspace,  but 
only  about  an  ounce  and  a  half  of  bloody  serum  was  obtained.  The  needle  was 
then  withdrawn  and  immediately  inserted  in  the  fourth  right  space  near  the  sternal 
border  with  absolutely  negative  result.  The  gravity  of  the  symptoms  led  to  two 
more  punctures  on  the  left  some  days  later,  one  with  small  though  positive  result, 
the  other  with  negative.     Absorption  and  recovery  ultimately  took  place. 

The  recommendation  of  the  author  to  make  a  preliminary  puncture  with  a 
hypodermic  syringe  for  diagnostic  purposes  seems  unnecessary,  just  as  with  pleural 
effusions. 

Roberts  has  tabulated  sixty  cases  of  paracentesis  of  the  pericardium,  with 
twenty-four  recoveries.] 

If  there  is  a  condition  of  cardiac  weakness,  stimulants  are  indicated — strong 
wine,  subcutaneous  injections  of  ether  or  camphor,  or  wine  of  musk.  We  try  to 
keep  up  the  patient's  strength  by  the  best  of  nourishment. 

The  resulting  conditions  of  disturbance  of  the  circulation,  like  oedema,  in 
chronic  pericarditis,  are  treated  in  the  same  way  as  in  valvular  disease  (vide 
supra).     Digitalis,  in  small  doses,  and  diuretics,  are  the  chief  remedies. 


CHAPTER  II. 


HYDRO-PERICARDIUM,   H2EMO-PERICARDIUM,   AND   PNEUMO- 
PERICARDIUM. 

1.  Hydro-Pericardium. 

(Dropsy  of  the  Pericardium.) 

The  collection  of  a  serous  transudation  in  the  pericardial  sac,  without  any  in- 
flammatory symptoms  in  the  serous  membrane  itself,  we  term  hydro-pericardium, 
or  dropsy  of  the  pericardium.  Dropsy  of  the  pericardium,  which  formerly  played 
quite  a  great  role  in  pathology,  is  never  a  disease  of  itself,  but  is  always  a  sec- 
ondary condition.  It  may  occur  in  anaämic  and  cachectic  people  as  a  result  of 
hydraemia,  but  it  usually  depends  upon  a  local  or  general  venous  stasis  in  the 
pericardium.     In  the  latter  case  the  hydro-pericardium  is  one  symptom  of  general 


330  DISEASES  OF  THE  CIKCULATOKY  OKGANS. 

dropsy,  and  hence  is  found  chiefly  in  heart  disease,  renal  disease,  or  pulmonary 
emphysema. 

The  clinical  symptoms  of  hydro-pericardium  are  only  exceptionally  distinct, 
being  obscured  by  the  underlying  affection.  Large  amounts  of  fluid  in  the  peri- 
cardial sac,  which  may  amount  to  a  quart  (a  litre)  or  more,  must  of  course  impair 
the  action  of  the  heart,  weaken  the  heart-beat  objectively,  and  cause  an  increase  in 
the  cardiac  dullness.  The  distinction  from  pericarditis  is  rendered  possible  by 
the  absence  of  a  friction-rub,  but  especially  by  attention  to  the  existence  of  an 
underlying  disease.  In  other  respects  the  distinction  between  a  pericardial  transu- 
dation and  an  effusion  during  life  is  not  always  easy. 

The  prognosis  and  treatment  depend  wholly  upon  the  nature  of  the  underlying 
disease.  Only  exceptionally  do  we  need  to  puncture,  when  the  exudation  is  very 
large. 

2.  Heemo-Pericardium. 

(Blood  in  the  Pericardial  Sac.) 

In  rare  cases  haemorrhages  occur  into  the  pericardial  sac.  The  source  of  the 
haemorrhage  is  most  frequently  an  aneurism  of  the  aorta,  which  perforates  into 
the  pericardium.  Other  causes  of  haemorrhage  are  the  bursting  of  aneurisms  of 
the  coronary  arteries  and  rupture  of  the  heart.  The  latter  has  been  seen  after 
injuries,  and  also  as  a  result  of  cardiac  aneurism  and  the  cicatricial  formations  in 
myocarditis  (see  Myocarditis).  Finally,  direct  injuries  to  the  heart,  especially 
bullet-wounds,  may  also  cause  haemorrhages  into  the  pericardial  sac. 

In  most  cases  death  occurs  in  a  few  moments  from  compression  of  the  heart, 
when  a  haemo-pericardium  comes  on.  Hence  the  amount  of  blood  poured  out  into 
the  pericardial  sac  is  usually  not  very  considerable.  Only  in  the  cases  where  the 
blood  oozes  out  more  slowly  can  a  great  distention  of  the  pericardial  sac  be  reached. 
The  diagnosis  is  only  rarely  possible.  With  regard  to  treatment  we  can  merely 
note  that,  in  some  traumatic  cases,  the  aspiration  of  the  blood  has  been  performed 
with  success. 

3.  Pneumo-Pericardium. 

(Air  in  the  Pericardial  Sac.) 

The  entrance  of  air  or  gas  into  the  pericardial  sac  has  been  observed  in  rare 
cases,  apart  from  external  wounds,  as  a  result  of  the  perforation  of  a  pyopneumo- 
thorax, or  of  some  other  suppurating  process  in  organs  that  contain  air.  Thus 
cases  are  known  where  the  rupture  into  the  pericardial  sac  comes  from  the 
oesophagus,  as  in  cancer ;  from  the  stomach,  in  cancer  or  ulcer ;  or  from  the  lungs, 
in  tubercular  or  gangrenous  cavities.  Since  the  agents  of  inflammation  enter  the 
pericardium  along  with  the  air,  a  purulent  pericarditis  almost  always  develops, 
besides  the  pneumopericardium,  or  it  may  rarely  be  simply  a  sero-fibrinous  peri- 
carditis. 

The  most  characteristic  and  striking  sign  of  pneumopericardium  is  the  pres- 
ence of  a  metallic  sound,  due  to  the  movements  of  the  heart.  Either  the  heart- 
sounds  themselves,  or  some  existing  friction-rub,  may  acquire  a  metallic  timbre 
from  the  increased  resonance,  or  splashing  metallic  sounds  may  be  produced  in 
the  pericardial  sac  from  the  movements  of  the  air  and  the  fluid,  which  may  even 
be  heard  at  a  distance  from  the  patient.  In  regard  to  diagnosis,  however,  it  is  im- 
portant to  know  that  signs  similar  to  those  of  metallic  resonance  in  the  heart 
may  arise  from  the  stomach,  when  it  is  drawn  or  pushed  upward. 

In  true  pneumo-pericardium  percussion  gives  a  more  or  less  complete  absence 
of  the  cardiac  dullness.     On  rod-percussion  (see  page  269)  a  metallic  sound  is  some- 


ARTERIOSCLEROSIS.  331 

times  heard,  whose  pitch  may  vary  somewhat  with  the  phase  of  the  heart's  action. 
If  fluid  is  also  present  in  the  pericardial  sac  besides  the  air,  the  dullness  caused  by 
this  will  rise  on  raising  up  the  patient. 

The  other  symptoms  of  the  disease  and  the  treatment  are  the  same  as  in  a 
severe  pericarditis.  The  prognosis,  however,  corresponding  to  the  primary  dis- 
ease, is  wholly  unfavorable. 


SECTION    III. 
Diseases  of  the  Vessels. 

CHAPTER  I. 

ARTERIO-SCLEROSIS. 

(Endarteritis  chronica  deformans.     Atheroma  of  the  Vessels.) 

JEtiology. — Atheromatous  degeneration  of  the  arteries  is  chiefly  a  disease  of 
advanced  life,  in  persons  over  forty.  It  is  often  to  be  regarded,  especially  in  old 
people,  not  as  a  disease,  but  as  attributable  to  conditions  of  senile  involution. 

Besides  age  there  are  also  a  number  of  astiological  factors  which  favor  an 
earlier  occurrence  and  a  greater  extension  of  the  atheroma.  Among  these  are, 
first  of  all,  chronic  alcoholism;  also  syphilis,  gout,  chronic  nephritis,  articular 
rheumatism,  and  chronic  lead-poisoning.  It  is,  however,  hard  to  find  more  positive 
evidence  for  the  connection  between  atheroma  and  the  conditions  mentioned, 
although  the  special  connection  between  alcoholism,  and  perhaps  syphilis  and 
arterio-sclerosis,  is  made  probable  by  many  observations.  We  must  mention  that 
in  many  families  there  is  a  pronounced  hereditary  tendency  to  atheroma  of  the 
vessels  and  its  results.  Men  are  decidedly  more  liable  to  the  disease  than 
women. 

Pathological  Anatomy. — Atheroma  is  almost  exclusively  confined  to  the  arte- 
ries ;  only  exceptionally  do  like  processes  occur  in  the  veins.  Among  the  arteries 
the  aorta  is  almost  always  the  most  intensely  and  extensively  diseased ;  we  also 
find  disease  in  the  iliac  and  femoi'al  arteries,  the  brachial,  radial,  and  ulnar,  the 
coronary  arteries  of  the  heart,  and  the  arteries  of  the  brain.  In  some  of  the  other 
arteries,  however,  like  the  gastric  artery,  the  hepatic,  and  the  mesenteric,  we  very 
rarely  find  atheromatous  changes. 

The  atheromatous  process  is  easy  to  recognize  macroscopically.  Instead  of  the 
normal  smooth  internal  surface,  we  find  more  or  less  numerous  irregularities  and 
thickenings  on  the  intima,  which  appear  either  more  or  less  gelatinous  and  trans- 
lucent, or  dense  and  fibrous,  or  ossified  as  a  result  of  calcification,  in  which  case 
they  also  feel  perfectly  hard.  In  extensive  calcification  the  whole  artery  is 
changed  to  a  hard,  stiff  tube.  In  many  cases  we  find  the  surface  of  the  thicken- 
ings destroyed — atheromatous  ulcers — and  covered  with  masses  of  thrombi. 

Microscopic  examination  shows  that  the  chief  changes  are  situated  in  the 
intima  of  the  arteries.  This  appears  three  or  four  times  as  thick  as  normal, 
partly  from  the  swelling  of  its  elements  and  partly  from  the  new  growth  of  con- 
nective tissue  and  the  deposit  of  round  cells.  In  the  connective-tissue  cells  of  the 
intima,  and  in  the  endothelial  cells  of  its  surface,  we  usually  find  a  marked  fatty 
degeneration,  to  which  the  yellowish,  translucent  appearance  of  the  surface  is  due. 
Finally,  in  the  deeper  layers  there  is  a  complete  breaking  down  of  the  tissue  into 


332  DISEASES  OF  THE  CIRCULATORY   ORGANS. 

a  mixture  of  fat,  detritus,  and  Cholesterine  crystals,  which  has  given  the  whole 
process  the  name  of  atheroma  [=  pulp].  If  this  destruction  extends  to  the  sur- 
face, an  atheromatous  ulcer  is  formed.  In  other  places,  however,  it  does  not 
reach  ulceration,  hut  the  superficial  layers  of  the  intima  become  sclerosed,  and 
are  finally  changed  to  lamella?  of  bony  hardness  from  the  deposition  of  lime- 
salts.  The  atheromatous  spots  on  the  intima  of  the  vessels  often  give  rise  to  the 
formation  of  parietal  thrombi. 

The  media  and  adventitia  of  the  arteries  also  show  changes  in  the  later  stages 
of  the  process.  Here,  too,  we  may  finally  get  fatty  degeneration  and  calcification. 
In  other  cases,  howevei*,  there  is  a  marked  atrophy  of  the  media. 

The  immediate  result  of  the  atheromatous  changes  is  a  loss  of  elasticity  in  the 
walls  of  the  vessels.  The  ability  to  resist  the  blood-pressure  is  reduced,  and  this  is 
why  diffuse  or  circumscribed  aneurismal  dilatations  of  the  vessels  so  often  arise 
as  a  result  of  arterio-sclerosis  (see  the  following  chapters). 

Another  result  of  extensive  atheromatous  degeneration  of  the  vessels  is  an 
increase  of  the  resistance  to  the  blood-current,  and  a  consequent  elevation  of  the 
arterial  pressure.  Furthermore,  the  loss  of  elasticity  in  the  coats  of  the  medium- 
sized  and  smaller  arteries  removes  an  important  factor  for  the  propulsion  of  the 
blood.  The  left  ventricle,  in  consequence  of  these  additions  to  its  task,  becomes 
almost  invariably  hypertrophied  in  cases  of  extensive  arterio-sclerosis,  provided 
the  general  nutrition  of  the  patient  is  still  well  maintained. 

The  thickening  of  the  intima  in  the  smaller  vessels  often  causes  so  marked  a 
diminution  of  the  blood-supply  that  secondary  disturbances  of  nutrition  are  not 
wanting  in  the  various  organs.  The  lumina  of  the  vessels  may  be  still  further 
narrowed,  or  even  completely  closed,  by  the  formation  of  thrombi  on  such 
portions  of  the  wall  of  the  vessels  as  have  undergone  atheromatous  changes.  We 
have  already  in  part  learned  to  recognize  the  sequelae  which  necessarily  arise  in 
the  various  organs,  such  as  indurations  in  the  heart  as  a  result  of  atheroma  of 
the  coronary  arteries,  and  we  will  return  later  on  to  the  analogous  changes  in 
some  other  organs,  like  cerebral  softening  and  certain  forms  of  contracted  kidney. 

Clinical  Symptoms. — In  order  to  decide  whether  an  arterio-sclerosis  is  present 
in  the  living  subject,  we  are  of  course  exclusively  restricted  to  the  examination  of 
those  peripheral  arteries  that  are  accessible  to  palpation.  We  must  examine, 
first  of  all,  the  radial,  brachial,  femoral,  and  temporal  arteries.  If  there  is  ath- 
eroma, we  feel  the  hard  and  partly  bony  vessel-wall.  In  marked  cases  we  have  a 
feeling,  especially  in  the  radial,  as  if  we  had  hold  of  a  goose's  neck.  We  some- 
times notice  a  diffuse  dilatation  of  the  femoral  arteries.  In  many  cases  the 
marked  spiral  form  of  the  vessels  is  very  striking,  and  it  is  a  direct  result  of  the 
loss  of  elasticity  of  their  walls  and  of  the  increased  blood-pressure.  The  spiral 
form  is  most  frequently  observed  in  the  temporal,  brachial,  and  radial  arteries. 

Although  we  can  often  directly  demonstrate  atheroma  in  the  vessels  men 
tioned,  we  must  always  be  cautious  in  deciding  from  this  that  there  is  also  au 
atheroma  of  the  internal  arteries,  for  the  radial  arteries  often  feel  very  rigid, 
while  the  autopsy  later  on  shows  little  or  absolutely  no  atheroma  of  the  internal 
arteries.  In  other  cases,  however,  we  find  at  the  autopsy  marked  atheromatous 
changes  in  the  arteries  of  the  brain,  the  kidneys,  the  heart,  etc.,  although  the 
external  arteries  during  life  felt  perfectly  normal.  We  see  from  this  how  hard  it 
is  to  make  an  absolute  diagnosis  of  general  arterio-sclerosis. 

It  is  impossible  to  give  a  uniform  picture  of  arterio-sclerosis,  since  its  results 
appear  now  chiefly  in  this  organ  and  now  chiefly  in  that,  whereby  entirely  dis- 
tinct types  of  disease  arise.  Hence  we  must  confine  ourselves  here  only  to  men- 
tioning briefly  the  most  important  sequelae.  For  the  most  part,  they  are  described 
separately  in  other  portions  of  this  work. 


AKTERIO- SCLEROSIS.  333 

In  the  heart  we  find  a  hypertrophy  of  the  left  ventricle  as  a  result  of  the 
increased  resistance  to  the  arterial  circulation.  This  is  often  apparent  during  life 
from  the  strength  of  the  apex -heat  and  its  displacement  to  the  left,  and  also  from 
the  extension  of  the  area  of  cardiac  dullness  to  the  left.  On  auscultation,  the 
increased  tension  in  the  aortic  system  is  made  manifest  by  the  strength  of  the 
aortic  second  sound.  The  examination  of  the  heart,  however,  is  often  rendered 
difficult  by  the  presence  of  pulmonary  emphysema.  On  the  other  hand,  we  some- 
times can  not  decide  how  far  a  manifest  hypertrophy  of  the  left  ventricle  is  due 
to  an  arterio-sclerosis,  and  not  to  other  co-existing  processes,  like  contracted  kidney. 
We  often  find  other  anatomical  changes  in  the  heart  besides  hypertrophy  of  the 
left  ventricle.  We  have  already  spoken  of  the  important  and  intei'esting  results 
of  atheroma  of  the  coronary  arteries,  the  formation  of  the  so-called  indurations  of 
myocarditis  in  the  heart  (see  page  308  et  seq.).  Sometimes,  from  an  invasion  of 
the  aortic  valves  by  the  atheromatous  process,  we  get  an  insufficiency,  or  much 
more  rarely  a  stenosis  of  the  aortic  orifice.  Finally,  we  may  also  mention  here 
that  atheroma,  especially  of  the  ascending  aorta  or  the  arcb,  is  the  commonest 
cause  of  the  formation  of  aneurism  of  the  aorta. 

YJ~e  have  already  described  the  character  of  the  peripheral  arteries.  The 
radial  pulse  is  hard  and  tense,  and  the  wave  is  either  quite  large,  or,  where  the 
tube  is  very  narrow,  small.  Since  the  wall  of  the  vessel  contracts  only  slowly, 
in  consequence  of  its  loss  of  elasticity,  the  radial  pulse  is  usually  sluggish— piJ.sn.s 
tardus.  This  condition  is  also  pronounced  in  the  sphygmographic  tracing,  which 
shows  a  slow  ascent,  and  a  still  slower  descent,  of  the  pulse-curve,  and  an  absence 
of  the  elevation  in  the  descending  limb  of  the  curve,  due  to  the  normal  elasticity. 
The  frequency  of  the  pulse  is  quite  different  in  different  cases;  it  is  often  rather 
slow  as  a  result  of  sclerosis  of  the  coronary  arteries  (q.  v.).  The  pulse  is  very 
often  irregular  as  a  consequence  of  changes  in  the  heart.  We  sometimes  find  an 
abnormal  delay  in  the  radial  pulse,  or  in  the  pulse  in  other  arteries,  in  compari- 
son with  the  heart-beat,  from  the  lessened  rapidity  of  transmission  of  the  pulse- 
wave. 

Besides  the  heart,  the  brain  is  the  chief  place  in  which  we  observe  definite 
results  of  arterial  sclerosis.  The  increased  tendency  to  rupture  which  the  athe- 
romatous vessel -walls  show,  and  the  co-existing  heightened  blood-pressure,  explain 
the  comparatively  frequent  occurrence  of  cerebral  haemorrhages.  Cerebral  haem- 
orrhages very  often  (always,  according  to  some  authors)  result  from  little  miliary 
aneurisms,  which  have  formed  in  the  atheromatous  cerebral  arteries.  Atheroma 
is  also  the  most  frequent  cause  for  the  formation  of  foci  of  softening  in  the  brain, 
since  the  arterial  changes  may  give  rise  to  a  closure  of  the  cerebral  arteries  both 
from  thrombosis  and  embolism.  We  will  later  describe  in  full  the  clinical  symp- 
toms of  the  affections  mentioned. 

In  the  kidneys,  too,  atrophic  processes  often  develop  from  the  diminution  of 
the  blood-supply  owing  to  the  narrowed  lumina  of  the  vessels,  and  they  lead  to 
a  special  form  of  contracted  kidney.  The  origin  of  the  granulated  "  senile  kid- 
ney "  is  in  large  part  due  to  atheroma  of  the  renal  arteries. 

Gangrene  of  the  extremities  may  arise  from  a  plugging  of  their  arteries  by 
thrombosis,  or  more  rarely  by  embolism.  The  so-called  "  senile  gangrene  "  almost 
always  depends  upon  arterio-sclerosis. 

From  all  this  it  follows  that  the  type  of  the  disease  may  he  very  different 
in  different  cases.  The  symptoms  in  the  vascular  apparatus  often  predominate 
over  all  others.  The  heart,  which  is  simply  hypertrophied,  or  has  undergone  in 
part  cicatricial  degeneration,  is  finally  paralyzed,  and  then  all  the  symptoms  of  a 
chronic  heart  disease  develop — dyspnoea,  oedema,  etc.  If  there  is  also  albuminuria, 
a  type  of  disease  is  produced  which  resembles  that  of  contracted  kidney.    In  other 


334  DISEASES  OF  THE  CIRCULATORY   ORGANS. 

cases,  however,  the  symptoms  in  the  brain  are  especially  manifest,  either  alone  or 
in  combination  with  the  other  symptoms  mentioned. 

We  must  remark,  however,  in  conclusion,  that  all  the  results  of  arterio- 
sclerosis mentioned  may  be  absent  for  a  long  time  or  altogether.  Many  people 
have  practically  no  symptoms  at  all  from  their  arterio-sclerosis,  and  reach  an 
advanced  age,  but  we  must  always  consider  the  possibility  of  the  sudden  occur- 
rence of  severe  symptoms,  and  make  our  prognosis  accordingly. 

There  is  no  question  of  a  special  treatment  of  arterio-sclerosis,  since  we  are  not 
in  a  position  to  affect  the  process  by  any  remedy.  In  the  individual  case  the 
treatment  is  directed  according  to  the  symptomatic  indications  resulting  from  the 
sequelae.  Prophylaxis,  by  avoiding  the  injurious  influences  mentioned  as  aetio- 
logical  factors,  is  more  important,  as  this  may  perhaps  prevent,  or  at  least  delay, 
the  development  of  the  process. 


CHAPTER  II. 
ANEURISM  OF  THE  THORACIC  AORTA. 

iEtiology  and  Pathological  Anatomy. — The  circumscribed  dilatation  of  an 
artery  is  termed  an  aneurism.  The  cause  of  its  formation  is  almost  always  to 
be  sought  in  a  primary  disease  of  the  vessel-wall,  which  weakens  its  resistance  to 
the  blood-pressure.  As  we  have  already  said  in  the  previous  chapter,  it  is  chiefly 
arterio-sclerosis  which  lies  at  the  foundation  of  aneurisms  in  many  cases.  The 
same  factors,  therefore,  which  favor  the  origin  of  arterio-sclerosis  belong  to  the 
aetiology  of  aneurisms.  It  is  also  repeatedly  asserted  that  severe  physical  exertion 
plays  a  part  in  the  aetiology  of  aneurism  of  the  aorta. 

[The  occurrence  of  aneurism  in  early  middle  rather  than  in  advanced  life  shows 
that  too  much  stress  can  be  laid  on  atheroma  as  a  cause.  That  sudden  strain  often 
plays  an  important  part  in  the  aetiology  can  scarcely  be  doubted,  though  the  cases 
in  which  a  perfectly  healthy  aorta  yields  locally  to  internal  pressure  must  be  very 
rare.  It  is  highly  probable  that  violent  exertion  tends  to  produce  changes  in  the 
walls  of  the  aorta.  The  far  greater  frequency  of  aneurism  in  the  male  sex  is 
notable.  Syphilis,  gout,  alcoholic  excess,  and  lead-poisoning  appear  to  be  factors 
in  some  cases.] 

The  size  of  aneurisms  of  the  aorta  varies  very  much,  of  course,  in  different 
cases.  They  most  frequently  are  about  the  size  of  an  apple  or  the  fist ;  but  in  rare 
cases  much  larger  aneurisms  are  observed.  According  to  their  shape  we  distin- 
guish the  more  diffuse  or  spindle-shaped  dilatations  from  the  saccular  aneurisms 
(anenrisma  diffusum  seu  cylindricum,  aneurisma  fusiforme,  et  aneurisma  sac- 
ciforme).  Intermediate  forms  and  combinations  of  the  different  forms  occur  in 
manifold  ways. 

As  we  should  expect  from  its  origin,  we  never  find  the  wall  of  the  aneurism 
formed  of  a  normal  vessel-wall.  The  intima  almost  always  shows  the  same 
changes  as  are  characteristic  of  arterio-sclerosis,  only  in  a  much  higher  degree. 
The  media,  too,  is  usually  changed,  and  its  muscular  structure  is  often  fatty- 
degenerated.  The  adventitia  is  usually  thickened  by  chronic  inflammatory  pro- 
cesses. The  media,  and  sometimes  the  intima,  are  in  many  cases  so  much  atro- 
phied that  the  wall  of  the  aneurism,  at  least  in  part,  is  formed  only  of  the  adven- 
titia. 

In  the  cavity  of  the  aneurism  the  blood  is  only  partly  fluid.  We  usually  find 
it  more  or  less  full  of  new  and  old  masses  of  thrombi.     The  oldest  thrombi,  which 


ANEURISM  OF  THE  THORACIC  AORTA.  335 

lie  upon  the  wall  of  the  aneurism,  are  firm,  yellowish,  adherent  to  the  wall,  ai,d 
sometimes  calcified.  At  other  points  the  thrombi  are  softened  and  broken  down. 
The  most  marked  coagulation  is  usually  found  in  the  saccular  aneurisms  with  a 
narrow  entrance,  because  in  this  form  of  aneurism  the  blood  is  almost  completely 
stagnant  in  the  aneurism  al  sac. 

Aneurisms  of  the  aorta  usually  have  their  seat  in  the  ascending  aorta,  or  in  the 
arch.  Aneurisms  of  the  descending  thoracic  and  of  the  abdominal  aorta  are  far 
more  rare.  The  following  description  refers  principally  to  aneurisms  at  the  be- 
ginning of  the  aorta.  The  other  aneurisms  will  receive  a  brief  separate  descrip- 
tion farther  on. 

Clinical  Symptoms. — The  subjective  sensations  of  the  patient,  relating  directly 
to  the  aneurism,  are  of  a  very  uncertain  nature,  and  are  often  entirely  absent.  In 
other  cases  there  is  pain  in  the  region  of  the  aneurism,  either  only  a  slight  sense  of 
pressure,  or  very  severe  and  subject  to  paroxysmal  increase.  Sometimes,  too,  the 
patient  feels  the  beating  and  pulsation  of  the  aneurism.  The  remaining  symp- 
toms of  aneurism  may  be  divided  into  two  groups.  The  first  group  embraces 
those  symptoms  which  are  directly  related  to  the  aneurism  itself,  and  most  promi- 
nent in  this  group  are  the  physical  signs.  The  second  group  of  symptoms  includes 
the  resultant  phenomena  which  the  aneurism  occasions  in  the  circulatory  appa- 
ratus and  by  pressure  upon  the  neighboring  parts. 

1.  Physical  Signs. — It  depends  entirely  upon  the  position  of  an  aneurism  of 
the  aorta  whether  it  causes  physical  signs  or  not.  Deep  aneurisms,  which  no- 
where approach  the  chest-wall,  may,  of  course,  be  quite  inaccessible  to  direct  ex- 
amination. 

Aneurisms  of  the  ascending  aorta,  however,  and  of  the  arch,  often  extend  so 
near  to  the  anterior  wall  of  the  chest  that  they  cause  an  abnormal  pulsation.  We 
feel  this  most  frequently  at  the  sternal  end  of  the  second  right  intercostal  space, 
or  over  the  upper  part  of  the  sternum.  The  pulsation  of  an  aneurism  of  the  arch 
of  the  aorta  may  sometimes  be  felt  in  the  root  of  the  neck.  It  ofteu  occurs  a  mo- 
ment later  than  the  systole  of  the  heart.  In  many  cases  the  pulsation  is  clearly 
double,  analogous  to  the  normal  dicrotism  of  the  pulse.  We  sometimes  feel  a  slight 
systolic  thrill  with  the  flat  of  the  hand.  In  the  rare  aneurism  of  the  descend 
ing  thoracic  aorta  the  pulsating  swelling  may  make  its  appearance  in  the  back, 
between  the  vertebral  column  and  the  left  scapula.  If  the  aneurism  has  reached  a 
certain  size,  the  pulsating  part  protrudes  as  a  tumor.  The  protrusion  is  either 
merely  slight,  or  in  many  cases  it  forms  a  large  prominent  swelling.  It  then  shows 
usually  a  marked  pulsation,  not  only  from  below  upward,  but  also  in  a  lateral 
direction,  which  is  of  diagnostic  significance.  In  large  aneurisms,  however,  the 
pulsation  sometimes  is  only  very  weak,  and  feels  obscure,  from  the  formation  of 
many  coagula. 

The  marked  prominence  of  large  aneurisms  is  possible  only  because  the  cover- 
ing parts,  not  only  the  muscles  and  skin,  but  also  the  cartilages  and  bones,  the 
ribs  and  sternum,  are  brought  to  a  gradual  atrophy  and  wasting  by  the  persistent 
pressure.  The  skin  over  large  aneurisms  gradually  becomes  thinner  and  thinner, 
until  finally  it  may  even  become  necrotic. 

In  many  cases  percussion  gives  a  positive  result,  since  the  resonance  over  the 
aneurism  is  necessarily  more  or  less  dull.  The  dullness  is  usually  evident  in  the 
upper  right  intercostal  spaces,  or  the  adjacent  parts  of  the  sternum.  Sometimes 
it  even  precedes  the  palpable  pulsation,  although  then  its  significance  is  usually 
still  very  uncertain.  In  rare  cases  of  aneurisms  of  the  ascending  aorta  and  of 
the  arch,  dullness  and  abnormal  pulsation  have  been  observed  to  the  left  of  the 
sternum. 

Auscultation  gives  varying  results.     In  some  cases  (probably  chiefly  when 


336  DISEASES  OF  THE  CIRCULATORY  ORGANS. 

many  coagula  form)  we  hear  nothing  at  all  over  the  aneurism.  In  other  cases  we 
hear  one  or  two  sounds,  which  are  usually  the  audible  heart-sounds  transmitted. 
Perhaps  a  systolic  sound  may  also  arise  from  vibration  of  the  wall  of  the  aneu- 
rism. In  other  cases,  we  hear  a  murmur  over  the  aneurism.  A  dull  and  usually 
not  very  loud  systolic  murmur  often  arises  from  the  formation  of  eddies  in  the 
aneurisrnal  sac.  If  we  also  hear  a  diastolic  murmur,  it  is  almost  always  due  to  a 
co-existing  insufficiency  of  the  semi-lunar  valves  of  the  aorta  (vide  supra). 

2.  Sequelce. — An  aneurism  of  the  aorta  by  itself  probably  never  causes  such  an 
increased  resistance  to  the  blood-current  as  to  give  rise  to  the  development  of 
a  hypertrophy  of  the  left  ventricle.  In  the  quite  frequent  cases  where  hyper- 
trophy of  the  left  side  of  the  heart  exists,  it  may  almost  always  be  referred  to  a 
co-existing  insufficiency  of  the  aortic  valves,  and  sometimes  to  very  extensive 
atheroma  of  the  arteries.  During  life  a  hypertrophy  of  the  heart  may  be  simu- 
lated, because  the  heart  is  pushed  to  the  left  by  the  aneurism. 

In  many  cases  the  signs  in  the  peripheral  arteries  are  important.  Marked 
inequality  of  the  pulse  in  symmetrical  arteries  is  often  an  especially  valuable 
diagnostic  sign.  Either  the  trunk  of  an  efferent  vessel  is  compressed  by  the 
aneurism,  or  the  lumen  of  the  exit  of  the  vessel  is  itself  involved  in  the  aneurism, 
and  hence  the  opening  of  the  vessel  is  distorted  or  contracted,  or  partly  stopped 
by  a  coagulum.  This  readily  explains  why,  in  aneurism  of  the  ascending  aorta, 
the  radial,  and  sometimes  the  carotid  pulse,  are  plainly  weaker  on  the  right  than 
on  the  left,  as  a  result  of  implication  of  the  trunk  of  the  innominate,  while  in 
aneurism  of  the  arch  or  of  the  beginning  of  the  descending  aorta  the  opposite 
condition  may  obtain.  Abnormal  differences,  too,  in  the  intensity  of  the  pulse  in 
the  upper  and  lower  halves  of  the  body  may  arise  under  some  circumstances. 

[W.  S.  Oliver  has  described  a  valuable  sign  to  which  he  gives  the  name  of 
"tracheal  tugging."  In  aneurism  of  the  transverse  arch  with  pressure  on  the 
left  primary  bronchus,  a  distinct  downward  pull,  synchronous  with  the  heart- 
beat, can  be  felt  by  the  thumb  and  forefinger  on  either  side  of  the  inferior  bor- 
der of  the  cricoid  cartilage,  when  the  patient,  in  the  erect  or  sitting  posture  and 
with  the  mouth  shut,  raises  the  chin  as  far  as  he  can.  The  late  R.  L.  MacDon- 
nell,  of  Montreal,  has  shown  that  non-aneurismal  tumors  in  this  region  are  not 
accompanied  by  this  sign,  and  that  pressure  on  the  trachea,  from  whatever  cause, 
does  not  produce  it.  It  may  be  the  sole  sign  of  aneurism  present,  and  may  then 
possess  the  double  diagnostic  value  of  indicating  both  the  nature  and  exact  seat  of 
the  disease.] 

A  marked  delay  of  the  pulse  in  the  arteries  arising  below  the  aneurism  is  a 
symptom  that  is  occasionally  seen.  Thus,  we  see  in  aneurism  of  the  arch  of  the 
aorta  that  the  left  radial  pulse  is  later  than  the  right,  and  that  in  aneurism  of  the 
descending  aorta  the  pulse  in  the  lower  extremities  is  later  than  the  radial  pulse. 

We  see  very  striking  signs  in  the  veins  if  the  large  venous  trunks  in  the  tho- 
rax, the  superior  vena  cava,  or  an  innominate  vein,  are  compressed  by  the  aneu- 
rism. The  veins  swell  in  the  neck,  in  the  upper  extremities,  or  upon  the  surface 
of  the  thorax,  according  to  the  seat  of  the  compression.  Local  oedema  may  also 
be  produced  in  this  way. 

The  respiratory  organs  are  exposed  to  the  pressure  of  aortic  aneurisms  in  many 
ways.  Compression  of  the  lungs  by  large  aneurisms  actually  contributes  toward 
increasing  the  dyspnoea  in  many  cases.  This  may  be  still  more  distressing  if  the 
trachea  be  compressed.  Of  the  two  main  bronchi,  the  left  bronchus,  which  lies 
beneath  the  arch  of  the  aorta,  is  more  apt  to  be  compressed.  This  produces  the 
symptoms  of  a  unilateral  bronchial  stenosis  (vide  supra).  The  comparatively  fre- 
quent compression  of  one  recurrent  nerve,  especially  the  left,  is  also  of  diagnostic 
importance,  as  it  results  in  paralysis  of  one  vocal  cord.     We  refer  the  occasional 


ANEURISM  OF  THE  THOEACIC  AORTA.  :;.;7 

paroxysms  of  severe  dyspnoea  to  a  compression  of  the  branches  of  the  vagus,  but 
no  post-mortem  lesion  has  been  found. 

Very  prominent  symptoms  sometimes  arise  from  compression  of  the  intercostal 
nerves  or  branches  of  the  brachial  plexus  by  the  aneurism.  As  a  result  of  this 
pressure,  extremely  severe  and  distressing  neuralgias  are  felt  in  the  nerve  terri- 
tories affected,  and  sometimes  we  see  motor  paresis  in  the  arm. 

Finally,  disturbances  of  deglutition  arise  in  many  cases  from  compression  of  the 
oesophagus.  If  this  be  falsely  interpreted,  it  may  lead  to  a  mischievous  use  of  the 
oesophageal  sound.  Cases  have  repeatedly  occurred  where  perforation  of  the 
aneurism  has  been  caused  by  passing  a  sound  into  the  oesophagus.  Hence  we 
must  always  remember  this  possibility  in  practice. 

Course  and  Termination  of  the  Disease.— Aneurisms  may  remain  latent  for  a 
long  time  without  causing  any  symptoms.  In  such  cases  a  sudden  perforation 
may  lead  to  a  speedy  and  unexpected  death. 

In  the  cases  which  have  shown  the  above  symptoms  to  a  greater  or  less  extent 
for  a  long  time,  and  often  for  years,  sudden  death  quite  frequently  results  from 
rupture  of  the  aneurismal  sac  and  perforation  into  a  neighboring  organ.  In 
perforation  into  the  pericardium  death  follows  almost  instantly  from  cessation  of 
the  heart's  action.  In  perforation  into  the  oesophagus  a  fatal  haemorrhage  occurs. 
In  perforation  of  the  aneurism  into  the  air-passages,  the  trachea  or  bronchi,  or 
into  one  pleural  cavity,  two  factors,  haemorrhage  and  suffocation,  unite  in  causing 
death.  In  aneurisms  which  gradually  erode  the  anterior  wall  of  the  chest,  the 
perforation  is  in  rare  cases  external ;  but  here  a  sudden,  immediately  fatal  haemor- 
rhage rarely  ensues ;  much  more  commonly  a  slowly  increasing  anaemia  develops 
as  a  result  of  repeated  slight  haemorrhages  which  may  sometimes  go  on  for  weeks. 
Death  then  is  due  to  the  gradually  increasing  weakness,  or  to  a  final  severe 
haemorrhage.  Perforation  of  an  aneurism  into  the  right  side  of  the  heart,  into 
the  pulmonary  arteries,  or  the  vena  cava,  is  a  rare  termination.  Here  death  does 
not  follow  at  once,  but  severe  general  disturbances  of  the  circulation,  like  dropsy, 
soon  arise.  In  many  of  these  rare  cases  peculiar  physical  signs  also  appear — a 
venous  pulse,  a  loud  systolic  murmur  over  the  point  of  perforation,  etc. 

If,  in  patients  with  aneurism  of  the  aorta,  death  does  not  ensue  from  a  sudden 
perforation,  the  general  type  of  the  disease  takes  a  form  similar  to  chronic  heart 
disease.  The  aneurism,  as  we  have  said,  is  often  also  combined  with  aortic  insuffi- 
ciency. The  left  ventricle  gradually  becomes  paralyzed,  and  the  well-known  dis- 
turbances of  compensation  set  in — increasing  dyspnoea,  oedema,  etc.  In  other 
cases  the  patient  gradually  becomes  duller  and  weaker  from  the  distressing  pain, 
the  sleeplessness,  and  the  other  symptoms,  and  dies  with  the  signs  of  increasing 
general  weakness. 

Recovery  from  aneurism  of  the  aorta  scarcely  ever  occurs. 

Diagnosis. — The  diagnosis  of  aneurism  of  the  aorta  can  in  many  cases  be  made 
with  great  ease  and  certainty,  but  in  other  cases  it  is  very  difficult  and  even 
impossible.  If  the  direct  physical  signs  are  plain,  especially  if  we  feel  an  abnor- 
mal pulsation,  we  shall  not  be  apt  to  commit  an  error;  but  the  diagnosis  presents 
great  difficulties  in  those  cases  where  the  aneurism  is  not  accessible  at  all,  or  acces- 
sible only  with  great  difficulty,  where  it  merely  causes  indefinite  symptoms,  pain 
in  the  chest,  occasional  oppression,  symptoms  of  pressure  on  neighboring  organs, 
etc.  A  very  stubborn  intercostal  neuralgia,  which  no  remedy  can  relieve,  may 
be  for  a  long  time  the  only  symptom,  often  misinterpreted,  of  a  latent  aneurism. 
The  disease  is  often  not  recognized,  however,  because  in  such  cases  we  do  not  gen- 
erally think  of  the  possibility  of  an  aneurism,  and  hence  we  neglect  a  careful 
examination  of  the  heart  and  the  arteries,  and  also  the  search  for  other  symptoms 
of  compression,  like  paralysis  of  the  vocal  cords;  but  sometimes,  even  with  the 
23 


338  DISEASES  OF  THE  CIRCULATORY  ORGANS. 

most  careful  examination,  the  diagnosis  can  not  amount  to  more  than  a  sus- 
picion. 

The  distinction  between  aneurism  and  other  tumors  in  and  about  the  thorax 
sometimes  presents  difficulties  in  diagnosis.  Mediastinal  sarcomata  and  abscesses. 
circumscribed  empyemas,  tumors  arising  from  the  sternum,  or  new  growths  in 
the  lungs  and  bronchial  glands,  may  all  give  rise  to  confusion.  We  can  scarcely 
lay  down  any  general  rules  for  diagnosis,  since  the  conditions  differ  in  almost 
every  case.  If  we  feel  a  swelling,  its  pulsation  is  the  symptom  which  points  most 
to  an  aneurism,  but  we  must  be  certain  that  the  pulsation  is  not  merely  trans- 
mitted, but  that  it  really  takes  place  in  all  directions  within  the  swelling  itself. 
We  must  also  consider  the  auscultatory  symptoms,  the  condition  of  the  heart  and 
the  arteries,  and  also  any  symptoms  of  compression ;  yet  in  such  cases  we  can  not 
always  make  a  definite  diagnosis. 

Treatment. — Many  attempts  have  been  made  to  bring  about  an  obliteration  of 
the  aneurism,  and  thus  a  recovery.  Although  the  methods  of  treatment  aiming 
at  this  have  obtained  decisive  results  in  the  aneurisms  of  peripheral  arteries, 
their  results  in  aneurism  of  the  aorta  are  still  of  a  very  doubtful  character ;  yet 
we  are  always  justified  in  any  given  case  in  trying  one  of  the  methods  recom- 
mended. 

Persistent  compression  by  a  pad  can  of  course  be  employed  only  in  those  cases 
where  the  aneurism  projects  at  one  part  of  the  chest-wall.  The  pressure,  how- 
ever, usually  causes  great  pain,  and  hence  is  ill  borne. 

Tying  the  carotid,  the  subclavian,  or  both  vessels,  has  also  been  repeatedly 
performed  in  aneurism  of  the  arch  of  the  aorta,  sometimes  with  apparent  success, 
but  offener  without  any  benefit. 

"  Acupuncture  "  of  the  aneurism  (Velpeau)  consists  in  inserting  a  needle  or  an 
iron  wire  into  the  aneurismal  sac  in  order  to  excite  coagulation  in  it.  The 
results  obtained  by  it  in  aneurism  of  the  aorta  are  not  very  encouraging. 

Better  results  are  reported  from  galvano-puncture.  Two  needles  inserted  into 
the  aneurism  are  connected  with  the  poles  of  a  galvanic  battery,  by  which  a  weak 
current  is  passed  through  the  aneurism.  Here  we  must  regard  the  chemical  and 
electrolytic  action  of  the  current  as  well  as  the  mechanical  action  of  the  needles. 

Injections  of  chemical  substances  into  the  aneurismal  sac,  in  order  to  produce 
coagulation,  are  dangerous,  since  the  coagula  caused  by  them  may  give  rise  to 
emboli.  Hence  we  have  abandoned  making  trial  of  liquor  ferri  sesquichloridi 
and  similar  substances.  We  can  better  recommend  injections  of  ergotine  into  the 
vicinity  of  the  sac,  two  to  five  grains  (grm.  O'l-O'S)  of  the  aqueous  extract  of  ergot 
dissolved  in  water  or  glycerine,  injected  every  day  or  two.  This  method  was  first 
employed  with  success  by  Langenbeck  in  peripheral  aneurisms.  Its  action  depends 
upon  a  contraction  of  the  smooth  muscles  in  the  wall  of  the  aneurism,  caused  by 
the  ergotine. 

We  can  expect  little  action  on  an  aneurism  from  the  use  of  internal  remedies, 
although  favorable  results  have  been  repeatedly  reported.  Acetate  of  lead,  five 
to  ten  grains  (grm.  0-3-0"6)  a  day,  and  iodide  of  potassium,  half  a. drachm  to  a 
drachm  (grm.  2-4)  a  day,  are  most  praised. 

The  symptomatic  treatment  of  aneurism,  which  tries  to  relieve  the  patient's 
sufferings,  and  the  dietetic  measures  prescribed,  follow  the  generally  customary 
principles.  In  a  rupture  of  the  aneurism  externally  we  try  to  avert  the  fatal 
catastrophe  by  absolute  rest,  ice-bags,  styptic  cotton,  etc.  Treatment  is  powerless 
against  internal  perforations. 

[Tufnell's  method,  so-called,  which  has  given  good  results  in  abdominal  and 
peripheral  aneurisms,  proves  sometimes  useful  in  palliating  the  symptoms  and 
lengthening  the  course  of  aortic  aneurism.     The  aim  of  this  method  is  to  diminish 


ANEURISMS  OF  THE  OTHER  VESSELS.  339 

the  force  and  rapidity  of  the  circulation,  and,  if  possible,  to  increase  the  fibrinous 
deposit.  It  is  carried  out  by  enforcing  absolute  rest  in  the  recumbent  position, 
and  by  limiting  the  amount  of  food,  especially  of  liquids.  About  ten  ounces  of 
solid  food  and  eight  of  liquid  are  allowed  daily,  divided  into  three  meals.J 


CHAPTER  III. 
ANEURISMS  OF  THE   OTHER  VESSELS. 

Aneurism  of  the  Abdominal  Aorta. — Its  favorite  seat  is  the  vicinity  of  the 
cceliac  axis.  In  many  cases  it  may  be  felt  through  the  abdominal  wall  as  a  pul- 
sating tumor,  over  which  a  systolic  sound  or  a  whirring  murmur  can  be  heard. 
The  possible  symptoms  of  compression  are  very  numerous.  The  stomach,  intestine, 
and  liver  (jaundice)  may  be  implicated.  Pressure  of  the  aneurism  upon  the  nerve 
trunks,  or  even  pressure  on  the  spinal  cord  after  gradual  erosion  of  the  vertebrae, 
with  consequent  severe  neuralgia,  paralysis,  etc.,  has  been  repeatedly  observed. 
Death  usually  ensues  from  rupture  of  the  aneurismal  sac  and  internal  haemorrhage. 

Aneurism  of  the  trunk  of  the  innominate  is  rare.  Its  symptoms  are  very 
much  like  those  of  an  aneurism  of  the  ai-ch  of  the  aorta.  If  we  feel  a  pulsating 
tumor,  it  is  usually  situated  somewhat  higher  up  than  the  aneurism  of  the  aorta, 
in  the  first  right  intercostal  space,  or  the  tumor  even  extends  into  the  supra- 
clavicular fossa.  In  rare  cases  aneurisms  of  the  subclavian  and  of  the  carotid  have 
been  observed.  We  have  ourselves  seen  an  aneurism  of  the  internal  carotid  the 
size  of  a  cherry  pressing  on  the  Gasserian  ganglion,  which  caused  an  extremely 
severe  trigeminal  neuralgia  lasting  for  years. 

Aneurism  of  the  pulmonary  artery  may  appear  as  a  pulsating  tumor  in  the 
second  left  intercostal  space.  It  is  usually  impossible  to  distinguish  it  with  cer- 
tainty from  an  aneurism  of  the  aorta. 

We  have  already  mentioned,  in  the  description  of  pulmonary  tuberculosis,  the 
great  importance  of  small  aneurisms  of  the  branches  of  the  pulmonary  artery  in 
pulmonary  cavities,  as  a  frequent  cause  of  haemorrhage. 

Aneurisms  of  the  arteries  of  the  brain,  which  are  relatively  most  frequent  in 
the  basilar  artery  and  the  artery  of  the  fissure  of  Sylvius  (the  middle  cerebral 
artery),  may  cause  severe  cerebral  and  bulbar  symptoms  (see  page  693).  As  has 
already  been  mentioned,  miliary  aneurisms  of  the  cerebral  arteries  play  an  impor- 
tant part  in  the  aetiology  of  cerebral  haemorrhage  (q.  v.). 

The  symptomatology  and  treatment  of  aneurisms  of  the  peripheral  arteries 
belong  to  the  domain  of  surgery. 


CHAPTER  IV. 

RUPTURE   OP  THE  AORTA. 

A  RUPTURE  of  a  previously  healthy  aorta,  with  fatal  haemorrhage,  after  violent 
traumatic  influences,  has  been  seen  only  in  a  very  few  cases.  In  the  majority  of 
the  very  rare  cases  of  rupture  of  the  aorta  we  have  to  do  with  a  vessel  that  is 
already  atheromatous.  In  some  cases  a  special  exciting  cause  is  present,  and  in 
others  it  is  absent.  We  once  saw  sudden  death  caused  by  rupture  of  the  ascend- 
ing aorta  in  a  young  man  about  twenty-five,  who  before  that  seemed  perfectly 


340  DISEASES  OF  THE  CIRCULATORY  ORGANS. 

healthy.  No  trace  of  atheroma  was  found ;  but  at  the  point  of  rupture  there  was 
a  slight  protrusion  and  a  decided  thinning  of  the  wall,  which  was  probably  con- 
genital. The  formation  of  a  so-called  dissecting  aneurism,  which  has  often  been 
seen  in  the  aorta,  is  of  anatomical  interest.  Here  only  the  intima  and  media  are 
torn.  The  blood  burrows  between  them  and  the  adventitia  or  between  the  layers 
of  the  media.  Most  of  the  cases  of  dissecting  aneurism  of  the  aorta  also  result, 
like  rupture  of  the  aorta,  in  sudden  death.  In  many  cases  death  results  from  the 
secondary  perforation  of  the  aneurism  into  the  pericardium.  On  the  other  hand,  a 
sort  of  recovery  from  dissecting  aneurism  may  occur.  A  secondary  perforation 
takes  place  into  another  part  of  the  aorta  itself  (Boström).  Cases  of  this  sort  were 
formerly  more  than  once  mistaken  for  double  aorta.  If  the  capsule  containing  the 
blood  is  preserved  for  a  considerable  length  of  time,  the  symptoms  may  assume  the 
character  presented  in  ordinary  aortic  aneurism. 


CHAPTER  V. 
NARROWING   OF   THE   AORTA. 

Congenital  narrowness  of  the  aorta  and  its  branches  is  a  condition  to  which 
Rokitansky  first,  and  later  Virchow,  have  directed  attention.  "We  find  this 
anomaly  especially  in  those,  mostly  women,  who  during  life  have  shown  the 
signs  of  persistent  chlorosis.  Sometimes  such  persons  are  backwai'd  in  their 
whole  development;  they  retain  a  puerile  habit,  and  show  a  defective  develop- 
ment of  the  genitals.  They  often  suffer  from  palpitation,  faintness,  and  a  tend- 
ency to  haemorrhages.  In  many  cases  the  heart  is  also  small,  but  in  others  it 
is  dilated  and  hypertrophied.  Valvular  disease  of  the  heart  has  been  repeatedly 
found  combined  with  general  narrowness  of  the  arterial  system.  During  life 
this  anomaly  of  the  vascular  system  may  sometimes  be  suspected,  but  it  can  never 
be  recognized  with  certainty. 

Narrowing  of  the  aorta  at  the  pt>int  of  insertion  of  the  ductus  arteriosus  is  a 
lesion  observed  in  rare  cases,  whose  origin  probably  always  falls  in  the  period 
directly  after  birth,  and  is  associated  with  obliteration  of  the  foetal  ductus  arteriosus. 
Other  congenital  anomalies  of  the  heart  are  usually  present  at  the  same  time.  If 
the  narrowing  of  the  aorta  is  not  very  marked,  it  may  be  properly  equalized  by 
a  secondary  hypertrophy  of  the  left  ventricle  and  the  development  of  a  collateral 
circulation.  The  latter  is  brought  about  by  dilatation  of  the  anastomoses  between 
the  first  intercostal  artery,  the  dorsalis  scapulae,  the  subscapular  is,  and  the  trans- 
versalis  colli  on  one  side,  and  the  lower  intercostal  arteries,  which  come  off  from 
the  descending  aorta  below  the  narrowing,  on  the  other.  Anastomoses  are  also 
formed  between  the  mammary  and  the  superior  epigastric  on  one  side  and  the 
lumbar  and  femoral  arteries  on  the  other.  During  life  the  dilated  arteries  are 
prominent,  in  part  abnormally  distoi'ted,  and  perceptibly  pulsating,  especially  the 
dorsales  scapulas,  the  subscapulars,  the  mammaries,  and  the  epigastrics.  In  some 
cases  a  systolic  murmur  has  been  heard  over  some  of  these  vessels.  The  pulse 
in  the  arteries  of  the  lower  extremities,  the  femoral  and  popliteal,  is  very  weak 
and  scarcely  perceptible. 

In  many  cases  the  collateral  circulation  is  so  complete  that  the  person  affected 
may  feel  no  subjective  disturbance  at  all,  and  may  attain  an  advanced  age,  but  in 
other  cases  disturbances  of  the  circulation  appear  sooner  or  later,  and  the  patient 
finally  succumbs  to  dropsy.  Sudden  death  from  rupture  of  the  heart  or  of  the 
aorta  has  also  been  observed. 


DISEASES   OF   THE   DIGESTIVE   ORGANS. 


SECTION   I. 

Diseases  of  the  Mouth,  Tongue,  and  Salivary  Glands. 

CHAPTER  I. 

STOMATITIS. 

{Inflammation  of  the  Mouth.) 

JEtiology. — Inflammation  of  the  buccal  mucous  membrane  is  not  infrequently 
the  direct  result  of  mechanical  or  chemical  causes.  As  mechanical  causes  we  may 
mention  particularly  the  sharp  edges  of  broken  or  carious  teeth.  Chemical  irri- 
tation may  come  from  highly  spiced  food,  or  from  tobacco-chewing  or  excessive 
smoking.  Very  intense  inflammation  is  caused  by  acids,  alkalies,  and  the  like, 
attacking  the  mucous  membrane.  Mercurial  stomatitis  is  also  of  practical  impor- 
tance. It  is  caused  by  mercurial  poisoning,  or  not  infrequently  by  the  therapeutic 
employment  of  the  drug.  The  stomatitis  attendant  upon  the  cutting  of  teeth  in 
children  will  be  discussed  below. 

In  many  instances  stomatitis  comes  from  a  direct  propagation  of  inflammation 
from  neighboring  parts.  It  thus  forms  a  frequent  complication  of  pharyngeal 
catarrh,  and  less  often  of  rhinitis. 

Infection  plays  an  important  part  in  the  aetiology  of  stomatitis.  The  local  in- 
flammation may  be  merely  part  of  a  constitutional  infectious  disease,  as  in  measles, 
variola,  and  syphilis.  Stomatitis  is  still  more  frequently  a  complication  of  some 
severe  and  protracted  illness,  where  the  mouth  is  not  properly  attended  to  and 
cleansed.  The  bits  of  food  and  the  mucus  quickly  begin  to  decay.  Great  num- 
bers of  fungi  and  bacteria  invade  the  buccal  cavity,  and  excite  inflammation  in  its 
mucous  membrane. 

Scorbutic  stomatitis  will  be  considered  under  scurvy. 

Clinical  History. — The  usual  symptoms  of  an  inflammation  of  mucous  mem- 
brane— namely,  redness,  swelling,  and  increased  secretion — are  exhibited  in  stoma- 
titis. The  redness  is  usually  most  intense  on  the  inside  of  the  cheeks  and  on  the 
gums.  Indeed,  we  have  tbe  special  name — gingivitis — for  inflammation  of  the 
latter.  The  swelling  is  best  shown  by  the  indentations  made  by  the  teeth  in  the 
cheeks  and  the  edges  of  the  tongue.  The  tongue  and  gums  are  smeared  with 
mucus.  There  is  often  considerable  salivation.  If  the  inflammation  is  more 
active,  we  find  a  purulent  coating  on  a  greater  or  less  portion  of  the  membrane. 
The  tongue  is  almost  always  thickly  coated.  If  we  scrape  off  a  little  of  the  coat- 
ing and  put  it  under  the  microscope,  we  find  a  great  abundance  of  pavement  epi- 
thelium, in  part  fatty-degenerated,  pus,  micrococci,  bacilli,  occasionally  mold- 
fungi,  and  remains  of  food.  White  spots  made  up  of  epithelium  may  also  be 
formed  elsewhere  than  on  the  tongue.  Here  and  there  little  vesicles  appear  which 
burst  and  leave  superficial  ulcers. 

(341) 


342  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

The  local  discomfort  of  severe  stomatitis  is  by  no  means  trifling.  There  is 
burning  pain,  which  interferes  with  taking  food,  and  usually  the  processes  of 
decomposition  occasion  a  constant  bitter  or  disgusting  taste  in  the  mouth,  as  well 
as  a  foul  and  offensive  breath. 

The  duration  of  the  disease  depends  on  the  nature  of  the  immediate  cause  or 
the  character  of  the  primary  disorder.  Usually  a  stomatitis  which  gets  well  in 
one  or  two  weeks  is  called  acute,  and  a  more  tedious  attack,  chronic.  The  chronic 
form  is  seen  in  topers  and  inveterate  smokers.  It  may  last  for  years,  with  the 
symptoms  described  above,  only  milder.     (For  lingual  psoriasis,  vide  infra). 

Treatment. — If  the  inflammation  is  considerable,  the  diet  must  be  liquid. 
Sometimes  cold  drinks  are  most  agreeable,  sometimes  lukewarm.  Often  the  pain 
is  relieved  by  taking  from  time  to  time  a  sip  of  iced  water  or  a  bit  of  ice ;  but  it 
may  happen  that  the  patient  will  prefer  to  rinse  the  mouth  with  lukewarm  water. 
The  important  indication,  to  keep  the  mouth  as  clean  and  pure  as  possible,  is  best 
met  by  having  the  mouth  frequently  rinsed  out  with  a  one-  or  two-per-cent.  solu- 
tion of  carbolic  acid,  a  two-per-cent.  solution  of  chlorate  of  potash,  or  one  or  two 
teaspoonfuls  of  a  one-per-cent.  solution  of  permanganate  of  potash  to  a  glass  of 
water.  In  children  who  can  not  do  this,  the  mouth  is  to  be  carefully  washed  or 
sprayed.  If  the  gums  are  spongy,  they  should  be  painted  with  a  mixture  con 
taining  equal  parts  of  tincture  of  myrrh  and  tincture  of  rhatany.  If  there  are 
superficial  ulcers  scattered  about,  it  is  sometimes  an  excellent  plan  to  touch  them 
lightly  with  lunar  caustic,  to  hasten  their  healing. 

Chronic  stomatitis  is  often  very  obstinate,  resisting  all  sorts  of  treatment  for  a 
long  time.  The  first  thing  is  to  remove  any  such  injurious  agencies  as  tobacco 
or  bad  teeth.  It  is  recommended  to  swab  out  the  mouth  with  a  solution  of  cor- 
rosive sublimate  (1  to  5,000)  or  of  lunar  caustic  (1  to  30-50).  A  well-known 
household  prescription  is  to  chew  bits  of  rhubarb. 


CHAPTER  II. 

ULCERATIVE   STOMATITIS. 

(Stomacace.) 

iEtiology.— By  ulcerative  stomatitis  is  meant  a  severe  disease  of  the  buccal 
mucous  membrane,  with  superficial  necrosis  and  the  consequent  formation  of 
ulcers.  The  abnormal  processes  are  not  in  all  cases  identical,  and  their  cause  may 
vary.  Still  it  is  probable  that  infection  is  the  important  factor,  at  least  in  most 
cases.  The  disease  has  repeatedly  been  epidemic,  chiefly  among  soldiers  in  bar- 
racks or  on  a  campaign,  and  among  the  inmates  of  jails.  It  also  occurs  in  chil- 
dren, principally  at  the  time  of  the  second  dentition ;  and  in  such  cases,  also,  the 
evidence  of  contagion  and  of  endemic  influences  is  often  very  striking.  Mercurial 
stomatitis,  if  severe,  always  assumes  the  form  of  ulcerative  stomatitis.  (For  the 
scorbutic  form,  see  page  959.) 

Symptoms. — The  disease  usually  attacks  the  gums  of  the  lower  jaw  first,  gradu- 
ally spreading  thence  to  neighboring  portions  of  the  lips  and  cheeks.  The 
tongue  and  palate  are  generally  not  very  much  affected,  though  often  the  seat  of 
a  simple  catarrhal  inflammation. 

Inspection  shows  that  the  mucous  membrane  in  the  places  mentioned  has  a 
thick,  soft,  purulent  coating.  The  gums  are  swollen,  spongy,  and  red,  and  bleed 
easily.  In  severe  cases  the  incisors  become  loose,  and  may  fall  out.  There  is 
usually  profuse  salivation.     The  lymph-glands  at  the  angle  of  the  lower  jaw  and 


APHTHÖS.  343 

on  the  chin  are  generally  swollen.  The  breath  is  very  offensive,  poisoning  the 
air  of  the  whole  room. 

The  local  discomfort  of  the  patient  is  the  same  as  in  simple  stomatitis,  only 
much  worse.  It  is  very  difficult  to  take  nourishment.  In  many  cases  there  are 
marked  constitutional  symptoms.  The  patient  feels  very  weak  and  languid. 
There  may  be  moderate  elevations  of  temperature,  particularly  in  children.  Now 
and  then  severe  symptoms  of  constitutional  sepsis  have  followed  the  disease. 

The  course  of  ulcerative  stomatitis  is  favorable  in  the  great  majority  of  cases. 
With  good  treatment  and  nursing,  the  ulcers  gradually  clean  up,  and  at  the  end 
of  one  or  two  weeks  recovery  is  complete.  Exceptionally,  the  disease  may  be 
more  chronic.  The  most  frequent  way  in  which  recovery  is  delayed  is  that  the 
disease  extends  to  the  periosteum  of  the  lower  jaw,  causing  necrosis  of  small 
portions  of  the  bone,  which  must  be  expelled  before  the  patient  gets  well. 

The  treatment  does  not  differ  essentially  from  that  of  the  milder  forms  of 
stomatitis.  The  mouth  must  be  still  more  carefully  and  more  frequently  cleansed 
and  disinfected.  A  solution  of  potassic  chlorate  (1  to  30)  is  the  favorite  mouth- 
wash. Some  authors  strongly  recommend  the  simultaneous  internal  administra- 
tion of  this  remedy;  but  we  must  employ  it  cautiously  in  children,  as  it  has 
repeatedly  caused  poisoning.  For  children  two  or  three  years  old  we  ought  not 
to  give  over  fifteen  to  thirty  grains  (grm.  1-2)  in  a  day. 

As  to  prophylaxis,  we  should  mention  that  all  patients  who  are  using  mercury 
should  employ  a  gargle  of  potassic  chlorate  faithfully  from  the  beginning  of 
treatment,  in  order  to  prevent  the  occurrence  of  mercurial  stomatitis.  If  saliva- 
tion occurs,  the  mercury  must  be  stopped. 


CHAPTER  III. 

APHTHiE. 

(Aphthous  Stomatitis.) 

Aphthae  is  a  name  given  by  physicians  to  several  entirely  distinct  diseases. 
Many  doctors  call  every  disease  aphthae  in  which  there  are  white  spots  upon  the 
buccal  mucous  membrane.  It  is  thus  frequently  confounded  with  thrush.  Ger- 
man mothers  often  apply  the  same  name  (Schwämmchen,  or  fungus)  indifferently 
to  thrush  and  to  aphtha?. 

There  is  a  special  form,  known  as  Bednar's  aphthae.  In  new-born  children 
white  patches  are  not  infrequently  found  lying  symmetrically  on  both  halves  of 
the  hard  palate  near  the  alveolar  processes,  and  persisting  till  about  the  third 
month.  These  plaques  are  not  syphilitic,  although  often  thought  to  be.  They 
are  probably  merely  due  to  the  tongue  pressing  upon  the  thin  mucous  membrane 
during  nursing.  Generally  they  do  no  harm ;  but  in  marantic,  ill-cared-f or  chil- 
dren, they  may  develop  into  quite  deep  ulcers.  In  that  case,  repeated  cauterization 
with  a  five-per-cent.  solution  of  argentic  nitrate  is  required. 

The  genuine  aphthae  are  roundish  spots  upon  the  mucous  membrane,  grayish 
white,  and  of  small  size,  unless  made  larger  by  the  confluence  of  several  into  one 
another.  They  usually  have  a  narrow,  red  areola.  They  are  most  numerous  on 
the  edges  and  dorsum  of  the  tongue  and  on  the  fraenum,  but  they  also  occur 
on  the  lips  and  cheeks.  The  attempt  to  remove  the  white  spot  with  forceps 
never  succeeds,  but  does  cause  bleeding.  In  addition  to  the  genuine  aphthae  there 
are  almost  always  the  signs  of  a  common  stomatitis,  which  may  be  mild  or  severe. 
The  white  spots  are  in  part  due  to  a  thickening  and  opacity  of  the  epithelium,  and 


344  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

in  part  are  said  to  be  caused  by  tbe  formation  of  a  fibrinous  exudation,  which 
penetrates  tbe  most  superficial  layers  of  the  mucous  membrane. 

The  disease  occurs  chiefly  in  children,  and  at  the  time  of  the  first  dentition. 
The  child  is  usually  restless,  often  somewhat  feverish,  and  evidently  suffers  pain 
when  nursing.  Generally  there  is  considerable  salivation.  The  lymph-glands 
may  be  a  little  enlarged.  Herpetiform  vesicles  may  appear  on  the  lips.  The  dis- 
ease is  not  rare  in  adults.  Many  individuals  seem  especially  liable  to  it,  and  very 
frequently  have  little,  white,  and  often  very  painful  spots  here  and  there  on  the 
tongue  or  elsewhere  in  the  mouth.  These  have  a  tendency  to  develop  into  super- 
ficial ulcers.  They  may  prove  very  troublesome,  from  their  frequent  recurrence 
and  the  hindrance  they  cause  to  speaking  and  mastication. 

The  prognosis,  except  as  just  described,  is  always  favorable.  There  is  usually 
complete  recovery  in  a  week  or  two.  The  treatment  of  children  consists  in  care- 
fully washing  out  the  mouth  with  cold  water,  and  in  administering  potassic  chlo- 
rate. Of  a  mixture  consisting  of  three  parts  of  potassic  chlorate,  twenty  of  syrup, 
and  a  hundred  of  water,  we  may  give  a  dessertspoonful  every  two  hours.  If  the 
spots  do  not  disappear,  we  can  paint  them  with  a  five-per-cent.  solution  of  sulphate 
of  zinc,  or  a  solution  of  borax  (1  to  30).  If  come  of  the  places  are  especially  pain- 
ful, particularly  in  adults,  we  may  touch  them  with  lunar  caustic,  when  they  usu- 
ally are  soon  cured.  In  the  constantly  recurring  form,  treatment  sometimes 
proves  almost  unavailing.  Local  cauterization,  which  unfortunately  in  such 
cases  is  often  of  no  benefit  whatever,  and  the  use  of  a  mouth-wash  containing 
chlorate  of  potash  or  carbolic  acid  in  weak  solution,  may  be  employed,  and,  fur- 
thermore, some  physicians  strongly  recommend  the  internal  administration  of 
iodide  of  potash.     Calomel  also  appears  sometimes  to  have  a  beneficial  influence. 

In  conclusion,  as  to  aetiology,  infection  is  a  not  unlikely  cause,  if  we  consider 
that  small  epidemics  or  endemics  have  repeatedly  occurred.  Lately  attention  has 
been  called  to  the  possibility  that  the  milk  of  cows  suffering  from  hoof-and- 
mouth  disease  may  be  a  source  of  infection.  That  this  may  happen  seems 
indubitable;  but  how  frequently  it  occurs,  future  observations  must  determine. 
The  cause  of  the  above-described  chronic  form  is  unknown. 


CHAPTER  IV. 

THRUSH. 

{Soor.     Muguet.) 

iEtiology. — Weak  and  artificially  nourished  children  are  particularly  liable  to 
this  disease ;  but  it  also  attacks  adults  who  are  suffering  from  phthisis,  carcinoma, 
and  severe  typhoid  or  typhus  fever.  In  it,  grayish-white  deposits  are  developed 
upon  the  buccal  and  pharyngeal  mucous  membrane.  The  microscope  shows  these 
collections  to  be  fungi;  there  are  a  multitude  of  oval  spores,  or  conidia,  and  a 
tangled  mass  of  long  mycelium  threads.  Until  lately  the  fungus  of  thrush  was 
called  oiclium  albicans,  and  was  held  to  be  identical  with  the  o'idium  lactis  found 
in  sour  milk.  A  more  recent  investigation  of  Grawitz  has  rendered  it  very  prob- 
able, however,  that  the  thrush  fungus  is  a  budding  fungus,  and  is  closely  related 
to  the  comb  fungi  (mycoderma  vini*  or  saccharomyces  albicans,  according  to 
Rees).     It  seems  to  be  a  sort  of  transition  form  between  the  budding  fungi  and 

*  Mycoderma  vini  is  a  fungus  which  is  found  associated  with  the  formation  of  acetic  acid  out  of 
alcohol,  that  is,  when  alcoholic  beverages  "  sour." 


GLOSSITIS.  345 

the  thread  fungi,  inasmuch  as  it  appears  both  in  a  form  resembling  yeast  and 
also  in  the  form  of  long  thread-like  mycelia.  At  any  rate,  the  thrush  fungus 
is  widely  distributed,  for  the  development  of  thrush  upon  the  mucous  membrane 
of  the  mouth  and  throat  is  a  frequent  phenomenon.  Nursing-bottles  and  the 
nipples  used  upon  them  are  probably  not  infrequently  the  agents  by  which  the 
disease  is  conveyed. 

Symptoms. — The  mucous  membrane  of  the  tongue,  cheeks,  and  soft  palate  is 
usually  somewhat  red  and  swollen.  Upon  it  we  see  at  first  small  white  spots, 
which  may  gradually  spread.  Microscopic  investigations  have  shown  that  the 
fungus  develops  first  in  the  middle  layers  of  the  epithelium.  From  this  starting- 
point  it  grows  not  only  upward,  but  also  downward  into  the  mucous  membrane. 
If  the  growth  is  abundant,  it  is  easy  to  scrape  off  the  upper  layers,  and  make  a 
diagnosis  by  aid  of  the  microscope.  In  exaggerated  cases  the  growth  may  even 
extend  from  the  pharynx  into  the  upper  part  of  the  oesophagus  and  the  entrance 
of  the  larynx.  But  we  never  find  thrush  in  the  larynx  itself,  or  the  nostrils,  or 
the  stomach — briefly,  in  no  place  where  there  is  cylindrical  epithelium. 

As  a  rule,  thrush  is  accompanied  by  a  more  or  less  severe  stomatitis.  The  fluids 
of  the  mouth  have  an  acid  reaction.  Nursing,  or  chewing,  and  swallowing,  are 
painful.  Still,  it  is  a  question  whether  the  stomatitis  is  due  to  the  fungus,  or 
whether  it  prepares  the  territory  for  the  fungus  to  settle  in.  Nursing  infants,  who 
suffer  from  thrush,  often  have  diarrhoea  or  marasmus  at  the  same  time,  which 
latter  affections  are  more  probably  the  cause  than  the  result  of  the  thrush.  If 
vigorous  and  healthy  sucklings  are  attacked  by  thrush,  the  disease  is  usually 
quite  harmless,  quickly  vanishing  if  proper  cleanliness  is  maintained.  In  sickly 
children,  particularly  if  bottle-fed,  the  appearance  of  the  disease  is  very  ominous. 
In  adults,  thrush  is  seldom  seen  except  when  there  is  great  general  prostration ; 
and  it  is  therefore,  to  a  certain  extent,  an  unfavorable  symptom. 

Treatment. — To  prevent  the  development  of  thrush  in  children,  the  mouth 
must,  if  possible,  be  wiped  out,  each  time  they  drink,  with  a  cloth  wet  in  cold  water ; 
and  if  adults  are  very  ill,  they  require  eqtial  attention  in  this  regard.  As  soon  as 
we  see  the  first  traces  of  the  disease,  we  should  touch  the  parts  attacked  with  a 
brush  wet  in  aqueous  solution  of  borax  (1  to  30)  or  of  sodic  carbonate  (1  to  20). 
Honey  should  not  be  added  to  the  borax  solution,  as  is  often  unwisely  done.  If 
the  thrush  has  once  got  a  vigorous  start  in  the  mouth  of  marantic  children,  or  of 
adults  suffering  from  an  incurable  disease,  it  must  be  confessed  that  we  often  fail 
to  check  its  growth. 


CHAPTEE  V. 
GLOSSITIS. 


(Parenchymatous  Inflammation  of  the  Tongue.) 

Inflammation  of  the  true  lingual  parenchyma  is  rare,  although  the  tongue's 
mucous  surface  is  frequently  involved  in  the  various  diseases  of  the  mouth. 

1.  Acute  parenchymatous  glossitis  is  the  name  given  to  an  inflammatory  infil- 
tration of  the  whole  or  a  part  of  the  tongue,  usually  ending  in  abscess.  The  most 
frequent  cause  is  the  sting  of  a  bee  or  wasp,  or  it  may  follow  burns  or  severe  cau- 
terization. In  the  rare  instances  where  it  is  apparently  spontaneous,  it  is  probable 
that  some  little  wound  has  afforded  ingress  to  the  inflammatory  poison. 

The  symptoms  of  acute  glossitis  are  very  violent  in  the  severer  cases.  The 
tongue  is  enormously  swollen,  so  as  sometimes  to  protrude  from  the  mouth.  It 
has  a  thick,  soft,  purulent  coating,  and  often  presents  excoriations  and  ulcerations. 


346  DISEASES  OE  THE  DIGESTIVE  ORGANS. 

The  subjective  symptoms  are  very  disagreeable.  The  patient  has  violent  pain. 
Talking  and  eating  are  almost  impossible.  There  is  usually  catarrhal  inflamma- 
tion of  the  rest  of  the  mouth.  The  cervical  lymphatic  glands  are  swollen.  The 
salivation  is  profuse  and  very  annoying.  In  many  cases  the  tongue  swells  so 
much  as  to  cause  dyspnoea  and  more  or  less  suffocation.     There  is  usually  fever. 

Treatment  consists  in  the  employment  of  ice,  which  the  patient  should  keep 
constantly  in  his  mouth,  if  possible.  Very  great  relief  follows  deep  scarification 
done  in  a  few  places  where  the  swelling  is  greatest.  As  soon  as  fluctuation  is  ob- 
tained, we  must  give  exit  to  the  pus.  This  is  usually  followed  by  a  rapid  abate- 
ment of  the  discomfort,  and  complete  recovery.  It  is  the  exception  that  the 
increasing  dyspnoea  necessitates  tracheotomy. 

2.  Glossitis  Dissecans. — This  is  a  chronic  disease,  of  rare  occurrence  and 
unknown  aetiology.  It  causes  the  gradual  development  upon  the  surface  of  the 
tongue  of  a  number  of  deep  fissures  and  indentations,  giving  the  organ  an  uneven 
and  ragged  look.  The  pain  is  due  to  the  frequent  presence  of  excoriations  and 
ulcers  in  these  fissures. 

The  trouble  is  not  intrinsically  dangerous,  nor  does  it  need  special  treatment. 
We  should  prescribe  cleanliness  and  the  use  of  some  disinfectant  mouth-wash. 
Ulcers,  if  present,  must  be  touched  with  lunar  caustic. 

3.  Lingual  Psoriasis.  Leucoplacia.  {Tylosis;  Ichthyosis  linguae,  et  oris.) — This, 
again,  is  a  superficial  disease,  the  aetiology  of  which  is  unknown.  It  consists  in 
localized  hyperplasiae  of  the  epithelium  of  the  tongue,  sometimes  conjoined  with 
similar  spots  upon  the  cheeks  and  lips.  Usually  the  tongue  gets  to  look  like  a 
map  ("  lingua  geographica  ").  The  disease  generally  lasts  years,  but  causes  dis- 
comfort only  when  extraordinarily  severe.  Still,  it  may  cause  a  hypochondriac 
endless  anxiety,  especially  if  he  takes  it  to  be  syphilitic. 

This  last  statement  applies  still  better  to  a  peculiar  disease  allied  to  psoriasis. 
It  is  called  leucoplacia,  and  affects  the  mucous  membrane  of  the  tongue  and  mouth. 
Usually  it  causes  the  appearance,  on  the  lateral  borders  of  the  tongue,  of  dull- 
whitish  spots,  which  have  the  look  of  scars,  and  are  generally  somewhat  notched. 
As  a  rule,  the  cheeks  display  at  the  same  time  similar  white  spots,  which  are  evi- 
dently due  merely  to  thickening  of  the  epithelium.  Certain  spots  may  disappear, 
but  are  sure  to  be  replaced  by  others,  so  that,  as  far  as  has  yet  been  observed,  the 
disease  must  be  regarded  as  incurable.  Still,  it  is  not  of  great  importance,  for  in 
many  cases  the  local  discomfort  is  very  slight.  If  the  indentations  along  the 
sides  of  the  tongue  become  cracked  or  ulcerated,  then  there  may  be  great  pain. 
The  cause  of  leucoplacia  is  not  yet  known.  It  certainly  is  not  syphilitic,  although 
the  disease  is  said  to  be  especially  prone  to  attack  those  who  have  at  some  former 
time  been  infected  with  syphilis.  This  does  not  apply  to  all  cases.  Nor  is  exces- 
sive smoking  connected  with  the  disease;  we  have  seen  leucoplacia  in  women. 
Treatment  is,  as  we  have  said,  usually  unsuccessful.  Still,  thorough  cleanliness 
and  good  care  of  the  mouth  may  avert  any  great  discomfort.  We  may  try  the 
effect  of  painting  the  spots  with  a  five-per-cent.  solution  of  chromic  acid.  The 
chief  importance  of  knowing  the  disease  is  to  prevent  our  confounding  it  with 
syphilitic  affections,  and  thus  to  save  the  patient  groundless  apprehension  and 
needless  mercurialization. 


NOMA.  347 


CHAPTER  VI. 

NOMA. 

( Water-cancer.     Cancrum  oris.) 

Noma  is  a  gangrene  of  the  cheek,  apparently  of  spontaneous  origin,  and  attack- 
ing chiefly  feeble  and  sickly  children.  The  disease  is  rare.  It  may  be  primary, 
but  is  usually  a  sequel  of  severe  diseases,  like  measles,  scarlet  fever,  typhus  and 
typhoid  fevers,  and  pneumonia.  Now  and  then  it  has  been  observed  in  adults. 
A  priori,  it  is  extremely  probable  that  noma  is  due  to  some  parasitic  micro-organ- 
ism ;  but  the  matter  has  not  yet  been  minutely  investigated.  It  deserves  mention 
that  noma  is  said  to  occur  with  much  greater  relative  frequency  in  moist  regions 
along  the  coast — for  example,  in  Holland — than  among  us  in  Germany. 

The  disease  begins,  without  any  evident  occasion,  in  an  insignificant  spot  of 
gangrene  on  the  inner  surface  of  the  cheek — that  is,  in  the  mucous  membrane.  It 
is  usually  situated  near  the  corner  of  the  mouth.  Externally,  the  parts  are  soon 
swollen  by  collateral  oedema,  and  the  whole  cheek  gradually  becomes  hard  and 
infiltrated.  At  first,  all  we  see  upon  the  mucous  membrane  is  a  dirty-greenish 
spot  not  much  larger  than  a  silver  dime,  but  soon  the  whole  cheek  and  the 
neighboring  parts  are  one  mass  of  gangrene.  Bits  of  dead  tissue  come  away,  and 
foul-smelling  ichor  flows  continuously  into  the  mouth.  The  collateral  oedema 
may  finally  pervade  that  entire  half  of  the  face.  The  neighboring  lymph-glands 
are  always  greatly  swollen. 

This  condition  is  almost  always  accompanied  by  fever,  often  reaching  or  ex- 
ceeding 104°  (40°  C).  The  general  health  may  indeed  for  a  time  be  astonish- 
ingly little  affected ;  but  gradually  prostration  comes  on,  or  even  general  sepsis 
develops,  with  fever,  stupor,  and  delirium.  Frequently  lobular  pneumonia,  which 
may  have  a  gangrenous  character,  is  produced  by  the  inhalation  of  sloughing  bits 
of  tissue;  and  often  the  ichor,  being  swallowed,  excites  violent  and  offensive 
diarrhoea.  The  local  discomfort  is  not  really  very  considerable  in  most  cases, 
compared  to  the  severity  of  the  disease.  There  may  even  be  no  pain  felt  what- 
ever. 

The  prognosis  is  almost  always  fatal.  Death  sometimes  occurs  suddenly  from 
collapse.  Sometimes  it  comes  at  the  end  of  three  or  four  weeks,  from  a  gradual 
sinking  of  the  bodily  powers.  Recovery  has  been  seen  in  only  a  few  cases:  there 
is  a  line  of  demarkation  formed,  the  sloughs  come  away,  and  a  slow  convalescence 
follows,  leaving  extensive  and  usually  very  disfiguring  scars  behind. 

Treatment  must  have  for  its  chief  object  to  check  further  extension  of  the 
gangrene,  by  removing  all  parts  that  are  already  destroyed.  Local  cauterization 
with  concentrated  hydrochloric  acid,  or  fuming  nitric  acid,  or  lunar  caustic,  or 
chloride  of  iron,  is  usually  futile.  It  is  probably  the  best  way  to  remove  all  the 
gangrenous  portion  by  means  of  Paquelin's  thermo-cautery.  At  least  in  the  early 
stages  of  noma  we  may  hope  something  from  this  method  of  treatment ;  but  if  the 
case  is  far  advanced,  we  can  hardly  expect  to  accomplish  much. 

We  should  also  disinfect  the  mouth  as  thoroughly  as  possible.  The  most 
efficient  means  is  to  syringe  it  out  with  solutions  of  salicylic  or  carbolic  acids,  or 
permanganate  of  potash,  and  to  dust  it  with  iodoform,  We  should  do  our  best 
to  maintain  the  patient's  strength. 


348  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

CHAPTER  VII. 

PAROTITIS. 

{Mumps). 

Parotitis,  or  inflammation  of  the  parotid  gland,  appears  not  only  as  a  pe- 
culiar, primary,  infectious  disease,  usually  epidemic,  but  also  as  a  secondary  com- 
plication of  numerous  other  severe  diseases.  These  two  forms  should  be  consid- 
ered separately. 

1.  Idiopathic,  Primary  Parotitis  (Epidemic  Mumps). 

./Etiology. — The  disease  occurs  in  epidemics  that,  although  not  very  frequent, 
may  be  quite  extensive.  Here  and  there  a  sporadic  case  is  seen.  Children  and 
young  adults  are  most  liable  to  it.  Nursing  infants  enjoy  a  marked  immunity,  as 
well  as  elderly  persons.     Males  are  much  oftener  attacked  than  females. 

There  can  be  no  doubt  that  mumps  is  a  specific  infectious  disease;  but  we  pos- 
sess no  minute  knowledge  of  the  infectious  agent.  Still,  it  is  natural  to  suppose 
that  the  infectious  matter  reaches  the  gland  by  way  of  Steno's  duct. 

Numerous  observations  support  the  view  that  the  disease  is  directly  contagious. 
The  period  of  incubation  seems  to  vary.  On  the  average,  it  is  about  fourteen 
days. 

Clinical  History. — There  may  be  a  prodromal  stage  of  one  or  two  days,  with 
mild  feverish  symptoms.  The  disease  itself  begins  with  swelling  of  one  parotid 
gland.  The  swelling  is  directly  below  and  in  front  of  the  lobe  of  the  ear,  which 
is  gradually  pushed  upward.  In  the  next  few  days  the  swelling  rapidly  increases, 
and  it  and  the  collateral  cedema  of  the  cheek  and  floor  of  the  mouth  may  become 
very  considerable,  The  face  is  much  distorted,  but  often  makes  a  very  comical 
impression,  especially  as  everybody  knows  how  harmless  the  disease  is.  In  most 
cases  the  other  gland  also  swells  a  few  days  later. 

An  abscess  hardly  ever  forms  in  genuine  mumps,  nor  does  the  swelling  often 
become  very  hard.  Generally  it  has  a  somewhat  doughy  consistence.  The  cor- 
responding portion  of  skin  is  usually  pale  and  shiny.  The  submaxillary  gland 
not  infrequently  swells  also  in  addition  to  the  parotid,  and  this  may  occur  upon 
one  or  both  sides  of  the  neck.  Penzoldt  has  observed  cases  where  the  submaxil- 
lary and  sublingual  were  swollen,  but  not  the  parotid.  We  ourselves  have  seen 
a  swelling  of  the  submaxillary  precede  the  parotitis. 

The  local  discomfort  is  moderate  in  most  cases.  There  is  difficulty  in  chewing, 
swallowing,  and  talking.  Often  quite  a  severe  stomatitis  develops,  with  foul 
breath. 

There  often  seems  to  be  no  fever  whatever.  Sometimes  there  may  be  a  mod- 
erate elevation  of  temperature,  seldom  exceeding  102-5°  (39°  C).  Only  occasion- 
ally has  there  been  a  case  with  grave  typhoidal  symptoms. 

Complications. — It  is  not  rare  for  men  to  have  a  swollen  testicle,  which  may 
be  quite  painful,  but  usually  subsides  in  a  few  days.  Resultant  suppuration  is  a 
rare  occurrence.  Double  orchitis  is  rare.  In  boys  this  complication  is  much  more 
exceptional  than  in  adults.  Some  observers  have  mentioned  analogous  swellings 
of  the  female  genitals  and  mamma?,  but  this  is  doubtful. 

The  prognosis  of  epidemic  parotitis  is,  as  we  have  said,  almost  always  favor- 
able. The  trouble  seldom  lasts  more  than  a  week  or  ten  days,  when  the  swelling 
goes  down,  and  the  patient  completely  recovers. 

The  diagnosis  is  easy.'  The  only  thing  to  exclude  is  swelling  of  the  lymph- 
glands,  and  they  never  have  exactly  the  same  location  as  the  parotid. 

Special  treatment  is  hardly  necessary.      Children   should  be   kept  in  bed. 


ANGINA  LUDOVICI.  :>AU 

Usually  some  salve,  like  vaseline,  is  applied  to  lessen  the  feeling  of  tension.  If 
resolution  is  tedious,  we  may  paint  the  swelling  with  iodoform  collodion  (1-15) 
or  with  tincture  of  iodine;  or  we  may  prescribe  iodoform  ointment  (1-15).  If 
there  is  orchitis,  the  testicle  must  he  elevated,  as  by  a  suspensory  bandage.  If  the 
pain  and  swelling  are  marked,  an  ice-bag  should  be  applied. 

2.  Secondary  Parotitis,  or  " Metastatic  Parotitis."— This  secondary  form  may 
be  a  complication  of  any  grave  disease.  In  most  cases  it  is  due  to  inflammatory 
agents  generated  by  decomposition  of  matters  in  the  mouth,  which  agents  reach, 
the  gland  through  Steno's  duct.  It  was  formerly  the  universal  belief  that  the  in- 
fection was  metastatic,  being  conveyed  through  the  blood-vessels ;  but  it  is  doubt- 
ful whether  this  does  occur.  It  is  probable  that  the  pysemic  form  is  in  many 
instances  thus  produced.  Secondary  parotitis  is  most  frequently  observed  in 
typhus  and  typhoid  fevers.  It  is  also  seen  occasionally  in  all  other  severe  acute 
diseases,  and  in  phthisis  and  carcinoma. 

The  parotid  gland  swells,  just  as  in  the  primary  disease.  It  is,  however,  much 
oftener  of  excessive  size,  and  in  the  majority  of  cases  suppurates.  If  one  has  an 
opportunity  to  make  an  autopsy  on  such  a  case  of  secondary  parotitis  in  its  early 
stages,  the  cross-section  of  the  swollen  gland  presents  a  large  number  of  rather 
small  discrete  abscesses.  These  finally  unite  to  form  one  larger  abscess,  which 
usually  discharges  outward,  or  into  the  external  auditory  meatus.  Sometimes 
the  parotid  suffers  from  gangrenous  inflammation,  and  there  is  extensive  slough- 
ing. If  such  a  case  finally  gets  well,  still,  as  a  rulef some  permanent  injuries  have 
been  inflicted :  there  is  facial  paralysis,  due  to  destruction  of  the  facial  nerve,  or 
deafness,  caused  by  an  extension  of  the  inflammation  to  the  middle  ear. 

The  treatment  of  secondary  parotitis  is  that  of  any  phlegmonous  inflammation. 
We  may  at  first  try  to  scatter  the  swelling  by  ice  or  iodoform  ointment,  but  this 
usually  fails.  As  soon  as  fluctuation  is  detected,  the  spot  must  be  incised,  and  a 
drainage-tube  inserted.  The  prognosis  depends  chiefly  on  the  nature  and  course 
of  the  original  disease. 


CHAPTER  VIII. 
ANGINA  LUDOVICI. 

The  name  angina  Ludovici  is  applied  to  a  rather  rare  phlegmonous  inflam- 
mation of  the  floor  of  the  mouth.  Its  starting  place  seems  to  be  the  submaxillary 
gland,  at  least  in  most  cases.  It  may  be  primary,  or  a  complication  of  other  severe 
acute  diseases. 

Angina  Ludovici  usually  begins  with  swelling  in  the  neighborhood  of  the  sub- 
maxillary gland.  The  swelling  rapidly  increases,  and  comes  to  involve  the  whole 
floor  of  the  mouth  and  the  anterior  surface  of  the  throat.  It  causes  great  discom- 
fort. Talking,  chewing,  and  swallowing  are  almost  impossible.  There  is  usually 
fever,  and  in  many  cases  we  even  find  the  symptoms  of  general  sepsis.  There 
may  be  great  dyspnoea,  due  either  to  compression  of  the  larynx  or  to  oedema  of 
the  glottis.  The  final  result  in  some  cases  is  an  extensive  sloughing  of  the  soft 
parts.  This  has  the  special  name  of  cynanche  gangraenosa.  In  other  cases  an 
abscess  forms,  and  points  outward  or  into  the  oral  cavity.  The  swelling  is  some- 
times, though  seldom,  reabsorbed. 

The  prognosis  should  always  be  guarded,  for  severe  constitutional  symptoms 
and  a  fatal  ending  are  not  infrequently  seen,  particularly  if  the  patient  has  a 
weakly  constitution.     There  may  also  be  repeated  exacei'bations  and  relapses. 

Treatment. — At  the  commencement  of  tbe  disease  we  may  make  the  attempt. 


350  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

in  suitable  cases,  to  cheek  the  process  by  local  depletion  and  by  ice ;  but,  as  soon 
as  suppuration  or  gangrene  begins,  the  case  becomes  a  surgical  one.  Now  and 
then  the  threatening  asphyxia  demands  tracheotomy. 


CHAPTER  IX. 
ANOMALIES   OF  DENTITION. 

(Difficult  Dentition.) 

The  processes  of  dentition  play  so  important  a  role  in  the  disorders  of  child- 
hood that  we  feel  obliged  to  discuss  the  subject,  at  least  briefly. 

The  first  appearance  of  any  of  the  milk-teeth  usually  takes  place  when  the 
child  is  seven  to  nine  months  old ;  it  may,  however,  occur  either  earlier  or  later 
than  this  period.  As  a  rule,  the  two  lower  central  incisors  are  cut  first ;  then  the 
upper  central  incisors  appear,  a  few  weeks  later,  and  next  the  lateral  incisors  of 
the  upper  jaw.  In  the  beginning  of  the  second  year  come  the  lower  lateral  inci- 
sors, and  almost  simultaneously  the  four  anterior  molars.  The  four  canine,  or 
"  eye  "  and  "  stomach  "  teeth,  are  cut  in  the  second  half  of  the  second  year ;  and 
last  of  all  comes  the  eruption  of  the  four  posterior  molars.  The  first  dentition  is 
4  a  a  2  s  therefore  completed  by  the  end  of  the  second 

or  in  the  beginning  of  the  third  year,  with 
the  development  of  all  the  twenty  milk-teeth. 
The  accompanying  diagram  (Fig.  33),  after 
Vogel,  represents  the  order  in  which  the  sep- 
arate teeth  appear.  In  the  fifth  or  sixth  year 
the  milk-teeth  begin  to  be  replaced  by  the 
permanent  teeth  of  the  second  dentition. 
"  Trouble  with  teething,"  however,  almost  invariably  refers  to  anomalies  of  the 
first  dentition. 

Noticeable  delay  in  teething  is  frequent  in  weakly,  and  particularly  in  rachitic 
children.  In  such  cases,  sometimes,  all  the  teeth  are  not  cut  till  the  end  of  the 
third  year. 

On  the  other  hand,  it  sometimes  happens  that  certain  teeth  appear  very  early, 
or  even  are  present  at  birth.  If  an  abnormally  early  tooth  is  only  loosely  in- 
serted in  the  gums,  it  should  be  removed  with  the  forceps ;  for  it  interferes  with 
nursing,  and  injures  the  opposing  surface  of  the  mouth.  But  if  the  tooth  is  firm 
in  its  place,  we  let  it  be. 

During  the  eruption  of  the  teeth  there  is  in  every  child  considerable  redness  of 
the  mucous  membrane  and  an  increased  flow  of  saliva.  The  child  evidently  feels 
an  itching  in  the  mouth,  and  therefore  a  constant  desire  to  bite  something.  This 
simple  catarrh  is  sometimes  accompanied  by  a  slight  rise  in  temperature.  Occa- 
sionally there  is  a  severe  stomatitis,  with  which  thrush  may  be  associated.  These 
troubles  should  be  treated  as  already  described. 

In  consequence  of  the  salivation,  and  the  large  amount  of  saliva  which  is  swal- 
lowed, in  which  the  various  processes  of  decomposition  are  apt  to  develop,  we 
often  see  gastro-intestinal  diseases  in  teething  children.  In  most  children  a  tem- 
porary and  mild  diarrhoea  occurs.  We  should  be  particularly  careful  at  this 
period  about  the  child's  nourishment,  and  in  treating  any  marked  gastro-intestinal 
symptoms.  Experience  shows  also  that  teething  children  are  unusually  liable  to 
simple  or  even  capillary  bronchitis,  and  catarrhal  pneumonia. 

Nervous  disturbances  are  often  referred  to  dentition.     The  most  important 


SORE  THROAT.  35  J 

symptom  of  this  kind  is  eclampsia.  The  attacks  are  sometimes  called  "  teething- 
convulsions."  Although  the  laity  go  too  far  in  ascribing  all  sorts  of  nervous  dis- 
orders to  teething-,  still  experienced  specialists  do  recognize  the  possibility  of  such 
an  origin  for  many  cases.  Some  of  the  convulsions  may  in  fact  be  regarded  as 
reflex  {vide  infra  the  chapter  on  the  convulsions  of  children,  page  779;. 

When  the  upper  canines,  or  "eye-teeth,"  are  being  cut,  there  is  sometimes  a 
unilateral  purulent  conjunctivitis,  which  is  perhaps  to  be  explained  as  an  exten- 
sion of  the  inflammation  by  way  of  the  antrum  of  Highmore  and  the  nostrils. 

Eczema  and  other  cutaneous  eruptions  have  been  often  ascribed  to  dentition ; 
whether  justly,  is  doubtful. 

There  is,  of  course,  no  special  treatment  for  difficult  dentition;  and  the  various 
disturbances  which  it  may  indirectly  produce  are  to  be  treated  on  general  princi- 
ples. 


SECTION  II. 

Diseases  of  the  Soft  Palate,  Tonsils,  Pharynx,  and  Naso- 
pharynx. 

CHAPTER  I. 

SORE   THROAT. 

( Tonsillitis.     Angina.) 

iEtiology. — Acute  inflammation  of  the  soft  palate  and  tonsils,  in  its  various 
forms,  is  one  of  the  commonest  of  diseases.  Almost  everybody  has  had  personal 
experience  with  it.  It  is  chiefly  a  disease  of  early  life,  being  infrequent  after  the 
thirty-fifth  year.  Individual  predisposition  to  it  varies  greatly.  There  are  per- 
sons who  have  one  or  more  attacks  almost  every  year,  while  with  others  attacks 
are  rare  and  insignificant.  In  many  instances  exciting  causes  have  evidently 
been  potent.  Chief  among  these  is  catching  cold;  the  sufferer  has  had  wet  feet, 
or  has  been  talking  in  a  damp,  cold  atmosphere.  Most  cases,  therefore,  occur  in 
cool  weather,  although  now  and  then  attacks  may  occur  in  the  hottest  days  of 
summer.  Again,  direct  injuries  of  the  pharynx  may  produce  the  disease,  e.  g., 
the  smoky  atmosphere  of  inns,  combined  with  loud  talking  or  shouting;  the 
inspiration  of  poisonous  vapors;  cauterization  of  the  mucous  membrane  with 
concentrated  acids,  alkalies,  and  other  chemical  agents ;  and  burns. 

[Especially  when  tonsillitis  recurs  in  an  individual,  or  attacks  several  members 
of  the  same  household  about  the  same  time,  it  is  well  to  have  the  drainage  care- 
fully examined.  The  precise  connection  between  bad  drainage  and  sore  throats 
we  do  not  know,  but  that  they  are  often  connected  there  seems  to  be  no  doubt.] 

Frequently  the  inflammation  is  due  to  extension  from  neighboring  parts,  as 
in  coryza,  laryngitis,  and  stomatitis.  In  many  cases  both  affections  are  simulta- 
neous results  of  one  common  cause. 

Finally,  sore  throat  may  be  a  symptom  of  many  acute  infectious  diseases,  such 
as  scarlet  fever,  measles,  small-pox,  and  erysipelas.  It  is  also  very  probable  that 
at  least  some  of  the  primary  cases  of  sore  throat  are  to  be  regarded  as  a  special 
acute  infectious  disease;  but  this  has  not  yet  been  really  proved. 

To  distinguish  between  an  inflammation  of  the  soft  palate  by  itself  and  an 
affection  of  the  tonsils  is  not  practicable.  In  most  cases  the  tonsils  are  the  strong- 
hold of  the  disease ;  less  often  we  find  the  inflammation  limited  to  the  soft  palate. 


352  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

Clinical  History. — The  most  important  subjective  symptom  of  sore  throat,  and 
that  by  which  it  is  usually  first  recognized,  is  the  difficult  and  painful  deglutition. 
The  pain  is  sometimes  manifest  before  any  objective  changes  are  to  be  seen.  It 
may  in  a  severe  case  be  very  violent  and  distressing.  The  pain  has  a  "darting" 
character,  or  sometimes  is  "  burning  " ;  and  it  is  most  acute  whenever  the  patient 
swallows,  although  in  well-marked  cases  it  seldom  entirely  intermits.  Swallow- 
ing is  not  only  painful,  but  it  is  laborious ;  it  requires  more  than  usual  effort  and 
time.  The  patient  feels  constantly  as  if  he  had  to  swallow  a  big  lump.  This  sen- 
sation is  worse  if  the  tonsils  are  swollen.  It  is  a  matter  of  experience  that  not 
infrequently  an  "  empty "  swallowing  hurts  more  than  swallowing  a  liquid  or 
some  half -solid  substance. 

Talking  is  also  difficult.  Every  word  may  be  painful,  so  that  the  patient 
expresses  his  wishes  as  briefly  as  possible.  Even  in  a  mild  case,  speaking  for  any 
length  of  time  will  produce  a  burning  pain  in  the  throat.  The  impaired  mobility 
of  the  soft  palate  often  prevents  the  complete  cutting  off  of  the  nasal  passages  in 
talking,  so  that  the  voice  has  a  nasal  twang ;  and  often  it  sounds  as  if  the  patient 
were  talking  with  his  mouth  full:  he  has  the  "voice  of  sore  throat." 

Further  local  discomfort  results  from  the  mucus  and  saliva  collecting  in  the 
mouth.  Salivation  is  not  infrequent,  probably  as  a  result  of  the  stomatitis  usually 
present.  In  other  cases  the  patient  complains  that  his  mouth  feels  dry  and  sticky. 
Frequently  there  is  a  persistent  bad  taste  in  the  mouth,  and  the  breath  is  dis- 
agreeable. 

With  these  local  disturbances,  more  or  less  severe  constitutional  symptoms  are 
almost  always  conjoined.  Indeed,  these  latter  may  begin  a  day  or  two  earlier 
than  the  local  symptoms.  The  patient  is  indisposed,  languid,  has  anorexia  and 
headache.  The  general  disturbance  may  be  surprisingly  great  in  comparison 
with  the  slight  objective  changes  in  the  tonsils. 

There  is  fever  in  most  of  the  well-marked  cases;  it  may  even  be  quite  high. 
Temperatures  of  103°  or  104°  (39"5°-40°  C),  or  even  higher,  are  not  rare.  Sore 
throat  can  not  be  said  to  have  one  particular  type  of  fever.  Usually  the  fever 
appears  rather  abruptly,  remains  high  for  several  days,  with  an  occasional  slight 
interruption,  and  then  falls  with  equal  abruptness  to  normal  again. 

The  entire  attack  usually  lasts  only  a  few  days,  seldom  more  than  a  week. 
Even  where  a  person  is  quite  ill  for  several  days,  convalescence  is  almost  always 
rapid  and  complete — that  is,  if  the  patient  has  a  good  constitution. 

Special  complications  are  very  infrequent,  except  that  the  neighboring  parts — 
the  larynx,  mouth,  and  throat — are  not  seldom  involved.  Herpes  labialis  is  quite 
frequent.     Beyond  this  there  is  nothing  to  mention. 

Various  Forms  of  Sore  Throat. 

The  symptoms  thus  far  mentioned  are  much  the  same  in  all  cases  of  sore 
throat,  varying  only  in  intensity  and  duration.  But  the  objective  changes  to  be 
observed  in  the  soft  palate  and  tonsils  ai-e  noticeably  different  in  different  cases. 
Whether  the  aetiology  differs  also  we  have  no  certain  information.  In  some 
instances  it  seems  probable  that  it  does. 

We  shall  distinguish  five  chief  varieties  of  acute  sore  throat.  Transitional 
forms  are,  however,  by  no  means  rare.  Genuine  diphtheria,  which  is  a  specific, 
acute,  infectious  disease,  and  has  already  been  discussed,  does  not  need  to  be 
brought  up  again  here. 

1.  Catarrhal  Sore  Throat  {Simple  Catarrhal  Inflammation  of  the  Mucous 
Membrane  of  the  Soft  Palate). — There  is  a  more  or  less  vivid  reddening  of  the 
mucous  membrane,  either  uniform  or  in  patches.     The  swelling  is  most  marked 


SOEE  THROAT.  353 

in  the  pillars  of  the  fauces  and  the  uvula.  The  surface  of  the  tonsils  is  likewise; 
reddened;  their  size  may  be  somewhat  increased,  or  remain  unchanged.  The 
mucous  membrane  of  the  palate  and  uvula  may  be  covered  here  and  there  with  a 
thin  layer  of  muco-pus,  which  can  easily  be  wiped  off.  The  tonsils  may  present 
small,  superficial  erosions,  scattered  about.  These  little  ulcers  are  apt  to  lie  at  the 
openings  of  the  follicles.  The  small  "blisters"  which  are  often  seen  on  tin; 
mucous  membrane  of  the  soft  palate  may  be  caused  in  various  ways.  Either  they 
are  mucous  glands  or  solitary  follicles,  swollen ;  or,  rarely,  they  are  real  vesicles 
filled  with  a  clear  fluid  and  produced  by  a  raising  up  of  the  epithelium.  The  cer- 
vical lymph-glands  are  usually  but  slightly  swollen,  if  at  all. 

This  is  the  common  and  mildest  form  of  sore  throat ;  and  it  may  be  over  in  a 
day  or  two.  In  some  instances,  however,  it  causes  considerable  local  and  gen- 
eral discomfort ;  but  the  disease  seldom  lasts  longer  than  five  to  eight  days. 

2.  Follicular  Tonsillitis. — In  this  form  there  is  not  only  more  or  less  catarrhal 
inflammation  of  the  soft  palate,  but  a  decided  swelling  of  one  or  both  fcmsils. 
On  the  reddened  surface  of  these  swollen  bodies  are  whitish-yellow  spots,  varying 
in  number  from  two  or  three  to  ten  or  more,  and  corresponding  to  the  follicles. 
These  spots  are  often  seen  to  be  plugs  projecting  from  the  openings  of  the  folli- 
cles. It  is  usually  easy  to  press  out  the  pasty  contents  of  the  follicle,  represented 
by  the  white  speck,  with  a  spatula.  The  microscope  shows  it  to  consist  of  numer- 
ous epithelial  cells  and  pus- corpuscles,  bacteria,  and  detritus,  and  sometimes  there 
are  also  crystals  of  the  fat  acids  and  Cholesterine.  The  pus-corpuscles  may  so 
predominate  that  we  may  have  small  follicular  abscesses,  which,  on  being  opened, 
leave  superficial  ulcers  behind.  The  parenchyma  of  the  tonsil  is  swollen  with  a 
serous  and  cellular  infiltration,  increasing  the  bulk  of  the  part.  The  trouble  is 
usually  bilateral,  though  often  more  marked  and  extensive  on  one  side  than  on 
the  otber.     In  the  severer  cases  the  cervical  lymph-glands  are  swollen. 

The  clinical  symptoms  do  not  differ  essentially  from  those  of  the  other  forms. 
The  attack  may  be  mild  or  severe.  Usually  the  contents  of  the  follicles  are  dis- 
charged after  a  few  days,  and  the  tonsils  become  normal  again.  Yet  the  contents 
may  be  retained  some  time,  and  become  calcified.  It  is  not  a  rare  thing  to  find 
such  plugs  in  the  tonsils  of  those  who  are  subject  to  sore  throat.  Timid  and 
hypochondriacal  individuals  are  sometimes  badly  frightened  by  expectorating 
these  old  chalky  plugs,  which  they  believe  to  be  "tubercles"!  From  an  astio- 
logical  standpoint,  follicular  tonsillitis  is  in  most  cases  entirely  distinct  from 
genuine  diphtheria;  still  it  is  noteworthy  that  precisely  at  the  time  of  diphtheria 
epidemics  follicular  tonsillitis  is  remarkably  frequent.  It  might,  after  all,  be  pos- 
sible that  the  mildest  degrees  of  diphtheria  present  themselves  in  the  garb  of  an 
apparently  simple  follicular  tonsillitis.  The  latter  is  very  probably  an  infectious 
disease. 

3.  Tonsillar  Abscess  (Parenchymatous  Sore  Throat) . — In  this  form  the  swell- 
ing of  the  tonsils  is  the  most  striking  symptom.  They  may  be  more  than  twice 
their  natural  size.  The  anterior  pillars  of  the  fauces  are  pushed  forward  and 
become  convex.  The  swelling  extends  so  far  toward  the  median  line  that  the 
tonsil  touches  the  uvula;  or,  if  the  affection  is  bilateral,  the  two  tonsils  press 
against  each  other,  grasping  the  uvula  between  them,  or  pushing  it  forward. 
The  soft  palate  is  very  much  reddened,  particularly  at  first.  Its  surface  is  usually 
thickly  covered  with  mucus.  If  this  be  wiped  off,  the  mucous  membrane  is  seen 
to  have  a  moist,  cedematous  luster.  The  mucous  membrane  of  the  tonsils  not 
infrequently  suffers  a  superficial  necrosis.  Follicular  and  parenchymatous  ton- 
sillitis are  often  combined. 

In  well-marked  cases  of  abscess  the  local  discomfort  is  usually  great.     The 
patient  is  in  a  pitiable  condition ;  he  can  neither  talk,  nor  swallow,  nor  gargle. 
23 


354  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

The  few  words  which  he  painfully  utters  have  in  an  extreme  degree  the  nasal 
quality  of  the  "  voice  of  sore  throat." 

In  the  milder  cases  the  trouble  seldom  lasts  hut  a  few  days  before  the  swell- 
ing goes  down,  and  the  discomfort  and  usually  rather  high  fever  gradually  abate. 
In  other  cases,  however,  a  tonsillar  abscess  forms,  usually  on  only  one  side. 
The  mucous  membrane  bulges  out  more  and  more  in  one  spot;  fluctuation  is 
detected;  and,  finally,  the  abscess  breaks.  With  the  discharge  of  the  pus  the 
pain  is  relieved  very  rapidly,  or  it  may  vanish  at  once.  The  rest  of  the  tonsil 
soon  regains  its  former  size,  and  in  a  few  days  the  patient  is  well.  Relapses  are 
possible,  but  rare. 

Parenchymatous  or  (as  it  is  called)  phlegmonous  sore  throat,  in  which  the  soft 
palate  and  not  the  tonsil  is  chiefly  affected,  is  infrequent.  Its  usual  cause  is  some 
severe  external  injury,  like  burns,  and  cauterizations  with  concentrated  acids  or 
alkalies.  The  swelling  extends  deep  down  into  the  submucous  tissue.  The  uvula 
may  have  the  diameter  of  one's  finger.  There  is  intense  hyperemia.  Sometimes 
there  are  haemorrhages  into  the  mucous  membrane :  this  is  called  hemorrhagic 
sore  throat.* 

There  are  also  a  peri-tonsillar  and  a  retro-tonsillar  abscess,  which  from  a  clin- 
ical standpoint  are  not  essentially  different  from  the  more  common  form.  They 
are  almost  always  unilateral,  and  are  due  to  a  suppurative  inflammation  of  the 
peri-tonsillar  connective  tissue,  lying  between  the  tonsil  and  one  of  the  pillars  of 
the  fauces,  usually  the  anterior  one. 

4.  Necrotic  Tonsillitis,  or  Necrotic  Sore  Throat. — In  this  form  the  tonsils 
are  chiefly  involved.  The  pillars  of  the  fauces  and  the  uvula  are  but  slightly 
affected  with  a  simple  catarrhal  inflammation.  The  tonsils  are,  as  a  rule,  mod- 
erately swollen,  seldom  attaining  great  size.  The  mucous  membrane  covering 
them  presents  a  whitish  or  grayish-white  discoloration,  often  quite  extensive,  and 
most  marked  on  the  side  toward  the  uvula.  These  spots  are  often  erroneously 
said  to  be  a  white  "  coating  " ;  but  a  more  careful  investigation  shows  that  there 
is  in  reality  a  necrosis.  The  process  may  be  superficial  ;  sometimes  it  reaches 
quite  deeply  into  the  structure  of  the  mucous  membrane.  It  is  not  possible  to 
pull  off  this  white  matter,  as  one  can  loosen  croupous  membranes,  although  little 
bits  may  perhaps  be  scratched  off  with  a  spatula  or  a  pair  of  forceps.  These 
particles  are  found,  on  microscopic  examination,  to  be  made  up  merely  of  detritus, 
bacteria,  epithelium,  and  pus-corpuscles.  The  necrosis  is  almost  invariably  con- 
fined to  the  tonsils,  and  a  sharp  boundary-line  separates  it  from  the  reddened 
and  inflamed  pillars  of  the  fauces.  After  a  few  days  the  slough  may  come  away, 
leaving  behind  an  ulcer,  which,  though  usually  shallow,  has  sometimes  a  con- 
siderable depth.  This  generally  cleans  up  rapidly.  In  severe  cases,  however, 
the  floor  of  the  ulcer  consists  for  a  number  of  days  of  a  dirty  necrotic  material, 
which  comes  away  only  gradually.  The  worst  cases  may  be  properly  called 
"gangrenous  tonsillitis." 

Necrotic  tonsillitis  is  almost  always  attended  by  considerable  fever  and  marked 
constitutional  disturbance.  Children  particularly  seem  very  ill  in  the  first  days 
of  the  attack.  The  cervical  glands  are  usually  swollen,  but  seldom  as  much  so  as 
in  genuine  diphtheria. 

Despite  the  rather  ominous  commencement,  the  disease  does  not  last  a  great 
deal  longer  than  the  other  forms  of  sore  throat.  It  seldom  continues  more  than 
five  to  eight  days  before  a  speedy  convalescence  begins. 

*  Another  form  with  the  same  name  occurs  where  there  is  violent  tonsillitis  with  necrosis  or  gan- 
grene. There  is  also  a  necrotic,  hemorrhagic  sore  throat  accompanying  scurvy,  leukaemia,  and  analo- 
gous diseases. 


SORE  THROAT.  355 

The  necrotic  tonsillitis  is  distinguished  from  the  follicular  form  by  the  greater 
area  of  the  white  or  grayish-white  spots.  Still  it  should  be  particularly  noted 
tbat  sometimes  combinations  of  these  two  varieties,  or  transitional  forms,  occur. 

^Etiology. — In  our  opinion,  necrotic  tonsillitis  is  in  many  instances  an  entirely 
different  disease  from  genuine  diphtheria.  On  the  other  hand,  our  experience  in 
several  epidemics  of  diphtheria  in  Leipsic  and  Erlangen  has  taught  us  that  in  all 
probability  mild  cases  of  genuine  diphtheria  of  the  tonsils  do  occur,  and  that  these 
objectively  resemble  necrotic  tonsillitis.  This  is  the  only  way  to  explain  what 
other  physicians  as  well  as  ourselves  have  often  observed— namely,  that  necrotic 
tonsillitis  appears  not  infrequently  in  families  at  the  same  time  with  severe  cases 
of  genuine  diphtheria.  Besides,  these  cases  of  necrotic  tonsillitis  are  sometimes 
followed  by  the  characteristic  "  diphtheritic  "  paralysis. 

[The  reader  will  observe  that  the  author  distinctly  admits  the  frequent  impos- 
sibility of  distinguishing  between  his  necrotic  and  croupous  forms  of  sore  throat 
and  diphtheria.  It  is  furthermore  stated  that  the  follicular  form  occurs  in  com- 
bination with  either  or  both  of  the  necrotic  and  croupous  forms,  the  vague  nature 
of  which  is  thus  apparent. 

A  membrane  or  membraniform  layer  which  is  not  confined  to  the  tonsils,  or 
which  is  seen  on  the  soft  palate  or  pillars  of  the  fauces  alone,  should  be  regarded 
with  great  suspicion.  A  few  days'  isolation  can  do  no  harm  in  such  a  case,  and 
may  save  bitter  regrets. 

Similar  deposits  limited  to  the  tonsils  consist  not  infrequently  of  follicular 
secretion  which  has  coalesced;  careful  examination  will  show  the  follicular  origin 
in  these  cases. 

A  protest  should  be  entered  against  the  use  of  the  term  "  diphtheritic  sore 
throat,"  so  often  applied  to  severe  simple  inflammations  as  well  as  to  mild  or 
doubtful  cases  of  diphtheria.  A  case  is  either  one  of  diphtheria  or  it  is  not.  It 
is  our  duty  neither  to  excite  needless  alarm  nor  to  encourage  a  false  security.  In 
doubtful  cases  the  only  safe  way  is  frankly  to  express  the  doubt  and  prepare  for 
the  worse  alternative.] 

Diagnosis  and  Prognosis. — It  is  never  very  difficult  to  recognize  a  sore  throat, 
and  a  little  practice  makes  it  easy  in  most  cases  to  decide  what  particular  variety 
is  present,  if  we  examine  the  objective  changes  carefully.  It  is  very  important 
in  practice  to  distinguish  diphtheria  from  the  benign  forms  of  inflammation. 
Follicular  and  necrotic  tonsillitis  are  very  frequently  mistaken  for  diphtheria— an 
error  which  explains  the  success  of  a  large  number  of  remedies  said  to  cure  diph- 
theria. Many  physicians  call  every  case  of  sore  throat,  where  there  is  anything 
white  to  be  seen,  "  diphtheria."  Certainty  in  diagnosis  of  genuine  diphtheria  can 
only  be  gained  by  practice;  no  description,  however  complete,  can  take  the  place 
of  personal  observation.  It  may  be  a  help  to  remember  that  in  both  follicular 
and  necrotic  tonsillitis  the  white  spots  are  usually  limited  to  the  tonsils,  while  in 
croupous  sore  throat  the  deposits  are  generally  from  the  very  first  also  situated 
upon  the  pillars  of  the  fauces  and  the  uvula.  The  white  spots  of  the  follicular 
variety  can  generally  be  recognized  by  their  arrangement.  The  plugs  are  seen 
projecting  from  the  follicles.  In  necrotic  sore  throat  there  is  never  a  separable 
croupous  membrane  with  its  characteristic  histological  structure,  but  there  is  sim- 
ply a  superficial  necrosis  of  the  mucous  membrane  and  parenchyma.  In  doubtful 
cases  the  condition  of  the  cervical  lymph-glands  is  not  unimportant ;  as  a  rule, 
they  are  much  more  affected  in  diphtheria  than  in  the  benign  cases.  Inasmuch 
as  we  have  seen  that  the  milder  forms  of  tonsillitis  may  be  aetiologically  related 
to  diphtheria,  it  is  well  in  practice  to  make  a  guarded  prognosis,  even  in  cases  of 
follicular  and  necrotic  angina,  particularly  in  children.  And  we  should  always 
isolate  the  patient  from  other  children. 


356  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

Treatment. — These  troubles  run  so  favorable  a  course  that  active  treatment  is 
very  seldom  needed.  The  gargle  usually  prescribed  generally  gives  the  patient 
more  discomfort  than  relief.  The  most  common  pi'escriptions  are :  Solutions  of 
potassic  chlorate  (5-10:  300),  of  alum  (5-10:  500),  or  of  borax  (10:  300);  salt  and 
water ;  and  weak  solutions  of  carbolic  acid  or  of  permanganate  of  potash.  To 
paint  the  parts  is  a  useless  and  now  almost  obsolete  proceeding.  Inhalations  of 
spray  are  better,  with  alum,  tannin,  or  carbolized  water.  It  is  beneficial  to  put  a 
cold  wet  compress  around  the  throat.  Children  must  be  kept  in  bed,  and  adults 
are  generally  forced  to  go  to  bed,  if  the  constitutional  symptoms  are  well  marked. 

In  parenchymatous  tonsillitis,  ice  will  sometimes  alleviate  the  pain.  Often, 
however,  the  patient  can  not  bear  it.  If  there  is  evident  fluctuation,  we  can  make 
an  incision  with  a  spear-pointed  bistoury,  after  guarding  a  portion  of  the  blade 
with  sticking-plaster.  Great  relief  follows;  and,  even  if  there  is  no  abscess,  scaii- 
fication  of  the  tonsils,  if  they  are  excessively  swollen,  usually  lessens  the  pain. 
The  operation  causes  little  discomfort. 

We  may  add  that  if  a  person  is  subject  to  sore  throat,  he  can  lessen  his  liability 
to  attacks  by  hardening  his  skin  through  the  use  of  cold  baths. 


CHAPTER   II. 
CHRONIC   HYPERTROPHY   OF   THE   TONSILS. 

Chronic  hypertrophy  of  the  tonsils  occurs  not  only  in  those  who  have  had 
repeated  attacks  of  tonsillitis,  but  also  in  cases  where  no  occasion  for  it  can  be 
found.  Even  in  childhood  there  may  be  well-marked  hypertrophy,  which  must 
be  due  to  a  congenital  predisposition. 

The  condition  is  at  once  revealed  by  inspection.  There  may  be  no  signs  what- 
ever of  any  acute  or  chronic  inflammation,  or  there  may  be  an  accompanying 
chronic  pharyngitis.  The  tonsils  bulge  out  in  two  great  lumps.  They  may  be  so 
large  as  to  touch  the  uvula  on  each  side.  Histologically,  there  is  a  genuine  hyper- 
trophy of  the  organ — that  is,  an  increase  of  all  its  component  tissues. 

In  many  cases,  where  the  swelling  is  moderate,  there  is  no  discomfort.  The 
possessor  of  the  tonsils  is  not  aware  that  they  are  enlarged.  In  other  cases  the 
hypertrophy  proves  of  clinical  importance,  inasmuch  as  all  forms  of  sore  throat 
are  found  to  occur  more  frequently  if  the  tonsils  are  enlarged,  and  to  cause  more 
trouble  when  they  do  appear.  The  hypertrophied  organs  may  also  be  the  seat  of 
a  chronic  catarrh,  which  by  extension  gives  rise  to  chronic  nasal  catarrh,  catarrh 
of  the  Eustachian  tubes,  or  hoarseness. 

If  the  hypertrophy  is  considerable,  the  local  discomfort  may  be  quite  marked. 
Swallowing  is  rendered  difficult,  if  not  painful.  Frequently  there  is  evident 
dyspnoea.  The  patient  has  to  breathe  through  his  mouth,  and  sometimes  when 
asleep  snores  and  snorts  in  a  way  to  frighten  one.  Children  are  particularly  apt 
to  suffer  in  this  manner.  Many  instances  of  pavor  nocturnus,  or  "  night  terrors," 
in  children  are  referable  to  this  cause.  We  have  already  mentioned  that  cases  of 
bronchial  asthma  sometimes  seem  to  be  connected  with  hypertrophy  of  the  tonsils 
(see  page  171). 

Treatment. — The  attempt  to  reduce  the  enlargement  by  applying  lunar  caustic, 
tincture  of  iodine,  etc.,  usually  fails.  If  there  is  much  distress,  if  the  patient  is 
subject  to  frequent  sore  throats,  or  if  the  hypertrophy  of  the  tonsils  keeps  up  a 
chronic  nasal  or  pharyngeal  catarrh,  then  the  simplest  remedy  is  to  remove  the 
tonsils.     The  operation  is  free  from  any  danger.     The  extirpation  can  be  accom- 


CHRONIC  PHARYNGITIS.  357 

plished  either  with  the  tonsillotome  or  with  scissors  and  forceps.     The  latter  way- 
is  the  simpler,  and  is  almost  equally  easy. 


CHAPTER  III. 
CHRONIC   PHARYNGITIS. 

iEtiology. — It  is  not  practicable  to  distinguish  between  chronic  catarrh  of  the 
soft  palate  and  of  the  pharynx,  for,  as  a  rule,  the  two  are  combined.  Sometimes 
the  condition  is  the  result  of  repeated  acute  attacks ;  sometimes — and  probably 
offener — it  is  due  to  persistent,  injurious,  local  influences.  A  large  number  of 
cases  originate  in  bad  habits,  or  in  abuse  incident  to  certain  vocations.  Examples 
are  seen  in  smokers,  drunkards,  singers,  preachers,  teachers,  and  men  who  work 
out-doors.  In  talking  and  singing,  the  soft  palate  is  strained ;  or  the  disease  is 
excited  by  breathing  cold  or  impure  air,  or  by  such  chemical  irritants  as  alcohol 
or  tobacco.  In  many  cases,  chronic  pharyngitis  follows  chronic  rhinitis  or  chronic 
laryngitis.  The  general  passive  congestion  due  to  cardiac  disease  or  pulmonary 
emphysema  may  sometimes  promote  the  development,  or  prolong  the  existence, 
of  a  chronic  pharyngitis. 

Symptoms. — The  local  discomfort  is  often  slight.  The  patient  gets  used  to  it, 
and  does  not  mind  it  except  when  there  is  some  exacerbation.  It  becomes  a  more 
important  matter  if  the  calling  of  the  patient  is  interfered  with,  as  in  a  preacher, 
singer,  or  teacher. 

Deglutition  is  seldom  impaired.  There  is  often,  however,  a  constant  feeling  of 
dryness,  or  burning,  or  scratching  in  the  throat.  The  patient  has  to  clear  his 
throat  frequently,  and  often  acquires  an  habitual,  short,  sudden  cough,  which  may 
be  dry.  The  uvula  becomes  so  long  that  its  tip  rests  on  the  tongue  or  the  poste- 
rior wall  of  the  pharynx;  and  this  gives  rise  to  a  peculiar  and  disagreeable  sensa- 
tion of  tickling.  All  these  uncomfortable  feelings  are  temporarily  increased  if 
anything  affects  the  throat  unfavorably;  and  they  ai*e  generally  at  their  worst  on 
rising  in  the  morning,  apparently  because  the  mucous  membrane  has  become  dry, 
or  a  collection  of  tough  muccus  has  formed  during  the  night.  Every  one  knows 
how  drunkards  have  to  hem  and  cough  mornings,  so  that  often  they  almost 
strangle  or  vomit. 

On  inspection,  we  generally  find  the  mucous  membrane  reddened.  Very  often 
a  number  of  dilated  and  tortuous  veins  are  visible  both  on  the  soft  palate  and  in 
the  back  of  the  throat.  Of  equal  frequency  is  the  appearance  of  numerous  small 
gray  projections,  corresponding  to  swollen  follicles  or  hypertrophied  mucous 
glands.  This  is  called  granular  pharyngitis.  Small  follicular  ulcers  are  not 
infrequent.  Exceptionally  there  are  more  extensive  catarrhal  ulcers.  The  mucous 
membrane  of  the  posterior  wall  of  the  pharynx  may  present  patches  of  opaque  or 
thickened  epithelium,  giving  the  surface  a  grayish-white  appearance. 

Frequently  chronic  pharyngitis  is  combined  with  chronic  laryngitis,  evidenced 
by  hoarseness ;  or  with  posterior  nasal  catarrh,  or  catarrh  of  the  Eustachian  tube, 
producing  deafness  and  ringing  in  the  ears. 

Varieties  of  Chronic  Pharyngitis. 

1.  Chronic  Catarrh  of  the  Naso-pharynx,  or  Chronic  Posterior  Nasal  Catarrh. — 
This  has  the  same  aetiology  as  the  ordinary  form.  It  is  practically  important 
because  the  nose  and  ear  are  frequently  involved. 


358  DISEASES  OF  THE  DIGESTIVE  OKGANS. 

The  anatomical  changes  are  essentially  those  already  depicted  under  chronic 
pharyngitis.  The  region  affected  can  not  be  seen  by  direct  inspection,  so  that 
accuracy  in  diagnosis  requires  the  use  of  a  nasal  speculum  (see  particulars  in  the 
works  mentioned  on  page  125).  The  ordinary  examination  of  the  throat  may 
reveal  a  condition  which  is  quite  characteristic  of  posterior  nasal  catarrh :  a  col- 
lection of  muco-pus,  or  of  firmly  adherent  dry  crusts,  rests  upon  the  posterior 
wall  of  the  pharynx,  and  can  be  seen  to  extend  upward  toward  the  naso-pharynx. 

The  local  discomfort  is  somewhat  similar  to  that  experienced  in  chronic 
pharyngitis.  There  is  a  scratchy  feeling,  or  a  feeling  as  if  there  were  a  foreign 
body  in  the  back  of  the  throat,  accompanied  by  a  constant  desire  to  blow  the  nose, 
hawk  or  cough.  Dried  and  decomposing  secretion  often  causes  extremely  foul 
breath.     There  is  often  also  vertigo,  and  occipital  headache. 

In  many  cases  the  nostrils  are  stopped  up.  The  posterior  opening  of  the  nos- 
trils is  closed  in  part  by  the  swelling  and  hypertrophy  of  the  mucous  membrane, 
and  in  part  by  the  accumulated  secretions.  The  patient,  therefore,  usually  has 
to  breathe  through  the  mouth.  The  ear  is  frequently  involved.  The  catarrh 
extends  into  the  Eustachian  tubes  and  the  tympanic  cavity,  or  the  opening  of  the 
tubes  is  occluded  with  the  secretions.  For  a  detailed  consideration  of  the  deaf- 
ness, tinnitus,  etc.,  thus  produced,  consult  works  on  otology. 

2.  Pharyngitis  Sicca,  or  "  Dry  Atrophic  Catarrh  of  the  Throat  and  Naso- 
pharynx."— This  name  is  applied  to  an  atrophy  of  the  mucous  membrane,  which 
sometimes  is  spontaneous  and  sometimes  is  ä  sequel  of  chronic  pharyngitis.  The 
whole  mucous  membrane  of  the  pharynx  and  the  naso-pharynx  (seen  with  the 
rhinoscope)  seems  pale,  smooth,  and  perfectly  dry,  and  has  a  peculiar  luster,  as  if 
varnished.  Here  and  there  tortuous  veins  project  from  the  general  anaemic 
surface. 

If  an  opportunity  is  afforded  to  examine  the  mucous  membrane  microscopic- 
ally, it  will  be  found  that  the  atrophy  involves  all  the  elements  of  the  tissue, 
though  the  follicles  and  mucous  glands  suffer  most. 

This  condition  may  not  cause  any  symptoms,  but,  in  many  cases,  the  patient 
suffers  constantly  and  considerably.  The  chief  trouble  is  a  feeling  of  dryness  in 
the  throat,  rendering  deglutition  difficult  or  even  painful.  There  is  also  a  con- 
stant desire  to  clear  the  throat.  The  secretion  hawked  up  may  be  scanty  and 
tough  or  more  abundant,  and  it  is  often  tinged  with  blood.  Actual  coughing 
may  also  be  due  to  pharyngeal  trouble  ("throat-cough  ").  Talking  is  often  ren- 
dered difficult,  the  voice  grows  weak  and  it  becomes  easily  tired.  In  severe 
cases  there  is  considerable  general  debility.  Not  infrequently  pharyngitis  sicca 
is  associated  with  atrophic  rhinitis  (q.  v.),  but  it  occurs  also  in  cases  where  there 
is  no  nasal  disease. 

The  disease  is  most  frequently  seen  in  the  elderly,  but  it  also  occurs  in  children 
and  young  persons.  It  is  especially  common  in  ill-nourished  individuals  or  in 
those  who  are  suffering  from  such  diseases  as  tuberculosis  or  chronic  nephritis. 

3.  Hypertrophic  Catarrh  of  the  Pharynx  and  Naso-pharynx. — An  opposite 
condition  of  hypertrophy  sometimes  results  from  chronic  catarrh.  The  changes 
consist  mainly  in  hyperplasia  of  the  lymphatic  tissue,  and  they  are  usually 
termed  "adenoid  growths."  The  choanse  and  the  posterior  extremity  of  the 
nasal  septum  may  be  almost  completely  hidden  by  these  growths,  as  they  ex- 
tend down  from  the  roof  of  the  pharynx  in  grayish-red,  uneven  masses.  In 
many  cases  the  hypertrophy  seems  to  originate  chiefly  in  Kölliker's  "  pharyngeal 
tonsil." 

The  adenoid  growths  are  especially  common  in  childhood.  The  symptoms 
consist  in  a  change  of  the  voice  (which  loses  its  reverberating  quality  and  becomes 
nasal),  frequent  snuffling  and  hawking,  and  a  tough   mucous  secretion,  often 


CHRONIC  PHARYNGITIS.  359 

tinged  with  blood.     Not  infrequently  there  is  headache.    Of  greater  importance  is 
ear-trouble,  which  is  often  occasioned  by  the  growths. 

An  accurate  diagnosis  requires  rhinoscopy.  Positive  results  are  also  often  ob- 
tained by  palpation.  The  index -finger,  being  passed  backward  and  bent  upward,  can 
touch  the  protuberances  and  the  enlarged  pharyngeal  tonsil  in  the  naso-pharynx. 

Prognosis. — The  prognosis  in  all  forms  of  chronic  pharyngeal  catarrh  should 
be  somewhat  guarded,  for  all  severe  cases  are  very  obstinate  and  can  seldom  be 
permanently  cured.  Success  may  be  depended  upon  only  in  cases  where  all  unfa- 
vorable influences  can  be  completely  removed.  We  may  afford  great  relief,  but 
there  will  be  a  persistent  tendency  to  acute  exacerbations  and  to  relapses  long 
afterward. 

Treatment. — Many  of  the  milder  cases  never  apply  to  a  physician.  The  pa- 
tient uses  some  domestic  remedy  or  gargle,  or  becomes  so  accustomed  to  the  dis- 
agreeable sensations  that  he  does  not  consider  it  necessary  to  do  anything  in 
particular  about  them. 

The  treatment  of  a  well-developed  case  requires  great  patience  and  persistence 
on  the  part  of  all  concerned.  If  there  is  some  underlying  disease,  such  as  pulmo- 
nary or  cardiac  disease,  that  must  be  treated.  All  exciting  causes  must  be  avoided. 
Energetic  local  treatment  is  also  indispensable.  This  has  been  greatly  elaborated 
by  specialists,  and  for  the  many  details  we  must  refer  to  their  writings ;  but  the 
following  remarks  will  meet  the  requirements  of  ordinary  practice : 

Gargles  are  seldom  satisfactory,  for  they  never  reach  farther  than  the  soft 
palate.  Inhalations  are  better ;  we  can  use  solutions  of  alum  or  tannin,  or,  in 
mild  cases,  of  common  salt.  Still  more  efficient  is  the  painting  of  the  entire  sur- 
face of  the  pharynx  with  some  concentrated  solution.  The  physician  usually  has 
to  perform  this,  although  some  patients  learn  to  do  it  for  themselves.  Proper 
solutions  are:  Argentic  nitrate,  five  or  ten  per  cent. ;  tannin,  eight  to  twenty  per 
cent. ;  tincture  of  iodine,  either  pure  or  diluted ;  or  iodized  glycerine,  composed  of 
pure'  iodine,  parts  1"5;  iodide  of  potassium,  5;  glycerine,  500.  These  applications 
must  reach  all  the  diseased  surface.  If  the  naso-pharynx  is  involved,  the  brush 
must  accordingly  be  bent  upward,  to  reach  that  region.  For  this  a  mirror  may  be 
needed.  It  is  very  important  to  make  the  applications  to  the  mucous  membrane 
itself,  freed  from  any  interposing  secretions. 

In  the  treatment  of  chronic  posterior  nasal  catarrh  the  nasal  douche  {vide  Dis- 
eases of  the  Nose)  plays  an  important  part.  It  should  be  used  two  or  three  times 
a  day.  It  not  only  removes  the  collected  secretions,  but  is  a  means  of  making 
local  *  applications.  The  instrument  is  merely  a  fountain-syringe.  The  nozzle 
must  be  of  a  size  to  fill  the  nostril  completely.  The  force  of  the  current  should 
always  be  moderate,  and  the  patient's  head  should  be  sharply  flexed  forward. 
The  fluid  used — the  best  is  a  one-per-cent.  solution  of  sodic  chloride  or  bicarbonate 
— must  have  about  the  temperature  of  the  body.  Other  medicated  solutions  must 
be  very  weak,  such  as  sulphate  of  zinc,  1  to  1,000. 

The  insufflation  of  powders  into  the  throat  can  be  made  through  any  small 
glass  tube,  three  to  six  times  a  week.  Alum  or  tannin  may  be  used,  either  pure 
or  mixed  with  equal  parts  of  pulvis  gummosus  [P.  G.,  made  of  gum-arabic,  three 
parts;  licorice-root,  two  parts;  and  sugar,  one  part].  For  the  naso-pharynx,  a 
bent  tube  of  glass  or  hard  rubber  is  to  be  introduced  through  the  mouth.  There 
are  numerous  "  insufflators  "  to  be  had  at  the  instrument-makers. 

Many  baths  enjoy  a  great  reputation  for  the  cure  of  chronic  pharyngitis. 
Besides  Ems,  there  are  Reichenhall,  Kreuznach,  Salzungen,  the  cold  sulphur 
springs,  such  as  Weilbach,  and  many  others.  Good  results  are  also  achieved  in 
Kissingen  and  Marienbad,  if  these  places  are  favorable  to  the  patient's  general 
constitution. 


360  DISEASES   OF  THE  DIGESTIVE   ORGANS. 

In  pharyngitis  sicca,  the  nasal  douche  with  a  one-per-cent.  salt  solution  is  to 
be  recommended.  It  is  sometimes  also  beneficial  to  paint  the  parts  with  solution 
of  argentic  nitrate,  iodized  glycerine,  etc.  Many  irritating  influences  which  do 
harm  in  common  pharyngitis  seem  sometimes  actually  to  benefit  this  form — such 
as  smoking  and  taking  snuff. 

In  treating  the .  hypertrophic  forms  of  pharyngitis  and  the  adenoid  growths, 
cauterization  with  nitrate  of  silver  suffices  for  the  milder  cases  alone.  A  thorough 
and  permanent  cure  can  be  achieved  only  by  removing  the  growths  with  the  gal- 
vano-cautery. 

[To  Hooper,  of  Boston,  belongs  the  credit  of  showing  that  a  radical  operation 
for  the  removal  of  adenoid  growths  of  the  naso-pharynx  can  safely  be  done  under 
anaesthesia.  The  blood  does  not,  as  was  feared,  run  into  the  air-passages,  but 
either  into  the  stomach  or  outwardly.  Anaesthesia  thus  renders  it  possible  to 
scrape  away  with  the  finger  or  tear  away  with  forceps  the  hypertrophied  tissue  at 
one  sitting,  and  to  do  it  in  the  child  before  secondary  changes  have  taken  place  in 
the  facial  expression,  the  jaw,  the  ears,  or  the  form  of  the  chest.] 


CHAPTER  IV. 
RETROPHARYNGEAL   ABSCESS. 

Retropharyngeal  abscess  is  formed  by  a  suppurative  inflammation  of  the 
connective  tissue  lying  between  the  posterior  wall  of  the  pharynx  and  the  spinal 
column.  It  is  a  serious  disease,  although  a  rare  one.  If  unrecognized,  it  proves 
fatal  in  many  instances;  while,  if  a  correct  and  timely  diagnosis  is  made,  the 
patient  can  usually  be  easily  cured.  It  is  commonest  in  childhood,  and  before 
the  second  year.  It  almost  always  appears  as  a  primary,  acute  disease,  without 
any  special  cause  being  evident.  Probably  the  agents  which  excite  the  inflamma- 
tion penetrate  into  the  tissue  from  the  pharynx.  The  idea  that  the  inflammation 
originates  in  the  small  lymphatic  glands  which  lie  in  front  of  the  vertebrae  lacks 
pi'oof  as  yet. 

The  disease  attacks  not  only  weakly  children,  but  those  who  have  been  per- 
fectly healthy  and  vigorous.  The  child  grows  restless  and  fretful,  and  does  not 
nurse  well.  Apparently,  deglutition  soon  becomes  painful,  but  one  can  not  be 
certain  about  this  except  in  older  children.  Generally,  the  respiration  quickly 
takes  on  a  peculiar  stertorous  character,  particularly  during  sleep.  Mucus  collects 
in  the  mouth  and  throat.  Upon  swallowing,  there  is  often  regurgitation  through 
the  mouth  or  nose,  or  some  of  the  food  gets  into  the  windpipe  and  causes  violent 
coughing.  The  lymph-glands  of  the  jaws  are  usually  somewhat  swollen,  and  the 
neighboring  parts  may  seem  slightly  cedematous.  After  a  week  or  two  the  dysp- 
noea gradually  increases.  Respiration  becomes  more  and  more  laborious,  with 
loud  rattling,  and  the  signs  of  stenosis.  The  jugular  veins  become  distended,  the 
lips  cyanotic,  and  portions  of  the  thorax  are  redacted  during  inspiration.  The 
voice  is  feeble«  and  may  be  hoarse  and  indistinct. 

The  correct  interpretation  of  these  symptoms,  which  are  common  to  various 
disorders,  requires  a  careful  examination  of  the  throat.  It  must  be  confessed  that 
this  has  its  difficulties  in  an  infant.  Still,  we  can  sometimes  see  distinctly  a  swell- 
ing in  the  posterior  wall  of  the  pharynx.  This  may  be  either  in  the  median  line 
or  on  one  side.  All  doubt  is  removed  by  digital  examination,  in  making  which, 
however,  we  must  insert  a  wedge  between  the  teeth,  to  avoid  being  bitten.  The 
finger  detects  fluctuation. 


INFLAMMATION  AND  ULCER  OF  THE  (ESOPHAGUS.  361 

The  diagnosis  once  established,  the  abscess  must  be  opened  at  once.  We 
should  not  delay,  even  if  the  dyspnoea  has  not  yet  become  extreme.  To  use  the 
finger-nail  for  the  purpose,  as  has  been  recommended,  is  permissible  only  in  an 
emergency.  As  a  rule,  incision  is  made  with  a  bistoury,  of  which  all  but  the 
point  is  guarded  with  sticking-plaster.  The  left  index-finger  is  placed  upon  the 
abscess,  and  used  as  a  guide.  Meanwhile,  the  child's  head  is  kept  upright,  and,  as 
soon  as  the  cut  is  made,  bent  over  forward.  The  pus  pours  out  in  abundance.  It 
is  advisable  to  syringe  out  the  mouth  repeatedly  with  lukewarm  water.  The 
threatening  symptoms  vanish  almost  instantly  upon  the  escape  of  the  pus. 
Exceptionally,  the  abscess  refills  and  requires  a  second  incision. 

If  the  trouble  is  not  correctly  diagnosticated,  or  if  the  abscess  is  not  opened 
promptly,  the  patient  may  suffocate.  Or  the  abscess  may  burst  spontaneously ; 
then  there  is  either  speedy  recovery,  or  asphyxia  from  the  pus  filling  the  larynx. 
In  some  instances,  where  a  retropharyngeal  abscess  has  not  been  properly  treated, 
the  pus  has  gravitated  far  down  into  the  neck  and  posterior  mediastinum.  The 
recognition  and  incision  of  the  abscess  may  prove  very  difficult  if  from  the  start 
it  is  situated  lower  down  in  the  throat  than  usual. 

Analogous  to  this  acute  idiopathic  abscess  of  which  we  have  been  speaking  is 
the  chronic  abscess  due  to  caries  of  the  cervical  vertebrae.  This  should  not  be 
opened  unless  there  is  danger  of  asphyxia. 

Retropharyngeal  abscesses  sometimes  occur  in  pyaemia  or  other  severe  acute 
infectious  diseases,  but  have  hardly  any  interest  except  to  the  pathologist.* 


SECTION  TIT. 
Diseases  of  the  (Esophagus. 

CHAPTER  I. 
INFLAMMATION   AND   ULCER   OF   THE   OESOPHAGUS. 

^Etiology  and  Pathology. — The  various  forms  of  oesophageal  inflammation  and 
ulceration  are  not  of  very  great  clinical  importance.  The  processes  are  seldom  of 
a  severe  grade,  or,  if  so,  they  are  generally  a  part  of  some  complicated  disease,  to 
which  they  seldom  contribute  prominent  symptoms.  Very  likely  the  milder  forms 
of  inflammation  occur  frequently,  but  the  symptoms  are  hardly  ever  character- 
istic. 

A  simple  catarrhal  inflammation  of  the  oesophageal  mucous  membrane  may 
be  caused  by  swallowing  substances  which  are  injurious  mechanically,  chem- 
ically, or  from  their  temperature.  It  may  also  occur  in  the  general  infectious 
diseases,  such  as  typhoid  and  typhus  fevers,  and  the  acute  exanthemata.  Any 
inflammation  of  neighboring  tissues  may  extend  into  the  oesophagus.  Chronic 
catarrh  is  seen  in  heart  disease,  from  the  passive  congestion.  It  is  also  found  in 
the  vicinity  of  other  chronic  oesophageal  diseases,  particularly  cancers  and  diver- 
ticula (vide  infra). 

The  acute  catarrh  is  distinguished  by  not  having  the  usual  increase  of  secre- 
tion.    The  epithelium  grows  spongy,  as  a  rule,  and  is  cast  off  more  rapidly  than 

*  Tuberculosis  of  the  pharynx  is  spoken  of  in  the  chapter  on  pulmonary  tuberculosis,  p.  226.  New 
growths  in  the  mouth  or  pharynx  belong  to  the  domain  of  surgery. 


362  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

usual,  so  as  to  suggest  the  name  of  a  desquamative  catarrh.  It  is  in  only  a  few 
cases  that  the  scanty  mucous  glands  become  swollen  and  look  like  papules  upon 
the  surface  of  the  membrane;  this  form  is  called  follicular  catarrh.  In  limited 
areas  the  desquamation  may  be  complete,  giving  rise  to  small  catarrhal  erosions. 
Likewise,  the  swollen  follicles  may  break  down  into  small  follicular  ulcers. 

In  chronic  catarrh  there  is  a  moderate  increase  in  the  secretion  of  mucus,  and 
a  marked  thickening  of  the  epithelium.  In  very  protracted  cases  actual  papillo- 
mata  may  finally  be  formed.     In  some  cases  ulcers  are  seen. 

Croupous  and  diphtheritic  inflammations  of  the  oesophagus  are  very  rare.  We 
have  already  said  that  the  specific  pharyngeal  diphtheria  frequently  extends  into 
the  larynx,  but  only  exceptionally  into  the  gullet.  Still,  we  have  ourselves  seen 
in  a  child  a  stricture  in  the  upper  third  of  the  oesophagus,  which  was  said  to  have 
been  a  result  of  a  severe  attack  of  diphtheria.  Isolated  cases  of  diphtheritic 
oesophagitis  have  also  been  seen  in  connection  with  severe  infectious  diseases, 
such  as  typhus,  typhoid,  small-pox,  cholera,  pyaemia,  and  pulmonary  tuberculosis, 
as  well  as  in  the  course  of  Bright's  disease  and  cancer.  In  variola  it  is  not  un- 
usual for  pocks  to  appear  upon  the  oesophageal  mucous  membrane. 

A  purulent,  phlegmonous  oesophagitis  now  and  then  attacks  the  submucous 
layer.  It  may  be  either  diffuse  or  circumscribed.  The  mucous  membrane  is  dis- 
sected up  from  the  muscular  layer  by  the  pus,  and  pushed  inward,  so  as  to  dimin- 
ish the  lumen  of  the  oesophagus  more  or  less.  Most  of  the  cases  end  by  the  dis- 
charge of  matter  into  the  tube,  when  complete  recovery  may  ensue.  If  the  mu- 
cous membrane,  however,  has  been  extensively  undermined,  Zenker  states  that  a 
fissure-like  cavity  may  be  left,  even  after  healing  has  taken  place.  Its  walls  grow 
smooth,  and  finally  acquire  a  layer  of  fresh  epithelium. 

Purulent  oesophagitis  is  caused  either  by  the  presence  of  foreign  bodies  in  the 
oesophagus,  or  by  purulent  inflammation  in  neighboring  parts,  as  in  glandular 
abscess,  vertebral  abscess,  or  laryngeal  perichondritis.  It  has  now  and  then 
resulted  from  the  action  of  concentrated  acids  and  the  like  upon  the  mucous 
membrane. 

The  action  of  corrosive  poisons  (corrosive  oesophagitis)  is  to  cause  necrosis 
of  the  tissues,  which  in  its  turn  produces  inflammation.  The  inner  surface  of 
the  oesophagus  is  converted  into  a  rotten,  haemorrhagic,  sloughing  mass,  of  a 
dirty  gray  or  almost  black  color.  The  muscular  layer  itself  may  be  partly  de- 
stroyed. If  death  does  not  occur  speedily,  the  necrosed  portions  come  away,  leav- 
ing extensive  purulent  ulcers  behind.  These,  if  they  heal  at  all,  cause  large  cica- 
trices and  stenosis. 

Symptoms. — The  milder  cases,  as  we  have  stated,  produce  almost  no  distinctive 
symptoms.  Possibly  there  may  be  pain  along  the  oesophagus,  or  at  some  one  point 
in  it,  during  deglutition.  In  a  more  severe  case  the  pain  may  be  great ;  but  the 
other  symptoms  are  usually  too  grave  for  this  to  excite  special  attention.  Labo- 
rious deglutition,  and  the  feeling  as  if  the  food  were  inclined  to  stick  in  the  throat, 
result  from  implication  of  the  muscular  layer.  A  diagnosis  of  the  particular  form 
of  oesophagitis  is  attainable  only  when  the  aetiology  guides  us  to  it. 

Treatment  must  be  purely  symptomatic.  No  solid  food  should  be  taken.  The 
pain  is  to  be  allayed  by  bits  of  ice,  or  by  morphine. 


DILATATION  OF  THE  (ESOPHAGUS.  363 

CHAPTER   II. 

DILATATION   OF   THE   (ESOPHAGUS. 

1.  Diffuse  Dilatation. 

Diffuse,  spindle-shaped  dilatation  of  the  oesophagus  is  observed  as  a  result  of 
stricture  of  the  cardiac  orifice.  At  first  the  muscular  coat  hypertrophies  as  the 
orifice  contracts,  and  is  able  to  overcome  the  obstruction,  so  that  there  is  no  dila- 
tation; hut  as  soon  as  the  muscles  are  paralyzed,  and  food  collects  behind  the 
stricture,  the  dilatation  begins  and  keeps  on  increasing.  The  ectasis  is  greatest  at 
the  lower  end  of  the  tube,  as  is  natural  from  its  mode  of  origin,  and  gradually 
diminishes  upward. 

There  have  been  a  very  few  well-substantiated  instances  of  this  diffuse  spindle- 
shaped  dilatation,  without  any  demonstrable  stenosis  of  the  cardiac  orifice.  Their 
cause  is  unknown.  Sometimes  the  walls  of  the  oesophagus  may  have  been  ren- 
dered more  yielding  and  less  contractile  by  a  precedent  inflammation  or  other 
disorder.  In  other  cases,  some  chance  bend  or  distortion  of  the  lower  end  of  the 
oesophagus  may  have  produced  a  mechanical  obstruction.  In  some  cases  the  ex- 
citing cause  is  said  to  be  a  blow  on  the  chest,  or  the  lifting  of  a  heavy  weight. 

The  symptom  of  this  condition,  when  well  developed,  is  a  chronic  difficulty  in 
deglutition,  lasting  perhaps  for  years.  The  patient  himself  feels  that  most  of  the 
food  he  eats  does  not  reach  the  stomach,  but  lodges  higher  up.  Usually  the  food 
is  soon  afterward  vomited,  or  rather  gulped  up.  When  there  is  stenosis  of  the 
cardiac  orifice,  the  explanation  of  these  symptoms  is  easy.  It  is  much  harder 
to  explain  the  almost  equal  dysphagia  where  there  is  dilatation  without  stenosis. 
Sometimes  a  localized  bulging  of  the  wall  causes  the  food  to  collect  in  that  spot, 
and  thus  to  obstruct  the  lumen.  As  is  to  be  expected,  the  partial  or  complete 
hindrance  to  the  ingestion  of  food  results  in  marasmus. 

If  there  is  stenosis,  it  can  easily  be  detected  with  the  oesophageal  sound,  and 
all  the  symptoms  thus  explained.  In  the  rare  cases,  however,  of  diffuse  dilata- 
tion without  stenosis,  the  use  of  the  sound  does  not  give  us  so  much  information. 
If  the  instrument  passes  readily  into  the  stomach,  we  may  safely  exclude  strict- 
ure ;  but,  in  one  case  of  our  own,  we  made  an  erroneous  diagnosis  of  a  diverticu- 
lum, because  the  sound  sometimes  glided  readily  into  the  stomach,  and  sometimes 
could  not  be  passed.  A  pocket  must  have  been  formed  at  the  lower  end  of  the 
dilated  tube,  in  which  the  sound  caught. 

The  treatment  is  directed  chiefly  to  the  satisfactory  nourishment  of  the  patient; 
for  the  oesophageal  trouble  itself  is  dangerous  only  as  its  prevents  the  taking  of 
food  and  leads  to  starvation.  We  do  not  speak  of  the  initial  lesion,  if  there  be 
one,  which  causes  the  dilatation.  If  nourishment  can  be  given  through  a  stomach- 
tube,  the  patient  almost  invariably  shows  a  rapid  improvement,  which  lasts  as 
long  as  the  artificial  feeding  can  be  kept  up.  If,  however,  any  cause  prevents  the 
introduction  of  the  tube,  we  must  resort  either  to  nutrient  enemata  {vide  infra) — 
and  these  will  not  support  the  system  indefinitely — or  we  must  make  a  gastric 
fistula.  In  the  latter  case  the  prognosis  depends  on  the  success  of  the  operation 
and  the  nature  of  the  original  lesion. 

2.  Diverticula. 

iEtiology  and  Pathology. — Circumscribed  pouches  in  the  wall  of  the  oesopha- 
gus are  termed  diverticula.  They  are  divided  into  two  essentially  distinct  varie- 
ties, according  to  their  mode  of  origin.  Zenker  has  given  them  the  names  of 
pressure  and  traction  diverticula. 


364  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

The  diverticulum  due  to  pressure  is  extremely  rare.  It  is  caused  by  pressure 
upou  the  mucous  membraue  from  within,  by  which  some  abnormally  weak  spot 
is  forced  outward.  All  cases  that  have  been  carefully  examined  thus  far  have 
shown  that,  histologically,  the  wall  of  the  diverticulum  is  not  the  distended  but 
otherwise  unchanged  wall  of  the  oesophagus,  but  is  composed  exclusively  of  the 
mucous  membrane  and  the  thickened  submucous  coat.  We  are  therefore  obliged 
to  suppose  that  the  mucous  membrane  is  pushed  out  like  a  hernia  through  some 
gap  in  the  muscular  coat.  It  is  only  about  the  neck  of  the  diverticulum  that  any 
muscular  fibers  are  found. 

The  original  factor,  therefore,  in  the  occurrence  of  a  pressure  diverticulum  is 
apparently  to  be  sought  in  some  circumscribed  lesion  of  the  muscular  coat.  As  a 
result  of  several  observations,  it  is  established  that  a  foreign  body,  sticking  in  the 
throat,  may  separate  some  of  the  muscular  fibers  and  push  the  mucous  membrane 
through  the  gap  thus  formed.  Or  a  severe  injury  leads  to  a  trifling  rupture  of 
the  muscular  coat,  and  then  the  food,  as  it  is  being  swallowed,  presses  out  the 
mucous  membrane  at  this  weakened  spot.  There  are  still  many  other  cases  where 
the  true  origin  of  the  diverticulum  remains  obscure. 

As  soon,  however,  as  the  formation  of  the  pouch  has  once  begun,  there  are 
many  influences  to  make  it  grow  larger.  Each  successive  bit  of  food,  as  it 
glides  by,  presses  upon  this  yielding  and  inelastic  spot.  Gradually  a  little  sac  is 
formed,  in  which  bits  of  food  lodge.  These  exercise  a  constant  pressure  upon  the 
walls  of  the  pouch,  and  by  their  weight  drag  it  bodily  downward.  The  larger  the 
pouch,  the  more  it  holds,  and  consequently  the  more  it  grows.  Thus  a  pressure 
diverticulum  of  the  smallest  size  originally  may  gradually  attain  to  a  diameter  of 
four  inches  or  more.  The  general  shape  of  the  diverticulum  may  approach  the 
hemispherical,  or  it  may  be  more  cylindrical  or  pear-shaped. 

It  is  remarkable  that,  with  very  rare  exceptions,  these  pressure  diverticula  are 
always  situated  at  the  beginning  of  the  oesophagus,  or  rather  between  it  and 
the  pharynx,  and  almost  invariably  affect  the  posterior  wall.  The  pouch  hangs, 
therefore,  in  front  of  the  spinal  column.  It  pushes  out  through  the  lowest  fibers 
of  the  inferior  constrictor  of  the  pharynx;  and  the  feebleness  of  this  muscle  is 
apparently  a  potent  factor  in  determining  the  precise  point  of  origin. 

The  cases  thus  far  seen  have  been  almost  all  in  men,  and  at  a  rather  advanced 
age.     A  few  cases  have  occurred  in  children. 

Traction  diverticula  are  much  more  common,  but  in  most  instances  have  little 
interest  except  for  the  pathologist.  They  are  not  infrequently  found  unexpectedly 
at  the  autopsy.  Rokitansky,  and  later  Zenker,  have  given  explanations  of  their 
occurrence :  some  tissue,  which  has  formed  adhesions  to  the  oesophagus,  contracts 
and  gradually  pulls  out  the  oesophageal  wall  in  the  shape  of  a  funnel.  Bronchial 
glands  are  apt  to  be  the  seat  of  the  contractile  change.  These  glands  are  situated 
near  the  bifurcation  of  the  trachea,  and  accordingly  the  traction  diverticula  occur 
oftenest  at  this  level.  There  may  be  two  or  three  in  one  subject.  They  are  rarely 
over  a  third  of  an  inch  in  depth.  From  within,  the  mucous  membrane,  much 
wrinkled  transversely,  is  seen  to  be  drawn  toward  the  apex  of  the  diverticulum. 
The  wall  of  the  latter  consists  either  of  the  mucous  membrane  alone,  bulging  out 
like  a  hernia,  or  of  the  mucous  membrane  covered  by  the  muscular  layer.  Inas- 
much as  children  quite  often  suffer  from  suppuration  and  caseation  of  bronchial 
glands,  with  subsequent  shrinkage,  we  see  why  traction  diverticula  are  frequent 
in  children. 

Clinical  History. — The  large  pressure  diverticula  always  cause  grave  symptoms, 
for  they  obstruct  more  and  more  each  day  the  passage  of  food.  At  first  there  is 
scarcely  any  disturbance.  Gradually,  however,  deglutition  is  impeded.  A  por- 
tion of  the  food  lodges  in  the  pouch,  and  is  either  wholly  or  in  part  regurgitated, 


DILATATION   OF  THE  OESOPHAGUS.  365 

though  perhaps  not  immediately.  Decomposition  is  apt  to  take  place  in  the  con- 
tents of  the  diverticulum,  giving1  rise  to  foulness  of  the  breath  and  to  nausea.  The 
danger  reaches  its  climax  when  the  distended  sac  presses  sidewise  upon  the 
oesophagus  and  closes  its  lumen,  so  that  no  food  reaches  the  stomach.  After 
protracted  strangling  and  vomiting,  the  material  may  be  in  part  ejected,  and  the 
patient  enabled  once  more  to  swallow. 

Of  course  the  symptoms  in  individual  cases  depend  upon  the  mechanical  con- 
ditions present,  and  may  vary  greatly.  Patients  contrive  all  sorts  of  manipula- 
tions, by  which  they  manage  to  get  at  least  some  portion  of  their  food  down.  Such 
individuals  may  maintain  a  tolerable  degree  of  nutrition  for  years,  although  they 
scarcely  ever  are  in  a  normal  condition.  But  at  last  some  cause  or  other  renders 
the  amount  of  food  ingested  inadequate ;  whereupon  a  rapidly  progressive  maras- 
mus sets  in,  and  the  patient  will  inevitably  starve  to  death  unless  some  relief  is 
afforded. 

The  most  valuable  objective  evidence  in  these  cases  is  gained  by  the  use  of  the 
oesophageal  sound.  If  the  sound  enters  the  sac,  its  passage  is  impeded.  If  it 
happens  to  slip  by  the  mouth  of  the  diverticulum,  it  glides  readily  into  the 
stomach.  This  varying  result  may  sometimes  be  obtained  at  one  sitting  by 
repeated  trials,  and  is  of  the  greatest  importance  in  making  the  diagnosis. 

In  some  instances  where  the  sac  was  large,  a  tumor  in  the  neck  has  been 
observed  at  one  side  of  the  trachea,  appearing  after  eating  and  disappearing  when 
the  sac  emptied  itself.  Symptoms  due  to  compression  of  the  recurrent  and 
phrenic  nerves  and  of  the  blood-vessels  have  been  noticed  in  some  cases. 

Auscultation  of  the  oesophagus  during  the  act  of  swallowing  has  been  practiced, 
and,  of  late,  attempts  have  been  made  to  examine  it  with  a  speculum.  Whether 
these  methods  of  investigation  will  prove  valuable  for  diagnosticating  diverticula, 
experience  must  determine. 

The  traction  diverticula  are  usually  of  no  clinical  importance.  They  do  not 
affect  deglutition  at  all,  and  their  size  is  too  limited  to  permit  any  great  accumu- 
lation of  food  in  them.  There  is  but  one  way  in  which  they  are  dangerous:  the 
apex  of  the  funnel  may  undergo  ulceration  and  perforation.  A  foreign  body,  like 
some  bit  of  food,  produces  necrosis  of  the  wall,  by  what  is  probably  at  first  a  purely 
mechanical  irritation.  The  tissue  ulcerates;  and  then  the  inflammation  may 
gradually  progress  till  it  causes  a  severe  and  usually  fatal  illness.  The  most  fre- 
quent event  is  perforation  into  a  bronchus,  followed  by  the  aspiration  of  food  and 
pulmonary  gangrene.  Or  the  perforation  takes  place  into  the  pleural  cavity, 
exciting  an  ichorous  empyema.  In  other  cases  the  pericardium  or  a  large  vein 
has  been  perforated.  Many  a  case  of  apparently  spontaneous  pulmonary  gan- 
grene or  purulent  inflammation  of  the  anterior  mediastinum  or  empyema  has 
been  found  at  the  autopsy  to  have  been  brought  aboiit  in  the  way  above  indicated. 
These  occurrences  are  fortunately,  however,  exceptional. 

Treatment. — The  only  possible  way  of  treating  the  large  pressure  diverticula 
successfully  would  be  by  operation.  Perhaps  surgery  will  some  day  win  victories 
in  this  domain.  In  the  mean  while  our  efforts  are  confined  to  sustaining  the 
patient.  If  he  can  not  swallow,  we  must  try  to  feed  him  through  a  tube.  As 
long  as  this  is  possible,  starvation  is  averted.  The  best  way  is  to  have  the  patient 
pass  the  tube  himself.  He  will  find  out  how  best  to  avoid  the  sac  and  reach  the 
stomach.  If  food  can  no  longer  be  given  in  this  way,  there  remain  two  alterna- 
tives: rectal  feeding  {vide  infra),  or  making  a  gastric  fistula.  As  to  the  latter, 
there  has  been  thus  far  very  little  practical  experience,  because  cases  are  so  rare. 

The  traction  diverticula  admit  of  no  special  treatment.  If  the  events  above 
mentioned  occur,  we  must  endeavor  to  meet  the  indications  of  the  individual  case. 


366  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

CHAPTER  III. 
STENOSIS   OF   THE  (ESOPHAGUS. 

etiology  and  Pathology. — Contractions  of  the  oesophagus  occur  with  such 
relatively  great  frequency  that  they  are  the  most  important  of  all  its  disorders. 
They  originate  in  various  ways.  By  far  the  commonest  cause  is  ring-shaped  car- 
cinoma of  the  tube.  The  new  growth  in  the  mucous  membrane  encroaches  more 
and  more  upon  the  lumen  of  the  oesophagus,  until  finally  it  fills  it.  Carcinoma 
will  be  discussed  at  length  in  the  next  chapter.  We  shall  here  confine  our  atten- 
tion to  its  purely  mechanical  action  in  causing  stenosis. 

(Esophageal  tumors  other  than  cancer  are  very  rare.  Fibrous  pedunculated 
polypi  have  been  observed  a  few  times.  They  usually  originate  in  the  lowest 
portion  of  the  anterior  wall  of  the  pharynx,  hanging  down  into  the  oesophagus, 
which  they  may  thus  obstruct. 

A  second  cause  of  stenosis  is  the  contraction  of  cicatrices  of  the  oesophageal 
wall.  The  most  frequent  occasion  for  this  is  the  extensive  ulceration  caused  by 
caustic  poisons,  such  as  concentrated  acids  or  alkalies.  If  the  victim  escapes  a 
speedy  death,  he  is  almost  certain  to  have  extensive  scars  formed  in  the  wall  of 
the  oesophagus.  These  scars  radiate  irregularly  in  all  directions,  and,  contracting, 
may  almost  completely  close  the  tube. 

Ulcers  from  other  causes,  resulting  in  stenosis  due  to  the  scars  they  leave,  are 
among  the  greatest  rarities.  Syphilis  has  been  the  well-established  cause  in  some 
instances,  and  Quincke  has  described  a  few  cases  where  there  were  ulcers  at  the 
lower  end  of  the  oesophagus  analogous  to  the  round  ulcer  of  the  stomach,  or 
"  ulcer  due  to  digestion  "  (vide  infra).  These  ulcers  also  may  eventually  produce 
cicatricial  stenosis. 

A  third  and  rare  cause  of  stenosis  of  the  oesophagus  is  compression  from 
tumors  external  to  it.  Such  swellings  may  originate  in  the  thyroid  gland,  or  in 
the  lymph-glands  of  the  neck  or  the  anterior  mediastinum;  or  the  swelling  may 
be  due  to  a  vertebral  abscess  or  an  aortic  aneurism.  This  form  of  stenosis  is  sel- 
dom extreme,  for  the  portion  of  the  tube  pressed  upon  is  usually  limited. 

Next  on  the  list  after  stenosis  due  to  compression  is  usually  placed  what  is 
called  intermittent  dysphagia  [dysphagia  lusoria).  This  term  is  applied  to  the 
difficulty  in  swallowing  which  is  said  to  be  caused  by  an  anomaly  in  the  course  of 
the  right  subclavian  artery.  The  artery  is  given  off  as  the  last  branch  from  the 
arch  of  the  aorta,  and  runs  toward  the  right  side  just  behind  or  just  in  front  of  the 
oesophagus.  It  seems,  however,  a  priori  improbable  that  the  feeble  pressure  of 
this  vessel  as  it  pulsates  should  impede  deglutition ;  nor  has  it  yet  been  proved 
to  do  so.  It  would  be  more  natural  to  believe,  what  was  indeed  the  original  ex- 
planation of  the  phenomenon,  that  a  large  morsel  of  food  passing  down  the  oesoph- 
agus compresses  the  vessel  and  thus  excites  uneasiness  and  palpitation. 

Stenosis  due  to  foreign  bodies  belongs  to  surgery.  It  need  not  be  said  that 
the  clinical  symptoms  differ  greatly  in  different  cases.  Not  only  the  obstruction, 
but  also  a  possible  laceration  and  consequent  inflammation  are  to  be  considered. 
Occasionally  thrush  has  been  abundant  enough  to  cause  pronounced  symptoms  of 
stenosis. 

Above  the  point  of  stenosis,  no  matter  how  the  condition  arose,  if  only  it  is 
well  developed  and  has  lasted  a  certain  length  of  time,  the  circular  fibers  of  the 
muscular  coat  are  more  or  less  hypertrophied.  This  hypertrophy  is  due  to  the 
increased  force  required  to  propel  the  ingesta  downward.  In  many  cases  the  tube 
is  also  diffusely  dilated  above  the  stenosis. 

Symptoms. — The  effect  of  every  oesophageal  stenosis  is  to  render  deglutition 


STENOSIS  OF  THE  OESOPHAGUS.  S61 

difficult.  If  the  case  is  a  mild  one,  the  patient  experiences  nothing  more  than  a 
moderate  pressure  in  the  oesophagus  upon  swallowing.  He  feels  that  the  mor  el 
is  longer  than  usual  in  reaching  the  stomach.  Very  soon  he  notices  that  solid 
food  and  large  morsels  can  he  swallowed  only  with  difficulty.  Accordingly,  he 
is  gradually  led  to  confine  himself  to  a  liquid  diet,  takes  only  small  mouthfuls, 
and  always  washing  down  any  solid  food  with  a  swallow  or  two  of  liquid.  The 
narrower  the  stenosis,  the  more  he  is  troubled.  Finally,  even  liquids  can  he 
taken  only  slowly  and  in  sips. 

It  must  not  be  thought  that  the  dysphagia  just  described  is  due  exclusively  to 
the  mechanical  obstruction  of  the  lumen.  Sometimes  a  patient  is  almost  entirely 
unable  to  take  nourishment,  and  yet  at  the  autopsy  no  adequate  mechanical 
obstruction  is  found.  The  dysphagia  must  therefore  be  due  to  some  lesion  of  the 
muscular  coat  of  the  oesophagus.  The  impaired  contractility  of  the  muscular  coat 
at  the  affected  spot  is  always  a  potent  factor  in  impeding  deglutition. 

As  soon  as  the  dysphagia  has  become  considerable  there  is  usually  regurgita- 
tion of  food.  At  first  only  a  portion  of  the  food  comes  up,  but  at  last  all  of  it.  If 
the  tube  has  become  dilated  above  the  stenosis,  food  may  collect  for  some  hours, 
and  then  be  regurgitated,  mixed  with  an  abundance  of  very  tenacious  mucus. 
We  saw  a  case  of  this  kind  where  the  patient  could  fill  the  sac  above  the  stricture 
with  quite  a  large  amount  of  fluid  without  a  drop  reaching  the  stomach.  If  he 
bent  his  head  sharply  forward,  the  collected  fluid  would  run  out  again  through 
his  mouth.  It  was  not  until  the  pouch  was  completely  filled  that  a  small  amount 
of  liquid  would  trickle  through  the  stenosis  into  the  stomach. 

Although  the  dysphagic  symptoms  above  described  generally  imply  oesophag- 
eal stenosis,  the  diagnosis  can  not  be  really  established  without  using  a  sound. 
Upon  introducing  this,  it  is  usually  easy  to  detect  the  obstacle,  which  may  either 
allow  the  instrument  to  pass,  with  a  noticeable  jerk,  or  else  prevent  its  further 
progress.  By  measuring  the  length  of  the  portion  introduced  before  the  stenosis 
is  reached  we  can  learn  its  position.  On  the  average,  the  entire  distance  from  the 
teeth  to  the  cardiac  sphincter  is  in  adults  sixteen  inches  (40  cm.) ;  from  the  teeth 
to  the  beginning  of  the  oesophagus,  six  inches  (15  cm.);  and  consequently  the 
length  of  the  latter  is  about  ten  inches  (25  cm.).  If  we  succeed  in  passing  a 
smaller  sound  through  the  stricture,  the  feeling  as  we  move  it  back  and  forth  will 
give  us  some  idea  of  the  length  of  the  stenosis,  or  will  detect  the  existence  of 
several  lying  one  below  the  other,  etc.  If  the  end  of  the  sound  can  be  moved 
about  very  freely  above  the  stenosis,  we  may  conclude  that  the  tube  is  dilated 
there. 

Hamburger  has  employed  auscultation  of  the  oesophagus  for  diagnostic  pur- 
poses. If  we  listen  behind,  to  the  left  of  the  upper  dorsal  vertebrae  during  deglu- 
tition, we  hear  a  gurgling  sound,  due  to  the  act  of  swallowing,  extending  down 
the  tube  to  the  stenosis,  but  no  farther.  Then  come  all  sorts  of  sounds,  some  of 
them  caused  by  the  fluid  trickling  slowly  through  the  narrow  part,  and  some 
caused  by  regurgitation.  In  general,  the  results  obtained  by  auscultation  are 
rather  variable  and  uncertain. 

Having  established  the  fact  of  the  existence  of  a  stenosis,  we  have  next  to  deter- 
mine its  nature,  which  is  our  chief  guide  to  prognosis  and  treatment.  In  certain 
instances  the  history  of  the  case  gives  us  the  needed  information.  The  diagnosis 
of  cicatricial  stricture  can  hardly  be  made  unless  the  patient  himself  tells  us  of 
being  burned  or  injured  by  caustic  poisons.  The  previous  history  is  likewise  of 
great  importance  if  the  stenosis  be  due  to  foreign  bodies  or  to  syphilis.  If  no  de- 
cisive serological  factor  can  be  elicited,  we  must  carefully  examine  the  neck  and 
thorax,  with  regard  to  the  possible  existence  of  a  swelling  compressing  the  oesoph- 
agus.    In  cases  where  an  aortic  aneurism  has  acted  in  this  way,  a  rhythmical 


368  DISEASES  OF  THE  DIGESTIVE  OEGANS. 

movement  has  sometimes  been  communicated  to  the  free  end  of  a  sound  intro- 
duced as  far  as  the  stenosis.  If  the  physical  examination  does  not  reveal  a  com- 
pressing  tumor,  and  particularly  if  the  stenosis  has  developed  gradually  and  in  an 
elderly  person,  we  are  almost  compelled  to  assume  that  there  is  cancer  of  the 
oesophagus.  This  is,  after  all,  by  far  the  most  frequent  cause  of  oesophageal  strict- 
ure. If  the  new  growth  has  ulcerated,  a  little  portion  of  it  may  adhere  to  the 
end  of  the  probe,  and,"  on  microscopic  examination,  render  our  diagnosis  of  carci- 
noma certain. 

The  prevailing  characteristic  in  stenosis  of  the  oesophagus  is  inanition,  increas- 
ing as  the  dysphagia  increases.  The  patient  gets  to  be  very  much  emaciated,  and 
so  feeble  that  he  can  not  leave  his  bed.  The  temperature  is  subnormal;  for  weeks 
it  keeps  at  95°  to  97°  (35°-36°  C).  The  pulse  grows  very  small  and  slow,  being 
40  to  60  per  minute.  The  heart-sounds  are  soft.  Respiration  is  superficial  and 
slow;  and  toward  the  close  of  life  short  pauses  occur  after  expiration,  before 
inspiration  begins.  The  stomach  and  intestines  are  so  empty  that  the  abdomen 
is  very  concave,  while  the  abdominal  walls  usually  feel  tense  and  resistant.  In 
all  cases  where  the  nature  of  the  stenosis  precludes  the  possibility  of  cure  or 
improvement,  death  results  from  increasing  exhaustion,  the  lamp  of  life  gradu- 
ally flickering  out. 

Prognosis  and  Treatment. — In  prognosis  the  main  factor  is  of  course  the 
nature  of  the  stenosis.  If  it  is  due  to  foreign  bodies  or  to  cicatrices,  it  may  be 
completely  cured.  In  stenosis  from  other  causes  it  is  often  possible  to  produce 
considerable  improvement,  at  least  temporarily.  The  final  result  must  be  con- 
fessed to  be  usually  unfavorable,  as  we  should  expect  from  the  nature  of  the  origi- 
nal trouble. 

The  treatment  is  chiefly  mechanical.  We  shall  not  speak  of  operations  for 
the  removal  of  new  growths,  etc.  What  we  do  refer  to  is  a  methodical  and  grad- 
ual dilatation  of  the  stricture.  Its  results  are  sometimes  brilliant,  particularly  in 
cicatricial  stenosis.  Other  varieties,  like  the  stenosis  from  cancer,  may  sometimes 
undergo  considerable  though  but  temporary  improvement  with  this  treatment. 

The  best  instrument  to  employ  is  the  flexible,  so-called  English,  oesophageal 
bougie.  It  is  made  in  all  sizes.  If  the  stenosis  is  very  narrow  indeed,  we  may 
have  to  resort  to  catgut  at  first.  Whalebone  bougies,  with  olive-shaped  ivory  tips 
of  various  sizes  to  screw  on  the  end,  are  also  good,  except  that,  being  stirrer,  there 
is  more  danger  in  using  them.  For  introduction  of  the  bougie,  the  patient  should 
be  seated,  with  the  head  slightly  extended  backward.  The  first  two  fingers  of  the 
left  hand  are  introduced  into  the  throat  and  guide  the  instrument,  previously 
well  oiled,  over  the  back  of  the  tongue  and  the  epiglottis  into  the  oesophagus.  Of 
course,  no  violence  must  be  used.  Otherwise  a  perforation  might  occur  if  there 
were  a  soft,  broken-down  cancer,  or  an  aortic  aneurism.  However,  such  a  mis- 
fortune is  very  exceptional. 

The  use  of  the  bougie  is  almost  invariably  beneficial  if  the  stricture  can  be 
passed.  The  patient  generally  finds  that  he  can  swallow  easier  than  before,  and 
will  himself  request  a  repetition  of  the  performance.  If  the  patient  is  an  intelli- 
gent person,  it  is  advisable  to  have  him  introduce  the  bougie  himself.  Patients 
often  acquire  even  greater  skill  with  it  than  the  physician  has.  The  bougie  should 
oe  passed  regularly  once  a  day,  or,  at  most,  twice  daily ;  and  in  favorable  cases  we 
shall  be  able  gradually  to  increase  the  size.  If  so,  the  symptoms  speedily  abate, 
and,  with  the  increased  ingestion  of  food,  the  patient  gains  flesh  very  fast. 

If  the  stenosis  is  extreme,  and,  although  it  admits  the  bougie,  does  not  allow 
of  sufficient  nourishment,  we  must  pass  a  tube  into  the  stomach  through  which 
to  introduce  liquid  food.  Milk  is  the  best  food  to  choose.  Raw  eggs,  sugar,  wine, 
etc.,  may  be  mixed  with  it.     The  various  infant's  foods  and  Hartenstein's  "legu- 


CANCER  OF  THE  OESOPHAGUS.  369 

minose"  are  also  excellent.  Their  consistence  is  favorable  for  the  purpose,  and 
they  supply  a  considerable  amount  of  nourishment  in  a  small  bulk. 

If  this  means  also  fails  us,  two  alternatives  are  left,  unless  we  are  to  resign 
our  patient  to  death  by  starvation  :  (1)  operative  interference,  cesophagotomy  if 
the  stenosis  is  high  up,  otherwise  gastrostomy ;  (2)  rectal  feeding. 

For  information  about  the  operations  we  mast  refer  to  surgical  literature. 
As  to  feeding  per  rectum,  its  results  are  never  brilliant.  It  is  indeed  probable 
that  life  may  be  by  this  means  somewhat  prolonged,  but  not  indefinitely.  But 
the  moral  effect  is  very  valuable,  when  the  patient  could  otherwise  receive  no 
nourishment  whatever.  The  sufferer  feels  that  something  is  being  done  to  avert 
absolute  starvation. 

The  simplest  materials  for  the  nutrient  enemata  are  milk,  eggs,  and  wine;  to 
which  we  may  add  pepsine  and  pancreatine  in  the  hope  of  promoting  absorption. 
Leube's  pancreatic  meat  emulsion  is  still  better,  although  more  troublesome  in  its 
preparation.  Leube1s  directions  are  as  follows:  About  five  ounces  (150  grm.)  of 
meat,  cut  very  thin  and  then  minced  finely,  and  about  two  ounces  (50  grm.j  of 
minced  pancreas  (from  the  calf)  free  from  fat,  are  to  be  stirred  with  about  three 
ounces  (100  grm.)  of  lukewarm  water  until  the  mixture  has  the  consistence  of 
gruel.  Before  it  is  injected,  the  rectum  should  be  cleansed  by  an  enema  of  plain 
water.     One  such  enema  is  to  be  given  daily. 


CHAPTER  IV. 
CANCER   OF   THE   OESOPHAGUS. 

iEtiology  and  Pathology. — Cancer  is  the  most  important  and  most  frequent 
affection  of  the  oesophagus.  We  have  already  mentioned  in  the  preceding  chap- 
ter that  often  stenosis  is  the  result  of  carcinoma  in  the  oesophageal  walls. 

Little  is  known  about  the  astiology.  It  has  been  often  maintained  that 
mechanical,  chemical,  or  thermic  irritation  of  the  mucous  membrane  may  result 
in  the  development  of  cancer;  but  this  is  not  certain.  It  receives  some  support 
from  the  remarkably  frequent  occurrence  of  oesophageal  cancer  in  hard  drinkers. 
Now7  and  then  the  patient  himself  will  allege  a  perfectly  definite  cause  for  his 
disease,  such  as  the  lodging  of  a  foreign  body,  or  the  swallowing  of  a  very  large 
or  very  hot  morsel.  Still  it  is  hardly  possible  in  any  particular  case  to  decide 
how  much  value  such  statements  have.  It  has  been  maintained  that  the  carci- 
noma sometimes  develops  in  the  scars  of  old  ulcers.  This  is  of  interest  when  we 
recall  the  similar  fact  in  regard  to  gastric  carcinoma  {vide  infra). 

Oesophageal  cancer  follows  the  general  rule  in  being  most  frequent  in  elderly 
people — somewhere  between  forty  and  sixty  years  of  age.  The  male  sex  is  de- 
cidedly more  often  attacked  than  the  female. 

As  we  might  expect  from  the  histological  character  of  the  epithelium  lining 
the  oesophagus,  primary  cancer  here  is  invariably  composed  of  pavement  cells. 
The  new  growth  may  be  either  hard,  firm,  and  fibrous,  or  it  may  be  soft,  succulent, 
and  but  scantily  supplied  with  connective  tissue.  The  first  variety  corresponds  to 
the  "scirrhus"  of  older  writers,  and  the  second  to  "medullary"  cancer.  Usually 
the  new  formation  encircles  the  entire  tube  like  a  ring,  extending  three  to  ten 
centimetres  longitudinally.  Exceptionally  a  still  larger  portion  of  the  oesophagus 
is  involved,  sometimes  almost  all  the  mucous  membrane.  The  tumor  is  usually 
seated  in  the  lower  and  middle  thirds  of  the  oesophagus,  being  much  rarer  above. 

Symptoms  and  Complications. — In  the  great  majority  of  cases  the  symptoms 

24 


370  DISEASES  OP  THE  DIGESTIVE  ORGANS. 

are  those  of  a  gradually  increasing  stenosis,  with,  its  results.  We  may  therefore 
refer  to  the  preceding  chapter  for  most  of  the  particulars.  There  are,  however, 
exceptional  cases  Where  the  carcinoma  is  flat  and  entails  no  dysphagia,  or  so  little 
that  oesophageal  trouble  may  not  be  suspected.  We  have  repeatedly  seen  cases  of 
extensive  secondary  hepatic  cancer,  or  of  pulmonary  gangrene  (vide  infra),  where 
the  real  primary  disease  was  a  flat  cancer  of  the  oesophagus  which  gave  no  clin- 
ical signs  of  its  existence,  and  was  therefore  not  diagnosticated. 

It  is  characteristic  of  the  stenotic  symptoms  produced  by  oesophageal  cancer 
that  sometimes  a  considerable  and  apparently  spontaneous  amelioration  occurs. 
This  is  the  result  of  an  ulceration  of  the  new  growth.  It  crumbles  away,  as  the 
result  of  superficial  disintegration.  The  tumor  is  transformed  into  an  ulcer,  and 
one  can  easily  understand  how  this  may  result  in  a  temporary  improvement  in 
deglutition. 

Important  clinical  symptoms  may  result  from  conditions  secondary  to  the  new 
growth.  The  cancer  may  extend  to  neighboring  organs.  Not  infrequently  the 
cardiac  extremity  of  the  stomach  is  thus  involved.  Sometimes  such  a  tumor  may 
be  felt  in  the  epigastrium ;  but  in  most  cases  there  is  nothing  to  indicate  that  the 
stomach  is  attacked. 

The  neighboring  parts  of  the  trachea  or  bronchi  are  sometimes  affected,  and 
important  symptoms  result  from  such  a  complication.  If  perforation  occurs,  an 
almost  certain  result  is  the  inhalation  of  food  or  of  decaying  bits  of  the  tumor, 
with  consequent  pulmonary  gangrene,  and,  as  a  rule,  speedy  death.  The  disease 
has  also  been  observed  to  attack  the  pleura,  and  end  in  perforation.  The  same 
is  true  of  the  pericardium  and  the  aorta.  A  few  instances  are  known  where  the 
vertebra?  have  been  involved,  the  spinal  cord  compressed,  and  paraplegia  thus  in- 
duced.    We  have  ourselves  seen  one  such  case. 

Quite  frequently  the  recurrent  nerve  is  affected,  and  a  paralysis  of  the  vocal 
cords  is  produced,  which  can  be  detected  by  the  laryngoscope.  This  nerve  lies 
so  close  to  the  oesophagus  that  it  is  peculiarly  exposed  to  hi  jury  from  the  new 
gi-owth  itself,  or  from  any  inflammatory  process  which  may  be  set  up  around  it. 

Metastatic  cancer  in  distant  organs  is  not  infrequent,  and  may  give  rise  to 
important  symptoms.  It  attacks  most  frequently  the  liver  and  the  lungs.  The 
kidneys,  pancreas,  bones,  and  brain  are  also  liable  to  it. 

Pulmonary  gangrene  must  be  mentioned  as  a  relatively  frequent  complication, 
and  one  which  has  serious  consequences.  We  have  already  stated  that  it  may 
result  from  perforation.  A  still  more  frequent  cause  is  the  inspiration  of  decaying 
masses  vomited  or  regurgitated  by  the  patient. 

Clinical  History,  Termination,  Prognosis,  and  Treatment.— The  disease  is 
incurable.  Operative  removal  has  never  been  successful.  The  entire  duration  of 
the  disease  seldom  exceeds  a  year,  or  a  year  and  a  half.  At  the  end  of  this  period 
the  patient  dies  either  from  lack  of  nourishment  or  as  a  result  of  some  one  of  the 
complications  above  enumerated.  Treatment  is  purely  symptomatic.  Temporary 
improvement  may  be  obtained  by  mechanical  treatment  of  the  stenosis.  The  par- 
ticulars about  this  may  be  found  in  the  preceding  chapter. 


RUPTURE  OP  THE  OESOPHAGUS.  371 

CHAPTER  V. 
RUPTURE   OF  THE   OESOPHAGUS. 

Medical  literature  records  a  small  number  of  cases  which  prove  that  the  sud- 
den rupture  of  the  oesophagus  in  persons  previously  perfectly  well  is  possible, 
although  of  course  very  rare.  The  first  and  most  famous  instance  was  described 
by  Boerhaave  in  1724. 

The  symptoms,  according  to  the  observations  thus  far  reported,  usually  com- 
mence with  sudden  nausea  and  vomiting,  during  or  shortly  after  a  hearty  meal. 
There  is  simultaneously  an  extreme,  general  collapse.  There  is  pallor  of  the  face 
and  extremities,  cold  perspiration,  and  an  extremely  feeble  pulse.  Sometimes  the 
patient  feels  a  sudden  darting  pain  in  the  chest.  Almost  invariably  an  extensive 
emphysema  overspreads  the  neck  and  thorax.  Death  results  in  a  few  hours,  or 
at  latest  in  a  few  days. 

The  autopsy  reveals  a  tear  in  the  oesophagus,  invariably  situated  in  its  lower 
half.  It  may  be  five  centimetres  long,  and  is  almost  always  longitudinal.  Food 
has  usually  escaped  into  the  surrounding  tissues,  in  which  case  a  secondary  puru- 
lent inflammation  exists,  if  death  was  not  immediate. 

Zenker  has  attempted  to  explain  this  remarkable  phenomenon  by  a  supposition 
which  is  really  very  plausible,  namely,  that  oesophagomalacia  always  precedes 
these  so-called  spontaneous  ruptures.  The  cause  of  this  softening  of  the  oesophag- 
eal walls  is  probably  the  action  of  gastric  juice  escaping  into  the  tube  and  attack- 
ing a  surface  which,  through  some  temporary  disturbance  in  the  circulation,  has 
lost  its  normal  powers  of  resistance. 


CHAPTER  VI. 
NEUROSES  OF  THE  OESOPHAGUS. 

1.  Spasm  of  the  (Esophagus. — In  rare  instances  oesophageal  disturbances  are 
observed,  which  appear  to  result  from  spasmodic  contraction  of  its  muscular  coat. 
Nervous  and  hysterical  subjects  are  particularly  apt  to  present  temporarily  the 
symptoms  of  extreme  stenosis,  for  which  there  can  be  no  anatomical  basis.  Such 
cases  are  termed  "  spastic  stenosis ?'  of  the  oesophagus,  or  "  cesophagismus. "  It  is, 
of  course,  possible  that  there  may  exceptionally  be  some  real  lesion  at  the  founda- 
tion of  the  trouble,  and  that  the  spasm  is  the  reflex  result  of  an  ulcer  or  inflamma- 
tion affecting  the  oesophagus.  It  is  even  affirmed  that  the  reflex  influence  may 
sometimes  originate  in  distant  organs,  such  as  the  uterus.  The  dysphagia  is  usu- 
ally attended  by  a  painful  sense  of  consti'iction  in  the  throat  and  chest.  The 
bougie  comes  upon  an  obstruction,  which  usually  soon  yields.  The  diagnosis  is 
confirmed  by  the  easy  passage  of  the  bougie  after  the  spasm  is  over.  Other  impor- 
tant factors  are,  the  character  of  the  symptoms  as  a  whole  and  the  other  attendant 
nervous  and  hysterical  disturbances.  Some  atithors  also  explain  the  "  globus 
hystericus  " — that  feeling  as  if  a  lump  were  passing  up  or  down  in  the  throat  and 
chest — as  a  spasm  of  the  oesophagus. 

2.  Paralysis  of  the  (Esophagus. — Of  this  subject  we  have  little  accurate  knowl- 
edge. It  is  not  improbable  that  an  extensive  bulbar  paralysis,  affecting  the  mus- 
cles of  the  pharynx  and  larynx,  may  sometimes  involve  the  oesophagus ;  although 
such  a  disturbance  hardly  ever  gives  rise  to  prominent  symptoms  in  this  disease. 


372  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

Ziemssen  asserts  that  sometimes  the  oesophagus  seems  to  participate  in  post-diph- 
theritic paralysis,  when  extensive. 


SECTION  IV. 
Diseases  of  the  Stomach. 

CHAPTER    I. 

ACUTE    GASTRIC   CATARRH. 

(Acute  Gastritis.) 


iEtiology. — As  the  gastric  mucous  membrane  is  not  open  to  direct  inspection, 
we  usually  have  to  base  our  conclusion  that  an  acute  gastric  catarrh  exists,  lipon 
the  analogy  of  the  symptoms  with  those  which  we  have  seen  in  other  mucous 
membranes.  The  pathology  of  gastric  catarrh  has  thus  far  been  very  little  studied, 
for  the  disease  almost  always  ends  in  recovery ;  and  in  those  cases  which,  on 
account  of  some  other  disease,  do  terminate  fatally,  the  signs  of  catarrh  become 
very  indistinct.  Nevertheless,  we  are  fully  justified  in  assuming  that  a  catarrh  of 
the  gastric  mucous  membrane  is  the  cause  of  most  of  the  brief  gastric  disturbances 
which  occur.  That  there  may  be  other  acute  disorders  of  the  stomach,  in  which 
there  is  no  anatomical  change  whatever,  but  merely  some  functional  anomaly 
("dyspepsia,"  in  the  narrower  meaning  of  the  word),  is  possible,  but  has  not  yet 
been  proved. 

The  most  frequent  cause  of  acute  gastric  catarrh  is  some  direct  injury  of  the 
mucous  membrane ;  the  injury  may  be  thermic,  as  by  taking  food  too  hot  or  too 
cold,  or  mechanical,  or  chemical.  The  last  is  the  most  important.  It  is  irritation 
that  produces  the  frequent  cases  of  catarrh  which  follow  over-eating,  or  the  inges- 
tion of  improper,  indigestible,  highly  spiced,  or  very  sour  articles.  In  the  same 
way  arise  the  disorders  caused  by  excess  in  alcohol,  or  by  taking  certain  medi- 
cines, as  well  as  a  large  portion  of  the  milder  cases  of  poisoning  from  all  sorts  of 
injurious  substances. 

A  special  importance  attaches  to  the  ingestion  of  decaying  substances.  The 
incautious  use  of  tainted  meat  or  fish  may  be  followed  by  relatively  severe  forms 
of  acute  gastric  catarrh.  The  products  of  decomposition  act  as  chemical  irritants 
upon  the  mucous  membrane ;  and  the  ferments  and  putrefactive  agents  likewise 
continue  in  activity  after  reaching  the  stomach,  and  thus  contribute  to  produce 
the  inflammation. 

It  is  universally  assumed  that  catching  cold  may  excite  gastric  catarrh ;  but 
the  importance  of  this  factor  can  seldom  be  demonstrated. 

Individual  predisposition  to  the  disease  varies  greatly.  Weakly  children  are 
peculiarly  liable  to  it;  also  anaemic  persons,  fever  patients,  convalescents  from 
severe  diseases,  and  chronic  invalids  whose  general  nutrition  and  vigor  are 
impaired.  Such  persons  may  be  affected  by  things  which  the  strong  and  healthy 
would  not  feel  at  all.  The  probable  explanation  of  this  especial  liability  to  the 
disease  is  that,  under  the  circumstances  enumerated,  the  physiological  functions  of 
the  stomach  are  not  a  little  restricted.  It  has  been  experimentally  proved  that  in 
fever,  and  in  most  anaemic  or  weakly  persons,  the  secretion  of  the  gastric  acids  is 
subnormal  in  amount.  Digestion  is  thus  considerably  protracted.  The  contrac- 
tions of  the  muscular  coat  of  the  stomach,  which  are  set  up  by  the  normal  gastric 


ACUTE  GASTRIC  CATARRH.  -7.; 

secretions,  are  also  rendered  less  vigorous.  And,  further,  it  is  probable  that  the 
muscular  fibers  themselves  may  participate  in  the  general  debility.  Thus  it 
happens  that  the  food  is  not  carried  on  into  the  duodenum,  but  remains  undi- 
gested in  the  stomach.  It  undergoes  abnormal  decomposition  to  a  certain  extent, 
and  acts  both  as  a  mechanical  and  as  a  chemical  irritant  upon  tbe  gastric  mucous 
membrane. 

Symptoms. — The  most  constant  subjective  symptom  is  anorexia.  In  many 
cases  the  very  thought  of  food  excites  disgust.  What  the  patient  does  eat  tastes 
flat,  and  he  is  therefore  very  eager  for  piquant  dishes,  higbly  spiced  or  very  sour. 
Thirst  is  often  present,  and  a  feeling  of  dryness  in  the  mouth. 

The  subjective  gastric  sensations  are  seldom  those  of  marked  pain.  The  usual 
complaint  is  of  constant  pressure  and  fullness.  Sometimes  the  patient  is  conscious 
of  the  peristaltic  movements  of  the  stomach.     He  has  "  rumbling  "  of  the  bowels. 

There  is  nausea,  and  often  even  vomiting.  The  vomitus  consists  for  the  most 
part  of  undigested  food,  with  which  mucus,  and  sometimes  bile,  is  mingled.  Eruc- 
tations of  gas  or  liquid  are  frequent. 

Physical  examination  reveals  little.  The  epigastrium  may  be  somewhat  promi- 
nent as  a  whole,  and  may  be  tender  on  pressure.  The  tongue  is  almost  always 
thickly  coated  and  dry.  The  breath  is  usually  disagreeable,  and  there  is  a  persist- 
ent flat  or  bitter  taste  in  the  mouth. 

In  all  well-marked  cases  of  acute  gastric  catarrh  the  general  health  is  consider- 
ably impaired.  The  patient  is  languid,  and  disinclined  to  exertion.  Moderate 
elevations  of  temperature,  with  chilliness  and  feverishness,  are  not  infrequent. 
Now  and  then  there  is  a  decidedly  typhoidal  condition,  with  marked  nervous 
symptoms,  such  as  intense  headache,  vertigo,  and  dullness.  The  term  "gastric 
fever  "  is  applied  to  such  cases,  and  it  is  possible  that  they  may  sometimes  be  the 
result  of  a  constitutional  infection.  It  is  also  probable  that  toxic  influences  are 
exerted  by  the  abnormal  products  of  the  fermentation  which  takes  place  in  the 
stomach.  For  example,  Senator  mentions  sulphuretted  hydrogen  as  thus  gen- 
erated. A  short  time  ago  Litten  described  a  few  cases  in  which  at  first  there  were 
such  dyspeptic  symptoms  as  nausea,  vomiting,  flatulence,  and  a  coated  tongue,  but 
which  soon  gave  evidence,  by  restlessness,  headache,  great  muscular  weakness,  and 
somnolence,  of  rather  severe  nervous  disturbance  in  addition.  The  breath  had  a 
marked  "  fruity "  odor ;  and,  on  adding  chloride  of  iron  to  the  urine,  a  strong 
reddish  color  was  developed,  as  in  the  so-called  acetone-reaction.  So  that  it  seems 
probable  that  an  auto-intoxication  had  occurred,  somewhat  resembling  diabetic 
coma. 

Chief  among  complications  are  the  intestinal  symptoms,  which  are  frequently 
coincident  with  the  gastric  disorder.  Constipation  is  the  rule.  There  may  be 
diarrhoea.  The  gastric  catarrh  may  by  extension  involve  the  duodenum,  and  give 
rise  to  jaundice.  Sometimes  herpes  appears  upon  the  skin.  This  fact  argues  for 
the  infectious  nature  of  many  cases  of  gastric  catarrh. 

The  course  of  acute  gastric  catarrh  is  invariably  brief.  Usually  after  a  few 
days  there  is  complete  recovery. 

Treatment. — If,  at  the  beginning  of  the  disease,  there  is  reason  to  suppose  that 
the  stomach  is  loaded  with  undigested  food,  an  emetic  is  indicated.  If  it  is  desired 
to  avoid  the  irritative  action  of  an  emetic  upon  the  gastric  mucous  membrane,  a 
subcutaneous  injection  of  one  sixth  grain  (0-01)  apomorphine  may  be  given. 

In  most  cases,  however,  emetics  may  be  dispensed  with.  The  treatment  in  such 
cases  consists  mainly  in  a  strict  regulation  of  the  diet,  allowing  only  such  tilings 
as  milk  porridge  or  iced  milk.  Of  internal  remedies,  ten  to  fifteen  drops  of  dilute 
hydrochloric  acid  in  half  a  wine-glass  of  water  sometimes  seems  beneficial ;  while 
in  other  cases,  where  there  are  sour  eructations  and  vomiting,  alkalies  are  to  be 


374  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

given.  We  may  order  as  much  bicarbonate  of  soda  or  as  much  magnesia  as  will 
rest  on  the  point  of  a  pen-knife.  The  so-called  stomachics  and  bitters  are  also 
often  prescribed,  such  as  compound  tincture  of  gentian  or  tincture  of  rhubarb. 
If  the  vomiting  is  obstinate,  the  best  remedies  are  bits  of  ice,  sips  of  cold  seltzer 
water,  or  small  doses  of  opium.  If  the  bowels  are  constipated,  Carlsbad  salts, 
Hunyadi  water,  or  rhubarb  may  be  given. 


CHAPTER  II. 


CHRONIC  GASTRIC   CATARRH. 

( Chronic  Gastritis.     Chronic  Dyspepsia.) 

JEtiology. — The  same  injurious  influences  which  produce  acute  gastric  catarrh 
if  frequently  recurring,  excite  the  chronic  form  of  the  disease.  The  most  potent 
causes  are  improper  diet  and  the  improper  use  of  alcohol.  Individual  predisposi- 
tion is  important  in  this  as  well  as  in  the  acute  disease.  Sometimes  it  even  seems 
to  be  a  matter  of  inheritance.  It  is  not  a  rare  thing  to  find  that  a  large  number 
of  the  members  of  a  family  have  a  "weak  stomach." 

Chronic  gastric  catarrh  is  not  always  a  primary  affection.  It  may  be  secondary 
to  some  other  disease.  All  diseases  which  result  in  passive  hyperaemia  of  the 
portal  system,  such  as  cirrhosis  of  the  liver  or  thrombosis  of  the  portal  vein,  are 
not  infrequently  followed  by  gastric  catarrh;  and  when  the  disease  occurs  in  per- 
sons afflicted  with  chronic  cardiac  or  pulmonary  disease,  it  is  to  be  regarded  as  in 
part  due  to  stasis. 

Pathology. — The  macroscopic  changes  in  the  gastric  mucous  membrane  are  in 
most  cases  very  slight.  Usually  it  is  coated  with  a  layer  of  tough,  grayish-white 
mucus,  in  which  is  suspended  a  greater  or  less  amount  of  detached  epithelium. 
The  membrane  is  red,  unless  rendered  gray  by  excessive  pigmentation.  The 
changes  are  almost  always  most  extensive  in  the  pyloric  region. 

If  the  catarrh  is  of  long  duration,  thei-e  may  be  still  further  changes.  The 
mucous  membrane  often  seems  smooth  and  atrophied.  The  glands  are  narrower 
and  shorter  than  normal,  and  the  connective  tissue  between  them  is  increased  in 
amount.  Other  cases  present  hyperplasia  of  the  mucous  membrane.  The  internal 
surface  of  the  stomach  is  thickened  and  mammillated.  The  hyperplasia  in  these 
cases  affects  chiefly  the  tubes  of  the  glands  in  the  mucous  membrane,  although  the 
submucous  layer  may  also  be  considerably  thickened. 

Symptoms. — The  symptoms  of  disturbed  gastric  digestion,  or  dyspepsia,  to  be 
observed  in  all  sufferers  from  chronic  gastric  catarrh,  are  referable  to  the  follow- 
ing functional  anomalies : 

The  secretion  of  the  gastric  juice  depends  upon  the  maintenance  of  the  circula- 
tion of  the  blood  in  the  gastric  mucous  membrane.  This  is  merely  in  accoi'dance 
with  a  general  rule.  It  is  easy,  therefore,  to  comprehend  that  any  inflammation,  dis- 
turbing as  it  does  the  circulation  of  the  blood,  must  modify  the  gastric  secretions. 
We  may  also  assume  that  a  deficiency  in  the  secretion  of  the  gastric  juice  is  the 
chief  factor  in  producing  the  dyspepsia  which  accompanies  both  the  primary  and 
inflammatory  catarrh  and  that  resulting  from  venous  stasis.  The  possible  diminu- 
tion in  the  production  of  pepsine  is  probably  not  of  great  importance  in  this  con- 
nection ;  for,  like  any  other  ferment,  a  very  small  amount  of  it  would  prove  efficient 
under  favorable  circumstances.  What  seems  of  more  importance  is  the  dimin- 
ished proportion  of  hydrochloric  acid  in  the  gastric  juice  of  patients  with  chronic 
gastric  catarrh — a  condition  which  has  been  repeatedly  proved  to  exist.     The  pro- 


CHRONIC  GASTRIC  CATARRH.  375 

cesses  of  digestion  are  thereby  not  a  little  lowered  and  impeded.  It  is  self-evident 
that  in  cases  where  there  is  actual  atrophy  of  the  mucous  membrane  and  of  the 
glands  in  particular,  the  normal  pi'ocesses  of  gastric  secretion  may  be  still  more 
seriously  impaired. 

A  further  unfavorable  result  of  the  imperfect  digestion  dependent  on  the  lack  of 
hydrochloric  acid  is  that  the  undigested  food  is  very  apt  to  undergo  abnormal  fer- 
mentation and  decomposition.  These  fermentative  processes  give  rise  to  lactic, 
butyric,  and  acetic  acids,  and  to  alcohol.  The  direct  cause  of  their  production  is 
that  the  ferment-producing  spores  are  not  destroyed  by  the  gastric  juice,  as  they 
would  be  under  normal  conditions.  On  the  contrary,  they  find  in  the  food 
stagnating  within  the  stomach  the  most  favorable  conditions  for  the  development 
of  their  activity.  These  products  of  abnormal  fermentation  in  their  turn  irritate 
the  gastric  mucous  membrane  and  prolong  the  catarrh. 

Another  factor  contributes  to  the  disturbance  of  the  normal  digestive  processes, 
namely,  the  excessive  secretion  of  mucus.  As  mucus  has  an  alkaline  reaction,  its 
presence  neutralizes  a  portion  of  the  acid  in  the  gastric  juice  and  lessens  the 
potency  of  the  latter.  The  mucus  also  does  harm  in  a  purely  mechanical  way.  It 
envelops  all  the  ingesta,  and  thus  to  no  small  degree  prevents  the  gastric  juice 
from  reaching  them.  Morsels  completely  covered  with  mucus  can  remain  for 
quite  a  long  time  in  the  stomach  without  being  digested. 

A  very  great  importance  attaches  to  the  motor  disturbances  which  the  stomach 
suffers  in  chronic  catarrh.  The  normal  peristalsis  is  of  course  an  essential  factor 
in  the  process  of  digestion.  It  is  its  function  to  bring  all  portions  of  the  contents 
of  the  stomach  successively  into  adequate  contact  with  the  mucous  membrane. 
Thus  alone  is  the  uniform  digestion  of  the  entire  mass  rendered  possible ;  and,  as 
physiology  has  taught  us,  the  gastric  secretions  are  continually  being  stimulated 
by  the  contact  of  the  still  undigested  food  with  the  lining  membrane.  Lastly,  it  is 
the  peristalsis  again  which  pushes  on  the  already  digested  food  into  the  duode- 
num, and  thereby  prevents  the  useless  accumulation  of  matter  within  the  stomach. 

Now,  gastric  peristalsis  is  undoubtedly  much  impaired  in  catarrh.  One  reason 
for  this  is  the  actual  harm  done  the  muscular  coat.  Every  decided  inflammation 
renders  the  muscular  layer  cedematous,  and  thus  impedes  its  activity.  In  all 
cases  where  food  accumulates  in  undue  amount  in  the  stomach,  the  muscular  coat 
is  gradually  so  stretched  as  to  become  still  more  incapacitated  for  its  proper  func- 
tions. A  factor  which  is  perhaps  of  still  greater  importance  than  these  lesions  is 
the  diminished  vigor  of  the  normal  excitants  of  the  peristaltic  movements.  We 
learn  from  physiology  that  the  chief  part  in  arousing  peristalsis  is  played  by  the 
normally  constituted  gastric  juice,  and  more  especially  by  the  acid  therein  con- 
tained. It  follows  that  all  influences  which  modify  the  amount  or  composition  of 
the  gastric  juice  must  have  the  remote  effect  of  diminishing  the  gastric  peristalsis. 
The  resulting  evils  can  be  inferred  from  what  has  been  already  stated.  Digestion 
is  impaired,  and  abnormal  decomposition  promoted ;  and  each  effect  becomes  in 
turn  a  cause  of  further  derangement — a  condition  of  things  which  we  are  con- 
stantly meeting  in  the  pathology  of  digestion. 

It  remains  to  be  stated  that  absorption  is  impeded  in  chronic  gastric  catarrh. 
It  has  been  shown  in  Ludwig's  physiological  laboratory,  in  Leipsic,  that  no  incon- 
siderable portion  of  the  peptones  manufactured  in  the  stomach  are  absorbed  by 
the  blood-vessels  in  its  walls.  Now,  as  the  circulation  is  disturbed  by  the  in- 
flammation, we  should  expect  the  absorption  of  peptones  to  be  thereby  diminished. 
The  peptones  remaining  in  solution  within  the  stomach  and  not  absorbed  have 
been  shown  by  experiment  to  disturb  and  delay  the  transformation  of  fresh  albu- 
minous substances  into  peptones.  The  diminished  peristaltic  action  also  tends  to 
prolong  the  time  during  which  the  peptones  remain  in  the  stomach ;  and  numer- 


370  DISEASES  OP  THE  DIGESTIVE  OEGANS. 

ous  observations  teach  that  normal  peristalsis  has  a  direct  influence  in  promoting 
absorption,  so  that,  if  it  be  diminished,  absorption  is  checked. 

We  have  therefore  a  whole  series  of  factors,  all  of  which  contribute  to  distm^b 
the  normal  processes  of  digestion.  We  have  discussed  them  at  some  length,  be- 
cause they  serve  to  explain  not  only  the  digestive  symptoms  of  chronic  gastric 
catarrh,  but  those  of  almost  all  the  other  gastric  diseases. 

If  we  now  proceed  to  the  symptoms  which  lead  us  to  a  diagnosis  of  dyspepsia  or 
chronic  gastric  catarrh,  we  find  first  anorexia.  This  symptom  is  common  to  all 
gastric  disorders.  There  is  sometimes  a  moderate  appetite,  but  it  is  soon  changed 
to  a  feeling  of  repletion  upon  the  ingestion  of  even  a  slight  amount  of  food.  In 
other  cases  there  is  actual  dislike  for  any  form  of  nourishment ;  the  patient  eats 
little,  and  prefers  highly  spiced,  piquant  dishes.  There  is  often  a  persistent  bitter, 
flat,  or  otherwise  abnormal  and  disagreeable  taste  in  the  mouth. 

Subjective  sensations  in  the  region  of  the  stomach  are  rarely  entirely  absent. 
As  a  rule,  there  is  a  feeling  of  fullness  or  pressure  and  of  dull  pain.  These  troubles 
may  either  be  constant,  or  occur  after  meals. 

The  eructation  of  gas  is  a  very  frequent  and  annoying  symptom.  Often  a  sour 
liquid  comes  up  with  the  gas  ("sour  stomach").  The  gas  is  a  mixture  of  atmos- 
pheric air  and  the  abnormal  gaseous  products  of  the  decomposition  which  takes 
place  in  the  stomach.  Hydrogen,  carbonic  dioxide,  and  occasionally  inflammable 
gases,  such  as  marsh  gas,  have  been  detected.  The  sour  masses  regurgitated  irri- 
tate the  oesophagus,  and  give  rise  to  a  sharp,  burning  sensation,  known  as  "  heart- 
burn." 

In  many  instances  the  feeling  of  nausea  is  superseded  by  actual  vomiting.  This 
almost  always  takes  place  either  directly  after  eating  or  an  hour  or  two  later. 
The  vomitus  consists  mainly  of  undigested  food,  usually  mixed  with  a  large 
amount  of  mucus.  The  chemical  reaction  may  he  either  neutral  or  strongly  acid. 
If  acid,  however,  it  is  often  not  made  so  by  hydrochloric 
acid,  but  by  the  acetic,  lactic,  or  fatty  acids  generated  by  the 
abnormal  fermentation  going  on  within  the  stomach.  That 
the  contents  of  the  stomach  have  an  acid  reaction  is  no 
proof  that  the  gastric  juice  has  peptonizing  properties,  for 
§  f-L  ^  none  of  these  other  acids  have  nearly  so  much  efficiency  in 
J)     ^  promoting  digestion  as  has  hydrochloric  acid.     They  may 

Fig.  34.— a,  Sarcina  ven-    even  at  times  check  the  process.     A  small  amount  of  blood 

triculi      ö  ^t  ClLSl-cgIIs 

may  be  mixed  with  the  matter  vomited,  but  need  not  excite 
apprehension.  Microscopic  examination  reveals  little  that  is  characteristic.  The 
cells  of  the  yeast  fungus  are  frequently  found,  and  also  the  sarcina  ventriculi 
(see  Fig.  34).  We  may  add  that  this  latter  has  apparently  no  connection  with 
the  abnormal  processes  of  fermentation. 

A  peculiar  kind  of  vomiting  is  extremely  frequent  in  the  chronic  gastric  catarrh 
of  drunkards.  We  refer  to  the  well-known  morning  vomiting  of  a  watery  fluid, 
which  is  usually  alkaline  in  reaction,  and  apparently  consists  at  least  in  part  of 
saliva  that  has  been  swallowed.     (Vide  also  page  357.) 

The  physical  examination  shows  malnutrition  (vide  infra),  but  not  much  that 
is  distinctive  of  the  disease.  The  center  of  the  tongue  is  often  coated,  while  its 
point  and  edges  are  red.     Considerable  salivation  not  infrequently  exists. 

The  epigastrium  seems  in  many  cases  unchanged.  Sometimes  the  stomach  is 
distended,  and  somewhat  tender  on  pressure.  On  palpation,  a  splashing  can  some- 
times be  both  heard  and  felt.  Its  presence  usually  indicates  dilatation  of  the  stom- 
ach (q.  v.). 


CHRONIC  GASTRIC  CATARRH.  377 

Examination  op  the  Contents  of  the  Stomach  by  means  op  the 

Stomach-tube. 

The  examination  of  the  contents  of  the  stomach  with  the  aid  of  the  stomach- 
tube  is  much  more  important  tlvan  the  mere  external  examination  of  the  stomach, 
which  usually  affords  little  information.  This  newer  method  of  research  was 
introduced  mainly  by  Leube,  and  by  its  means  we  are  able  to  learn  about  many 
of  the  processes  of  digestion,  and  to  obtain  a  somewhat  clearer  insight  into  the 
especial  forms  of  digestive  disturbance  which  may  be  present.  The  use  of  the 
stomach-tube  for  this  purpose  has  indeed  certain  inconveniences  for  the  patient, 
and  therefore  it  will  not,  of  course,  be  used  immediately  in  every  case.  If,  how- 
ever, we  have  to  deal  with  any  obstinate  disorder  of  the  stomach,  investigation  by 
means  of  the  tube  is  the  more  desirable  because  we  may  thus  obtain  data  valuable 
not  only  from  a  diagnostic  but  also  from  a  therapeutic  point  of  view. 

The  first  question  which  can  be  determined  with  the  aid  of  the  stomach-tube 
relates  to  the  time  occupied  in  digestion,  or,  in  other  words,  to  the  motor  power  of 
the  stomach.  The  best  tube  to  ftse  is  the  soft  catheter  of  Nelaton,  supplied  at  its 
lower  end  with  sufficiently  wide  openings.  Numerous  experiments  on  healthy 
human  beings  have  shown  that  under  ordinary  circumstances  gastric  digestion  is 
ended  in  six  or  seven  hours  at  the  latest,  so  that  we  should  find  the  healthy  stom- 
ach completely  empty  six  or  seven  hours  after  the  last  meal.  Indeed,  frequently 
this  is  the  case  much  earlier,  say  three  or  four  hours  after  a  meal.  The  investiga- 
tion of  this  point  in  disease  of  the  stomach  is  usually  carried  out  in  the  following 
way:  The  patient  is  given,  either  in  the  morning  fasting  or  at  noon,  a  so-called  test- 
meal  ;  this  consists  either  of  flesh,  such  as  minced  beef-steak,  with  a  roll,  or  merely 
of  a  roll  with  some  tea.  Six  or  seven  hours  after  this  meal  the  stomach  is  rinsed 
out  with  lukewarm  water.  In  normal  digestion  the  rinse-water  is  almost  per- 
fectly clear,  and  contains  at  most  a  few  small  bits  of  mucus  and  the  like,  while  in 
dyspepsia  there  are  still  present  in  the  stomach  numerous  remnants  of  the  ingesta. 
This  latter  condition  demonstrates  with  certainty  the  presence  of  disorders  of 
digestion ;  while  the  sufficiently  rapid  emptying  of  the  stomach  is  in  most  cases  a 
sign  of  normal  digestion,  although  it  may  sometimes  exist  despite  some  few  devia- 
tions from  perfect  health. 

We  must  therefore  endeavor  to  make  further  investigation  as  to  the  quality 
of  the  gastric  juice  and  the  digestive  power  of  the  stomach,  and  for  this  purpose 
also  the  stomach-tube  is  indispensable.  The  result  of  attempts  to  obtain  a  perfectly 
pure  and  undiluted  gastric  juice  has,  to  be  sure,  thus  far  been  unsatisfactory ;  still, 
we  are  able  to  get  most  of  the  reactions  in  a  satisfactory  way  from  the  total 
gastric  contents — that  is,  from  the  gastric  juice  mingled  with  portions  of  food. 
For  this  purpose  we  must,  of  course,  draw  out  the  gastric  contents  at  a  time  when 
the  secretion  of  the  gastric  juice  has  reached  its  highest  point,  and,  accordingly, 
the  tube  is  introduced  about  an  hour  or  an  hour  and  a  half  after  the  test-meal. 
By  coughing  and  pressing  the  patient  is  usually  able  to  squeeze  out  a  sufficient 
amount  of  the  gastric  contents  through  the  tube,  and  this  by  filtration  is  sepa- 
rated from  the  remnants  of  the  food.  The  filtrate  thus  obtained  may  now  be 
tested  in  various  ways.  If,  however,  we  can  obtain  none  of  the  contents  of  the 
stomach  by  mere  expression,  it  is  necessary  to  gain  our  result  by  pouring  some 
fluid  into  the  stomach  and  siphonage.  For  the  investigation  of  the  quality  of  the 
gastric  juice  it  is  in  general  preferable  to  give  the  so-called  test-breakfast,  consist- 
ing of  a  roll  and  tea,  because  if  we  give  a  larger  test-meal  the  secreted  hydro- 
chloric acid  is  at  once  and  completely  combined  with  the  abundant  nitrogenous 
substances  present.  In  that  case  the  test  for  free  hydrochloric  acid  proves  nega- 
tive, even  when  the  stomach  has  secreted  hydrochloric  acid  in  abundance. 


378  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

The  investigation  of  the  gastric  juice  thus  obtained  relates,  first,  to  its  richness 
in  acids,  and  in  particular  free  hydrochloric  acid,  and,  secondly,  to  its  digestive 
power. 

The  digestive  power  of  the  gastric  juice  is  tested  in  the  following  way :  A  thin 
shaving  of  coagulated  egg  albumen  is  allowed  to  stand  in  the  gastric  juice  for 
sixty  to  ninety  ininutes.  If  the  gastric  juice  possesses1  normal  efficiency,  the  albu- 
men will  be  completely  dissolved  at  the  expiration  of  this  time.  Under  patho- 
logical conditions  the  gastric  juice  requires  a  much  longer  time  for  this,  or  it  may 
not  digest  the  albumen  at  all  until  a  few  drops  of  hydrochloric  acid  are  added. 

Testing  the  gastric  juice  in  relation  to  the  acids  it  contains  has  become,  as  the 
result  of  numerous  investigations,  a  matter  of  great  importance  during  the  last 
few  years.  In  the  first  place,  we  must  determine  whether  the  juice  contains  any 
free  acid  at  all  or  not.  This  is  best  done  by  means  of  a  solution  of  tropasolin. 
Even  slight  amounts  of  acid  change  the  yellow  color  of  tropasolin  to  red.  Red 
Congo-paper  is  also  to  be  recommended  for  demonstrating  free  acids.  This  takes 
on  an  evident  blue  coloration  upon  the  application  of  a  drop  of  acid  gastric  con- 
tents. Both  reactions  take  place  only  if  free  acid»  are  present.  They  are  not  pro- 
duced by  acid  salts. 

If  the  gastric  juice  contains  free  acid,  the  next  question  is  whether  this  free 
acid  is  hydrochloric  or  lactic.  Hydrochloric  acid  is  certainly  the  acid  which  is 
by  far  more  important  and  absolutely  necessary  to  digestion,  while  lactic  acid  is 
probably  entirely  dependent  for  its  creation  upon  the  digestion  of  the  starches  in 
the  stomach.  In  the  case  of  normal  digestion  lactic  acid  alone  is  found  during 
the  first  half-hour,  the  amylolytic  stage  of  gastric  digestion.  Then  the  hydrochloric 
acid  begins  to  appear  along  with  the  lactic  acid.  The  latter  grows  less  and  less 
abundant,  and  at  the  end  of  an  hour  there  is  usually  found  hydrochloric  acid 
alone  without  any  lactic  acid.  The  most  certain  and  best  means  for  the  demon- 
stration of  free  hydrochloric  acid  is  the  phloroglucin-vanillin  test  of  Gtinzburg. 
The  solution  is  composed  as  follows  :  Phloroglucin  2,  vanillin  1,  absolute  alcohol 
30  parts.  A  few  drops  of  this  solution  are  mixed  in  a  porcelain  evaporating  dish 
with  a  few  drops  of  the  gastric  juice  whicb  is  to  be  examined,  and  warmed  over  a 
flame.  If  there  be  free  hydrochloric  acid  present  there  at  once  appears  at  the 
edge  of  the  heated  liquid  a  beautiful  red  border.  The  test  is  very  easy  to  carry 
out,  and  extremely  sensitive.  The  second  reaction  for  free  hydrochloric  acid  is 
with  methyl- violet.  Its  solution  has  a  violet  color,  which  changes  to  blue  upon 
the  addition  of  a  small  amount  of  hydrochloric  acid,  while  lactic  acid  does  not 
produce  this  change  in  color.  For  the  direct  demonstration  of  lactic  acid,  on  the 
other  hand,  we  may  use  Uffelmann's  chloride  of  iron  and  carbolic  test.  Upon 
the  addition  of  a  drop  of  liquor  ferri  perchloridi  to  a  two-per-cent.  solution  of  car- 
bolic acid,  there  is  at  once  developed  a  steel-blue  color.  Upon  adding  the  gastric 
juice  to  this  mixture  the  blue  color  will  at  once  change  to  yellow,  if  lactic  acid  be 
present. 

According  to  the  later  investigations  of  Cahn  and  Von  Mehring,  we  must  add 
that  the  failure  of  the  reactions  for  hydrochloric  acid  does  not  authorize  us  to 
assert  that  there  is  actually  a  complete  absence  of  hydrochloric  acid  in  the  gastric 
juice.  The  authors  just  named  have  demonstrated  hydrochloric  acid  where  the 
methyl-violet  reaction  has  failed.  Nevertheless,  the  negative  result  of  the  test, 
which,  it  seems,  must  be  caused  by  the  mixture  of  foreign  matter  with  the  gastric 
juice,  does  possess  practical  importance,  inasmuch  as  the  reaction  can  always  be 
demonstrated  if  digestion  is  normal. 

If  we  now  return  from  this  digression  to  the  conditions  present  in  chronic  gas- 
tric catarrh,  we  find  that  in  this  disease  digestion  is  often  decidedly  delayed  and 
incomplete.     The  gastric  juice  usually  contains  free  hydrochloric  acid,  but  the 


CHRONIC  GASTRIC  CATARRH.  379 

amount  of  it  is  often  appreciably  diminished.  Indeed,  there  are  severe  cases  of 
chronic  gastric  catarrh  where  the  secretion  of  hydrochloric  acid  seems  to  be  per- 
manently almost  nil.  This  is  probably  to  be  explained  by  the  final  occurrence  of 
an  atropby  of  the  mucous  membrane.  The  appearance  of  abnormal  organic  acids 
in  the  gastric  contents,  such  as  butyric  and  acetic  acids,  points  to  processes  of 
abnormal  fermentation  in  the  stomach. 

With  regard  to  those  disturbances  which  are  associated  with  an  increased 
secretion  and  an  abnormally  large  amount  of  acid  in  the  gastric  juice,  see  the 
appendix  to  this  chapter. 

Of  the  other  organs,  the  intestine  most  frequently  suffers  in  chronic  gastric 
catarrh.  The  combination  of  gastric  disease  and  intestinal  disease  is  not  infre- 
quent. In  almost  all  cases  of  chronic  gastric  catarrh  the  bowels  are  irregular. 
Habitual  constipation  is  the  rule,  but  sometimes  there  is  diarrhoea.  If  much  gas 
is  generated  in  the  stomach,  the  intestinal  canal  often  becomes  implicated,  and 
tympanites  and  flatulence  develop.  There  may  be  catarrh  of  the  duodenum 
leading  to  jaundice. 

The  urine  is  often  only  feebly  acid  in  reaction,  and  therefore  frequently  depos- 
its a  large  amount  of  phosphates.  The  diminished  acidity  is  probably  in  part  a, 
result  of  the  deficient  secretion  of  acid  by  the  stomacb,  though  excessive  vomiting 
(compare  the  chapter  on  dilatation)  may  also  have  some  influence,  because  of  the 
acid  thus  lost. 

It  has  been  often  maintained  that  eczema  and  other  chronic  cutaneous  diseases 
are  sometimes  referable  to  gastric  catarrh,  but  the  fact  has  not  yet  been  definitely 
established. 

There  is  a  more  evident  relation  between  chronic  gastric  catarrh  and  certain 
nervous  derangements.  The  disease  has  a  notable  influence  on  the  spirits.  In 
numerous  instances  it  is  accompanied  by  decided  hypochondriasis.  There  may  be 
other  nervous  symptoms,  such  as  headache,  vertigo,  and  dullness  or  listlessness. 
Vertigo  in  particular  is  a  familiar  concomitant  of  the  disease  ("  vertigo  a  stomacho 
Iceso  ").  It  is  possible  that  in  many  cases  these  symptoms  are  toxic,  resulting 
from  the  absorption  of  the  abnormal  matters  generated  within  the  stomach  (vide 
supra,  page  373).  In  the  majority  of  instances,  however,  they  are  due  to  the  neu- 
rasthenic and  hypochondriacal  condition  of  the  patient  (see  the  chapter  on  nerv- 
ous dyspepsia). 

Whenever  the  catarrh  is  of  any  duration  and  severity,  the  general  nutrition  is 
seriously  impaired.  The  diminished  appetite  and  the  imperfect  digestion  and  ab- 
sorption of  what  is  eaten  contribute  to  produce  a  gradual  and  considerable  loss  of 
weight.  The  fatty  and  muscular  tissues  atrophy.  The  skin  grows  dry  and  harsh, 
and  usually  has  a  dirty-pale  color. 

Individual  cases  differ  greatly  in  the  combination  of  symptoms  they  present 
and  in  their  course.  The  anorexia,  gastric  oppression,  eructations,  vomiting,  and 
other  important  disturbances  already  mentioned,  exhibit  the  greatest  diversity  in 
their  intensity  and  their  grouping.  In  the  milder  cases,  loss  of  appetite  and  mod- 
erate local  uneasiness  may  be  the  only  symptoms.  Frequent  vomiting  is  seen 
only  in  the  severer  cases.  The  disease  often  lasts  for  years,  especially  if  the 
patient  neglects  himself.  In  most  cases  there  are  frequent  remissions  and  exacer- 
bations, usually  dependent  upon  external  causes. 

The  disease  is  not  intrinsically  fatal,  but  the  general  debility  consequent  upon 
it  may  indirectly  shorten  life. 

Diagnosis. — The  diagnosis  is  based  upon  the  existence  of  chronic  gastric  symp- 
toms unattended  by  evidence  of  any  more  serious  lesion,  whether  of  the  stomach 
itself  or  of  some  other  organ.  For  example,  the  possibility  of  gastric  ulcer,  can- 
cer, or  dilatation  is  to  be  considered.     This  elimination  of  other  diseases  is  very 


380  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

important.  It  is  not  at  all  exceptional  to  meet  in  practice  cases  that  have  heen 
carelessly  diagnosticated  as  chronic  gastric  catarrh  where  a  more  thorough  exami- 
nation or  the  further  progress  of  the  case  leads  to  an  entirely  different  conclusion 
— chronic  pulmonary  or  cardiac  disease,  chronic  nephritis,  or  one  of  the  other 
gastric  affections  above  mentioned.  It  should  therefore  be  our  invariable  rule 
to  reach  the  diagnosis  by  exclusion,  after  making  a  careful  and  complete  physical 
examination,  in  order  to  detect  any  other  possible  disease  to  which  the  gastric 
symptoms  might  be  referred.  The  important  differential  diagnosis  between  chronic 
gastric  catarrh  and  so-called  nervous  dyspepsia  will  be  discussed  hereafter. 

Treatment. — If  the  disease  seems  to  be  merely  symptomatic — the  result,  for 
instance,  of  venous  stasis  due  to  chronic  cardiac,  pulmonary,  or  hepatic  disease — 
our  efforts  must,  of  course,  be  chiefly  directed  to  the  relief  of  the  original  trouble. 

Treatment  of  the  primary  form,  on  the  other  hand,  must  always  begin  with 
regulation  of  the  diet.  Such  vague  injunctions  as  '-  to  be  cautious  "  or  "to  avoid 
indigestible  articles  of  food  "  are  useless.  The  patient  must  have  a  perfectly 
definite  bill  of  fare  prescribed  for  him ;  nor  can  any  universal  one,  suitable  for 
all  cases,  be  drawn  up.  In  each  individual  instance  the  individual  circumstances 
must  be  considered.  The  personal  experiences  of  the  patient  himself  are  by  no 
means  to  be  disregarded.  One  man  may  be  quite  unable  to  digest  what  is  well 
borne  by  others,  and  vice  versa. 

In  the  first  place,  certain  foods  must  be  utterly  forbidden  to  such  patients  as  do 
not  themselves  avoid  whatever  disagrees  with  them.  All  articles  must  be  pro- 
hibited which  may  irritate  the  mucous  membrane,  either  mechanically  or  chem- 
ically. This  includes  all  the  coarser  soi'ts  of  vegetables  or  fruits,  containing  a  large 
proportion  of  indigestible  cellulose ;  and  all  dishes  that  are  very  sour,  strongly 
salted,  or  highly  spiced.  Potatoes,  farinaceous  food,  and  all  substances  mainly 
composed  of  hydrocarbons,  must  also  be  interdicted ;  because  almost  all  the  abnor- 
mal fermentative  processes,  the  evil  consequences  of  which  have  already  been 
considered,  are  promoted  by  the  hydrocarbons.  Fat  is  also  harmful.  It  impedes 
digestion  by  protecting  the  contents  of  the  stomach  from  the  action  of  the  gastric 
juice,  in  a  purely  mechanical  way;  and  then,  being  changed  into  the  fat  acids, 
it  causes  sour  eructations  and  pyrosis.  It  is  important  that  all  forms  of  alcohol 
should  be  forbidden.  Fleischer  and  others  have  proved  by  actual  experiment 
that  even  small  amounts  of  alcohol  prolong  and  hinder  the  digestive  process.  An 
injunction  to  abstain  totally  is  usually  better  obeyed  in  a  severe  case  than  the 
advice  to  be  very  moderate  in  the  use  of  liquors.  The  food  should  neither  be 
very  hot  nor  ice-cold. 

In  determining  what  the  patient  may  be  allowed  to  eat,  we  are  to  consider,  as 
already  mentioned,  his  own  personal  experience  as  well  as  our  more  general 
knowledge.  An  intelligent  patient  will  often  be  himself  the  best  judge  of  what 
agrees  or  disagrees  with  him.  The  following  foods  are  very  easy  to  digest :  Milk, 
soft-boiled  or  raw  eggs,  broths,  and  certain  artificial  preparations,  chief  among 
which  stand  the  Leu  be-Rosen  thai  meat  solution  and  the  meat  peptones  which 
have  been  lately  put  upon  the  market.  The  brain  and  sweetbread  of  calves  are 
easily  digestible;  also  birds,  such  as  pigeons,  chickens,  and  partridges,  and  thin 
shavings  of  raw  meat  or  raw  ham.  Gradually  we  may  proceed  to  somewhat 
heartier  food — veal,  game,  roast  beef,  and  light  farinaceous  dishes.  The  worse  the 
symptoms  are  in  any  case,  the  more  strict  must  we  be  in  regard  to  diet.  For 
drink,  besides  water  or  Seltzer  water,  very  weak  tea  and  non-oleaginous  cocoa  are 
good. — Shall  we  permit  coffee  ?  This  is  often  a  question  of  great  interest  to  the 
patient  :  it  must  be  answered  according  to  his  individual  experience.  Coarse 
bread  is  to  be  forbidden.  Ordinary  white  bread,  toasted,  if  it  seems  desirable,  may 
be  allowed  in  moderate  amount. 


CHRONIC  GASTRIC  CATARRH.  33] 

Solid  articles  of  diet  must  be  finely  cut  up  and  well  chewed  before  being 
swallowed.  It  is  sometimes  advantageous  to  take  more  than  three  meals  a  day, 
each  one  being  proportionally  smaller.  Other  patients  relish  their  food  better  if 
the  intervals  between  eating  are  prolonged. 

There  are  other  special  indications  to  be  met.  As  we  have  already  seen,  one  of 
the  chief  factors  in  maintaining  digestive  disturbance  is  the  abnormal  detention 
of  undigested  food  in  the  stomach.  If  we  can  only  empty  the  viscus  properly,  we 
thereby  relieve  it  of  the  abnormal  processes  of  decomposition  and  fermentation,  as 
well  as  of  mucus  which  may  have  collected  in  injurious  amount.  This  indication 
is  best  fulfilled  by  the  mechanical  treatment  of  chronic  gastric  catarrh  by  means 
of  the  stomach-pump.  Its  results  are  often  brilliant ;  but  rinsing  out  the  stomach 
is  never  agreeable  to  the  patient,  and  the  method  should  not  be  resorted  to  except 
in  severe  and  inveterate  cases.  The  most  suitable  are  those  where  an  examination 
of  the  contents  of  the  stomach,  made  as  above  described,  shows  that  abnormal  fer- 
mentative processes  are  going  on,  or  that  the  ingesta  stagnate  in  the  organ.  For 
further  particulars  we  refer  to  the  chapter  on  dilatation. 

If  we  now  turn  to  a  consideration  of  the  internal  remedies  used  in  chronic 
gastric  catarrh,  it  is  possible  to  decide  with  regard  to  their  employment  in  a  much 
more  intelligent  fashion  than  heretofore,  because  we  are  able  in  all  severer  cases 
to  prosecute  a  more  accurate  investigation  of  the  digestive  process.  If  the  exami- 
nation of  the  gastric  juice  shows  a  diminution  of  hydrochloric  acid,  this  may  be 
artificially  supplied.  We  prescribe,  thirty  to  sixty  minutes  after  each  meal,  ten  to 
fifteen  drops  of  dilute  hydrochloric  acid  in  half  a  glass  of  water.  The  benefit  to 
be  thus  derived  must  not  be  overestimated.  In  appropriate  cases,  however,  its 
influence  is  favorable.  One  may  also  make  a  trial  of  pepsin — pepsin  i  Germanici 
solubilis,  seven  and  a  half  grains  (grm.  0'5)  after  each  meal — or  of  pancreatin. 
The  popular  wines  of  pepsin  are  not  to  be  recommended,  because  of  the  alcohol 
they  contain. 

On  the  other  hand,  alkalies  have  been  long  employed  in  chronic  gastric 
catarrh  with  good  effect.  Their  value  is  more  easily  understood  to-day,  because 
we  know  (see  the  appendix  to  this  chapter)  that  many  disturbances  of  digestion 
are  associated  with  an  excessive  production  of  acid ;  still  it  can  not  be  denied  that 
even  in  other  cases  alkaline  remedies  are  sometimes  beneficial.  This  is  probably 
because  the  alkalies  may  contribute  to  the  neutralization  of  abnormally  formed 
acids ;  because  they  promote  the  discharge  of  the  gastric  contents ;  because  they 
tend  to  clear  away  the  mucus;  and  because,  finally,  as  has  been  experimentally 
shown,  bicarbonate  of  soda,  chloride  of  soda,  and  carbonic-dioxide  gas  exercise  a 
stimulating  influence  upon  the  secretion  of  the  gastric  juice.  As  is  well  known, 
the  alkalies  are  mainly  prescribed  in  the  form  of  alkaline  mineral  waters.  The 
springs  of  Carlsbad  possess  the  greatest  reputation.  Those  at  Ems,  Kissingen, 
Tarasp,  and  Vichy  also  deserve  to  be  mentioned  as  health  resorts  for  patients  with 
gastric  trouble.  A  good  portion  of  the  benefit  at  these  places  is,  to  be  sure,  de- 
pendent upon  the  fact  that  many  patients  are  much  more  apt  to  follow  a  strict 
regimen  when  they  make  use  of  a  particular  "  cure "  than  when  they  remain 
at  home. 

If  the  character  of  the  vomitus  or  of  the  gastric  contents  indicates  abnormal 
processes  of  fermentation  in  the  stomach,  the  best  remedy  is  probably  a  methodical 
lavage  of  the  stomach.  We  may  also  try  drugs  which  prevent  fermentation,  the 
most  important  of  which  is  again  hydrochloric  acid  in  rather  large  doses.  Other 
remedies  for  this  purpose  are  salicylic  acid  in  powders  of  eight  grains  (grm.  0"5) 
each;  creasote,  two  or  three  half -grain  pills  (grm.  0-03)  a  day;  and  benzine,  twenty 
drops  in  milk. 

The  best  drugs  to  stimulate  the  secretion  of  gastric  juice  are  the  bitters.     It  is 


382  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

this  property  which  has  earned  them  the  name  of  stomachic  tonics.  Compound 
tincture  of  gentian,  tincture  of  nux  vomica,  tinctura  amara,  and  tinctura  calami, 
P.  G.,  quassia  and  columbo — these  are  the  most  employed.  In  general,  however, 
they  are  not  very  efficient.  An  excellent  tonic  in  many  of  these  cases  is  cundu- 
rango  bark.  A  decoction  may  he  made  (15  parts  to  200  of  water) ;  or  we  may 
write  for  powders  of  seventy-five  grains  (grm.  5)  each,  one  powder  being  made 
into  one  or  two  cups  of  infusion  by  the  patient  himself. 

A  few  remedies  remain  to  be  mentioned,  which  are  said  to  exert  a  direct  bene- 
ficial influence  upon  the  catarrh,  and  which  many  physicians  extol  highly.  Their 
efficacy,  however,  is  somewhat  problematical.  We  refer  chiefly  to  subnitrate  of 
bismuth,  sulphate  of  zinc,  and  nitrate  of  silver. 

Certain  symptoms  may  demand  especial  treatment,  such  as  vomiting.  It  will 
usually  yield  to  regular  and  persistent  washing  out  of  the  stomach.  Other  reme- 
dies are  small  bits  of  ice,  and  minute  doses  of  opium  or  chloral.  Potassic  bromide 
may  also  be  tried. 

Violent  gastralgia  requires  narcotics,  such  as  hydrocyanic  acid  and  morphine. 
"  Sour  stomach  "  may  be  relieved  by  a  pinch  of  bicarbonate  of  soda,  or  of  calcined 
magnesia.  Persistent  anorexia  may  yield  to  the  bitters  mentioned  above,  or  to 
small  doses  of  quinine.  If  the  bad  taste  in  the  mouth  is  annoying,  the  mouth 
should  be  frequently  rinsed  out  with  Seltzer  water,  a  one-per-cent.  solution  of 
carbolic  acid,  or  five  drops  of  tincture  of  myrrh  to  a  glass  of  water.  For  habitual 
constipation,  enemata,  or  the  various  mineral  waters,  are  good;  also  Carlsbad 
salts.  In  obstinate  cases  pills  of  rhubarb  or  aloes  may  be  employed.  Still,  we 
ought  never  to  forget  that  the  infrequency  of  the  stools  is  often  merely  a  natural 
consequence  of  the  scanty  diet,  and  that  it  is  therefore  possible  to  do  harm  with 
our  purgatives.  Iron  is  often  prescribed  for  the  concomitant  anaemia;  but  it 
should  be  employed  cautiously,  for  it  is  often  ill  borne  in  gastric  disease. 


APPENDIX. 

HYPERACIDITY  AND  HYPERSECRETION  OF  THE  GASTRIC  JUICE.      ACID   DYSPEPSIA. 

It  was  formerly  believed  that  in  most  cases  of  disturbed  digestion  there  was  a 
diminished  secretion  of  the  gastric  juice,  and  in  particular  of  hydrochloric  acid; 
but  the  newer  investigations  of  Reichmann,  Riegel  and  others,  have  taught  us 
that  it  is  by  no  means  rare  to  find  in  these  cases  an  exaggeration  of  the  production 
of  acid  and  an  increased  secretion  of  the  gastric  juice.  Hyperacidity  is  the  term 
applied  to  that  condition  in  which  at  the  time  of  digestion  an  abnormally  large 
amount  of  hydrochloric  acid  (0.4  to  0.6  per  cent.)  is  found  in  the  gastric  juice. 
"  Hypersecretion "  refers  to  that  anomaly  where  at  other  times  than  when 
digestion  is  taking  place,  when  the  stomach  is  empty,  there  is  invariably  to 
be  found  a  considerable  amount  of  strongly  acid  gastric  juice  in  the  stomach. 
Hyperacidity  may  exist  independently  of  hypersecretion,  while  hypersecretion 
is  usually  conjoined  with  excessive  secretion  of  acid.  Probably,  therefore,  hy- 
persecretion is  merely  an  exaggeration  of  those  processes  which  lead  to  hyper- 
acidity. 

Hyperacidity  may  usually  be  demonstrated  merely  by  obtaining  an  unusually 
strong  reaction  for  hydrochloric  acid  with  methyl-violet  in  the  gastric  contents, 
but  a  more  accurate  diagnosis  of  course  requires  a  quantitative  estimation  of  the 
acidity.  The  recognition  of  hypersecretion  is  not  easy.  If  we  introduce  a  tube 
into  an  empty  stomach — the  best  time  being  early  in  the  morning — we  shall  find 
that  the  stomach  is  never  empty,  but  that  it  invariably  contains  a  larger  or 
smaller  amount  of  strongly  acid  liquid  unmixed  with  particles  of  food,  and  that 


PHLEGMONOUS  GASTRITIS.  383 

i 
this  liquid  evinces  its  character  as  gastric  juice  by  possessing  an  abundant  amount 
of  hydrochloric  acid  and  digestive  properties. 

As  to  the  causes  of  hyperacidity  and  hypersecretion,  little  as  yet  is  known. 
They  are  perhaps  occasioned  by  conditions  of  nervous  irritation,  or  perhaps  by 
special  forms  of  catarrh.  It  is  certain  that  gastric  ulcer  is  very  frequently  asso- 
ciated with  hyperacidity  (see  below). 

As  we  have  already  mentioned,  increased  production  of  acid  and  of  gastric 
juice  is  by  no  means  rare,  and  therefore  it  is  of  great  practical  importance.  These; 
conditions  occasion  quite  severe  dyspepsia,  which  is  usually  termed  dyspepsia 
acida.  The  symptoms  of  which  such  patients  complain  are  mainly  pain  and 
extremely  sour  eructations,  often  associated  with  pyrosis.  The  pain  is  usually 
described  as  burning,  and  it  is  located  mainly  in  the  region  of  the  stomach,  but 
usually  radiates  toward  the  navel.  It  occurs  sometimes  independently  of  the 
ingestion  of  food  (hypersecretion?),  sometimes  an  hour  or  an  hour  and  a  half  after 
eating  (hyperacidity?).  The  extremely  sour  eructations  take  place  usually  at  the 
time  of  digestion.  Vomiting  is  not  very  frequent,  but  it  may  occur.  The  appetite 
is  in  many  cases  diminished,  but  in  others  it  is  not  much  affected.  Often  there  is 
complaint  of  great  thirst.  The  general  nutrition  in  many  cases  remains  tolerably 
fair.     In  other  cases  the  patients  become  decidedly  emaciated. 

Although  the  above  symptoms,  and  in  particular  the  sour  eructations  and  the 
burning  pains  in  the  stomach,  often  of  themselves  arouse  a  suspicion  of  acid 
dyspepsia,  yet  the  absolute  diagnosis  requires  investigation  by  means  of  the 
stomach-tube.  The  particulars  relating  to  this  have  been  already  detailed.  It 
remains  only  to  add  that  in  testing  the  digestive  power  we  usually  find  a  satisfac- 
tory digestion  of  albumen,  but  a  very  incomplete  digestion  of  starchy  food.  This 
is  probably  in  main  part  dependent  upon  the  fact  that  the  excessive  acidity  of  the 
gastric  juice  inhibits  the  amylolytic  action  of  the  saliva  in  the  stomach  (Ewald 
and  Boas),  but  it  may  also  partially  result  from  the  hindrance  to  the  propulsion  of 
the  food  from  the  stomach,  because  of  a  spasmodic  closure  of  the  pylorus  (Riegel). 

The  treatment  of  acid  dyspepsia  consists  first  in  the  employment  of  alkalies, 
such  as  bicarbonate  of  soda,  in  sufficient  doses,  say  seventy -five  grains  (grm.  5), 
several  times  a  day.  The  use  of  alkaline  waters,  such  as  Carlsbad,  is  also  often 
attended  with  good  results,  particularly  as  these  dilute  the  gastric  juice  and  thus 
diminish  the  irritation  caused  by  the  acidity.  For  this  reason  many  patients  find 
great  relief  from  taking  warm  tea  at  the  time  of  the  pain.  If  the  discomfort  is 
great,  the  most  efficient  remedy  is  certainly  a  methodical  lavage  of  the  stomach. 
With  regard  to  the  best  diet,  we  may  allow  flesh  in  a  sufficient  amount,  while  car- 
bohydrates as  above  mentioned  must  be  enjoyed  in  moderation. 


CHAPTER  III. 

PHLEGMONOUS   GASTRITIS. 

{Purulent  Inflammation  of  the  Stomach.) 

PURULENT  inflammation  of  the  stomach  is  very  rare,  and  little  is  yet  known 
about  it.  In  most  cases  no  special  causes  for  it  have  been  ascertainable.  It  is 
occasionally  one  of  the  symptoms  of  grave  pysemic  or  puerperal  inflammation. 

Two  forms  are  distinguished — a  diffuse  and  a  limited  variety.  The  latter  is 
equivalent  to  gastric  abscess.  The  submucous  layer  is  almost  invariably  the  chief 
seat  of  suppuration.  From  this  starting-point  the  process  invades  the  muscular 
and  serous  coats  on  the  one  hand,  and  the  mucous  membrane  itself  on  the  other. 


384  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

The  usual  symptoms  are  violent  gastric  derangement,  with  pain  and  vomiting, 
high  fever,  and  the  indications  of  constitutional  infection,  namely,  headache, 
delirium,  and  general  prostration.  Sometimes  the  disease  is  quickly  fatal,  some- 
times it  runs  a  more  chronic  course.  The  few  cases  in  which  recovery  has  heen 
reported  are  somewhat  obscure. 

The  disease  can  never  be  diagnosticated  with  absolute  certainty.  Treatment 
must  be  purely  symptomatic.  Ice,  both  internally  aud  externally,  and  the  nar- 
cotics, are  chiefly  employed. 


CHAPTER  IV. 

GASTRIC   ULCER. 

{Simple  or  Bound  Ulcer  of  the  Stomach.) 

iEtiology. — Since  Cruveilhier  gave  the  first  accurate  description  of  gastric 
ulcer,  numerous  explanations  of  its  occurrence  have  been  propounded.  Even  yet 
there  is  no  universally  accepted  view.  There  is,  however,  one  point  about  wThieh 
most  authors  are  agreed,  namely,  that  the  ulcer  is  due  to  a  self-digestion  of  the 
stomach  at  one  limited  spot.  Hence  it  is  frequently  termed  "  peptic  ulcer  of  the 
stomach." 

Apart  from  the  inherent  vital  resisting  power  of  the  cells,  the  reason  that 
the  stomach  is  not  continually  being  digested  by  its  own  juices  is,  as  we  all 
know,  chiefly  the  alkalinity  of  the  blood,  which  is  constantly  coursing  through 
the  mucous  membraue.  Wherever  the  circulation  is  in  any  way  interfered 
with,  we  should  therefore  expect  to  find,  and  we  do  find,  that  the  mucous  mem- 
brane begins  to  be  digested.*  If,  as  a  result  of  inflammation,  a  minute  haeroor- 
rhage  occurs  at  any  point,  the  little  area  thus  deprived  of  its  blood-supply  is  at 
once  digested.  This  is  what  is  called  a  " haemorrhagic  erosion."  The  experi- 
ment of  occluding  the  arterioles  of  the  gastric  mucous  membrane  with  emboli  has 
been  tried  by  Panum  and  Cohnheim.  The  resulting  haemorrhagic  infarctions 
were  transformed  into  ulcers.  Just  what  the  essential  conditions  are,  in  man, 
under  which  a  local  disturbance  of  the  circulation  and  a  consequent  round  ulcer 
of  the  stomach  are  produced,  we  are  thus  far  confined  to  conjecture.  Virchow 
assumed  that  most  cases  were  the  result  of  thrombosis  or  embolism  of  the  minute 
blood-vessels,  caused  by  various  diseases.  Klebs  suggested  the  possibility  of  a 
local  spasm  in  the  vessel.  Böttcher  has  succeeded  in  detecting  numerous  colonies 
of  micrococci  in  the  margins  of  gastric  ulcers,  and  regards  them  as  the  cause. 
As  we  have  already  said,  however,  no  one  of  these  views  has  been  universally 
accepted. 

It  may  be  that  in  many  cases  some  local  injury  of  the  mucous  membrane  is  the 
original  cause  of  the  ulceration.  Such  possible  causes  are  burns  or  mechanical 
lesions,  including  blows  over  the  stomach.  But  even  then  we  are  unable  to 
explain  why  the  ulcers  should  spread  laterally  and  downward.  For  all  gastric 
ulcers  experimentally  produced,  whether  by  embolism,  contusion,  burning,  or 
even  cauterization  (as  practiced  by  Quincke),  exhibit  a  decided  tendency  to  rapid 
healing.  It  has  therefore  been  suggested  that  the  further  extension  of  the  ulcers, 
in  such  cases,  is  due  to  an  abnormally  great  acidity  of  the  gastric  juice  (vide 
infra). 

*  After  the  circulation  is  terminated  by  death,  this  digestive  process  at  once  begins,  producing  the 
softening  of  the  stomach,  or  gastromalacia,  frequently  found  at  autopsies.  There  has  been  much  dis- 
cussion as  to  the  origin  of  this  condition,  but  it  now  seems  indubitable  that  it  is  in  every  instance  a 
post-mortem  change. 


GASTRIC  ULCER.  385 

Ulcer  of  the  stomach  is  commonest  in  young  adults,  het ween  seventeen  and 
twenty-five  years  of  age.  It  is  rare  in  children;  less  so  in  older  people.  The 
disease  is  noticeably  more  frequent  in  females  than  in -males.  It  is  more  prone  to 
attack  the  weakly,  anaemic,  and  chlorotic  than  the  vigorous. 

Pathology. — The  ulcer  is  usually  of  a  circular  shape.  Its  borders  are  sharp; 
the  walls  often  slope  inward,  giving  the  ulcer  the  form  of  a  shallow  funnel.  Its 
base  is  almost  always  perfectly  clean.  If  superficial,  it  does  not  extend  farther 
than  to  the  muscular  coat,  but  it  may  be  deep  enough  to  expose  the  serous  mem- 
brane, or  even  to  perforate  it  (vide  infra).  The  size  varies  greatly.  Some  are 
hardly  as  large  as  a  pea;  others  may  measure  ten  to  fifteen  centimetres  in  tbeir 
greatest  diameter.  As  to  position,  most  of  them  are  found  near  the  pylorus. 
They  attack  the  posterior  wall  of  the  stomach,  particularly  the  neighborhood  of 
the  lesser  curvature,  more  frequently  than  the  anterior  wall.  As  a  rule,  we  find 
but  a  single  ulcer,  although  exceptions  to  this  statement  are  not  very  rare. 

If  an  ulcer  of  any  size  heals,  a  scar  is  formed,  with  radiating  lines  and  often  of 
considerable  size.  Cicatricial  contraction  may  alter  the  shape  of  the  stomach  con- 
siderably. Pyloric  ulcers  may  leave  scars  which  eventually  produce  stricture  of 
the  pylorus  and  consequent  dilatation  of  the  stomach. 

If  the  ulcer  attacks  the  serous  membrane,  perforation  may  finally  result,  unless 
an  adhesive  peritonitis  attaches  the  stomach,  at  the  point  threatened,  to  some  neigh- 
boring organ.  The  ulcers  being  usually  on  the  posterior  wall  of  the  stomach,  it 
is  oftenest  the  pancreas  to  which  the  stomach  becomes  adherent.  In  other 
instances  it  is  the  liver,  transverse  colon,  diaphragm,  or  spleen.  If  the  ulcer 
penetrates  organs  to  which  the  stomach  has  become  attached  in  this  way,  the 
inflammation  extends,  so  as  to  cause  empyema,  for  example,  or  hepatic  abscess ;  or 
the  pleura,  lungs,  pericardium,  or  transverse  colon  may  be  perforated.  We  shall 
revert  to  this  subject  under  the  symptomatology  of  gastric  ulcer. 

The  ulcer  may  cause  erosion  of  a  blood-vessel,  and  thus  give  rise  to  one  of  the 
most  important  symptoms  of  the  disease,  namely,  gastric  haemorrhage. 

Clinical  History. — There  may  be  absolutely  no  symptoms.  It  is  not  a  rare 
thing  to  find  at  autopsies  a  still  active  ulcer  of  the  stomach,  or  the  cicatrix  left  by 
one,  in  subjects  who  never  had  during  life  any  gastric  disturbances  whatever. 
Nor  is  it  exceptional  for  a  person  suddenly  to  exhibit  grave  symptoms,  like  gastric 
haemorrhage,  or  peritonitis  due  to  perforation,  where  there  has  been  no  reason 
previously  to  apprehend  the  existence  of  an  ulcer. 

In  other  instances  the  ulcer  does,  indeed,  give  rise  to  symptoms,  but  they  are 
not  sufficiently  characteristic  to  point  to  the  correct  diagnosis.  There  are  ano- 
rexia, occasional  gastralgia,  vomiting,  and  eructations — symptoms  which  might 
with  equal  probability  be  referred  to  a  simple  chronic  catarrh.  In  fact,  it  seems 
likely  that  the  ulcer  has  little  share  in  their  production,  and  that  they  are  mainly 
due  to  a  co-existing  catarrh.  In  these  cases,  also,  grave  symptoms  consequent 
upon  the  ulceration  may  suddenly  arise. 

In  a  third  class  of  cases  there  are  symptoms  which  are  to  a  certain  extent 
characteristic,  and  lead  with  more  or  less  definiteness  to  the  true  diagnosis.  These 
''  symptoms  of  ulcer  "  are  chiefly  a  peculiar  epigastinc  pain,  which  is  usually  inter- 
mittent, and  vomiting,  or,  what  is  yet  more  distinctive,  the  vomiting  of  blood,  or 
haematemesis.  These  symptoms  and  their  diagnostic  value  we  must  now  consider 
in  detail. 

Pain  in  the  stomach  is  one  of  the  most  frequent  symptoms  of  round  ulcer.  Its 
forms  are  very  diverse.  Often  the  patient  complains  only  of  a  diffuse,  painful 
sensation  of  pressure  referred  to  the  entire  region  of  the  stomach.  This  may  be 
uninterrupted,  or  it  may  occur  only  after  meals,  or  after  excessive  exertion,  or  as 
the  result  of  some  other  special  cause.  This  sort  of  pain  is  the  least  diagnostic  of 
25 


386  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

any,  inasmuch  as  exactly  similar  sensations  may  be  caused  by  a  simple  chronic 
catarrh.  More  characteristic  of  ulcer  is  a  decided  cardialgia — that  is,  a  very  vio- 
lent pain,  coming  on  at  intervals  like  neuralgia.  It  is  described  as  "  cutting," 
"  tearing,"  "  boring,"  and  the  like.  The  pain  may  come  on  irregularly  at  any 
hour;  or  it  may  occur  with  considerable  regularity  at  the  end  of  a  definite  time 
after  eating,  say  half  an  hour  or  an  hour.  It  is  felt  chiefly  in  the  epigastrium, 
but  not  infrequently  extends  toward  the  umbilicus,  backward  toward  the  verte- 
brae, into  the  thorax,  or  even  into  the  upper  extremities.  In  many  instances  a 
mai'ked  sensation  of  thoracic  oppression  accompanies  it.  Another  characteristic 
point  is  that  a  change  of  position  may  sometimes  affect  the  severity  of  the  pain. 
It  is  sometimes  observed  that  the  patient,  when  lying  upon  his  right  side,  feels 
violent  pain,  which  is  at  once  relieved  by  changing  to  the  left  side,  probably 
because  the  ulcer  is  located  near  the  pylorus.  An  attack  of  cardialgia  may  last 
for  a  few  minutes  or  for  several  hours.  It  is  commonly  thought  to  be  due  to 
the  direct  irritation  of  the  ends  of  nerves  lying  exposed  at  the  base  of  the  ulcer. 
As  an  isolated  symptom,  this  cardialgia  can  not  be  distinguished  from  the  purely 
nervous  variety,  but,  taken  in  connection  with  other  symptoms,  it  is  often  a  great 
aid  to  diagnosis.  We  should  add  that  precisely  similar  attacks  of  cardialgia  may 
be  produced  by  the  scars  of  ulcers  which  have  already  entirely  healed. 

A  third  variety  of  pain  may  be  observed  in  gastric  ulcer.  The  suffering  may 
be  localized  in  a  very  limited  area.  Such  pain  is  thought  to  be  due  to  irritation  of 
the  floor  of  the  ulcer  by  food,  or  to  its  edges  being  pulled  upon  during  the  move- 
ments of  the  organ.  It  generally  comes  on  after  eating,  and  ceases  if  the  stomach 
is  perfectly  quiet.  In  position,  this  pain  is  generally  epigastric,  but  sometimes  it 
is  umbilical,  or  even,  now  and  then,  more  toward  the  back.  In  many  cases  of 
gastric  ulcer  there  is  also  tenderness  on  pressure  in  a  quite  sharply  defined  area 
and  at  one  particular  spot.  Most  authors  regard  the  accurately  localized  pain  as 
the  most  nearly  pathognomonic ;  but  it  must  be  said  that  it  is  decidedly  the  least 
frequently  exhibited  of  any.  Transitional  forms  and  combinations  of  the  various 
kinds  of  pain  are  often  observed. 

Vomiting  is  a  very  frequent  symptom  of  gastric  ulcer,  but  if  the  vomitus  is 
composed  of  nothing  except  food,  or  food  mixed  with  mucus  or  bile,  the  symptom 
is  not  at  all  characteristic.  In  quite  a  large  proportion  of  cases,  however  (about 
one  third),  haematemesis  occurs  either  once  or  repeatedly.  The  vomiting  of  a 
considerable  amount  of  blood  is  beyond  doubt  the  most  important  factor  in 
diagnosticating  gastric  ulcer.  Often  the  sudden  occurrence  of  a  decided  haema 
temesis  enables  one  to  diagnosticate  a  gastric  ulcer  with  an  approach  to  certainty. 
If  there  is  no  vomiting  of  blood  whatever,  there  is  much  more  doubt  about  the 
existence  of  an  ulcer. 

Haematemesis  is  frequently  the  symptom  which  first  leads  the  patient  to  apply 
to  a  physician.  Up  to  this  time  he  may  have  felt  perfectly  well,  or,  although 
there  may  have  been  some  gastric  derangement,  he  has  not  thought  anything  of 
it.  The  patient  suddenly  becomes  faint,  perhaps  while  he  is  pursuing  his  regular 
occupation,  or  it  may  be  at  night.  He  feels  dizzy,  and  it  looks  black  before  his 
eyes.  Then  he  has  nausea,  and  finally  is  obliged  to  vomit.  The  vomitus  is  either 
pure  blood,  or  a  mixture  of  blood  and  food.  It  is  partly  coagulated,  and  often  has 
a  rather  dark  or  blackish  color.  This  change  in  color,  as  well  as  the  coagulation, 
is  due  to  the  action  of  the  gastric  juice.  The  amount  varies  greatly  in  different 
cases:  there  may  be  a  quart  or  more.  Not  infrequently  blood  is  repeatedly  vom- 
ited either  at  short  intervals  or  on  successive  days.  Part  of  the  blood  escapes 
through  the  pylorus,  so  that,  after  a  profuse  gastric  haemorrhage,  blood  is  sure  to 
be  found  in  the  stools.  In  them  it  is  black  and  tarry.  Exceptionally  it  happens 
that  all  the  blood,  beyond  what  is  absorbed  from  the  intestinal  canal,  passes  off 


GASTRIC  ULCER.  ZS1 

per  anum,  so  that  none  whatever  is  vomited.  In  such  cases  it  is  often  a  dillicult 
matter  to  locate  the  haemorrhage. 

The  consequences  of  gastric  haemorrhage  depend,  of  course,  chiefly  on  the 
amount  of  blood  lost.  Sometimes,  although  fortunately  rarely,  a  large  blood- 
vessel is  eroded  and  the  patient  dies.  This  event  may  be  sudden,  or  it  may  occur 
more  gradually  under  the  influence  of  repeated  haemorrhages  and  after  a  few 
days,  during  which  all  the  symptoms  of  acute  anaemia  are  exhibited.  On  the 
other  hand,  the  loss  of  blood  may  be  so  insignificant  as  to  produce  no  especial 
symptoms.  In  most  instances  life  is  not  actually  threatened,  but  yet  the  signs 
and  results  of  a  more  or  less  marked  general  anaemia  are  clearly  visible. 

In  such  cases  the  patient  feels  extremely  exhausted,  and  at  once  takes  to  his 
bed.  He  has  also  all  the  subjective  symptoms  of  cerebral  anaemia.  There  are 
vertigo,  tinnitus  aurium,  specks  before  the  eyes,  frequent  gaping,  and  sometimes 
headache.  To  assume  an  erect  posture  aggravates  the  disturbance.  There  is  usu- 
ally excessive  thirst.  Now  and  then  a  temporary  amaurosis  has  followed  an  ex- 
cessive haemorrhage. 

Objectively,  we  notice  at  once  the  excessive  pallor  of  the  skin,  particularly  of 
the  face.  The  lips  and  conjunctivae  are  also  blanched.  The  pulse  is  rapid,  and 
often  ill  sustained.  For  some  days  there  may  be  anaemic  murmurs  over  the  heart, 
and  there  is  a  distinct  sound  to  be  heard  in  the  femoral  arteries.  A  moderate  rise 
of  temperature  is  very  common.  This  is  known  as  the  anaemic  fever.  The  urine 
is  pale,  and  usually  rather  abundant.  Its  specific  gravity  is  not  infrequently  rela- 
tively high,  namely,  1015  to  1020.  All  these  symptoms  are  directly  referable  to 
the  loss  of  blood,  and  will  be  discussed  with  greater  detail  in  the  section  on 
anaemia. 

If  the  haemorrhage  is  not  repeated,  the  patient  gradually  regains  his  strength. 
To  be  sure,  the  pallor  usually  persists  for  a  long  while,  but  the  disagreeable  symp- 
toms gradually  abate.  Where  gastric  discomfort  has  existed  previously  to  the 
haemorrhage,  it  often  disappears  entirely  after  it — a  circumstance  which  is  prob- 
ably in  part  due  to  the  excessive  caution  of  the  patient  thereafter.  At  the  end  of  a 
few  weeks  the  patient  often  feels  perfectly  well  again ;  and,  indeed,  recovery  is  not 
infrequently  complete  and  permanent.  In  other  cases,  however,  the  symptoms  of 
ulcer  return,  sooner  or  later. 

Other  symptoms  than  those  already  discussed  are  more  uncertain.  Anorexia, 
eructations,  and  obstinate  constipation  may  be  present,  or  may  be  wholly  wanting. 
In  cases  of  suspected  ulcer,  it  is  usually  inadvisable  to  introduce  the  stomach-tube 
for  diagnostic  purposes,  because  bleeding  or  perforation  might  result.  Investiga- 
tions have  shown  that  frequently  there  is  no  serious  derangement  of  digestion.  It 
is  interesting,  however,  that  very  often  the  gastric  juice  is  excessively  acid  (hyper- 
acidity, Riegel).  If  there  be  imperfect  digestion,  it  is  probably  due  not  so  much 
to  the  ulcer  as  to  a  coincident  gastiäc  catarrh.  The  general  nutrition  often  suffers 
comparatively  little,  unless  there  are  persistent  anorexia  and  vomiting. 

An  event  which  has  been  already  mentioned  under  pathology — namely,  perfo- 
ration of  the  ulcer — is  of  great  clinical  importance.  It  would  be  impossible  to 
particularize  here  all  the  possibilities  incident  to  it.  We  shall  confine  ourselves 
to  the  two  most  important  because  most  frequent  varieties  of  perforation :  (1)  into 
the  peritoneal  cavity,  causing  peritonitis,  and  (2)  into  the  left  pleura,  or  left  lung. 

Perforation  into  the  peritoneal  cavity  leads  almost  invariably  to  a  quickly  fatal 
peritonitis.  When  the  ulcer  has  previously  caused  few  symptoms,  if  any,  the 
excruciating  abdominal  pain,  tympanites,  vomiting,  collapse,  and  sudden  death  of 
peritonitis  may  abruptly  supervene  upon  a  state  of  apparently  perfect  health.  It 
is  the  exception  to  have  the  peritonitis  limited.  This  is  more  apt  to  occur  if  adhe- 
sions have  been  formed  previously.     An  encapsulated  abscess  then  results,  which 


388  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

points  either  into  the  intestine  or  externally,  and  may  rarely  terminate  in  com- 
plete recovery. 

Perforation  into  the  left  pleural  cavity  we  have  observed  repeatedly.  It  causes 
a  purulent  or  septic  pleurisy  on  that  side,  and  pulmonary  gangrene  may  develop 
at  the  same  time  or  later,  as  a  result  of  perforation  into  the  lung.  Whenever  we 
meet  a  case  of  apparently  spontaneous,  left-sided  empyema,  we  should  at  any  rate 
always  think  of  the  possibility  of  gastric  ulcer. 

The  general  course  of  round  ulcer  of  the  stomach  varies,  as  we  can  see,  so 
greatly  in  different  cases  that  it  can  not  be  depicted  simply.  Complete  recovery 
is  by  no  means  rare.  In  other  cases  the  symptoms  persist  for  years  with  varying 
intensity.  We  have  already  spoken  of  the  haemorrhage  and  perforation  which 
may  suddenly  intervene,  and  of  their  significance.  Relapses  are  not  infrequent, 
even  after  apparent  recovery.  If  the  ulcer  cicatrizes,  the  scar  itself  may  give  rise 
to  persistent  disturbances ;  there  may  be  obstinate  cardialgia,  or,  if  the  scar  is  at 
the  pylorus,  dilatation  of  the  stomach  (vide  infra)  may  gradually  be  developed. 

Diagnosis. — The  diagnosis  can  be  made  only  when  the  above-mentioned  char- 
acteristic symptoms  are  present.  Of  these,  haematemesis  is  by  far  the  most  signifi- 
cant, for  it  is  with  very  few  exceptions  the  result  of  gastric  ulcer.  Particularly  is 
this  true  of  individuals  under  middle  age. — But  how  shall  we  determine  whether 
the  blood  ejected  did  not  come  from  the  nose  or  the  lungs,  rather  than  the  stom- 
ach ?  The  answer  is  not  always  easy.  If  an  epistaxis  occurs  at  night,  a  part  of 
the  blood  often  flows  back  into  the  naso-pharynx,  and,  being  swallowed,  excites 
vomiting,  so  that  a  gastric  haemorrhage  is  suggested.  It  is  also  very  important 
for  the  physician  to  remember  that  blood  may  be  "  vomited  "  in  hysterical  cases. 
If  there  is  also  nervous  cardialgia,  one  might  easily  be  misled  to  assume  the  exist- 
ence of  a  gastric  ulcer.  Other  hysterical  symptoms  (see  the  chapter  on  hysteria) 
and  the  character  of  the  blood  will  usually  guide  us  to  a  correct  diagnosis.  The 
blood  probably  comes  in  most  cases  not  from  the  stomach,  hut  from  the  gums 
or  pharynx,  and  it  is  consequently  of  a  comparatively  bright  color  and  rather 
watery. 

The  diagnosis  between  gastric  and  pulmonary  haemorrhage  in  doubtful  cases 
depends  on  the  following  factors :  1.  The  previous  condition  of  the  patient — whether 
he  has  had  cough,  expectoration,  and  other  pulmonary  symptoms,  or,  on  the  other 
hand,  gastric  pain  and  vomiting.  2.  On  the  character  of  the  haemorrhage,  whether 
accompanied  by  vomiting  or  by  cough.  But  there  may  have  been  both.  Violent 
vomiting  may  excite  a  cough ;  and,  on  the  other  hand,  blood  which  has  been 
coughed  up  may  be  in  part  swallowed  and  induce  vomiting.  3.  On  the  character 
of  the  blood :  if  from  the  lungs,  it  is  usually  bright-red  and  frothy,  containing 
bubbles  of  air,  with  few  clots,  and  of  alkaline  reaction.  In  gastric  haemorrhage  it 
is  usually  dark,  mixed  with  food,  partly  clotted,  and  acid  in  reaction.  4.  On  the 
results  of  physical  examination.  In  this,  of  course,  we  must  be  extremely  cautious 
after  a  haemorrhage,  lest  the  movements  of  the  patient  excite  fresh  bleeding;  and 
yet  we  may  be  able,  from  the  general  condition  of  the  patient,  or  from  dullness  at 
the  apices,  or  moist  rales,  to  demonstrate  pulmonary  disease.  If  the  blood  came 
from  the  stomach,  we  usually  detect  nothing  but  the  signs  of  anaemia.  5.  The 
subsequent  symptoms.  In  cases  of  pulmonary  haemorrhage  there  is  almost  sure 
to  be  an  expectoration,  for  the  next  few  days,  either  of  pure  blood  or  of  matter 
stained  with  blood;  and,  in  gastric  haemorrhage,  the  next  dejection  will  almost 
certainly  be  black,  from  the  presence  of  decomposed  blood.  In  doubtful  cases,  the 
appearance  of  blood  in  the  stools  almost  invariably  settles  the  question  in  favor  of 
gastric  haemorrhage. 

In  cases  of  gastric  ulcer,  unaccompanied  by  haematemesis,  the  diagnosis  is  only 
more  or  less  probable,  not  certain.     The  existence  of  cardialgia  and  localized  pain 


GASTRIC  ULCER.  389 

in  the  stomach  must  always  make  us  consider  the  possibility  of  an  ulcer,  but  we 
can  not  be  positive  about  it. 

The  differential  diagnosis  between  gastric  ulcer  and  purely  nervous  cardialgia, 
and  between  ulcer  and  cancer,  will  be  discussed  later  in  the  appropriate  chapters. 

Prognosis. — The  dangers  in  ulcer  of  the  stomach,  particularly  haemorrhage 
and  perforation,  have  already  been  spoken  of.  Whether  these  misfortunes  will 
actually  occur  in  any  individual  case,  and  when,  wo  can  not  determine. 

There  can  be  no  doubt  that  a  large  number  of  ulcers  heal  perfectly;  but,  as  we 
have  already  said,  even  the  resulting  scar  may  cause  trouble.  This  possibility 
must  be  borne  in  mind.  Of  these  persistent  symptoms,  cardialgia  is  the  most  fre- 
quent. Dilatation  is  also  possible.  And,  finally,  it  is  probably  not  a  very  rare 
event  that  cancer  eventually  develops  in  the  floor  of  the  old  ulcer.  We  shall 
revert  to  this  matter  under  cancer  of  the  stomach. 

Treatment. — If  the  diagnosis  of  gastric  ulcer  is  evident,  or  if  the  symptoms  are 
of  such  a  nature  that  there  is  a  justifiable  suspicion  of  an  ulcer,  the  patient  should 
be  urgently  advised  to  submit  himself  to  careful  and  methodical  treatment;  for  it 
is  only  by  means  of  a  sufficiently  persistent  and  properly  conducted  treatment 
that  we  can  hope  for  good  therapeutic  results  in  ulcer  of  the  stomach. 

The  essential  condition  is,  that  the  patient  should  keep  his  bed  for  the  first  part 
of  the  treatment,  at  least  for  two  or  three  weeks.  Complete  bodily  rest  is  certainly 
an  important  assistance  in  promoting  healing  of  the  ulcer.  The  patient  should 
also  have  moist  compresses,  or,  still  better,  as  Leube  has  advised,  warm  poultices 
applied  all  day  long  to  the  epigastrium.  These  poultices  give  great  relief  to  the 
pain.  In  the  third  place — and  this  is  probably  the  important  matter — the  patient 
must  keep  strictly  to  an  accurately  prescribed  diet.  Every  mechanical  and  chem- 
ical irritation  of  the  floor  of  the  ulcer  must  be  avoided,  and  therefore,  at  first,  liquid 
nourishment  alone  is  to  be  pei'mitted.  It  is  best  to  allow  the  patient,  for  the  first 
ten  days,  milk,  bouillon,  and  at  the  most  some  eggs  and  thoroughly  moistened 
bread.  A  very  suitable  article  of  diet  is  soup  made  out  of  the  Leube-Rosenthal 
solution  of  meat.  In  the  fourth  and  last  place,  we  should  consider  the  hyperacidity 
of  the  gastric  juice,  which,  as  has  been  already  said,  exists  in  the  case  of  ulcer. 
The  patient  therefore  should  be  given  every  day  a  tablespoonful  of  Carlsbad  salts, 
dissolved  in  a  pint  of  warm  water,  to  be  taken  in  three  or  four  divided  doses  during 
the  forenoon  and  afternoon.  If  treatment  of  this  sort  is  strictly  carried  out,  the 
discomforts  of  the  patient,  his  pain  and  vomiting,  will  abate  in  a  few  days.  After 
some  ten  days  have  passed,  if  the  patient  feels  well,  he  may  cautiously  begin  to  eat 
such  food  as  the  brain  of  calves  boiled,  boiled  pigeon,  boiled  fowl,  and  flour  gruel. 
If  this  dietary  makes  the  pain  return,  we  must  fall  back  upon  the  first  kinds  of 
nourishment.  Usually,  however,  the  above-named  foods  are  well  borne,  so  that 
after  another  period  of  eight  or  ten  days  the  patient  may  be  allowed  some  beef, 
such  as  sirloin  or  beefsteak,  shaved  raw  ham,  and,  later,  also  underdone  roast  meat, 
game,  veal,  fish,  and  the  like.  The  more  severe  the  earlier  symptoms  were,  the 
slower  and  more  cautiously  will  one  proceed  with  changes  in  diet.  If  desired, 
one  may  also  employ  either  artificial  nutriments,  such  as  the  meat  peptones  of 
Koch  and  of  Kemmerich,  and  leguminose,  and  also  various  kinds  of  infant 
foods. 

The  above  methods  will  usually  accomplish  all  that  we  can  hope  to  do,  and  it 
is  not  till  they  prove  unavailing  that,  while  persisting  in  our  dietetic  treatment,  we 
should  try  the  other  remedies,  whose  efficiency  is  often  extolled  but  has  never  been 
demonstrated.  Among  these,  the  favorite  is  subnitrate  of  bismuth  in  powders  of 
five  to  fifteen  grains  (grm.  O'30-l'OO)  each,  mixed  with  sugar.  To  this  we  may 
add  a  sixth  of  a  grain  (grm.  O'Ol)  of  morphine,  if  there  is  cardialgia.  One  powder 
is  to  be  given  three  times  a  day,  fifteen  minutes  before  meals.     Nitrate  of  silver  is 


390  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

also  frequently  administered  in  pills  of  one  sixth  of  a  grain  (grm.  0"01)  thrice 
daily;  or  in  a  solution  of  1  to  400,  of  which  the  dose  is  one  or  two  teaspoon- 
fuls. 

Finally,  there  are  special  symptoms  which  may  need  to  be  relieved.  Violent 
pain,  when  not  yielding  to  regulation  of  the  diet,  demands  morphine.  We  may 
also  try  warm  or  cold  applications,  or  chloroform,  externally.  Gerhardt  recom- 
mends three  or  four  drops  of  liquor  ferri  chloridi  in  a  wineglass  of  water,  for  the 
relief  of  pain. 

Excessive  vomiting  and  persistent  nausea  are  likewise  to  be  combated  by  the 
narcotics.  Opium  is  the  best;  morphine,  chloral,  and  bromide  of  potash  may  also 
be  tried.  If  there  be  no  improvement,  we  may  try  creasote,  or  three  or  four  drops 
of  tincture  of  iodine.  At  the  first  appearance  of  blood  in  the  vomitus  the  greatest 
bodily  quiet  and  most  careful  dieting  is  absolutely  indispensable.  For  the  first  day 
or  two  it  is  best  to  allow  nothing  except  ice-cold  milk  and  bits  of  ice  in  the  mouth 
to  appease  the  burning  thirst.  The  patient  must  lie  as  quietly  as  possible  in  bed. 
A  flat  ice-bag,  not  too  heavy,  should  be  placed  on  the  epigastrium.  In  case  of  per- 
sistent nausea  or  eructations,  small  doses  of  morphine  are  to  be  prescribed.  We 
must  wait  till  four  or  five  days  after  the  haemorrhage  before  we  cautiously  increase 
the  amount  of  nourishment,  wdiich  must  still  be  liquid. 

If  peritonitis  appears  as  the  result  of  perforation,  the  best  means  to  try  are  the 
outward  application  of  ice  to  the  epigastrium  and  the  internal  use  of  opium  in 
large  amounts — that  is,  half  a  grain  to  a  grain  (grm.  0 '03-0 "05)  every  one  or  two 
hours.  Unfortunately,  however,  the  cases  are  exceptional  in  which  the  perito- 
nitis does  not  become  general.  Then,  possibly,  operative  interference  might  be 
of  some  avail.  Other  measures  are  almost  hopeless.  We  may  try  to  alleviate  the 
pain  by  narcotics,  but  it  is  very  rarely  that  we  can  prevent  a  fatal  issue. 

[In  cases  of  recent  haemorrhage  or  markedly  painful  digestion,  the  editor  has 
pursued  the  following  plan  of  treatment  with  apparently  good  results :  The  most 
powerful  agent  in  the  promotion  of  cicatrization  is  rest.  Absolute  rest  in  bed  is 
therefore  enjoined,  with  the  secondary  end  in  view  of  reducing  the  demands  of  the 
system.  The  patient  is  then  fed  exclusively  by  the  rectum  for  at  least  one  week, 
generally  for  two  weeks,  nothing  but  a  little  water  being  given  by  the  mouth.  A 
simple  cleansing  enema  is  given  once  daily ;  and  at  six-hour  intervals  a  nutrient 
enema,  six  to  eight  ounces  in  bulk,  and  composed  of  one  or  two  raw  eggs,  an 
ounce  of  expressed  beef  juice,  and  fully  peptonized  milk,  is  administered.  Toler- 
ance by  the  rectum  is  promoted  by  the  addition  to  the  enema  of  a  few  drops  of 
laudanum.  After  one  or  two  weeks  small  quantities  of  milk  at  frequent  intervals 
are  given  by  the  mouth,  and  the  rectal  alimentation  is  gradually  diminished  as 
that  of  the  stomach  is  increased.  Pain  usually  ceases  immediately  on  the  cessa- 
tion of  gastric  ingestion,  and  the  loss  of  weight  during  a  fortnight  of  rectal  feed- 
ing is  surprisingly  small.] 

APPENDIX. 

MELJENA    NEONATORUM. 

We  desire  here  also  to  mention  the  condition  known  as  melcena  neonatorum. 
In  rare  instances  during  the  first  week  after  birth,  haemorrhages  occur  from  the 
stomach  (haematemesis),  which  are  sometimes  associated  with  dark,  bloody  stools. 
As  a  rule  the  haemorrhages  are  repeated,  so  that  after  a  few  days  death  occurs  with 
all  the  phenomena  of  anaemia;  but,  even  after  what  seem  to  be  the  worst  symp- 
toms, recovery  may  exceptionally  take  place. 

The  cause  of  melaena  neonatorum  is  by  no  means  clear,  but  in  some  of  the 
cases  small  ulcers  are   found   in   the  mucous  membi'ane  of  the   stomach   and 


CANCER  OF  THE  STOMACH.  391 

intestine,  as  to  the  origin  of  which  we  have  no  certain  information.     Passive  con- 
gestion, embolism,  and  infection  have  been  suggested  as  causos. 

The  treatment  consists  in  the  application  of  ice  poultices  to  the  abdomen. 
Liquor  ferri  perch] oridi  has  been  also  recommended,  in  doses  of  one  drop  every 
two  hours  in  oatmeal-water. 


CHAPTER  V. 
CANCER  OF  THE  STOMACH. 

iEtiology. — We  can  not  here  discuss  the  aetiology  of  carcinoma  in  general, 
and  we  shall  therefore  merely  enumerate  the  factors  which  experience  has  shown 
to  favor  the  development  of  cancer  in  the  stomach. 

Age  has  a  remarkable  influence.  Gastric  cancer  is  decidedly  most  frequent 
late  in  life,  between  the  fortieth  and  sixtieth  year.  Still  it  is  occasionally  seen  in 
younger  persons.  We  have  ourselves  seen  several  cases  in  persons  between 
twenty-two  and  twenty-five  years  of  age. 

Sex  is  of  no  importance. 

Heredity  has  a  slight  but  undeniable  influence.  The  most  famous  example  of 
the  transmission  of  cancer  is  presented  by  the  family  of  Napoleon. 

The  relation  of  gastric  cancer  to  other  antecedent  diseases  of  the  stomach  is 
very  interesting.  Whether  frequent  errors  in  diet  or  the  use  of  alcohol  increase 
the  liability  to  this  disease  is  uncertain.  On  various  sides  attention  has  been 
called  to  a  possible,  and  as  it  seems  to  us  very  probable,  connection  of  gastric  can- 
cer with  antecedent  ulcer.  Not  only  at  the  bedside,  but  at  the  post-mortem  table, 
a  relatively  large  number  of  cases  have  been  observed  where  cancer  had  developed 
on  the  floor  of  an  old  (and  usually  cicatrized)  ulcer.  Häuser  made  the  interesting 
discovery  of  a-typical  growths  of  epithelium  in  the  scars  of  gastric  ulcers — a 
phenomenon  which  points  strongly  toward  the  relation  suggested. 

Pathology. — The  stomach  is  a  favorite  seat  for  cancer.  About  a  third  of  all 
cases  of  cancer  are  gastric.  The  parts  of  the  organ  most  often  attacked  are  the 
pyloric  end  and  the  lesser  curvature.  Less  frequently  the  cardiac  end  and  the 
fundus  suffer. 

The  new  growth  takes  the  form  either  of  a  circumscribed  tumor  or  of  a  diffuse 
infiltration,  thickening  the  walls.  The  disease  invariably  originates  in  the  mucous 
layer,  extending  thence  into  the  submucous  and  muscular  coats.  The  connective 
and  muscular  tissues  in  the  neighborhood  of  the  cancer  are  quite  often  consider- 
ably hypertrophied. 

Histologically,  gastric  cancer  is  of  the  cylindrical-cell  variety,  starting  from  the 
glandular  epithelium.  The  soft  tumors  are  termed  medullary;  the  firm  and  hard, 
scirrhous  or  fibroid.  The  medullary  cancers  are  particularly  apt  to  be  quite  exten- 
sively broken  down  on  their  exposed  surface,  thus  forming  what  are  known  as 
cancerous  ulcers.  This  seems  to  be  mainly  the  result  of  the  gastric  juice  acting 
on  the  superficial  and  insufficiently  vascularized  portion  of  the  tumor.  The  base 
of  these  ulcers  is  usually  clean,  as  we  should  expect  from  the  mode  of  their  pro- 
duction. In  many  cases  of  rather  young  subjects,  and  also  in  others,  we  find 
colloid  cancer.  This  form  also  may  appear  either  in  nodules  or  as  a  diffuse 
growth,  infiltrating  the  tissues.     As  to  metastasis  of  gastric  cancer,  vide  infra. 

Clinical  History. — Most  cases  of  gastric  cancer  exhibit  a  combination  of  grave 
digestive  disturbances  with  a  relatively  rapid  loss  of  flesh  and  strength.  Now 
and  then  the  gastric  symptoms  assume  less  prominence.  The  chief  sign  of  dis- 
ease is  a  constantly  progressive  marasmus  or  anaemia,  the  true  cause  of  which 


392  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

is  either  entirely  latent  or  not  unmistakably  recognizable  till   late  in  the  ill- 
ness. 

Some  of  the  gastric  symptoms  are  not  very  characteristic.  They  merely  show- 
that  digestion  is  disordered.  There  is  loss  of  appetite  and  distress  after  meals. 
The  patient  complains  of  a  disagreeable  sensation  of  pres^ura  in  the  epigastrium, 
increased  by  food.  Sometimes  this  amounts  to  actual  cardialgia.  Many  patients 
are  annoyed  by  frequent  eructations.  Occasionally  vomiting  is  troublesome;  in 
other  instances  there  is  scarcely  any.  The  vomitus  may  contain  nothing  but 
mucus  and  the  ingesta;  or  it  may  assume,  from  the  admixture  of  blood,  a  very 
characteristic  and  somewhat  pathognomonic  appearance. 

Free  gastric  haemorrhage  and  consequent  hasmatemesis  is  exceptional,  or  at 
least  much  less  frequent  than  in  ulcer  of  the  stomach ;  but  the  vomitus  often 
contains  decomposed  blood,  and  in  many  cases  this  will  be  for  a  time  almost  a 
constant  appearance.     Most  of  the  ulcerated  cancers  bleed  frequently,  a  little  at  a 
time.     The  escaping  blood  is  broken  up  by  the  action  of  the  gastric  juice,  its  red 
hsemoglobine  being  transformed  into  the  black  haematine,  which  produces  that 
"  coffee-ground  "  or  "  chocolate-colored  "  appearance  of  the  vomitus  so  significant 
of  the  disease.     In  such  cases  the  presence  of  blood  can 
|"%    ^Jsf|  #^$       be  demonstrated  conclusively  by  the  spectroscope,  or  by 
^  Hi    %>.  %         means  of  the   so-called  haemine  reaction.     To  perform 

k  *a    ■    |       tn*s'  a  smaH  portion  of  the  vomitus  is  heated  to  boiling 

|s%   $  9  in  a  watch-glass,  having  first  been  mixed  with  a  little 

^  <j|)  ä|      glacial  acetic  acid  and  a  few  crystals  of  common  salt. 

I0®\    ®  \\      Ji^         ^  ^roP  °f  ^his  *s  then  allowed  to  dry  upon  an  object- 
■^  n      ^Lä        glass,  when  the  rhombic  crystals  of  haemine  are  quickly 

^  W  formed.     These  crystals  have  a  dark-brown  color,  and 

Fig  35.— Hsemine  crystals.      are  easuy  recognized  (vide  Fig.  35).     We  should  men- 
tion   that    in   the    case  of    ulcerating    carcinoma    ven« 
triculi  the  vomitus  may  have  so  foul  an  odor  that  it  may  even  be  regarded 
as  stercoraceous. 

Immediate  microscopic  examination  of  the  vomitus  may  reveal  red  blood- 
globules.  Other  characteristic  constituents  are  rare.  It  is  only  exceptionally 
that  bits  of  cancer  can  be  demonstrated.  Of  course,  if  seen,  they  end  all  doubt. 
Sarcinae  are  often  found,  just  as  in  other  gastric  diseases. 

Of  great  diagnostic  importance  is  the  investigation  of  the  gastric  juice  (vide 
supra,  page  378).  As  Von  den  Velden  first  pointed  out,  in  most  cases  of  gastric 
cancer  there  is  no  free  hydrochloric  acid  in  the  gastric  juice,  or  at  least  none  to 
be  detected  by  means  of  the  well-known  reaction  with  methyl-violet  and  the  other 
reagents;  while  on  the  other  hand  lactic  acid  is  not  infrequently  abundant,  and 
may  even  be  present  for  a  long  while  after  food  has  been  ingested.  The  digestive 
power  of  the  gastric  juice  in  persons  afflicted  with  carcinoma  is  consequently,  as 
may  be  easily  demonstrated  by  experiment,  decidedly  below  normal.  The  reason 
of  this  frequent  absence  of  free  hydrochloric  acid  in  carcinoma  is  not  yet  clear. 
Probably  this  phenomenon  does  not  depend  directly  upon  the  carcinoma,  but 
upon  the  catarrh  of  the  rest  of  the  gastric  mucous  membrane  which  is  usually 
present  in  cases  of  carcinoma ;  and  again,  when  the  gastric  mucous  membrane  is 
much  atrophied,  as  has  likewise  been  repeatedly  shown  to  be  the  case,  the  pro- 
duction of  hydrochloric  acid  ceases. 

Physical  examination  of  the  stomach,  and  palpation  in  particular,  are  of  the 
greatest  value.  In  a  large  number  of  cases  the  new  growth  can  be  more  or  less 
plainly  felt  through  the  abdominal  walls,  as  a  hard,  nodular  tumor.  The  tumor 
is  situated  in  the  epigastrium,  in  a  majority  of  cases,  but  it  may  be  lower  down 
or  more  to  one  side,  according  to  the  region  attacked.     It  should  be  remembered 


CANCER  OF  THE  STOMACH.  393 

always  that  a  permanent  tumor  may  essentially  alter  the  position  of  the  stomach 
to  which  it  is  attached.  As  an  illustration,  a  case  of  pyloric  cancer,  which  we  saw, 
with  secondary  dilatation  of  the  stomach,  had  resulted  in  such  a  displacement  of 
the  pylorus  that  the  tumor  was  to  be  felt  through  the  abdominal  walls,  about  a 
hand's  breadth  above  the  symphysis  pubis.  Sometimes  the  tumor  varies  in  posi- 
tion according  to  the  fullness  of  the  stomach.  The  effect  of  the  respiratory  move- 
ments upon  the  tumor  varies.  In  some  cases,  particularly  if  the  tumor  is  adherent 
to  the  liver,  it  can  be  plainly  felt  to  move  downward  with  each  inspiration,  while 
in  other  cases  it  remains  perfectly  stationary. 

In  a  minority  of  the  cases  no  tumor  can  be  felt  at  any  time.  Under  such  cir- 
cumstances the  diagnosis  can  not  often  be  definitely  established.  The  tumor  is 
undiscoverable,  first,  in  most  cases  of  diffuse  cancerous  infiltration  of  the  stomach- 
walls.  We  may,  indeed,  notice  an  increased  sense  of  resistance  and  hardness  in 
the  epigastrium,  but  can  not  refer  this  condition  with  certainty  to  a  new  growth. 
Secondly,  the  new  growth  may  extend  chiefly  inward,  toward  the  cavity  of  the 
organ,  and  may  thus  escape  detection.  And,  finally,  the  tumor  may  be  so  con- 
cealed by  the  liver  or  the  edge  of  the  ribs  that  it  is  inaccessible  to  the  touch.  Such 
cancers  as  attack  the  cardiac  extremity,  the  posterior  wall,  or  the  lesser  curvature 
of  the  stomach,  are  particularly  apt  to  be  out  of  reach  of  palpation. 

Percussion  of  the  cancer  rarely  gives  flatness,  but  instead  a  muffled  tympanitic 
resonance.  This  is  sometimes  an  influential  factor  in  the  differential  diagnosis 
from  cancer  of  the  liver. 

The  physical  examination  sometimes  yields  secondary  evidences  of  cancer,  in 
addition  to  those  which  are  due  directly  to  the  new  growth.  In  most  cases  of 
pyloric  cancer  a  resultant  dilatation  of  the  stomach  can  be  demonstrated. 

Next  in  importance  to  the  gastric  symptoms  is  the  disturbance  of  general 
nutrition.  Loss  of  flesh  is  not  rarely  the  very  first  symptom  which  calls  the 
patient's  attention  to  his  disease.  This  wasting  is  observed  earliest  in  cases  which 
are  attended  with  anorexia  and  vomiting.  The  patient  also  gradually  takes  on 
that  familiar  cachectic  look  which  is  characteristic  of  most  cases  of  cancer.  Some 
patients  become  excessively  anaemic.  The  skin  acquires  a  waxy  pallor,  and  there 
are  all  the  symptoms  which  result  from  great  anaemia,  such  as  cerebral  symptoms 
and  functional  cardiac  murmurs.  Sometimes  the  blood  itself  presents  decided 
peculiarities  in  such  cases.  Thus  we  may  find  microcytes  and  poikilocytes  in  it. 
Gastric  cancer  and  pernicious  anaemia  (q.  v.)  have  been  repeatedly  confounded. 
The  cause  of  this  excessive  anaemia  is  not  always  perfectly  clear.  In  one  such 
case  we  made  the  interesting  discovery  of  extremely  abundant  metastatic  cancer 
in  the  bones.  As  the  bone  marrow  is  known  to  have  something  to  do  with  the 
production  of  the  blood,  it  may  be  that  the  anaemia  was  due  to  this  abnormal  con- 
dition. At  any  rate,  the  grave  anaemia  which  results  from  cancer,  and  sometimes 
also  from  other  chronic  diseases  of  the  stomach,  particularly  gastric  ulcer,  can 
not  be  regarded  in  just  the  same  light  as  are  the  loss  of  flesh  and  the  cachexia. 
Often  the  anaemia  is  very  great  before  the  general  nutrition  has  suffered  much 
impairment. 

When  the  disease  is  pretty  well  advanced  there  may  be  moderate  oedema  of  the 
ankles  and  the  back  of  the  hands.  This  is  to  be  explained,  as  in  other  cachectic 
and  anaemic  conditions,  by  the  impaired  nutrition  of  the  vascular  walls,  the 
hydraemia,  and  the  cardiac  weakness. 

Special  derangements  of  other  organs  are  relatively  infrequent.  Metastatic 
cancer  is  of  importance.  It  attacks  the  liver  chiefly.  If  the  hepatic  new  growth 
is  considerable  it  may  quite  overshadow  the  primary  cancer.  Secondaiy  carci- 
nosis of  the  peritonaeum  is  also  apt  to  cause  marked  symptoms,  such  as  ascites  and 
abdominal  pain.     Secondary  cancer  may  also  involve  the  mesenteric  and  retro- 


394  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

peritoneal  lymph-glands,  the  lungs,  and  other  organs,  but  does  not  usually  give 
rise  to  striking  symptoms  when  so  situated.  It  may  be  added  that  patients  with 
cancer  of  the  stomach  sometimes  present  a  swelling  of  tbe  lymphatic  glands  above 
the  clavicle,  especially  on  the  left  side,  and  that  many  authors  regard  this  fact  as 
of  some  value  in  making  a  diagnosis. 

Direct  extension  of  the  new  growth  into  neighboring  organs  is  not  very  fre- 
quent. We  will  venture  to  mention  one  case  wThich  we  saw,  on  account  of  its 
great  rarity.  The  new  growth  caused  adhesion  of  the  anterior  wall  of  the  stomach 
to  the  abdominal  walls,  and  then,  penetrating  through  them  and  the  skin  of  the 
epigastrium,  finally  appeared  as  a  tumor,  of  about  the  size  of  one's  fist,  projecting 
outward.  If  a  cancer  ulcerates,  it  may  destroy  all  the  layers  of  the  stomach,  and 
result  in  perforation  and  secondary  peritonitis;  or,  if  previous  adhesions  have 
been  formed,  tbe  perforation  may  open  up  an  abnormal  communication  between 
the  stomach  and  some  neighboring  part  of  the  intestine.  The  transverse  colon  is 
the  part  visually  perforated ;  less  often  the  small  intestine. 

As  to  the  bowels,  constipation  is  the  rule.  Diarrhoea  is  rare.  The  urine  is 
usually  pale  and  but  slightly  acid.  Its  amount  is  diminished,  as  we  should  expect 
from  the  slight  amount  of  nourishment  taken,  and  from  the  vomiting.  Over  the 
heart  we  may  sometimes  hear  soft  anaemic  murmurs.  The  pulse  is  usually  accel- 
erated, although,  if  there  be  extreme  marasmus,  it  may  be  slow.  The  temperature 
is  normal,  or  even  subnormal.  If  there  is  some  inflammatory  complication,  or  if 
the  anaemia  is  extreme,  fever  may  occur. 

The  entire  duration  of  the  disease  may  occupy  one  or  two  years.  It  is  excep- 
tional for  it  to  last  longer,  except  where  the  cancer  develops  in  the  floor  of  a  pre- 
existing ulcer.  In  this  event,  the  symptoms  of  ulcer  gradually  give  place  to  those 
of  cancer.  In  individual  cases  the  disease,  of  course,  exhibits  many  variations 
and  departures  from  the  typical  course.  Sometimes  the  constitutional  symptoms 
of  weakness  and  emaciation  ai'e  more  prominent,  and  sometimes  the  distinctively 
gastric  disorders. 

The  fatal  termination  is  usually  preceded  by  the  symptoms  of  constantly  in- 
creasing weakness.  It  may  be  hastened  by  complications.  Now  and  then  grave 
nervous  symptoms  appear,  often  quite  suddenly.  The  patient  falls  into  a  condition 
resembling  that  of  diabetic  coma  (q.  f.),  he  is  somnolent,  and  has  a  peculiar  dysp- 
noea, with  deep  and  labored  respirations,  and  such  an  attack  almost  always  ends 
fatally.     Recovery  from  cancer  of  the  stomach  is  unknown. 

Diagnosis. — In  addition  to  the  ordinary  symptoms  common  to  most  gastric 
disorders,  such  as  pain,  eructations,  and  vomiting,  the  distinctive  factor  in  diag- 
nosis is  the  discovery  of  a  tumor  connected  with  the  stomach.  The  demonstration 
of  this  is  almost  conclusive.  Other  subsidiary  evidence  can  be  obtained  in  most 
instances.  The  patient  is  wasted,  has  a  cachectic  look,  and  is  somewhat  advanced 
in  years.  The  most  characteristic  gastric  symptom,  as  we  have  already  said,  is 
coffee-gi'ound  vomitus,  containing  blood. 

It  is  not  always  easy,  nor  even  possible,  to  make  sure  that  a  tumor  in  this 
region  is  really  of  gastric  origin.  The  chief  characteristics  of  the  tumor  of  gastric 
cancer  have  already  been  mentioned.  The  main  thing  to  exclude  is  cancer  of  the 
left  lobe  of  the  liver,  or  of  the  pancreas,  omentum,  or  transverse  colon.  No  gen- 
eral scheme  for  the  differential  diagnosis  between  these  and  the  gastric  disease 
can  be  given,  for  the  circumstances  and  diffictilties  vary  with  almost  every  case. 
A  careful  consideration  of  all  the  facts,  and  wide  personal  experience  at  the  bed- 
side and  the  post-mortem  table,  are  requisite  here ;  and  yet  the  most  practiced 
diagnostician  may  be  misled. 

We  may  be  able,  however,  to  feel  a  tumor  plainly,  and  to  be  sure  that  it  is 
gastric,  and  still  find  it  difficult,  or  even  impossible,  to  determine  whether  it  is 


CANCER  OF  THE  STOMACH.  395 

cancerous,  or  whether  it  is  not  a  circumscribed  induration  and  thickening  result- 
ing from  an  ulcer  of  the  stomach.  This  is  particularly  true  of  small  tumors  near 
the  pylorus,  attended  with  secondary  dilatation.  The  clinical  symptoms  are  usu- 
ally valueless  here,  for  stenosis  of  the  pylorus  must  produce  identically  the  same 
symptoms  in  either  case.  The  age  of  the  patient,  the  duration  of  the  disease,  and 
possibly  the  history  of  characteristic  symptoms  earlier  in  the  illness,  may  enable 
us  to  reach  a  probable  diagnosis.  In  this  connection  it  is  also  to  be  considered 
that,  as  already  mentioned,  the  scars  of  old  ulcers  not  infrequently  form  the  basis 
for  the  development  of  a  cancer.  The  previous  history  of  the  case  may  present 
such  symptoms  as  cardialgia  and  haBmatemesis,  indicating  that  an  ulcer  has  ex- 
isted, while  the  objective  examination,  by  demonstrating  a  tumor  and  the  absence 
of  free  hydrochloric  acid,  leads  us  to  diagnosticate  the  later  formation  of  a  car- 
cinoma. In  such  cases,  and  indeed  in  any  doubtful  ones,  we  may  test  the  con- 
tents of  the  stomach  for  free  hydrochloric  acid,  and,  if  this  is  invariably  absent, 
cancer  may  be  inferred. 

Here  we  should  add  that,  even  without  any  evidence  of  previous  ulceration, 
there  may  be  a  simple  non-cancerous  hypertrophy  of  the  pylorus  with  consequent 
stenosis.  This  occurrence  we  can  affirm  from  our  own  experience.  The  tumor 
can  not  be  distinguished  clinically  from  the  carcinoma  of  the  pylorus,  and  not 
infrequently  the  autopsy  itself  will  not  enable  us  to  determine  at  once  whether 
there  is  a  carcinoma  or  a  simple  ulcerative  scar  or  hypertrophy.  Absolute  cer- 
tainty is  to  be  gained  in  such  cases  by  a  microscopic  examination  of  the  tumor, 
and  by  the  discovery  of  metastatic  growths,  if  there  be  any. 

In  cases  of  gastric  carcinoma  where  there  is  no  tumor  to  be  felt,  it  is  always 
very  difficult  to  make  an  absolute  diagnosis.  In  general,  we  should  consider  the 
possibility  of  a  cancer  in  every  case  where  a  patient  of  advanced  years  complains 
of  severe  gastric  symptoms  without  any  other  demonstrable  cause.  The  more 
evident  the  constitutional  symptoms  of  cancer,  such  as  increasing  emaciation  and 
cachexia,  the  more  reason  is  there  for  fearing  the  existence  of  a  malignant  growth. 
Here  the  investigation  of  the  gastric  contents  is  very  important.  If  there  is 
good  evidence  of  hydrochloric  acid  in  the  gastric  juice  {vide  supra),  this  is  cer- 
tainly an  important  argument  against  the  assumption  of  a  cancer.  On  the  other 
hand,  if  there  is  no  hydrochloric-acid  reaction  the  suspicion  of  cancer  will  be  de- 
cidedly strengthened,  although  by  no  means  assured,  since  severe  atrophic  ca- 
tarrh of  the  stomach  may  be  associated  with  the  complete  absence  of  hydrochloric 
acid.  If  one  finds  decomposed  blood  in  the  gastric  contents  (coffee-ground  vomit- 
ing, vide  supra),  this,  as  has  been  stated,  is  an  almost  sure  sign  of  carcinoma. 

To  distinguish  between  ulcer  and  cancer  of  the  stomach  may  sometimes  be  a 
difficult  matter.  In  general,  however,  we  shall  be  enabled  to  form  a  diagnosis  by 
considering  the  much  longer  course  of  the  disease  in  ulcer,  as  well  as  the  usual 
youthfulness  of  the  patient,  the  abundant  presence  of  hydrochloric  acid  in  the 
gastric  juice,  the  characteristic  vomitus,  and  the  hasmatemesis. 

Treatment. — As  to  treatment,  we  must  be  content  if  we  relieve  the  patient's 
suffering.  We  possess  no  means  of  antagonizing  the  new  growth.  The  bark  of 
cundurango,  which  Friedreich  recommended  a  few  years  ago,  has  not  proved 
efficient.  It  may,  however,  be  given  with  some  advantage,  as  it  seems  to  be  a 
good  stomachic  tonic.  A  decoction  may  be  made  of  15  parts  of  the  bark  to  150  of 
water,  and  10  parts  of  syrup  of  orange-peel  may  be  added  to  improve  the  taste. 

The  only  possibility  of  a  cure  of  gastric  cancer  lies  in  the  operative  removal  of 
the  same,  as  first  carried  out  by  Billroth.  Numerous  attempts  at  operation  in  the 
last  few  years  have  many  of  them  resulted  unfortunately,  but  a  few  most  favor- 
ably. We  are  therefore  thoroughly  justified,  in  all  cases  where  we  see  any  possi- 
bility of  operative  interference,  to  propose  an  exploratory  incision.     After  the 


396  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

tumor  is  laid  bare,  we  may  then  determine  whether  the  case  is  operable  or  not. 
We  can  not  here  enter  into  particulars  upon  the  subject. 

Tbe  symptomatic  treatment  of  gastric  carcinoma  does  not  differ  greatly  from 
that  repeatedly  described  in  the  preceding  chapters.  The  diet  must  be  regulated, 
and  the  administration  of  hydrochloric  acid  is  important,  inasmuch  as  we  know  it 
to  be  absent  from  the  gastric  juice  in  this  disease;  otherwise  we  merely  fulfill 
such  indications  as  arise.  For  pain,  we  use  the  narcotics,  and  warm  or  cold  appli- 
cations. If  there  is  persistent  vomiting,  we  give  small  doses  of  opium  or  mor- 
phine, chloral,  bits  of  ice,  creasote,  or  tincture  of  iodine.  For  acid  eructations,  we 
prescribe  bicarbonate  of  soda  or  magnesia.  Very  considerable,  although  unfor- 
tunately only  temporary,  benefit  is  derived  from  washing  out  the  stomach.  The 
most  suitable  cases  for  this  are  those  of  pyloric  cancer  with  consequent  dilatation. 
The  various  stomachic  tonics  and  bitters  must  not  be  forgotten.  Our  chief  aim 
must  be  to  maintain  the  patient's  strength  as  long  as  possible,  and  to  do  what  we 
can,  morally  as  well  as  physically,  to  alleviate  his  unhappy  fate. 


CHAPTER  VI. 
DILATATION  OF   THE    STOMACH. 

iEtiology  and  Pathology. — Dilatation  of  the  stomach  is,  in  a  majority  of  in- 
stances, a  secondary  condition,  the  result  of  pyloric  constriction.  As  we  have 
already  seen  in  the  preceding  chapters,  this  constriction  is  usually  due  either  to 
cancer  or  some  other  new  growth,  or  to  the  scars  of  ulcers.  Narrowing  produced 
by  pressure  from  without  is  relatively  infrequent.  Tumors  in  the  neighborhood 
may,  however,  thus  cause  dilatation;  and,  if  Cartels  be  correct,  a  movable  right 
kidney  (q.  v.)  may  also  compress  the  pylorus  or  the  beginning  of  the  duodenum 
sufficiently  to  produce  the  same  result. 

The  manner  in  which  the  stenosis  leads  to  dilatation  is  perfectly  analogous 
with  that  in  which  stenosis  of  the  aorta  causes  dilatation  of  the  left  ventricle.  The 
propulsion  of  food  out  of  the  stomach  into  the  duodenum  becomes  more  difficult, 
and  consequently  the  muscular  fibers  of  the  stomach  are  aroused  to  abnormal 
activity,  that  this  hindrance  may  be  at  least  in  part  if  not  wholly  overcome.  As 
a  physiological  sequence,  we  find  in  most  cases  of  pyloric  stenosis  the  muscular 
coat  hypertrophied.  and  particulaidy  so  in  the  neighborhood  of  the  pylorus.  It 
is  not  till  the  muscle  proves  inadequate  to  overcome  the  obstruction  that  the 
dilatation  begins.  A  portion  of  the  ingesta  remains  in  the  stomach,  and  the  bulk 
of  this  stagnating  mass  gradually  increases.  Its  weight  and  pressure  have  a 
direct  mechanical  influence  in  promoting  the  gradual  expansion  of  the  organ.  In 
addition,  the  processes  of  decomposition  usually  attack  the  contents  of  the  stom- 
ach, and  the  gases  thus  generated  contribute  largely  to  the  mechanical  dilatation. 
Speedily  these  abnormal  chemical  and  other  irritants  excite  catarrh.  The  catarrh 
lessens  the  resisting  powers  of  the  tissues,  interferes  with  the  absorption  of  the 
contents  of  the  stomach,  and  in  both  ways  tends  to  increase  the  dilatation.  The 
united  effect  of  all  these  pernicious  influences  may  finally  be  to  produce  a  dilata- 
tion up  to  three  or  four  times  the  normal  volume  of  the  organ,  the  flabby  fundus 
hanging  down  like  a  great  bag  into  the  hypogastrium. 

In  a  smaller  number  of  cases  of  dilatation  we  find  no  stenosis  of  the  pylorus. 
A  large  dilatation  of  this  sort  is  very  rare.  Smaller  degrees  of  enlargement  may 
frequently  exist,  but  still  they  are  so  difficult  to  diagnosticate  with  certainty  that 
we  can  not  really  say  just  how  frequent  they  are.     The  cause  of  such  dilatations 


DILATATION   OF  THE  STOMACH.  397 

is  in  many  instances  an  impaired  pr>wer  of  resistance,  affecting  chiefly  the  muscu- 
lar layer.  This  condition  may  sometimes  be  due  to  congenital  weakness  of  the 
muscular  fibers,  which  not  only  makes  them  more  yielding,  but  also  favors  the 
retention  and  stagnation  of  food  in  the  stomach.  In  other  cases  the  walls  are 
weakened  by  disease.  Thus  a  persistent  chronic  catarrh  may  lead  to  moderate 
dilatation;  or  constitutional  weakness  resulting  from  anaemia  or  severe  illness 
sometimes  renders  the  gastric  muscular  fibers  so  weak  as  to  permit  dilatation.  In 
all  such  cases  muscular  insufficiency  is  the  chief  factor,  because  it  favors  the 
accumulation  of  ingesta  within  the  stomach.  In  chronic  gastric  catarrh,  it  is 
probable  that  the  muscular  fibers  become  not  merely  weak  but  paretic,  just  as  the 
muscles  of  the  larynx  frequently  do  in  laryngeal  catarrh. 

One  factor  of  gastric  dilatation  remains  to  be  mentioned.  It  is  the  habitual 
overloading  of  the  stomach  with  ingesta.  That  gluttons  and  drunkards  are  liable 
to  dilatation  of  the  stomach  has  long  been  a  familiar  fact.  It  also  occurs  among 
the  indigent,  who  are  obliged  to  make  up  for  the  poor  quality  of  their  nutriment 
(e.  g.,  potatoes)  by  taking  very  large  amounts  of  it.  Such  a  condition  may  well  be 
compared  to  cardiac  dilatation  from  excessive  arterial  tension,  and  may  be  termed 
''overstraining  of  the  stomach."  The  condition  does  not  become  strictly  patho- 
logical till  compensation  begins  to  be  insufficient,  so  that  even  the  hypertrophied 
muscles  are  no  longer  equal  to  the  task  of  propelling  the  food  properly  into  the 
duodenum.  In  diabetes,  excessive  ingestion  and  deficient  nutrition  combine  to 
produce  dilatation,  and  it  has  been  repeatedly  observed  in  this  disease. 

Symptoms  and  Diagnosis. — The  gastric  symptoms  are  only  in  part  due  to  the 
dilatation,  being  also  due  to  the  original  lesion  or  to  other  attendant  circumstances. 
Most  patients  complain  of  loss  of  appetite,  frequent  or  constant  pressure  in  the 
region  of  the  stomach,  heartburn,  eructations,*  and  vomiting.  The  vomiting  is 
frequently  to  a  certain  extent  characteristic.  It  occurs  at  rather  long  intervals, 
and  then  a  very  considerable  amount  is  vomited  at  once.  There  may  be  several 
quarts  ejected.  The  vomitus  not  infrequently  contains  bits  of  food  eaten  several 
days  previously.     Usually  vomiting  affords  the  patient  temporary  relief. 

We  must  have  recourse,  however,  to  physical  examination  in  order  to  be  cer- 
tain about  our  diagnosis.  In  many  cases,  although  by  no  means  in  all,  inspection 
reveals  the  contours  of  a  distended  stomach  through  the  abdominal  walls.  The 
fundus  and  the  greater  curvature  are  most  prominent.  Sometimes  we  can  observe 
the  peristaltic  movements  of  the  stomach,  which  if  not  present  may  perhaps  be 
started  up  by  the  mechanical  irritation  of  sudden  and  repeated  palpation.  If  we 
administer  to  the  patient  a  half -drachm  each  of  sodic  bicarbonate  and  tartaric  acid, 
one  after  the  other,  as  suggested  by  Frerichs,  the  consequent  distention  of  the 
stomach  with  carbonic-dioxide  gas  will  often  render  its  dimensions  much  more 
evident,  and  we  shall  also  be  able  to  ascertain  if  the  prominence  already  noticed 
is  really  gastric. 

By  palpation  it  is  often  possible  to  make  out  the  greater  curvature  and  the 
fundus  still  better  than  by  inspection,  particularly  if  the  muscular  coat  happens 
to  be  contracted.  A  splashing  sound  may  sometimes  be  evoked  by  giving  quick, 
short  blows  with  either  hand  alternately  upon  the  walls  of  the  stomach.  We  can 
hear  and  feel  the  contents  of  the  stomach  rushing  to  and  fro  with  great  distinct- 
ness.    This  is  very  characteristic,  though  not  pathognomonic. 

To  determine  the  size  of  the  stomach  by  percussion  is  so  difficult,  that  percus- 
sion is  seldom  as  reliable  as  inspection  and  palpation,  but  now  and  then  it  does 
aid  us.  The  patient  must  be  examined  in  both  the  erect  and  the  recumbent  post- 
ure, and  both  when  the  stomach  is  full  and  when  it  is  empty.      If  we  introduce 

*  In  some  instances  the  regurgitated  gases  have  proved  inflammable. 


398  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

about  a  quart  of  water  iuto  the  empty  stomach  and  then  fiud  a  line  of  dullness 
below  the  navel  which  was  not  there  before,  we  have  good  reason  to  believe  that 
the  organ  is  dilated.  This  is  Penzoldt's  test.  Sometimes  we  are  unable  to  define 
the  limits  of  the  stomach  by  percussion  until  we  have  dilated  it  with  carbonic 
dioxide ;  but  of  course  we  are  to  bear  in  mind  that  the  stomach  is  in  this  case 
expanded  beyond  its  usual  limits. 

The  use  of  the  bougie  is  valuable.  In  health  the  instrument  will  only  pene- 
trate about  sixty  centimetres,  measured  from  the  mouth,  while  in  dilatation  it  can 
often  be  introduced  as  far  as  seventy  centimetres.  Occasionally  we  may  be  able 
to  feel  the  end  of  the  bougie  through  the  lax  abdominal  walls,  as  Leube  first 
remarked.  In  such  a  case  the  nearer  the  point  is  to  a  horizontal  line  joining 
the  two  anterior  superior  spinous  processes  of  the  ilium,  the  greater  is  the  cer- 
tainty that  dilatation  exists.  Under  ordinary  conditions  the  bougie  probably  does 
not  extend  any  lower  than  the  level  of  the  umbilicus,  if  as  far  as  that. 

A  consideration  of  the  symptoms  already  enumerated,  combined  with  the 
above  methods  of  physical  examination,  will  in  many  cases  enable  us  to  diagnos- 
ticate with  certainty  any  considerable  dilatation  of  the  stomach ;  and  yet  it  must 
be  confessed  that  sometimes  quite  extensive  dilatation  may  escape  observation. 
In  such  instances  there  may  be  either  a  partial  or  complete  absence  of  symptoms 
suggestive  of  any  serious  gastric  derangement,  so  that  no  careful  examination  of 
the  organ  is  made,  or  the  methods  of  physical  examination  already  mentioned, 
when  employed,  yield  a  negative  or  ambiguous  result.  It  is  true  that  other 
methods  have  been  suggested  by  various  authorities  to  determine  the  size  of  the 
stomach  and  test  the  functional  capacity  of  its  muscular  tissue ;  but  none  of  these 
have  as  yet  been  generally  adopted.  Thus  Schreiber  introduced  an  India-rubber 
bag  on  the  end  of  a  catheter,  and  tried  by  blowing  it  up  to  gain  information  as  to 
the  size  and  position  of  the  organ.  With  the  same  end  in  view,  Eosenbach  prac- 
ticed auscultation  of  the  rales  caused  by  blowing  into  a  catheter,  the  opening  of 
which  was  placed  at  the  level  of  the  fluid  contained  in  the  stomach . 

Other  symptoms  are  mostly  analogous  to  those  seen  in  other  severe  gastric  dis- 
orders. The  general  nutrition  becomes  gradually  so  impaired,  particularly  if 
there  is  much  vomiting,  that  the  patient  may  seem  like  a  skeleton.  Kussmaul 
has  sometimes  observed  painful  cramps  in  the  flexors  of  the  arms,  the  calves,  and 
the  muscles  of  the  abdomen.  These  he  refers  to  the  abnormal  dryness  of  the 
muscular  tissue.  The  bowels  are  almost  always  very  much  constipated,  mainly  as 
a  result  of  the  diminished  amount  of  ingesta  which  reaches  the  intestine.  The 
urine  is  small  in  amount,  and  often  neutral  or  alkaline  in  reaction.  The  alkaline 
reaction  Quincke  believes  is  more  apt  to  be  present  while  the  stomach  is  being 
washed  out,  because  in  this  way  the  system  is  deprived  of  a  relatively  large 
amount  of  acid. 

Course  of  the  Disease  and  Prognosis. — The  course  and  duration  of  the  disease 
are  chiefly  dependent  upon  the  nature  of  the  original  lesion  from  which  the  dila- 
tation proceeds.  If  there  is  cancerous  stenosis  of  the  pylorus,  of  course  the  case 
is  hopeless.  Cicatricial  stenosis  with  secondary  dilatation  allows  a  more  favorable 
prognosis.  With  proper  treatment  and  a  sensible  mode  of  life,  the  patient  may 
be  tolerably  comfortable  for  years;  but  Anally  nutrition  becomes  more  and  more 
impaired,  and  death  ensues. 

The  general  course  of  the  disease  presents  all  sorts  of  vicissitudes.  As  long  as 
the  hypertrophied  muscles  are  able  to  overcome  the  abnormal  obstruction,  there 
may  be  no  symptoms  of  importance.  Just  as  in  cardiac  cases,  it  is  only  when 
compensation  becomes  disturbed  that  the  results  of  dilatation  are  observable.  If 
we  can  tone  up  the  muscles  again,  or  reduce  the  work  they  are  called  upon  to  per- 
form to  an  amount  which  they  are  capable  of  accomplishing,  marked  relief  follows. 


DILATATION   OF  THE  STOMACH. 


399 


Those  cases  of  dilatation  which  are  not  due  to  pyloric  stricture  have,  on  the 
whole,  the  best  prognosis.  In  milder  cases  of  this  kind  there  may  be  permanent 
recovery,  provided  proper  mechanical  and  dietetic  treatment  be  promptly  and  per- 
sistently employed. 

Treatment. — Our  first  aim  in  treatment  should  be  to  relieve  the  dilated  organ 
of  the  great  amount  of  material  it  contains  and  to  avoid  new  accumulations.  If 
this  double  effort  is  successful,  we  have  removed  the  injurious  influences,  both 
mechanical  and  chemical,  which  we  have  seen  to  maintain  and  persistently  to 
aggravate  the  dilatation. 

The  indication  is  best  met  by  the  "  mechanical  treatment  of  dilatation,"  for 
which  we  are  so  deeply  indebted  to  Kussmaul.  This  method  is  beneficial  to  the 
chronic  catarrh  which  accompanies  the  dilatation,  or  which  may  even  have  pro- 
duced it.  We  have  no  direct  means  of  treating  stenosis  of  the  pylorus,  if  it  exists, 
unless  possibly  by  surgical  operation.  The  operative  removal  of  cicatricial  steno- 
sis has  already  been  repeatedly  performed  with  success,  and  it  is  to  be  expected 
that  it  will  come  to  be  practiced  "more  and  more. 

For  emptying  and  rinsing  out  the  stomach  the  best  means  is  simple  siphonage. 
A  long,  soft  Nelaton's  catheter,  supplied  with  sufficiently  large  openings  on  its 
sides,  near  its  extremity,  is  joined  to  a  rubber  tube  of  about 
one  metre  in  length,  and  to  the  end  of  this  is  fitted  a  large 
glass  funnel  {vide  Fig.  36).  The  stomach-tube  being  intro- 
duced and  the  funnel  raised,  the  entire  tube  is  filled  with 
water  and  thereupon  lowered.  Thus  siphonage  is  pro- 
duced and  the  contents  of  the  stomach  flows  out.  By  alter- 
nate raising  and  lowering  of  the  funnel,  combined,  of 
course,  with  the  pouring  in  of  water  or  soda  solution,  and 
the  escape  of  the  same  again,  the  stomach  may  »be  thor- 
oughly cleansed.  It  is  still  more  convenient  to  have  a 
Y-tube  of  glass  fitted  to  the  upper  end  of  the  catheter  con- 
necting respectively  with  a  reservoir  of  water  and  with  a 
slop-jar  by  rubber  tubes,  the  alternate  opening  and  closing 
of  which  will  permit  water  to  run  into  the  stomach  from 
the  reservoir  and  then  out  again  into  the  jar. 

The  siphon  apparatus  and  the  necessary  manipulations 
are  so  simple  that  we  have  had  several  patients  with  gastric 
dilatation  who  daily  washed  out  their  own  stomachs.  This 
simple  tube  has  almost  completely  superseded  the  regula- 
tion stomach-pump.  The  latter  consists  of  a  catheter  at- 
tached to  a  syringe  which  has  two  openings  at  its  end,  one 
to  aspirate  and  one  to  allow  the  escape  of  liquid.  More  than 
once,  when  this  instrument  has  been  employed,  a  piece  of 
the  lining  membrane  of  the  stomach  has  been  sucked  into 
the  hole  at  the  end  of  the  stomach-tube  and  torn  off.  The 
assumption  that  the  pump  empties  the  stomach  more  com- 
pletely than  does  the  siphon  is  seldom  borne  out  by  facts. 

We  may  use  pure  water  for  lavage,  or,  as  already  men- 
tioned, a  one-  or  two-per-cent.  solution  of  soda  or  of  Carls- 
bad salts,  which  may  more  effectually  clear  away  the 
mucus.     If  there  is  reason  to  believe  that  fermentation  is 

particularly  active,  we  may  employ  a  one-per-cent.  solution  of  salicylic  acid  or  a 
two-per-cent.  solution  of  resorcin.  The  best  time  for  washing  out  the  stomach  is 
shortly  before  meals.     It  is  done  once  or  twice  a  day. 

The  patient's  diet  should  be  carefully  regulated.     The  food  should  be  nourish- 


Fig.    36.— Stomach    tube, 
with  Hegar's  funnel. 


400  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

ing,  easily  digestible,  and  of  the  least  possible  bulk.  We  should  therefore  try 
Leube's  meat  solution,  fine  shavings  of  raw  beef  or  ham,  soft-boiled  eggs,  and  milk 
in  small  amounts,  but  should  avoid  vegetables,  coarse  bread,  and  the  like.  In  this 
way  we  can  usually  succeed  in  improving  the  patient's  nutrition  decidedly,  and 
the  vomiting  and  sense  of  gastric  oppression  as  well  as  other  disagreeable  symp- 
toms will  cease.  Whether  the  improvement  will  be  permanent  depends,  as  has 
been  said,  upon  the  nature  of  the  dilatation  and  the  causal  lesion. 

In  conclusion,  we  should  mention  that  the  attempt  has  been  made  to  tone  up 
the  muscular  fibers  of  the  stomach  and  stimulate  them  to  more  vigorous  contrac- 
tion. Energetic  faradization  and  galvanization  of  the  stomach  have  been  recom- 
mended. The  application  may  be  made  through  the  abdominal  walls,  or  by 
means  of  an  electrode  introduced  through  a  stomach-tube.  Nux  vomica  has  also 
been  employed  to  meet  the  same  indication.  The  symptomatic  treatment  of  gastric 
dilatation  may  employ  also  all  the  other  remedies  mentioned  in  discussing  catarrh 
of  the  stomach.  It  is  advantageous  to  have  the  patient  wear  an  elastic  bandage 
firmly  applied  around  the  abdomen. 


CHAPTER  VII. 

NERVOUS  DISORDERS  OP  THE   STOMACH. 

(Nervous  Dyspepsia.     Gastric   Neurasthenia.) 

It  very  often  happens  that  persons  complain  of  gastric  symptoms  for  which  we 
can  assign  no  objective  lesion  of  the  stomach.  There  is  neither  any  certain  in- 
dication of  any  important  pathological  change,  such  as  dilatation,  cancer,  or  ulcer, 
nor  any  history  to  be  obtained  of  any  of  the  causes  of  chronic  gastric  catarrh.  On 
closer  study  of  the  cases  we  find,  however,  that  the  stomach  symptoms  are  most 
strikingly  dependent  on  certain  nervous  and  chiefly  psychical  conditions.  We 
are  therefore  justified  in  describing  such  affections  as  nervous  diseases  of  the 
stomach,  and  entirely  distinct  from  other  affections  of  that  organ. 

If  we  seek  to  give  a  more  accurate  account  of  the  precise  nature  of  these  nerv- 
ous disorders,  we  must  admit,  in  the  first  place,  that  there  may  be  in  some  cases 
actual  disease  of  the  nerves  of  the  stomach.  Thus,  for  example,  cases  of  pure 
"  nervous  cardialgia  "  occur,  the  foundation  of  which  is  probably  a  neuralgia  of  the 
nerves  of  the  stomach,  precisely  corresponding  to  the  neuralgias  of  other  sensory 
nerves.  Again,  motor  derangements  are  seen  which  are  evidently  caused  by  ab- 
normal excitement  of  the  motor  nerves  of  the  stomach,  or  else  of  the  correspond- 
ing nerve-centres.  To  this  class  belongs  Kussmaul's  "  peristaltic  restlessness  of 
the  stomach,"  characterized  by  a  marked  exaggeration  of  peristalsis,  which  is  both 
seen  and  felt  through  the  abdominal  walls,  is  sometimes  accompanied  by  all  sorts 
of  gurgling  noises,  and  of  which  the  patient  himself  is  often  painfully  conscious. 
Peculiar  attacks  of  nervous  vomiting  belong  in  the  same  category.  In  many  per- 
sons they  occur  from  time  to  time  without  special  cause  and  with  great  violence. 
They  may  last  for  hours,  or  even  days,  and  are  often  associated  with  cardialgia, 
general  prostration,  and  other  nervous  phenomena.  Leyden  observed  such  cases, 
and  described  them  under  the  name  of  "  periodical  vomiting  with  paroxysms  of 
gastealgia. "  The  cause  of  this  state  is  far  from  clear.  Except  at  the  time  of  the 
attack  there  are  no  symptoms  whatever  of  gastric  disease  or  any  other,  and  we 
are  therefore  obliged  to  assume  a  "  nervous  origin  "  for  it.  The  paroxysm  reminds 
one  decidedly  of  the  gastric  crisis  of  tabes  dorsalis  (vide  p.  643).  It  may  also  be 
related  to  migi'aine  (q.  v.). 


NERVOUS  DISORDERS  OF  THE  STOMACH  401 

If  in  these  cases  the  voraitus  is  abnormally  sour,  we  have  a  condition  which 
Rossbach  has  named  nervous  gastroxynsis.  Gastroxynsis  seems  to  be  associated, 
therefore,  with  secretory  disturbances,  and  recalls  the  above-described  acid  dys- 
pepsia {vide  p.  382).  There  is  also  a  form  of  persistent,  purely  nervous  vomiting. 
We  have  seen  it  with  particular  frequency  in  school  children  of  both  sexes,  in 
whom  about  the  only  symptom  was  that  they  would  vomit  after  every  meal. 

The  varieties  already  enumerated  are  not,  however,  nearly  so  common  as 
others  in  which  the  nervous  condition  is  not  so-  pronounced.  The  patient  com- 
plains almost  all  the  time  of  a  train  of  nervous  and  dyspeptic  sensations,  all  of 
which  occur  mainly  after  eating,  during  digestion,  and  which  may  therefore  be 
properly  classed  as  nervous  dyspepsia.  Such  a  patient  will  say  that  he  has  a 
sensation  of  pressure  and  pain  in  the  stomach  after  every  meal,  and  that  after  a 
few  mouthfuls  the  organ  feels  full  and  distended.  As  a  consequence,  there  are 
often  thoracic  oppression  and  palpitation.  The  patient  frequently  suffers  also 
from  eructations,  which  may  increase  to  actual  vomiting.  All  these  symptoms 
may  occur  in  the  same  way  where  there  is  actual  gastric  disease,  particularly  gas- 
tric catarrh,  but  in  the  present  instance  they  are  usually  associated  with  other 
phenomena  which  indicate  their  nervous  character.  In  the  first  place,  we  may 
notice  that  thei*e  is  often  a  striking  changeableness  in  their  severity.  The  same 
patient  who  to-day  complains  of  severe  gastric  oppression  after  a  few  spoonfuls  of 
soup,  will  to-morrow,  when  happy  and  excited,  enjoy  a  grand  dinner  without  being 
in  the  slightest  degree  reminded  of  his  stomach.  This  and  many  other  circum- 
stances show  most  plainly  the  influence  of  emotion  upon  the  state  of  the  stomach. 
We  all  know  how  appetite  may  at  once  vanish  under  the  influence  of  violent 
anger  or  keen  anxiety  or  lively  hope,  or  any  strong  emotion,  whether  pleasurable 
or  the  reverse,  and  that  great  excitement  not  infrequently  causes  vomiting  or  the 
like.  In  the  same  way,  sensitive  persons  are  affected  by  the  slightest  psychical 
influences.  And  of  all  such,  the  most  harmful  is  disquietude  with  regard  to  their 
own  bodily  condition.  The  fear  that  a  dish  they  have  eaten  may  harm  them,  the 
constant  dread  that  a  serious  disease  of  the  stomach  is  in  process  of  development 
— such  mental  disquietude  is  it  which  is  best  calculated  to  maintain  the  unhealthy 
state  and  gradually  to  aggravate  it.  In  this  way  a  peculiar  subjective  hyperes- 
thesia is  developed  which  feels  exquisite  "  pain "  in  the  stomach  when  there  is 
really  nothing  more  than  the  ordinary  normal  sensation.  And,  in  conclusion, 
there  are  developed  in  the  same  way  certain  half-unconscious,  half-voluntaiy 
movements  which  produce  eructations,  vomiting,  and  the  like. 

What  we  desire,  therefore,  especially  to  emphasize,  is  our  own  conviction  that 
in  the  large  majority  of  the  cases  of  so-called  nervous  dyspepsia  there  is  no  func- 
tional derangement  of  the  nerves  of  the  stomach  themselves,  but  a  diseased 
"  psychogenous "  excitation  of  the  nerve-centres,  the  consequences  of  which  are 
expressed  mainly  in  the  domain  of  the  digestive  functions.  Nervous  dyspepsia  is 
only  a  particular  example  of  that  great  class  of  nervous  diseases  which  owe  their 
origin  to  hypochondriacal  conditions  of  the  mind,  and  which  may  occur  in  the 
most  diverse  oi'gans  of  the  body.  This  explains  why  the  gastric  symptoms  are 
frequently  attended  by  other  nervous  phenomena,  among  which  may  be  men- 
tioned symptoms  of  increased  psychical  irritability,  headache,  pressure  in  the  head, 
vertigo,  and  abnormal  sensations  in  the  extremities  of  pain  or  cold  or  numbness. 
There  are  almost  always  also  some  intestinal  symptoms.  The  patient  complains 
of  distention  of  the  abdomen,  and  particularly  of  irregular  and  constipated 
bowels. 

Nervous  dyspepsia  may  become  a  rather  serious  matter,  if  the  patient's  anxiety 
to  avoid  errors  in  diet,  and  the  anorexia  occasioned  by  his  uneasy  sensations,  pre- 
vent his  taking  sufficient  nourishment.  In  this  way  there  may  be  gradually  pro- 
26 


402  DISEASES  OF  THE  DIGESTIVE  OKGANS. 

duced  a  considerable  oi'  even  excessive  emaciation,  with  corresponding  debility 
and  weakness.  Such  a  patient  may  become  completely  bedridden,  and  give  one  at 
first  the  impression  of  severe  illness. 

In  such  cases  the  diagnosis  is  not  always  easy,  although  it  can  usually  be 
formed  upon  careful  consideration  of  the  whole  course  of  the  disease  and  the 
character  of  the  patient.  Physical  examination  in  nervous  dyspepsia  is,  of  course, 
invariably  negative  in  its  results.  The  epigastrium  is  often  very  tender  on  press- 
ure, and  the  vertebrae  painful.  The  skin  over  the  stomach  is  often  noticeably 
insensible  to  pin-pricks.  This  fact  is  a  connecting  link  between  nervous  dyspep- 
sia and  the  allied  hysterical  affections  of  the  stomach.  If  it  is  possible  to  examine 
the  contents  of  the  stomach  with  the  aid  of  the  stomach-tube,  the  processes  of  di- 
gestion and  the  secretion  of  gastric  juice  are  found  to  be  undisturbed.  This  dis- 
covery often  has,  of  course,  great  diagnostic  value,  and  it  holds  true  at  least  for 
most  of  the  cases  which  rest  upon  a  purely  psychical,  hypochondriacal  basis.  If, 
on  the  other  hand,  the  patient  has  not  only  well-marked  nervous  symptoms,  but 
also  a  diminution  of  the  motor  power  of  the  stomach,  and  diminished  or  (as  is  not 
infrequent)  increased  secretion  of  acid  in  the  stomach,  the  diagnosis  is  usually  ob- 
scure. These  changes  may,  indeed,  depend  on  purely  nervous  causes ;  but  still  in 
the  individual  case  it  is  generally  difficult  or  even  impossible  to  exclude  with  cer- 
tainty the  simultaneous  existence  of  an  actual  catarrh  or  ulcer  of  the  stomach. 

In  many  severe  cases  it  requires  long-continued  observation  of  the  patient  to 
render  a  correct  diagnosis  possible.  We  may  be  aided  by  learning  what  remedies 
help  and  what  hurt  the  patient.  This  is  particularly  true  where  the  diagnosis 
lies  between  ulcer  and  nervous  dyspepsia,  where  it  may  be  very  difficult,  and  often, 
despite  careful  balancing  of  all  the  symptoms,  scarcely  possible  to  reach  a  sure 
conclusion.  A  patient  with  nervous  dyspepsia  subjected  to  the  strict  regimen 
suitable  for  ulcer  often  grows  worse  and  worse,  while  an  opposite  course  of  treat- 
ment (vide  infra)  may  achieve  the  most  surprising  success. 

The  prognosis  depends  mainly  on  the  outward  circumstances  of  the  patient.  If 
the  harmful  mental  influences  or  other  setiological  factors  are  persistently  active, 
actual  and  permanent  recovery  is  hardly  to  be  expected ;  but  if  the  cause  can  be 
removed,  complete  recovery  is  not  rare,  even  in  what  seem  to  be  grave  cases.  A 
liability  to  relapses  is,  of  course,  almost  always  left  behind. 

Treatment. — If  nervous  dyspepsia  has  once  been  diagnosticated,  the  proper  aim 
of  our  therapeutic  efforts  becomes  perfectly  definite.  We  must,  in  the  first  place, 
convince  the  patient  that  he  has  no  incurable  or  even  dangerous  gastric  disease, 
but  that,  on  the  contrary,  his  stomach  is  perfectly  capable  of  performing  its  func- 
tions in  a  normal  manner.  Nothing  could  be  more  harmful  to  a  sufferer  from 
nervous  dyspepsia  than  to  have  his  physician  manifest  great  anxiety  about  treat- 
ment, and  prescribe  a  very  strict  diet.  The  patient  must  rather  be  gradually  led 
to  use  an  abundance  of  nutritious  food.  It  is  in  this  way  alone  that  he  regains  a 
confidence  in  himself,  when  he  sees  that  the  hearty  food  does  him  no  harm,  that 
he  is  gaining  flesh,  and  that  the  bowels  are  becoming  regular. 

Internal  remedies  are  best  omitted  altogether  if  the  patient  has  already  taken  a 
good  deal  of  medicine.  We  should  particularly  warn  him  against  the  abuse  of 
purgatives.  If  we  must  prescribe  something,  a  bitter  tonic  is  very  good,  such  as 
tincture  of  nux  vomica.  Anaemic  patients  may  also  take  iron.  For  nervous 
vomiting  and  regurgitation  the  best  remedy  is  bromide  of  potash.  Antipyrin  also 
is  sometimes  useful. 

Those  methods  of  treatment  are  of  great  value  which  are  directed  to  the  ton- 
ing up  of  the  body  in  general  and  the  nervous  system  in  particular.  The  patient 
may  go  into  the  country  or  to  the  mountains  or  the  seashore.  Methodical  treat- 
ment with  cold  water  is  good ;  in  particular,  sponging,  combined  with  rubbing  of 


INTESTINAL  CATAEEH.  403 

the  trank  and  the  whole  body,  almost  always  gives  good  results.  On  the  other 
hand,  those  health  resorts  which  often  do  good  in  the  case  of  organic  gastric  dis- 
ease are  but  seldom  beneficial  in  nervous  dyspepsia.  Thus,  we  have  frequently 
seen  such  patients,  who  had  been  sent  by  their  physicians  to  Carlsbad,  return 
worse  rather  than  better.  We  have  repeatedly  found  electricity  valuable,  al- 
though we  are  not  prepared  to  deny  that  its  subjective  effect  may  be  of  chief  im- 
portance. Galvanism  is  applied  along  the  spinal  column,  and  also  through  the 
stomach  horizontally,  one  large  electrode  being  placed  upon  the  epigastrium  and 
the  other  on  the  back.  It  is  well  to  reverse  the  current  frequently.  Faradization 
of  the  abdominal  walls  is  indicated,  especially  when  there  is  constipation. 

We  need  hardly  add  that  the  a?tiological  factors  must  not  be  overlooked.  The 
patient  must  be  warned  against  useless  overexertion,  emotional  excitement,  etc. 
(Compare  the  chapter  on  neurasthenia.) 

The  main  point  is  to  aim  at  a  methodical  moral  training  of  the  patient.  He 
should  learn  to  feel  and  to  behave  like  a  healthy  person.  He  should  regain  his 
self-control,  and  not  allow  himself  to  be  upset  by  every  slight  psychical  shock, 
whether  subjective  or  coming  from  without.  It  is  self-evident  that  this  goal  is  to 
be  attained  not  by  baths  and  prescriptions,  but  by  correct  moral  guidance.  It  is 
therefore  true  of  nervous  dyspepsia,  as  of  all  similar  neurasthenic  conditions, 
that  it  is  to  be  cured  not  by  physic  but  by  the  physician. 


SECTION  V. 

Diseases  of  the  Intestines. 

CHAPTEE  I. 

INTESTINAL   CATARRH. 

(Catarrhal  Enteritis.) 

iEtiology. — The  majority  of  cases  of  intestinal  catarrh,  like  gastric  catarrh,  are 
due  to  an  abnormal  irritation  of  the  mucous  membrane  of  the  intestine  by  its 
contents.  In  most  cases  the  irritants  are  of  a  mechanical  or  a  chemical  nature, 
and  depend  upon  the  quantity  and  quality  of  the  food  taken,  which  explains  why 
catarrh  of  the  stomach  and  of  the  intestine  are  so  often  combined  with  each  other. 
Noxious  substances,  taken  into  the  system  by  the  ingestion  of  spoiled  food,  like 
spoiled  meat,  fish,  beer,  etc.,  very  often  play  a  part  in  the  origin  of  intestinal 
catarrh. 

To  the  intestinal  catarrhs  caused  by  improper  food  we  may  add  the  toxic 
catarrhs  which  are  produced  by  the  direct  ingestion  of  poisonous  substances  into 
the  digestive  tract.  Severe  inflammations  of  the  intestinal  mucous  membrane 
arise  from  poisoning  by  mineral  acids  and  corrosive  alkalies,  arsenic,  corrosive 
sublimate,  etc.  Intestinal  catarrh  may  also  arise  from  the  imprudent  use  of 
certain  drugs,  especially  active  cathartics. 

A  great  many  cases  of  intestinal  catarrh  are  due  to  infectious  influences,  in- 
cluding most  of  the  apparently  spontaneous  catarrhs,  and  also  many,  if  not  all,  of 
the  catarrhs  attributed  to  taking  cold  or  getting  wet,  and,  finally,  those  affections 
which  often  develop  epidemically  or  endemically  in  hot  weather,  and  which  we 
term  summer  complaint,  cholera  morbus,  etc.  Cholera  morbus  is  an  especially 
severe  form,  and  will  be  described  more  fully  later  on.     We  must  also  mention 


404  DISEASES  OF  THE  DIGESTIVE  OEGANS. 

here  that  intestinal  catarrh  is  very  often  one  symptom  of  other  general  infectious 
diseases,  like  typhoid,  dysentery,  septic  diseases,  or  severe  malaria. 

In  a  final  class  of  cases  intestinal  catarrh  develops  from  disturbances  of  the 
circulation,  which  cause  a  passive  hyperseniia  of  the  intestinal  mucous  membrane. 
Diseases  of  the  liver  and  portal  vein,  and  also  chronic  diseases  of  the  heart  and 
lungs,  are  the  chief  affections  which  produce  a  stasis  in  the  portal  system,  and 
thus  an  intestinal  catarrh ;  but  here  the  stasis  is  probably,  in  most  cases,  only  a 
predisposing  factor  in  the  development  of  the  catarrh,  since  the  action  of  all  other 
irritants  is  made  easier  by  the  disturbance  of  the  circulation. 

The  great  frequency  of  intestinal  catarrh  in  both  sexes,  and  at  every  age,  is 
well  known.  Children,  above  all,  have  a  pronounced  tendency  to  diseases  of 
the  intestine,  so  that,  by  a  probable  estimate,  almost  one  third  of  the  illnesses 
of  children  are  to  be  referred  to  the  intestinal  canal.  We  will  give  a  special 
description  of  intestinal  catarrh  in  children  on  account  of  this  fact. 

Pathological  Anatomy. — The  pathological  changes  in  catarrhal  inflammation 
of  the  intestines  are  essentially  the  same  as  are  met  with  in  the  inflammation 
of  any  other  mucous  membrane.  Eedness  and  swelling  of  the  mucous  coat, 
increased  secretion  of  mucus,  and  in  severe  cases  purulent  products  on  the  sur- 
face of  the  membrane,  and  a  cellular  infiltration  of  the  tissue  itself,  are  the  well- 
known  processes  characteristic  of  all  catarrhal  inflammations.  The  solitary  and 
agminated  follicles  often  swell  in  follicular  catarrh,  and  may  finally  become 
the  seat  of  superficial  follicular  ulcers.  We  often  find  superficial  erosions  on 
the  rest  of  the  mucous  membrane,  and  in  severe  cases  the  so-called  catarrhal 
ulcers. 

If  the  catarrh  has  lasted  a  long  time,  we  sometimes  find  quite  a  considerable 
thickening  of  the  mucous  membrane,  which  is  due  to  a  hyperplasia  of  the  con- 
nective tissue,  and  which  gives  an  uneven,  puffy  appearance  to  the  internal  sur- 
face of  the  intestine.  Circumscribed  hyperplasia  of  the  connective  tissue  may 
actually  lead  to  the  formation  of  polypi.  If  the  orifices  of  Lieberkühn's  follicles 
are  stopped,  we  have  a  cystic  degeneration  of  the  follicles  from  the  retention  of 
the  intestinal  juice. 

We  very  often  find,  however,  a  considerable  atrophy  of  the  mucous  membrane, 
especially  in  the  chronic  intestinal  catarrh  of  children.  This  atrophy,  which  has 
lately  been  carefully  investigated,  especially  by  Nothnagel,  affects  chiefly  the 
glandular  layer  of  the  mucous  coat.  In  place  of  the  glands,  which  in  many  parts 
may  wholly  disappear,  we  find  connective  tissue  more  or  less  rich  in  cells.  The 
atrophy  is  usually  most  pronounced  in  the  colon  and  the  lower  part  of  the  ileum. 
The  muscular  coat  may  also  take  part  in  the  atrophy. 

Certain  peculiarities  of  catarrh  affecting  single  portions  of  the  intestine  will  be 
mentioned  later  on. 

Symptomatology. — The  symptom  by  which  we  chiefly  determine  an  affection 
of  the  intestinal  canal,  and  which  in  the  milder  cases  is  often  almost  the  only  sign 
of  an  intestinal  catarrh,  is  diarrhoea — that  is,  abnormally  frequent  stools  of  a 
looser  consistency  than  usual;  yet,  strictly  speaking,  we  should  not  attribute 
every  diarrhoea  to  a  catarrh  of  the  intestinal  mucous  membrane,  since  a  large 
number  of  influences  may  directly  produce  an  increased  peristalsis  and  a  conse- 
quent diarrhoea.  Thus,  for  instance,  it  is  a  well-known  fact  that  sudden  terror  or 
great  anxiety  may  sometimes  cause  an  obstinate  diarrhoea  in  a  very  short  time. 
In  general  nervous  and  neurasthenic  conditions,  we  sometimes  have  a  chronic 
diarrhoea  which  can  be  due  only  to  abnormal  processes  of  innervation — "  nervous 
diarrhoea."  The  diarrhoea  which  may  arise  immediately  after  taking  cold  is  also 
merely  the  result  of  abnormally  great  peristaltic  movements  excited  in  a  reflex 
manner.     Probably  a  number  of  chemical  and  infectious  irritants  may  also  stimu- 


INTESTINAL  CATARRH.  405 

late  the  movements  of  the  intestines,  and  thus  set  up  a  diarrhoea,  without  causing 
at  the  same  time  a  catarrh  of  the  mucous  membrane.  Practically,  however,  we 
can  not  make  a  sharp  distinction  between  diarrhoea  and  intestinal  catarrh ;  and, 
in  most  of  the  diarrhoeas  which  have  lasted  for  some  time,  we  are  certainly  right 
in  supposing  that  there  are  actual  anatomical  lesions  of  the  intestine,  as  well  as 
functional  disturbances. 

There  are  two  chief  factors  which  cause  diarrhoea  in  intestinal  catarrh.  In  the 
first  place,  as  has  already  been  intimated,  the  same  injurious  substances  which 
cause  the  catarrh  also  excite  peristalsis.  The  many  products  of  the  abnormal 
processes  of  decomposition  in  the  intestine  also  exert  a  like  influence.  Besides  the 
abnormal  irritants,  however,  we  ought  also  to  consider  an  abnormally  great  irri- 
tability of  the  intestinal  walls  in  catarrh.  Thus  it  happens  that  the  fluid  contents 
of  the  intestine  are  expelled  by  the  vigorous  peristaltic  movements  (which  the 
patient  himself  often  feels  as  a  "  rumbling  in  the  abdomen  "),  before  the  normal 
consolidation  of  the  faeces  is  completed  by  the  absorption  of  water.  The  food, 
under  normal  conditions,  passes  through  the  small  intestine  in  two  or  three  hours, 
and  thus  the  consolidation  of  the  faeces  takes  place,  as  is  well  known,  almost  ex- 
clusively in  the  colon.  We  see,  therefore,  why  the  diarrhoea  owes  its  origin 
chiefly  to  the  increased  peristalsis  of  the  large  intestine ;  although  in  many  cases 
the  peristaltic  action  of  the  small  intestine  is  also  increased. 

Besides  increased  peristalsis,  another  circumstance  may  perhaps  contribute  to 
the  diarrhoea,  viz.,  the  greater  fluidity  of  the  contents  of  the  intestine  due  to  the 
increased  secretion  of  mucus  and  the  exudation  caused  by  the  catari'hal  inflam- 
mation. 

In  the  intestinal  catarrh  from  passive  congestion  we  must  consider  still  another 
factor,  to  explain  the  thin  and  watery  stools — namely,  the  diminished  absorption 
of  water  by  the  intestine  from  disturbance  of  the  circulation.  In  other  catarrhs 
this  factor  is  quite  subordinate  to  increased  peristalsis. 

The  diarrhceal  dejections  show  a  considerable  difference  in  regard  to  their 
minor  characteristics.  Their  number  varies  very  much.  There  are  sometimes 
two  or  three,  and  sometimes  ten  or  more,  evacuations  in  the  twenty-four  hours. 
The  consistency  of  the  stools  is  pap-like,  or  almost  wholly  watery.  This  is  due 
to  the  abnormal  amount  of  water  in  them,  amounting  to  ninety  or  ninety-five  per 
cent.,  while  the  amount  in  normal  stools  is  about  seventy-five  per  cent.  The 
color  of  the  thin  stools  in  intestinal  catarrh  is  usually  bright  yellow,  but  they  are 
sometimes  greenish  from  the  admixture  of  bile  pigment,  and  sometimes  slimy 
(vide  infra). 

In  only  a  part  of  the  cases  does  microscopic  examination  give  us  information 
as  to  the  extent  and  intensity  of  the  catarrh.  We  usually  find  the  remains  of  the 
food,  muscular  fibers,  starch-granules,  and  fat,  and  also  countless  bacteria,  and 
often  triple  phosphates,  occasional  pus-corpuscles,  and  cylindrical  epithelium — 
chiefly  the  constituents  which  are  found  in  normal  stools.  Further  peculiarities 
will  be  mentioned  below. 

Besides  the  diarrhoea,  there  is  often,  but  by  no  means  always,  abdominal  pain 
in  intestinal  catarrh,  either  continuous,  or  having  the  character  of  the  paroxysmal, 
so-called  colicky  pains.  In  catarrh  of  the  rectum  there  is  that  constant  painful 
desire  to  go  to  stool  which  we  term  tenesmus. 

Physical  examination  of  the  abdomen  gives,  on  the  whole,  few  important 
results.  Sometimes  the  abdomen  is  flat,  and  sometimes  there  is  meteorism. 
Marked  peristaltic  action  of  the  intestines  often  causes  gurgling  and  rumbling 
noises — borborygmi.  On  palpation,  the  abdomen  is  often  somewhat  sensitive. 
The  peculiar  colicky  pains,  however,  are,  as  a  rule,  alleviated  by  external  pressure. 
In  rare  cases  we  may  detect  a  fluctuation  on  palpation,  if  the  intestine  contains 


406  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

much  fluid.  The  results  of  percussion  depend  largely  upon  the  fullness  of  the 
intestines. 

In  many  cases  of  simple  diarrhoea  the  general  health  is  practically  unaffected, 
but  in  other  cases  of  acute  intestinal  catarrh,  especially  in  the  severe  infectious 
forms,  the  disturbance  of  the  general  health  may  be  quite  considerable.  The 
patient  feels  so  dull  and  weak  that  he  stays  in  bed.  We  often  see  a  moderate  rise 
of  temperature,  between  100°  and  102°  (38°-39°  C).  There  are  very  often  gastric 
symptoms  also,  especially  loss  of  appetite,  and  vomiting.  Other  organs  are  quite 
rarely  affected,  except  in  duodenal  catarrh,  when  the  liver  is  involved  (vide  infra). 
In  acute  infectious  intestinal  catarrhs,  there  is  sometimes  an  eruption  of  herpes  on 
the  lips.  We  have  repeatedly  seen,  in  severe  cases  of  acute  enteritis,  marked  mus- 
cular and  articular  pains,  and  even  slight  but  manifest  swelling  of  the  joints. 

Different  Forms  of  Intestinal  Catarrh.— Since  the  intestine  is  an  organ  which 
is  only  slightly  accessible  to  physical  examination  during  life,  and  since  we  can 
only  rarely  make  a  post-mortem  examination  in  the  mild  diseases  of  the  intes- 
tine, our  knowledge  as  to  the  different  forms  of  enteritis  is  defective  in  many 
respects.  In  practice  we  content  ourselves  in  most  cases  with  diagnosticating  an 
intestinal  catarrh  simply  from  the  existence  of  diarrhoea,  without  laying  much 
stress  upon  the  special  variety;  but  in  many  cases  some  points  can  be  obtained 
which  give  information  as  to  the  more  accurate  seat  of  the  catarrh.  The  distinc- 
tion between  acute  and  chronic  intestinal  catarrh  is  also  of  practical  significance. 

Duodenal  catarrh  can  be  diagnosticated  only  if  it  is  combined  with  jaundice. 
The  details  regarding  it  may  be  found  in  the  chapter  on  catarrhal  jaundice. 

Isolated  catarrh  of  the  small  intestines,  of  the  jejunum  and  ileum,  is  probably 
only  of  rare  occurrence,  except  when  the  upper  portions  of  the  colon  are  involved. 
We  can  very  rarely  diagnosticate  it  with  certainty,  but  there  are  a  number  of  fac- 
tors which  permit  us  to  decide  that  the  small  intestine  is  chiefly  affected,  or  at  least 
that  it  is  involved  in  the  disease.  In  the  first  place,  we  may  assume  an  affection 
of  the  small  intestine,  from  obvious  reasons,  in  all  those  cases  in  which  there  are 
also  gastric  disturbances.  It  is  evident  that,  in  the  frequent  combination  of  gas- 
tric and  intestinal  catarrh,  the  portions  of  the  intestine  nearest  the  stomach  will  be 
chiefly  affected.  Physical  examination  of  the  abdomen  also  gives  some  indica- 
tions, since  the  slight  sensitiveness  and  swelling  of  the  abdomen,  as  well  as  the 
visible  abnormal  peristaltic  action,  chiefly  affect  the  middle  and  lower  portions  of 
the  abdomen  in  catarrh  of  the  small  intestines,  while  the  analogous  symptoms  in 
catarrh  of  the  large  intestine  affect  the  lateral  and  upper  portions  of  the  abdomen, 
corresponding  to  the  anatomical  course  of  the  colon.  We  can  not  make  a  sharp 
distinction,  however,  in  this  respect.  The  results  which  auscultation  and  percus- 
sion over  the  abdomen  give  in  regard  to  the  point  of  origin  of  the  gurgling  sounds 
and  the  fullness  of  the  loops  of  intestine  are  very  rarely  unequivocal,  and  hence 
are  of  little  value  in  diagnosis. 

Careful  examination  of  the  stools  gives  us  more  information.  As  has  already 
been  said,  we  need  have  no  diarrhoea  in  a  catarrh  confined  to  the  small  intestines, 
since  diarrhoea  is  due  only  to  the  increased  peristalsis  of  the  large  intestine ;  hence 
diarrhoea  is  absent,  for  example,  in  most  cases  of  duodenal  catarrh  (catarrhal  jaun- 
dice). In  extensive  isolated  catarrh  of  the  small  intestines  the  firm  stools  passed 
may,  however,  be  regarded  as  pathological,  because,  on  microscopic  examination, 
they  appear  intimately  mixed  with  little  lumps  of  hyaline  mucus  (Nothnagel). 
As  a  rule,  of  course,  catarrh  of  the  small  intestines  is  combined  with  a  catarrh  of 
the  upper  portion  of  the  large  intestine.  Then  we  have  a  diarrhoea,  but  the  thin 
stools  show  some  peculiarities  which  point  to  an  implication  of  the  small  intes- 
tines. As  a  result  of  the  increased  peristalsis  of  the  small  intestines,  we  find  cer- 
tain constituents  in  the  stools  which  are  normally  contained  in  the  small  intes- 


INTESTINAL  CATARRH.  407 

tines,  but  which  under  normal  conditions  are  no  longer  to  be  met  with  in  the 
faeces  in  the  large  intestine.  We  find  here,  in  the  first  place,  undigested  constitu- 
ents of  the  food,  large  masses  of  muscular  fiber,  or  even  fragments  of  meat  which 
may  be  recognized  by  the  naked  eye,  and  also  starch  and  fat.  Of  course  tbe  oppo- 
site hypothesis  does  not  hold  good,  that,  if  we  find  a  large  amount  of  the  undi- 
gested portions  of  the  food  in  the  stools,  it  must  necessarily  always  point  to  a 
catarrh  of  the  small  intestines,  since  the  digestion  may  be  impaired  by  other  cir- 
cumstances, like  fever  or  anaemia,  and  increased  peristalsis  of  the  intestines,  from 
any  cause,  must  result  in  the  same  symptoms.  A  diarrhoea,  where  the  thin  stools 
contain  a  very  large  amount  of  undigested  particles  of  food  which  can  be  recog- 
nized by  the  naked  eye,  was  formerly  called  lientery,  and  the  term  is  still  occasion- 
ally used. 

If  the  stools  contain  bile  in  addition  to  some  portions  of  the  food,  it  is  to  a  cer- 
tain degree  characteristic  of  catarrh  of  the  small  intestines.  Under  normal  con- 
ditions the  contents  of  the  small  intestines  alone  show  Gmelin's  test  for  bile-pig- 
ment, while  the  contents  of  the  large  intestine,  and  also  the  normal  stools,  do  not. 
In  intestinal  catarrh,  with  increased  peristalsis  of  the  small  and  large  intestines, 
there  is,  however,  often  quite  a  large  admixture  of  still  undecomposed  bile-pig- 
ment. The  green  stools  which  are  so  often  seen  in  the  diarrhoea  of  children,  and 
more  rarely  in  that  of  adults,  are  also  well  known.  Such  stools  usually  show  a 
marked  color  reaction  with  nitric  acid.  In  other  cases  we  find  only  certain  con- 
stituents of  the  stools  stained  with  bile — a  fact  to  which  Nothnagel  has  called  spe- 
cial attention.  Yellow  pigmented  bits  of  mucus  and  cylindrical  epithelium,  and 
round  cells  stained  with  bile,  are  especially  characteristic  of  the  diarrhoea  of 
catarrh  of  the  small  intestines. 

Catarrh  of  the  large  intestine  is  probably  present  in  every  diarrhoea,  as  has 
been  repeatedly  stated,  inasmuch  as  the  thin  stools  can  be  explained  only  by  an 
increased  peristalsis  of  the  large  intestine ;  but  in  a  number  of  cases  we  have  symp- 
toms which  point  especially  to  a  disease  of  the  large  intestine,  particularly  of  its 
lower  portion. 

Physical  examination  of  the  abdomen  should  show  changes,  like  swelling, 
sensitiveness  to  pressure,  etc.,  chiefly  in  the  lateral  portions,  corresponding  to 
the  course  of  the  colon ;  but  this  is  rather  a  theoretical  hypothesis  than  a  sign  of 
practical  value.  We  can  not  definitely  affirm,  either,  that  "  colicky  pains "  are 
characteristic  of  catarrh  of  the  large  intestine  alone.  The  condition  of  the  stools, 
however,  is  of  importance.  In  the  first  place,  we  may  note  that,  if  the  stools  con- 
tain many  masses  of  mucus  which  may  be  recognized  by  the  naked  eye,  it  is  of 
diagnostic  significance.  As  we  have  seen  above,  the  stools  in  catarrh  of  the  small 
intestines  also  contain  mucus,  but  it  is  intimately  mixed  with  the  other  constitu- 
ents of  the  faeces,  and  hence  it  can  usually  be  recognized  only  by  the  microscope. 
In  catarrh  of  the  large  intestine,  however,  the  mucus  rather  adheres  to  the  outside 
of  the  other  constituents,  and  is  often  present  in  large  masses  visible  to  the  naked 
eye.  If  the  catarrh  affects  the  lower  part  of  the  large  intestine  chiefly,  it  may  be 
that  the  intestinal  contents  are  already  formed  into  firm  lumps,  which  may  some- 
times be  wholly  or  partly  inclosed  in  a  layer  of  mucus.  In  acute  catarrh  of  the 
lowest  part  of  the  large  intestine  the  evacuations  are  sometimes  composed  chiefly 
of  pure  mucus,  with  a  greater  or  less  admixture  of  pus,  as  is  seen  chiefly  in  the 
"  catarrhal  flux  "  (see  the  chapter  on  dysentery).  The  more  the  rectum  is  involved 
in  the  inflammation,  the  worse  is  that  painful  feeling  of  tension  and  pressure  at 
the  anus  during  and  after  the  evacuation,  which  we  term  tenesmus. 

Isolated  inflammation  of  the  rectum  (proctitis)  is,  at  least  in  part,  directly 
accessible  to  examination  by  the  finger  or  by  the  speculum.  Painful  tenesmus  and 
an  admixture  of  mucus,  and  especially  of  pus  in  the  stools,  are  the  chief  symp- 


408  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

toins  of  the  disease.  In  most  cases,  however,  we  have  to  do,  not  with  a  primary 
disease,  hut  with  a  secondary  catarrh  of  the  rectal  mucous  membrane,  as  a  result 
of  different  morbid  conditions  in  the  vicinity  of  the  rectum,  or  of  new  growths, 
syphilitic  processes,  etc.,  in  the  rectum  itself.  Periproctitis  (ischio-rectal  abscess) 
belongs  to  the  domain  of  surgery,  and  can  not  be  described  here. 

Intestinal  catarrh  is  divided  into  an  acute  and  a  chronic  form. 

In  the  acute  intestinal  catarrhs,  excluding  the  toxic  inflammations,  we  class 
simple  diarrboea,  which  usually  passes  off  in  a  few  days,  and  the  severe  enteritis, 
which  is  probably  usually  infectious,  and  which  is  attended  by  a  marked  disturb- 
ance of  the  general  health,  by  fever,  and  sometimes  by  gastric  symptoms  also,  as 
well  as  by  herpes,  by  occasional  slight  albuminuria,  by  articular  pains,  etc.  It 
lasts  from  three  to  ten  days.  Cbolera  morbus  (vide  infra)  is  to  be  regarded  as  a 
special  form  of  acute  infectious  inflammation  of  the  gastric  and  intestinal  mucous 
membranes. 

Chronic  intestinal  catarrh  either  comes  from  an  acute  disease  of  the  intestinal' 
mucous  membrane,  or  it  gradually  develops  independently.  In  adults  it  is  by  no 
means  a  frequent  disease,  at  least  as  regards  pronounced  cases,  and  is  much  rarer, 
for  example,  than  chronic  gastric  catarrh ;  but  we  have  already  mentioned  that  it 
is  very  common  in  practice  among  children. 

[Chronic  intestinal  catarrh  is  much  more  common  in  the  southern  than  in  the 
northern  portions  of  our  country.  It  was  the  great  scourge  of  camps  during 
our  late  civil  war,  and  there  are  many  men  alive  to-day,  pensioned  and  unpen- 
sioned,  who  have  never  recovered  from  the  diarrhoea  contracted  during  their  army 
life.] 

In  regard  to  the  aetiology  and  symptomatology,  much  the  same  may  be  said  of 
chronic  catarrh  which  we  have  learned  to  recognize  in  considei'ing  acute  catarrh. 
In  regard  to  aetiology  we  must  note,  in  adults,  chiefly  the  intestinal  affections 
remaining  after  an  attack  of  an  acute  disease,  like  dysentery,  severe  malaria,  or 
typhoid.  Among  the  most  prominent  symptoms  are  the  abnormal  evacuations, 
usually  alternating  between  diarrhoea  and  constipation,  but  sometimes  showing  per- 
sistent constipation,  due  chiefly  to  the  atrophy  of  the  muscular  coat  and  the  disturb- 
ance of  the  nervous  apparatus.  We  must  also  mention,  as  a  prominent  symptom, 
the  secondary  disturbances  of  the  general  nutrition,  like  emaciation  and  anaemia. 
In  regard  to  peculiarities  in  the  character  of  the  stools,  we  must  refer  to  what  has 
been  said  above.  As  chronic  catarrh  of  the  large  intestine  is  far  commoner  than 
chronic  catarrh  of  the  small  intestines,  we  very  often  find  large  amounts  of 
mucus  in  the  stools.  Special  mention  must  here  be  made  of  a  pai'ticular  form  of 
chronic  catarrh  of  the  large  intestine,  in  which  large  pieces  of  membrane  and  com- 
plete mucous  casts  of  the  intestinal  canal  are  evacuated. 

This  peculiar  condition,  of  which  we  have  seen  several  cases,  affects  women 
most  frequently,  but  it  is  also  met  with  in  men.  The  disease  is  almost  always 
associated  with  obstinate  constipation.  Either  at  the  same  time  with  hard  scybala, 
or  quite  independently,  large  masses  of  this  membrane  are  from  time  to  time 
evacuated,  and  the  passage  of  them  is  often  associated  with  quite  severe  colic. 
These  masses,  as  the  microscope  shows,  consist  of  mucus,  and  often  contain  also 
much  cylindrical  epithelium,  and  more  rarely  a  few  round  cells  and  occasional 
crystals  of  Cholesterine  and  triple  phosphate.  The  general  nutrition  sometimes 
suffers  but  little,  but  in  other  cases  quite  a  good  deal.  We  very  often  see  in 
women,  at  the  same  time,  all  sorts  of  hysterical  and  nervous  symptoms.  The  dis- 
ease, which  is  termed  membranous  enteritis,  desquamative  catarrh  of  the  large 
intestine,  or  mucous  colic  (colica  mucosa),  may  last  for  years.  No  thorough  ex- 
amination has  yet  been  made  into  the  aetiology  and  pathology  of  the  disease,  but 
it  is  most  probable  that  the  intestinal  mucus  collects  into  the  membranous  for- 


INTESTINAL  CATARRH.  400 

mations  above  described  in  the  bottom  of  the  longitudinal  fold«  of  the  spasmodic- 
ally contracted  large  intestine  (Marchand). 

Treatment. — Most  of  the  milder  cases  of  acute  intestinal  catarrh  need  only  a 
dietetic  treatment.  If  the  patient  avoids  all  injurious  suhstances  for  a  few  days, 
he  recovers  completely.  The  different  gruels,  like  barley  and  oatmeal  gruel,  and 
also  weak  broths  and  thoroughly  toasted  bread,  or  the  German  zwieback,  are  gen- 
erally regarded  as  the  most  suitable  food.  The  coarser  vegetable«  and  fruits,  fat 
meat  and  brown  bread,  are  to  be  avoided  as  much  as  possible.  In  other  respects 
we  may  refer  to  the  dietetic  rules  laid  down  under  the  treatment  of  chronic  gastric 
catarrh. 

It  is  also  an  important  rule,  confirmed  by  much  experience,  to  keep  the  abdo- 
men warm.  Children  should  always  stay  in  bed,  and  adults  should  do  so,  at  least 
in  all  severe  cases.  It  is  a  good  plan,  pai'ticularly  in  children,  to  protect  the  abdo- 
men from  cold  by  a  flannel  band. 

In  many  of  the  mild  cases  it  is  scarcely  necessary  to  use  internal  remedies. 
Gum  mixture  (P.  G.)  or  almond  mixture  is  a  good  prescription  if  there  is  no  special 
indication,  but  in  severe  cases  further  medication  may  be  proper.  If  we  have  rea- 
son to  suspect  some  irritating  ingesta  or  a  collection  of  faeces  as  a  cause  of  the  in- 
testinal catarrh,  a  cathartic  acts  favorably  at  the  beginning  of  the  treatment,  in 
spite  of  the  existence  of  diarrhoea.  0\w  best  cathartic  in  such  cases  is  castor-oil  or 
calomel.  In  all  those  cases  where  many  thin  dejections  point  to  a  greatly  increased 
peristalsis  of  the  intestine,  we  use  astringents,  especially  opium,  which  we  give  in 
the  form  of  the  simple  tincture  or  the  wine  in  doses  of  ten  or  fifteen  drops,  one 
to  three  times  a  day;  or  as  a  powder,  half  a  grain  to  a  grain  (grm.  0'03  to  0'05)  of 
opium  with  a  grain  (grm.  0'05)  of  sugar,  two  or  three  times  a  day.  It  is  also  rec- 
ommended to  combine  the  opium  with  some  mucilaginous  vehicle,  as  2  parts  of 
laudanum  to  150  of  gum  mixture  or  decoction  of  salep  (P.  G.),  a  teaspoonful  every 
two  or  three  hours. 

Besides  opium,  the  different  astringents  are  used  in  the  treatment  of  intestinal 
catarrh,  especially  tannic  acid,  acetate  of  lead,  logwood,  columbo,  catechu,  and 
many  others.  These  remedies  are  often  given  combined  with  opium,  as  in  the 
following  prescriptions : 

B   Opii gr.  ss. 

Acidi  tannici gr.  j. 

Sacchari  albi. ... gr.  j.     (   "       0-05).       M. 

S.  As  a  powder  two  or  three  times  a  day. 

B  Decoct,  radicis  calumba? (1-15)  §  v. 

Extract,  opii gr.  j. 

Syrup,  aurantii |  ss.     (   '         15-0).       M. 

S.  Tablespoonf  ul  every  two  hours. 

Good  results,  particularly  in  chronic  cases,  are  sometimes  obtained  from  the 
administration  of  bismuth.  Either  the  subnitrate  or  the  salicylate  may  be  given 
in  powders  containing  seven  or  eight  grains  (0 -4-0-5). 

If  there  is  severe  colic,  opium,  or,  under  some  circumstances,  an  injection  of 
morphine  is  the  best  remedy.  In  milder  cases  it  is  sufficient  to  apply  warmth  to 
the  abdomen,  by  warm  poultices  or  hot  towels.  The  colic,  however,  often  depends 
upon  the  presence  of  old  faecal  masses  in  the  intestine,  when  it  is  necessary  to 
prescribe  a  cathartic,  like  castor-oil. 

In  all  cases  where  the  symptoms  point  to  a  more  intense  disease  of  the  large 
intestine,  local  treatment  may  be  employed.  This  is  chiefly  of  importance  in  the 
treatment  of  chronic  intestinal  cataiTh  which  is  situated  mainly  in  the  large 


(grm. 

(   " 
(   " 

0-03); 
0-05); 
0-05). 

(grm. 
(  " 

(   " 

150-0); 
0-05); 
15-0). 

410  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

intestine.  We  irrigate  the  large  intestine  daily  with  weak  astringents,  and  some- 
times with  disinfectants.  The  necessary  apparatus  is  very  simple.  It  consists  of 
an  ordinary  irrigator,  to  which  a  rubber  tube,  about  half  a  metre  long  and  with  a 
proper  tip,  is  attached.  Instead  of  the  irrigator  we  can  use  an  ordinary  glass  fun- 
nel, a  "  Hegar's  funnel."  We  may  very  well  use,  for  an  end-piece  to  be  introduced 
into  the  rectum,  a  long,  soft,  clastic  oesophageal  tube,  which  can  easily  be  pushed 
quite  high  up.  The  fluids  used  for  irrigation  must  always  be  warmed  to  about 
85°  (30°  C),  and  should  be  allowed  to  run  in  gradually  and  slowly.  The  amount 
of  fluid  used  for  one  irrigation  should  be  two  or  three  pints  (1-1-jj-  litre),  or  some- 
times more.  The  patient  keeps  on  his  back  during  the  irrigation.  The  knee- 
elbow  position,  which  is  much  more  uncomfortable  than  the  dorsal,  is  only  occa- 
sionally necessary.  The  fluids  most  used  are  a  one-  or  two-per-cent.  solution  of 
salicylic  acid,  solutions  of  salicylic  and  boracic  acids  combined,  a  one-per-cent. 
tannin  solution,  or  a  solution  of  acetate  of  lead  (1  to  1,000). 

If  there  is  painful  tenesmus,  it  is  usually  relieved  by  suppositories  of  cocoa- 
butter  and  extract  of  opium. 

In  chronic  intestinal  catarrh  a  careful  regulation  of  the  diet  is  of  the  greatest 
importance.  Besides  local  treatment  we  must  consider  internal  remedies,  chiefly 
the  astringents  mentioned  above,  to  which  we  may  add  alum,  guarana,  and  kino. 
Furthermore,  the  preparations  of  strychnine,  and,  among  newer  remedies,  sali- 
cylate of  bismuth  and  naphthaline,  in  powders  of  two  to  five  grains  (O^IO-O'SO), 
deserve  mention.  Baths,  like  Carlsbad,  Kissingen,  Marienbad,  or  Tarasp,  often 
give  good  results,  especially  in  cases  where  there  is  at  times  constipation. 

[Saratoga,  Bedford  (Pa.),  and  the  Virginia  Springs  are  those  in  chief  repute  in 
this  country.  The  change  of  scene  and  the  regular  life,  to  which  patients  will 
more  readily  submit  in  these  and  similar  places  than  at  home,  have  probably  more 
effect  than  the  water  itself. 

I  have  known  the  Rockbridge  alum-water,  internally,  render  good  service.  A 
sea  voyage  is  sometimes  curative,  and,  in  general,  a  sufferer  from  chronic  diarrhoea 
should  shun  malarial  regions. 

Treatment  must  often  be  patient  and  prolonged;  relapses  are  liable  to  follow 
imprudence  of  any  kind.  Time  is,  of  course,  required  for  the  restoration  of  the 
intestine  to  its  normal  structure  and  function,  and  perseverance  is  not  infrequently 
rewarded  in  full  measure.  A  decided  change  of  climate  will  sometimes  be  found 
to  render  service  greater  than  that  of  diet  and  drugs.  ] 

The  symptoms  which  simulate  a  chronic  intestinal  catarrh  often  depend,  as 
we  have  said,  on  abnormal  processes  of  innervation.  These  are  the  cases  which 
are  associated  with  general  nervous  and  nervous-dyspeptic  symptoms.  Internal 
remedies  in  such  cases  are  of  but  little  assistance,  but  judicious  general  treatment, 
cold-water  cures,  electricity,  and  massage  may  be  attended  with  very  good  results. 
(See  the  chapters  on  nervous  dyspepsia  and  habitual  constipation.) 


CHAPTER  II. 

CHOLERA    MORBUS. 

(Cholera  Nostras.     Cholera  Infantum.) 

By  the  name  "  cholera  morbus  "  we  mean  an  acute  disease  of  the  stomach  and 
intestinal  canal,  of  a  definite  form,  whose  symptoms  in  severe  cases  greatly  resem- 
ble those  of  genuine  Asiatic  cholera.  It  is  in  the  highest  degree  probable,  from 
the  whole  course  of  the  disease,  that  cholera  morbus  also  depends  upon  an  acute 


CHOLERA  MORBUS.  411 

infection  of  the  body  by  a  specific,  organized  producer  of  disease,  but  tbis  has  not 
yet  been  definitely  discovered.  The  statement  of  Finkler  and  Prior,  that  bacilli 
are  found  in  the  intestinal  contents  in  cholera  morbus  which  can  not  be  distin- 
guished from  the  comma-bacilli  of  genuine  Asiatic  cholera  (q.  v.),  has  not  proved 
correct.  Finklers  bacilli  seem  to  have  no  pathogenic  significance  in  cholera 
morbus. 

Cholera  morbus  comes  on  usually  as  an  epidemic,  and  almost  exclusively  in 
the  hot  summer  months— June  to  August.  Hence  it  is  often  termed  summer 
cholera.  Children  in  the  first  two  years  of  life  are  chiefly  attacked,  especially 
those  who  are  artificially  fed  or  who  have  recently  been  weaned.  The  disease 
also  attacks  older  children  and  adults,  but  much  more  rarely. 

[Special  opportunities  are  afforded  in  this  country  for  the  study  of  cholera 
infantum.  The  causative  conditions  are,  briefly,  unsuitable  food,  a  high  tempera- 
ture, and  bad  hygiene— conditions  which  are  all  combined  and  attain  their  maxi- 
mum intensity  in  large  cities.  That  a  high  thermometric  range  alone  is  not  suffi- 
cient is  shown  by  the  comparative  immunity  of  all  country  districts.  Those  who 
live  in  the  country,  or  have  never  been  busied  among  the  city  poor,  have  no  idea 
of  the  atmosphere  breathed  by  the  children  of  the  poorer  classes,  especially  during 
the  heated  term,  nor  of  the  extreme  difficulty— impossibility  we  can  almost  say 
—of  getting  a  really  good  milk.  Even  if  the  milk  was  good  at  the  start  and  has 
not  been  tampered  with,  the  time  which  necessarily  elapses  after  it  is  drawn  from 
the  cow  and  before  it  reaches  the  consumer  permits  marked  fermentative  changes 
during  hot  weather.  And  milk  is  and  must  remain  the  main  article  of  diet  for 
children  under  two  years  of  age.] 

The  symptoms  of  cholera  morbus  are  those  of  a  severe  acute  gastro-enteritis. 
The  disease  begins  suddenly,  or  after  some  slight  warning,  with  violent  vomiting 
and  severe  diarrhoea.  In  some  cases  one  of  these  symptoms  predominates,  and  in 
others  the  other.  The  vomitus  consists  partly  of  the  food  taken,  and  partly  of  a 
slimy,  watery  substance.  The. stools  at  first  retain  their  faecal  character,  but  they 
soon  became  more  colorless  and  more  watery,  so  that  they  sometimes  approach 
the  well-known  rice-water  appearance  of  the  stools  in  genuine  cholera.  Abdomi- 
nal pain  is  usually  absent,  but  a  feeling  of  pressure  and  constraint  in  the  epigas- 
trium is  often  present.  The  diminished  secretion  of  urine  and  the  frequent  mus- 
cular pains  cause  the  whole  type  of  the  disease  to  resemble  genuine  cholera  still 
more  closely. 

The  severe  disturbance  of  the  general  condition  is  especially  characteristic. 
The  patient  becomes  extremely  dull  and  has  a  wasted  look,  the  voice  is  weak  and 
hoarse,  an  unquenchable  thirst  sets  in,  the  pulse  is  very  small,  the  skin  of  the  face 
and  the  extremities  is  cool  and  livid ;  in  short,  we  have  the  pronounced  picture  of 
a  general  collapse.  The  body  heat  also  falls,  although  at  the  first  stage  of  the 
disease  there  is  often  a  rise  of  temperature. 

[The  temperature  is  always  high,  even  during  the  stage  of  collapse,  when  the 
skin  and  extremities  are  cool  to  the  touch;  if  the  thermometer  is  introduced  into 
the  rectum— generally  the  best  place,  by  the  way,  to  take  the  temperature  in. 
young  children — it  will  rise  to  101  °  to  102°,  and  is  more  apt  to  reach  104°  to  107°. 
This  shows  that  inflammation  plays  a  large  part  in  the  pathology  of  the  disease.] 

The  picture  of  a  severe  general  disease  is  especially  prominent  in  cholei'a  infan- 
tum. In  severe  cases  of  this  form  of  the  disease  the  general  restlessness,  which  at 
first  exists,  rapidly  passes  into  somnolence.  The  child  lies  with  sunken,  half- 
closed  eyes,  the  conjunctiva?  are  slightly  injected,  the  cornea?  are  cloudy,  the  face 
is  pale  and  cyanotic,  the  fontanelies  are  depressed,  the  skin  is  cool,  and  the  pulse 
is  small  and  frequent  and  can  scarcely  be  counted.  Amid  these  symptoms, 
which  are  usually  termed  "  hydrocephaloid  "  by  specialists  in  children's  diseases 


412  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

[Marshall  Hall],  death  comes  on  in  coma  or  with  slight  convulsions.  There  can 
scarcely  remain  room  for  doubt  that  these  severe  cases  of  gastro-enteritis  are  of 
infectious  origin,  and  that  the  constitutional  symptoms  are  the  result  of  toxic 
matters  generated  in  the  intestine  under  the  influence  of  the  micro-organisms 
(vide  page  373). 

The  mortality  of  children  with  cholera  infantum  is  very  marked,  especially  in 
large  cities,  aud  among  the  poorer  classes  of  society.  Severe  cases  usually  end 
fatally  in  a  few  days,  but,  on  the  other  hand,  many  cases  recover,  either  because 
the  course  of  the  disease  from  the  first  is  not  so  severe,  or  because  cases  appar- 
ently hopeless  take  a  favorable  turn.  In  adults  it  is  extremely  rare  to  see  cholera 
morbus  terminate  unfavorably.  Patients  also  recover  quite  rapidly  from  appar- 
ently severe  conditions,  although  the  stomach  and  intestines  often  remain  rather 
sensitive  for  a  long  time. 

The  anatomical  appearances  in  children  who  die  of  cholera  infantum  con- 
trast, from  their  insignificance,  with  the  severe  symptoms  observed  during  life. 
The  catarrhal  affection  of  the  gastric  and  intestinal  mucous  membranes  is  not 
at  all  prominent  in  the  cadaver,  and  the  solitary  follicles  and  Peyer's  patches 
show  only  a  slight  swelling.  The  other  lesions  which  are  most  frequently  seen 
are  lobular  atelectases  in  the  lungs,  and  venous  hyperasmia  and  cedema  of  the  pia 
mater. 

The  diagnosis  of  cholera  morbus  presents  no  difficulty  if  the  characteristic 
symptoms  of  the  disease  are  present.  The  distinction  between  it  and  genuine 
Asiatic  cholera  used  to  be  occasionally  quite  difficult,  and  was  rendered  possible 
only  by  considering  the  aetiological  factors,  and  the  evident  connection  between 
the  individual  case  and  other  cases  of  undoubted  cholera.  By  Koch's  discovery  of 
the  comma-bacilli  in  Asiatic  cholera  the  distinction  between  the  two  diseases  has 
now  become  absolutely  certain.  In  all  suspicious  cases,  therefore,  we  must  ex- 
amine the  dejections  for  comma-bacilli,  and  upon  the  result  of  this  examination 
depends  the  determination  of  the  proper^means  of  prophylaxis. 

The  treatment  of  cholera  morbus  in  adults  must  be  first  to  take  special  care  to 
limit  the  diet.  The  food  should  be  only  gruels,  or  at  most  broth,  soft-boiled  eggs, 
and  milk.  It  is  a  good  plan  to  give  the  milk  iced,  and  in  small  amounts.  The 
distressing  thirst  is  best  relieved  by  cracked  ice.  Wine  (iced  champagne)  is  to  be 
given  if  the  general  weakness  becomes  marked. 

Among  drugs,  opium  is  the  most  effective  remedy,  and,  whether  in  powder,  as 
the  extract,  or  in  liquid  form,  as  laudanum,  is  the  first  thing  to  use  to  relieve  the 
diarrhoea  and  vomiting.  All  other  remedies  which  are  recommended  in  cholera 
morbus  in  adults,  like  nitrate  of  silver,  or  calomel,  are  quite  subordinate  to  opium. 
In  other  respects  we  may  refer  to  the  treatment  of  acute  gastric  and  intestinal 
catarrh. 

We  are  more  cautious  in  prescribing  opiates  for  children,  although  here  small 
doses  of  opium,  one  or  two  drops  of  laudanum  according  to  the  age  of  the  child, 
may  often  be  indispensable.  In  fresh  cases  calomel  has  obtained  a  great  reputa- 
tion, a  sixth  of  a  grain  (grm.  0-01)  two  or  three  times  a  day.  Ice-cold  cow's  milk, 
given  in  teaspoonfuls,  serves  best  as  food,  if  the  child  can  not  be  fed  naturally  by 
breast-milk.  As  soon  as  the  signs  of  marked  collapse  appear,  we  must  use  hot 
baths  of  chamomile  or  mustard,  hot  packs,  and  also  stimulants,  small  amounts  of 
wine  and  injections  of  camphor.  If  the  child's  stupor  increases,  we  may  under 
some  circumstances  use  cool  packs  and  shower-baths. 

We  will  pass  over  the  many  other  remedies  recommended  for  cholera  infan- 
tum, like  quinine,  salicylic  acid,  and  creosote,  since  in  severe  cases  they  unfor- 
tunately almost  always  leave  us  in  the  lurch.  In  practice,  of  course,  we  are  often 
obliged  to  try  one  or  another  of  these  remedies. 


INTESTINAL  CATAERH  OF  CHILDREN.  413 

[Treatment  must  be  prompt  and  judicious;  many  a  child  is  thus  saved  which 
would  otherwise  die. 

Calomel  is  less  used  in  this  country  than  in  Germany,  and  I  think  rightly.  It 
is  not  very  often  that  a  preliminary  purgation  is  required;  the  bowels  have  usu- 
ally been  quite  sufficiently  unloaded  before  the  physician  arrives,  and  the  indica- 
tion he  has  to  meet  is  to  check  the  vomiting  and  diarrhoea.  Opium,  either  in  the 
form  of  Dover's  powder  and  combined  with  bismuth,  or  as  paregoric,  is  nearly 
always  in  place  before  the  stage  of  collapse;  precise  directions  should  be  given  to 
omit  the  opium  or  diminish  the  dose  if  stupor  comes  on.  Opium  can  also  be  given 
by  enema  if  necessary.  One  should  not  wait  till  the  symptoms  are  desperate 
before  giving  brandy,  a  good  way  to  administer  which  is  by  dropping  it  on  a  tea- 
spoonful  of  shaved  ice.  Improvement  is  shown  by  decrease  or  cessation  of  the 
vomiting,  and  greater  consistency  with  less  frequency  of  the  dejections.  While 
the  symptoms  are  at  their  height  there  is  but  little  use  in  trying  to  give  nourish- 
ment, which  can  not  be  digested  even  if  it  is  retained. 

A  warm  mustard  bath  aids  in  the  re-establishment  of  the  cutaneous  circulation, 
and  thus  tends  to  relieve  the  gastro-intestinal  tract. 

The  diet  is  essentially  the  same  as  in  the  more  chronic  inflammatory  and  in 
the  non-inflammatory  diarrhoeas  of  young  children. 

Details  to  complete  the  above  brief  sketch  must  be  sought  in  works  devoted  to 
the  diseases  of  children.  It  should,  however,  be  added  that  removal  to  the  pure 
air  of  the  sea-shore  in  non-malarial  regions  will  sometimes  turn  the  scale  in  cases 
which  are  apparently  hopeless.  Pure  country  air  is  to  be  sought  if  the  seaside  can 
not  be  reached;  but  the  latter  is  the  better  of  the  two.] 


CHAPTER  III. 

INTESTINAL   CATARRH   OF   CHILDREN. 

(  Chronic  Dyspepsia  of  Children.     Pedatrophy.) 

The  great  frequency  and  the  practical  importance  of  the  "  dyspeptic  condi- 
tions "  in  children  in  the  first  years  of  life,  which  conditions  are  associated  with 
severe  disturbances  of  nutrition,  justify  a  short  description  of  them,  but  we  must 
refer  to  the  special  manuals  on  children's  diseases  for  a  detailed  account. 

That  diseases  of  the  digestive  organs  play  so  large  a  part  in  children's  troubles 
is  owing,  on  the  one  hand,  to  the  great  sensitiveness  which  the  digestive  apparatus 
in  children  shows  to  the  irritants  which  are  brought  in  contact  with  it,  and,  on 
the  other,  to  the  too  common  foolishness  and  carelessness  which  the  child's  parents 
and  nurses  show  in  its  feeding.  Of  course  it  is  not  always  ignorance  and  neglect, 
but  often,  unfortunately,  poverty  and  want  which  cause  children  to  suffer,  and 
explain  the  terrible  mortality  in  the  first  years  of  life. 

The  simple  fact  that  by  far  the  larger  number  of  children  who  suffer  from 
dyspeptic  and  atrophic  conditions  are  fed  artificially,  leads  us  to  the  belief  that  the 
cause  of  most  of  the  intestinal  diseases  in  children  is  to  be  found  in  faulty  and 
injudicious  feeding.  The  food,  which  is  not  suited  to  the  child's  digestive  powers, 
is  only  impei'fectly  absorbed;  it  undergoes  many  processes  of  decomposition, 
whose  products  irritate  the  intestinal  mucous  membrane  and  give  rise  to  increased 
peristaltic  action.  Thus  the  imperfect  digestion,  or  "  dyspepsia,"  excites  a  catarrh 
of  the  gastric  and  intestinal  mucous  membrane,  by  which  again,  in  a  vicious  cir- 
cle, the  digestive  power  is  still  further  reduced.  Hence  the  boundary  between 
"  dyspepsia  "  and  catarrh  can  be  drawn  only  artificially. 


414  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

The  anatomical  changes  of  the  intestinal  mucous  membrane  in  children  who 
die  of  ''chronic  intestinal  catarrh"  are,  as  a  rule,  only  slightly  marked,  and 
contrast,  in  their  apparent  insignificance,  with  the  severe  intestinal  symptoms 
observed  during  life.  Probably  here  also  the  toxic  influences  of  the  matters 
abnormally  generated  in  the  intestine,  play  a  more  important  part  than  do  the 
anatomical  changes.  .  We  must  remember,  however,  that  most  catai'rhal  condi- 
tions are  hard  to  recognize  in  the  cadaver  because  of  the  disappearance  of  the 
hyperaemia.  Sometimes  the  swelling  of  the  follicles  is  especially  marked — fol- 
licular catarrh.  Follicular  ulcers  are  also  seen.  In  other  cases  the  atrophy  of 
the  mucous  membrane,  which  is  often  seen  after  chronic  catarrhs,  is  the  chief 
lesion.  Chronic  thickening  and  swelling  of  the  mucous  membrane  is  of  rarer 
occurrence.  In  most  of  the  severe  cases  the  large  intestine,  and  also  the  lower 
portion  of  the  ileum,  are  the  chief  seat  of  the  changes.  We  often  find  a  swelling 
of  the  mesenteric  lymph-glands,  and  also  a  fatty  liver.  In  the  lungs  extensive 
atelectases  or  nodules  of  catarrhal  pneumonia  often  develop  as  a  result  of  the 
imperfect  respiration. 

The  symptoms  of  chronic  intestinal  catarrh  are,  in  the  first  place,  those  due 
directly  to  the  intestinal  trouble,  and,  secondly,  the  quite  rapid  disturbance  of  the 
child's  general  nutrition. 

The  condition  of  the  stools  is  the  most  important  intestinal  symptom.  The 
normal  dejection  in  children  until  they  are  weaned  is  of  the  color  of  the  yolk  of 
an  egg,  of  a  rather  pasty  consistency,  and  of  a  faintly  sour  smell.  In  intestinal 
catarrh  the  stools  are  more  frequent,  six  or  seven,  and  even  more,  a  day.  They  are 
thinner,  more  watery,  contain  large  flakes  and  lumps  of  undigested  bits  of  case- 
ine  and  other  remains  of  food,  and  smell  badly.  They  very  often  have  a  green 
color,  or  acquire  it  on  standing.  According  to  recent  French  investigations 
(Lesage),  this  green  coloring  matter  is  generated  by  a  specific  kind  of  bacilli,  which 
are  also  to  be  regarded  as  the  pathogenic  cause  of  intestinal  catarrhs  with  green 
evacuations.  We  may  find  admixtures  of  mucus,  sometimes  in  the  form  of  the 
so-called  "  sago  grains,"  especially  in  catarrh  of  the  large  intestine.  In  the  severe 
forms  we  often  find  pus-corpuscles  and  epithelium  under  the  microscope,  besides 
remains  of  the  food.     The  stools  may  contain  small  amounts  of  blood. 

There  is  no  definite  distinction  in  regard  to  the  dejections  in  catarrh  of  the 
large  and  of  the  small  intestines.  On  the  whole,  the  rule  holds  that,  in  catarrh 
of  the  small  intestines  chiefly,  the  stools  are  larger,  they  are  passed  with  more 
wind  or  gas,  and  show  a  more  uniform  consistency ;  while  in  catarrh  of  the  large 
intestine  they  are  smaller  but  more  frequent,  ten  or  twenty  a  day,  are  passed 
noiselessly,  are  associated  with  tenesmus,  and  show  a  different  consistency  in 
their  various  parts,  partly  normal,  partly  thin,  partly  slimy,  etc.  Examination 
of  the  abdomen  is  in  so  far  of  importance  that,  in  general,  in  catarrh  of  the  small 
intestines  the  abdomen  is  much  swollen,  while  in  catarrh  of  the  large  intestine  it 
is  often  deeply  sunken. 

We  often  find  disturbances  in  the  stomach,  vomiting,  eructations,  etc.,  as  well 
as  trouble  in  the  intestines.  There  may  be  thrush  in  the  mouth,  or  the  development 
of  aphthous  ulcers. 

In  almost  all  long-continued  cases,  however,  the  general  disturbance  of  nutri- 
tion, the  atrophy  (athrepsia)  of  the  child,  takes  the  first  place  in  the  picture  of 
the  disease.  The  muscles  become  shriveled  and  flabby,  and  the  whole  body  finally 
becomes  so  much  emaciated  that  the  pale,  dry  skin  hangs  in  broad  folds  and  wrin- 
kles about  the  bones,  whose  prominences  are  everywhere  visible.  The  face  is 
sharp,  and  has  an  aged  expression  from  the  many  little  folds  of  the  skin.  The 
eyes  are  dull,  lusterless,  and  wide  open;  the  voice  is  merely  a  low,  hoarse  whim- 
per.    The  abdomen  is  deeply  sunken,  or  in  some  cases  it  is  swollen  by  meteorism, 


INTESTINAL  CATARRH  OF  CHILDREN  415 

in  peculiar  contrast  to  the  emaciation  elsewhere;  and  its  surface  is  traversed  by 
bluish  veins. 

From  this  sad  picture,  unfortunately  so  frequently  seen  in  practice  among  chil- 
dren, we  can  usually  recognize  the  condition  of  tilings  at  the  first  glance,  for  by 
far  the  larger  part  of  the  cases  called  "pedatrophy"  are  due  to  chronic  digestive 
disturbances.  Very  often  it  is  combined  with  rachitic  changes  in  the  bones,  of 
whose  occurrence  we  shall  speak  further  in  the  description  of  rachitis.  Tubercu- 
lar changes,  too,  are  often  found  in  the  cadaver,  especially  in  the  lungs  and  the 
bronchial  and  mesenteric  lymph-glands.  In  such  cases,  of  course,  the  tuberculosis 
is  usually  to  be  regarded  as  the  main  disease,  upon  which  the  intestinal  affection 
which  may  be  simple  or  even  tubercular,  has  developed  secondarily.  During  life 
tuberculosis  in  little  atrophic  children  may  very  easily  be  overlooked. 

If  we  would  give  a  full  account  of  the  treatment  of  the  atrophic  conditions  in 
children  due  to  digestive  disturbances,  we  must  include  in  our  consideration  the 
entire  hygiene  and  care  of  children  in  health  and  disease,  for  all  children's  physi- 
cians are  united  in  the  opinion  that,  as  the  cause  of  most  intestinal  diseases  in  ' 
children  is  to  be  found  in  improper  feeding,  so  recovery  from  existing  digestive 
disturbances  can  take  place  primarily  only  by  a  corresponding  proper  and  judi- 
cious feeding.  In  what  follows  we  can  refer  only  to  the  most  important  princi 
pies  and  general  points  which  are  here  to  be  considered. 

The  only  proper  and  natural  food  for  a  child  in  its  first  year  is  breast-milk. 
All  dyspeptic  conditions  are  much  rarer  in  children  who  are  nursed  than  in  bot- 
tle-fed children,  and,  when  they  do  occur  in  children  at  the  breast,  they  often 
are  only  of  brief  duration.  They  are  then  to  be  referred  usually  to  certain  dis- 
turbances in  the  mother,  such  as  disease,  insufficient  diet,  or  severe  mental  excite- 
ment. The  return  of  menstruation  or  a  new  pregnancy  has  sometimes  an  unfa- 
vorable influence  on  the  character  of  the  milk.  Finally,  we  may  mention  that 
in  spite  of  the  best  of  milk,  if  the  breast  is  given  irregularly  and  too  frequently,  it 
may  cause  anomalies  of  digestion  in  nursing  children. 

Most  of  these  slight  disturbances  may  easily  be  readjusted,  but  sometimes  it 
happens  that,  without  any  discoverable  reason,  the  milk  of  a  wet-nurse  "  does  not 
agree "  with  the  child.  Then  we  must  change  the  nurse.  The  atrophic  condi- 
tions which  develop  and  progress  in  children,  in  spite  of  plenty  of  normal  food, 
are  usually  due,  not  to  simple  digestive  disturbances,  but  to  deep-seated,  general, 
constitutional  diseases  like  tuberculosis,  or  syphilis. 

The  great  majority  of  cases  of  chronic  intestinal  catarrh  and  chronic  atrophy 
are  found,  as  we  have  said,  in  bottle-fed  children.  The  first  question  which  every 
physician  should  ask  a  mother  who  brings  him  such  a  child  for  treatment,  must 
therefore  refer  to  the  sort  of  feeding  which  the  child  has.  If  the  mother,  for  any 
reason,  can  not  nurse  it  herself,  and  if  the  bottle-fed  child  has  digestive  disturb- 
ances, we  must  invariably  consider,  in  the  first  place,  the  possibility  of  procuring  a 
wet-nurse.  Feeding  by  the  milk  of  a  wet-nurse  is  a  remedy  which,  at  least  in 
many  cases,  by  saving  the  child's  life,  repays  the  many  annoyances  and  quite 
large  expense  which  a  wet-nurse  causes.  We  must  tell  the  parents  this,  and  repre- 
sent to  them,  without  reserve,  the  great  dangers  which  threaten  the  life  of  every 
bottle-fed  baby.  Complete,  and  sometimes  even  quite  rapid,  recovery  may  be  ob- 
tained through  a  wet-nurse,  even  in  cases  of  severe  chronic  intestinal  catarrh, 
where  atrophy  and  weakness  are  already  very  far  advanced. 

Often,  however,  it  is  impossible  to  hire  a  wet-nurse,  especially  in  the  poorer 
classes  of  society.  We  must  continue  bottle-feeding,  and  these  are  the  cases 
where  chronic  intestinal  catarrh  demands  the  greatest  number  of  victims;  yet 
even  here  the  physician  can  always  do  much  good  by  instructing  the  parents. 

The  best  substitute  for  mother's  milk  is  cow's  milk.     This  must  be  as  fresh  as 


41 G  DISEASES  OF  THE  DIGESTIVE  OKGANS. 

possible,  and  is  given  boiled.  Tbe  Soxhlet  apparatus  for  preparing  the  milk  is 
rather  troublesome,  but  very  appropriate  and  advantageous.  By  its  means  the 
milk  is  completely  sterilized.  One  part  of  the  milk  must  be  diluted,  according 
to  its  quality,  with  two  or  three  parts  of  boiled  water  in  the  first  months,  in 
children  from  four  to  six  months  old  with  equal  parts  of  Wftter,  and  in  older 
children  with  about  half  as  much  water.  From  nine  to  twelve  months,  the  child 
may  have  undiluted  milk.  In  general  we  give  the  milk  warmed  to  about  85° 
(28°  C),  but  children  with  gastro-in testin al  catarrh  often  bear  cold  milk,  given  in 
small  amounts,  better  than  warm.  Among  the  special  additions  to  the  milk,  by 
which  physicians  have  tried  to  make  cow's  milk  more  like  human  milk,  we  may 
mention  as  occasionally  advantageous  sugar  of  milk,  as  much  as  will  go  on  the 
point  of  a  small  knife,  added  to  each  portion  of  milk  given,  and  soda,  a  tablespoon- 
ful  of  a  one-  or  two-per-cent.  solution  to  a  pint  (half  a  litre)  of  milk.  The  much- 
practiced  dilution  of  milk  with  salep,  oat-meal,  and  barley  waters  is  always  inju- 
dicious,.and  it  should  be  a  principle,  especially  with  children  under  thi'ee  months, 
•to  avoid  entirely  any  starchy  food.  It  is  not  a  bad  plan  to  add  veal-broth  to  the 
milk,  as  it  is  sometimes  well  borne  even  by  weak  children. 

Cow's  milk,  properly  diluted,  is  better  for  children  with  chronic  intestinal 
catarrh,  in  many  cases,  than  any  other  food.  In  acute  digestive  disturbances, 
however,  it  is  sometimes  advisable  to  omit  the  milk  entirely  for  a  few  days,  and 
give  instead  of  it  only  a  little  mucilaginous  drink  like  decoction  of  salep.  In 
chronic  dyspepsia  we  must  first  try  good  cow's  milk.  If  the  milk  is  not  well  borne, 
if  the  diarrhoea  increases,  and  if  the  child  becomes  still  more  emaciated,  we  may 
try  to  get  milk  from  another  and  better  source;  but  it  often  happens  that  either 
we  can  not  procure  good  milk,  or  that  the  child  can  not  bear  even  the  best  cow's 
milk.  We  are  then  obliged  to  have  recourse  to  one  of  the  many  u  artificial  foods  " 
and  "substitutes  for  mothers'  milk"  in  the  market.  We  can  not  here  go  into  par- 
ticulars concerning  these.  Each  of  these  preparations  has  occasional  good  results 
to  show,  but  none  of  them  has  an  uncontested  pre-eminence  over  the  rest.  We 
will  mention  the  preparations  most  in  use  at  present,  of  whose  value  in  individual 
cases  we  have  convinced  ourselves :  Swiss  condensed  milk,  Nestle's  and  Frerich's 
infants'  foods,  Biedert's  cream  mixture,  and  Liebig's  soup.  Almost  every  physician 
has  his  special  favorite  preparation,  which  in  his  own  personal  experience  has 
done  him  relatively  the  best  service. 

If  we  keep  fast  to  the  principle  that  every  intestinal  catarrh  in  children  is  to 
be  treated  in  the  first  place  by  a  judicious  regulation  of  the  diet,  in  many  cases  we 
shall  not  have  to  use  any  drugs.  These  may  be  of  service  only  when  we  have  also 
carried  out  the  dietetic  measures  which  are  specially  necessary. 

Calomel  has  obtained  the  greatest  reputation  in  the  treatment  of  intestinal 
catarrh  in  children.  It  deserves  to  be  tried  in  fresh  cases,  in  doses  of  TV  to  ^  of  a 
grain  (grm.  0  "005-0  "01)  in  powder.  If  the  diarrhoea  lasts  a  long  time,  we  may 
very  well  use  opiates,  although  with  great  caution.  The  combination  of  calomel 
and  opium  often  does  good  service. 

YP  Calomel gr.  \  (grm.  0-01) ; 

Extractiopii gr.  j»  (     "     0-002); 

Pulv.  acacise gr.  ss  (     "    0"03). 

M.  et  ft.  pulv. 

Sig. :  One  such  powder,  three  or  four  times  a  day. 

With  little  children  we  may  put  two  to  four  drops  of  laudanum  in  three 
ounces  (grm.  100)  of  liquid,  like  gum  mixture,  salep  decoction,  muriatic-acid 
mixture,  etc.,  and  give  a  dessertspoonful  of  this  every  two  or  three  hours. 


INTESTINAL  CATARRH  OF  CHILDREN.  417 

Many  attempts  have  been  made  to  check  the  abnormal  processes  of  decomposi- 
tion in  the  intestine  by  prescribing  remedies  which  possess  antiseptic  and  anti- 
zymotic  properties.  Creasote  has  been  warmly  recommended  by  many,  four  to 
six  drops  in  two  ounces  (grm.  50)  of  water  with  half  an  ounce  (grm.  15)  of  syrup, 
a  teaspoonful  every  two  hours.  Other  drugs  used  for  the  same  purpose  are  naph- 
thalin,  one-half-  to  one-per-cent.  solution  of  dilute  muriatic  acid  in  water,  and  one- 
per-cent.  solution  of  chloral  in  water.    A  prescription  for  naphthalin  is  as  follows: 

B   Naphthalin 0"5  to  TO; 

Mucilag.  acaciae, 

Aquae  destillat ää  40'0 ; 

01.  menthae  pip gl-  j- 

M.     Sig. :  Shake.     Teaspoonful  every  two  hours. 

If  the  stools  have  a  green  color,  it  is  said  that  lactic  acid  is  especially  beneficial. 
A  teaspoonful  of  a  two-per-cent.  solution  may  be  given  fifteen  minutes  after  every 
meal. 

A  number  of  other  remedies,  "  astringents,"  are  given  to  act  directly  on  the 
diseased  mucous  membrane.  Those  most  to  be  recommended  in  chronic  diarrhoea 
are  subnitrate  of  bismuth,  one  or  two  grains  (grm.  O'Oö-O"!)  four  to  six  times  a 
day,  which  may  be  combined  with  opium,  nitrate  of  silver  (1  to  2,000  solution), 
alum  (1  to  200  solution),  guarana,  five  to  fifteen  grains  (grm.  0-3-l'0),  three  times 
a  day,  and  many  others. 

If  a  large  amount  of  mucus  in  the  stools  points  to  a  catarrh  of  the  large  intes- 
tine, we  may  sometimes  employ  irrigation  of  the  colon  with  excellent  results.  We 
inject  the  fluid,  one-per-cent.  solution  of  tannin  or  alum,  or  solution  of  acetate  of 
lead  (1  to  3  to  1,000),  once  or  twice  a  day.  The  amount  of  fluid  to  be  introduced  at 
once,  by  a  Hegar's  funnel,  with  a  gum-elastic  catheter,  may  reach  one  or  two 
pints  (half  a  litre  to  a  litre). 

In  conclusion,  we  must  mention  the  advantage  of  daily  warm  baths  in  atrophic 
children.  We  often  order  some  special  "  strengthening  "  additions  to  the  bath- 
water, such  as  salt,  iron,  or  sweet-flag. 

[In  view  of  the  great  importance  of  this  malady,  it  seems  desirable  to  remark 
on  one  or  two  points. 

In  the  first  place,  prophylactic  measures  are  deducible  directly  from  the  aeti- 
ology. No  child  should  be  kept  in  a  large  city  in  summer,  if  it  can  be  provided 
for  at  the  sea-shore  or  in  the  country.  The  vast  number  who  must  perforce  re- 
main are  to  be  kept  under  the  best  general  hygienic  conditions  possible.  Mothers 
should  be  encouraged  to  take  their  children  to  the  relatively  pure  air  of  the  public 
parks  as  much  as  they  can.  The  relation  between  diet  and  the  diarrhoea  of  chil- 
dren should  be  dwelt  upon  whenever  there  is  opportunity. 

The  establishment  of  boards  of  health  has  done  much,  and  will  do  more,  to 
check  the  ravages  of  summer  diarrhoea. 

Great  advances  have  been  made  in  the  artificial  digestion  of  cow's  milk  within 
a  few  years.  By  the  aid  of  the  preparations  of  Fairchild  Bros.  &  Foster  the 
caseine  is  digested  in  part,  and  the  remaining  portions  coagulate  in  light  flocculi ; 
at  the  same  time  no  appreciable  taste  is  imparted  to  the  milk,  provided  that  a 
moderate  amount  of  care  is  exercised.  The  importance  of  preventing  the  forma- 
tion of  large,  firm  curds  has  long  been  recognized,  and  an  older  means  of  attain- 
ing this  end  was  mechanically  to  separate  the  curd  by  adding  to  the  milk  a  barley 
or  other  similar  water-gruel. 

Mellin's,  Horlick's,  and  Ridge's  foods  also  deserve  mention  in  this  connec- 
tion. 

27 


418  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

The  quantities  of  food,  as  well  as  the  frequency  with  which  it  is  given,  must 
be  determined  in  each  case. 

The  system  of  milk  inspection  which  has  come  into  vogue  of  late  years  in  many 
places  does  much  to  improve  the  milk  supply,  as  does  also  an  improved  method  of 
transportation.  But  still,  especially  during  the  summer  heat,  a  really  fresh  and 
pure  article  is  nearly  impossible  of  attainment  by  the  poorer  classes  in  large  cities, 
and  it  is  these  classes  which  swell  the  mortality  from  infantile  diarrhoea.  For 
them,  in  particular,  the  modern  simple  and  inexpensive  methods  of  sterilizing 
milk  may  be  made  of  the  greatest  service.  The  seashore  homes  for  poor  children 
which  have  been  established  near  the  large  cities  on  the  Atlantic  seaboard  have 
fully  justified  themselves. 

It  seems  to  the  editor  that  the  author  has  insisted  more  strongly  than  is  neces- 
sary on  the  vital  importance  of  a  wet-nurse,  in  view  of  the  very  great  advances 
which  have  been  made  within  a  few  years  in  the  preparation  of  artificial  foods  for 
infants.  For  full  details  as  to  these  processes,  the  reader  must  be  referred  to 
modern  treatises  on  the  diseases  of  children. 

The  drugs  most  worthy  of  confidence  are,  in  the  opinion  of  the  editor,  opium 
and  bismuth;  in  mild  cases  the  former  is  often  not  required;  the  dose  varies 
greatly  with  circumstances  ;  the  latter  can  safely  be  given  in  ten-grain  doses, 
every  three  hours,  to  a  child  of  six  months.  Calomel  does  not  now  enjoy  the 
reputation  in  this  country  that  it  does  in  Germany,  though  it  has  its  advocates 
here.     For  more  minute  details  see  works  on  children's  diseases.] 


CHAPTER  IV. 

TYPHLITIS  AND   PERITYPHLITIS. 

{Typhlitis  Stercoralis.     Inflammation  of  the  Caecum.") 

iEtiology  and  Pathological  Anatomy.— Inflammation  of  the  caecum  and  its 
vicinity  has  a  special  place  among  the  diseases  of  single  portions  of  the  intes- 
tines. The  reason  why  circumscribed  inflammation  so  often  develops  here  is  to 
be  found  in  the  peculiar  anatomical  arrangement  of  the  caecum  and  its  appendix, 
the  vermiform  process.  This  arrangement  explains  why  faecal  masses  or  foreign 
bodies  are  easily  retained  in  the  caecum,  and  give  rise  to  an  inflammation  of  it. 

Inflammation  of  the  caecum  is  due,  in  most  cases,  to  an  accumulation  of  faeces 
in  it,  and  hence  it  is  usually  termed  typhlitis  stercoralis.  Since  the  causes  pro- 
ducing the  inflammation  are  usually  permanent  in  their  action,  the  anatomical 
inflammatory  changes  are  generally  much  more  intense  in  perityphlitis  than  in 
the  other  forms  of  intestinal  catarrh.  The  inflammation  attacks  the  whole  intes- 
tinal wall,  and  sometimes  even  invades  the  surrounding  connective  tissue,  being 
then  called  perityphlitis. 

The  great  majority  of  severe  cases  of  perityphlitis  do  not  start  from  the 
caecum  itself,  but  from  the  vermiform  appendix.  This  rudimentary  portion  -  of 
the  intestine,  so  unimportant  physiologically,  plays  a  great  part  in  pathology. 
Small  faecal  masses  from  the  caecum  often  enter  the  vermiform  appendix,  and, 
under  some  circumstances,  may  remain  there.  The  fluid  in  them  is  absorbed,  they 
are  very  often  incrusted  with  lime-salts,  and  thus  the  little  so-called  "faecal  cal- 
culi "  are  formed.  In  many  cases  the  return  of  faecal  masses  into  the  caecum  is 
probably  hindered  by  the  valve  at  the  orifice  of  the  vermiform  appendix,  Gerlach's 
valve.  Foreign  bodies,  like  little  seeds  of  fruit,  often  enter  the  vermiform  appen- 
dix and  give  rise  to  the  formation  of  a  faecal  calculus.     These  calculi  often  have 


TYPHLITIS  AND  PERITYPHLITIS.  419 

such  a  rounded  shape  that  they  were  formerly  considered,  very  erroneously,  to  he 
retained  cherry-stones. 

In  many  cases  faecal  calculi  may  remain  in  the  vermiform  appendix  for  a  long 
time  without  producing  any  further  injurious  results,  hut  as  a  rule  they  cause  a 
mechanical  irritation  of  the  mucous  memhrane  which  leads  to  inflammation,  and 
often,  in  some  circumscribed  spots,  to  a  pressure  necrosis,  and  later  to  ulceration 
of  the  vermiform  appendix.  If  the  ulcer  does  not  cicatrize — it  always  may — the 
ulceration  gradually  deepens.  When  there  is,  finally,  perforation  of  the  vermi- 
form appendix,  we  have  either  a  circumscribed  or  a  general  puralent  peritonitis, 
according  as  adhesions  have  or  have  not  formed  in  the  vicinity.  Although  gen- 
eral peritonitis  almost  always  ends  fatally,  the  circumscribed  purulent  perityphlitis 
may,  at  least  in  a  number  of  cases,  finally  recover  (vide  infra). 

Clinical  History. — The  symptoms  of  simple  typhlitis  stercoralis  sometimes 
develop  quite  rapidly,  but  in  other  cases  they  are  preceded  by  somewhat  protracted 
prodromata.  The  latter  are  chiefly  constipation,  which  may  at  times  be  inter- 
rupted by  diarrhoea,  and  occasional  dull  pain  in  the  ileo-caecal  region.  These 
symptoms  gradually  or  suddenly  increase.  The  pain  in  the  ileo-caecal  region,  in 
particular,  becomes  more  intense,  and  prevents  the  patient  from  making  any  con- 
siderable movement.  Sometimes  there  is  complete  stoppage,  but  in  other  cases 
small  amounts  of  faeces  are  still  passed.  The  patient  frequently  vomits  one  or 
more  times.  The  general  health  is  also  much  disturbed.  The  patient,  as  a  rule; 
is  dull,  has  no  appetite,  and  has  a  moderately  high  fever,  somewhere  between  101° 
and  104°  (38"5°-39'8°  C),  the  course  of  which  has  nothing  characteristic. 

The  most  important  signs  for  diagnosis  come  from  the  physical  examination 
of  the  abdomen.  The  abdomen  as  a  whole  is  often  moderately  swollen  by  meteor- 
ism.  The  collection  of  gas  probably  takes  place  chiefly  in  the  ileum,  above  the 
part  of  the  intestine  which  is  narrowed  by  the  accumulation  of  faeces.  The  nieteor- 
lsm  often  is  entirely  absent  or  is  only  slight,  and  then  we  may  notice  by  mere 
inspection  a  marked  prominence  in  the  region  of  the  caecum.  If  we  examine 
more  closely  we  perhaps  meet  with  very  considerable  sensitiveness  and  tenderness 
on  pressure  in  the  same  region.  We  also  feel  a  resistance,  which  is  either  diffuse 
or  well-defined,  exactly  like  a  tumor,  and  which  gives  flatness  or  a  diill  tympanitic 
resonance  on  percussion.  This  characteristic  ileo-caecal  tumor,  which  usually 
confirms  the  diagnosis,  is  caused  in  part  by  the  collection  of  masses  of  faeces, 
which  often  seem  quite  compressible,  and  permit  us  to  determine  approximately 
the  portion  of  intestine  affected,  and  in  part  by  the  materially  thickened  intestinal 
walls,  and  eventually  by  the  inflammatory  exudation  in  the  vicinity.  In  their 
clinical  relations  there  is  no  sharp  distinction  between  typhlitis  and  perityphlitis, 
and  inflammatory  processes  which  rise  from  the  vermiform  appendix.  The  fur- 
ther course  only  can  make  the  distinction  possible. 

Most  cases  of  simple  typhlitis  stercoralis  take  a  favorable  course.  If  the  patient 
has  timely  care  and  proper  treatment  the  pain  and  fever  gradually  disappear. 
Large  dejections  follow,  and  after  ten  days  to  three  weeks  complete  convalescence 
sets  in.  The  abnormal  resistance  in  the  region  of  the  caecum  due  to  the  thickened 
intestinal  walls  may  often  be  felt,  of  course,  for  a  much  longer  time.  A  tendency 
to  constipation  is  also  apt  to  be  present  for  a  long  time.  Relapses  are  not  uncom- 
mon, and  it  not  infrequently  happens  that  people  who  have  once  had  typhlitis 
may  be  again  attacked  later  on  by  the  same  affection. 

Typhlitis  takes  a  more  severe  course  in  the  happily  quite  rare  cases  where  the 
intestinal  stenosis  as  a  result  of  retention  of  faeces  is  well  marked.  The  meteor- 
ism  is  greater,  the  vomiting  is  more  frequent,  and  finally  assumes  a  decidedly 
stercoraceous  character.  The  constitutional  symptoms  are  much  more  severe. 
The  patient  is  extremely  dull,  the  skin  is  cool  and  livid,  the  pulse  is  small  and 


400  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

frequent.  In  such  cases  death  may  ensue  with  all  the  signs  of  general  collapse,  if 
we  do  not  finally  succeed  hi  causing  the  evacuation  of  faeces  and  hence  removing 
the  obstruction. 

The  symptoms  of  perityphlitis  are  essentially  the  same  as  those  of  typhlitis, 
but  they  are  usually  of  a  higher  degree  of  severity.  The  resistance  to  be  felt  in 
the  region  of  the  caecum  is  less  sharply  circumscribed  and  is  deeper  seated.  As  a 
rule  there  is  less  meteorism  where  perityphlitis  predominates  than  in  typhlitis. 
The  pain  is  usually  very  severe,  and  often  shoots  into  the  right  leg,  where  there 
may  be  numbness  and  formication;  but,  on  the  other  hand,  there  are  cases  in 
which  quite  extensive  perityphlitic  processes  cause  very  slight  subjective  symp- 
toms for  a  long  time. 

[It  is  to  be  remembered  that  the  relation  of  the  appendix  to  the  caecum  is  not  a 
constant  one,  and  that  the  seat  of  the  tumor  is  therefore  not  precisely  the  same  in 
all  cases.  The  induration  or  resistance  may  extend  well  up  toward  the  liver  or 
backward  into  the  flank.  Especially  in  those  cases  in  which  the  appendix  lies 
backward  near  or  over  the  brim  of  the  pelvis,  the  tumor  may  be  distinctly  felt  in 
the  rectum  or  vagina,  the  digital  exploration  of  which  should  never  be  neglected 
in  cases  attended  with  any  uncertainty.] 

The  course  of  perityphlitis  is  always  tedious,  but  in  favorable  cases  we  may  see 
complete  absorption  of  the  inflammatory  products  and  recovery.  Severe  cases 
often  end  by  forming  abscesses,  which  may  be  ichorous.  The  local  symptoms  do 
not  disappear,  the  fever  continues  and  assumes  a  septic  character.  Finally,  if  the 
abscess  tends  to  break  externally,  the  swelling  in  the  ileo-caecal  region  becomes 
more  prominent  and  more  sharply  defined,  the  skin  becomes  thin  and  red,  there 
is  fluctuation,  and  the  abscess  breaks  spontaneously,  if  it  has  not  been  opened 
previously.  Besides  perforation  outward,  we  also  meet  with  perforation  into  the 
abdominal  cavity,  with  a  consecutive  general  peritonitis,  and  sometimes  perfora- 
tion into  the  ascending  colon,  with  evacuation  of  pus  into  the  bowels  and  final 
recovery.     [Occasionally  the  pus  is  discharged  into  the  bladder.] 

An  unfavorable  complication  repeatedly  observed  in  perityphlitis  is  an  exten- 
sion of  the  inflammation  to  the  ileo-caecal  vein,  which  results  in  a  purulent  phle- 
bitis of  this  and  also  of  the  portal  vein.  A  general  pyaemic  condition  develops, 
with  chills  and  marked  elevation  of  temperature.  This  almost  always  ends  fatal- 
ly, and  at  the  autopsy  we  usually  find  many  metastatic  abscesses  in  the  liver. 

The  diagnosis  of  typhlitis  and  perityphlitis  may  easily  be  made  in  most  cases 
from  the  peculiar  localization  of  the  swelling  and  tenderness,  and  by  paying  atten- 
tion to  the  general  course  of  the  disease.  During  life  we  can  merely  conjecture 
whether  the  special  origin  of  the  inflammation  is  in  the  caecum  or  in  the  vermi- 
form appendix,  but  we  can  never  determine  this  with  certainty,  since  in  both  cases 
the  type  of  the  disease,  as  we  have  said,  is  almost  precisely  the  same.  The  further 
course  of  the  disease  is  the  only  means  of  deciding  whether  the  inflammation  has 
remained  circumscribed,  or  has  invaded  the  adjacent  parts  in  the  manner  men- 
tioned above. 

Chronic  cases  may  be  confused  with  new  growths,  especially  with  cancer,  aris- 
ing from  the  caecum  or  the  vermiform  appendix.  Tumors  of  the  right  kidney,  or 
the  right  ovary,  and  also  psoas  abscess,  after  caries  of  the  vertebrae,  have  in  some 
cases  given  rise  to  false  diagnoses.  In  such  doubtful  cases  we  are  usually  able  to 
form  a  definite  opinion  only  after  long  and  careful  observation. 

We  may  mention  here  in  addition  that  in  rare  cases  there  may  be  a  closure 
in  some  part  of  the  vermiform  appendix.  The  portion  behind  this  closure  is  then 
gradually  more  and  more  distended  by  the  secretion  of  the  mucous  membrane, 
and  thus  the  so-called  dropsy  of  the  vermiform  appendix  is  developed,  which  may 
give  rise  to  a  tumor  which  can  be  felt  in  the  ileo-caecal  region. 


TYPHLITIS  AND  PERITYPHLITIS.  421 

[In  brief  the  early  signs  and  symptoms  are  those  of  a  local  peritonitis,  the  seat 
of  which  is  generally  highly  suggestive  of  its  origin  in  the  appendix.  In  some 
cases  the  symptoms  are  not  indicative  of  serious  trouble,  and  patients  not  infre- 
quently walk  into  the  outpatient  departments  of  hospitals  for  advice.  It  is  un- 
necessary to  say  that  such  should  be  put  at  absolute  rest  in  bed  with  the  uimost 
promptitude. 

In  women  the  diagnosis  is  somewhat  complicated  by  the  possibility  of  acute 
inflammation  about  the  uterus  or  its  appendages.  In  both  sexes  the  possibility 
of  the  serious  error  of  mistaking  appendicitis  for  typhoid  fever  is  to  be  constantly 
borne  in  mind.  Acute  intestinal  obstruction  affords  another,  though  practically 
less  serious,  possibility  of  error. 

The  tumor  may  require  two  or  three  days  for  its  development.] 

The  prognosis  in  every  case  of  typhlitis  and  perityphlitis  is  to  be  given  with 
some  reserve,  since  we  can  not  foresee  the  further  course  of  the  disease.  A  favor- 
able termination,  however,  is  by  far  the  most  frequent,  and  the  rule  is  that  the 
cases  are  mild  and  the  inflammation  is  confined  to  the  caecum.  In  severe  cases  of 
perityphlitis,  which  end  in  suppuration,  all  depends  upon  whether  a  general  peri- 
tonitis ensues  or  not,  and  then,  if  the  inflammation  be  limited,  whether  the 
patient's  strength  is  sufficient  or  not  to  sustain  him  until  the  abscess  finally  heals. 
If  his  strength  holds  out,  he  may  sometimes  recover  after  the  disease  has  lasted 
for  months. 

The  treatment  of  typhlitis  has  two  tasks  to  accomplish :  first,  to  remove  the 
accumulation  of  faeces,  which  in  most  cases  has  caused  and  which  still  keeps  up 
the  inflammation,  and,  in  the  second  place,  to  prevent,  if  possible,  the  further 
extension  of  the  inflammation,  when  it  has  once  appeared.  Unfortunately,  the 
accomplishment  of  these  two  tasks  are  opposed  to  each  other,  and  thus,  in  a  given 
case,  it  is  often  hard  to  decide  whether  to  satisfy  the  first  indication  by  prescrib- 
ing cathartics,  or  the  second  by  prescribing  opium.  In  general,  as  we  believe,  the 
fear  of  the  harm  which  cathartics  may  do  by  tearing  any  adhesions  formed,  etc., 
need  not  be  carried  too  far.  In  fresh  cases  of  simple  typhlitis  stercoralis,  which 
come  on  with  manifest  stoppage  and  a  palpable  faecal  tumor  in  the  region  of  the 
caecum,  we  may  always  prescribe  cathartics  like  castor-oil  or  rhubarb,  if  only  we 
exercise  due  caution  about  it.  When  there  are  copious  dejections  after  a  few 
spoonfuls  of  castor-oil,  the  pain  and  fever  usually  speedily  disappear.  If  we  do 
not  wish  to  be  imprudent  in  cases  where  marked  tenderness  leads  us  to  suspect 
that  the  peritoneum  is  already  involved,  we  may  order  large  enemata  of  water 
instead  of  cathartics,  and  these  often  act  well.  In  cases,  too,  where  there  are  signs 
of  intestinal  stenosis,  we  may  hope  for  the  best  results  from  large  enemata  repeated 
three  or  four  times  a  day. 

If  the  inflammation  has  extended  to  the  parts  adjacent  to  the  caecum,  and  if, 
accordingly,  we  have  a  perityphlitis,  cathartics  are  no  longer  proper,  and  are  even 
sometimes  injurious.  The  treatment  then  is  chiefly  to  give  opium,  half  a  grain  to 
a  grain  (grm.  O'OS-O'Oß)  of  the  extract  every  hour  or  two,  according  to  the  severity 
of  the  case.  By  prescribing  opium  we  soonest  attain  a  cessation  of  the  pain  and 
a  limitation  of  the  inflammation.  If  we  suspect  a  large  accumidation  of  faeces 
besides  the  perityphlitis,  or  if  symptoms  of  intestinal  stenosis  appear,  the  opiuni 
treatment  can  be  combined  very  well  with  large  enemata. 

The  local  treatment  of  typhlitis  and  perityphlitis  is  often  of  great  service.  In 
most  cases  an  ice-bag  on  the  ileo-caecal  region  is  well  borne  and  relieves  the  pain. 
If  there  is  very  much  tenderness,  we  can  employ  local  blood-letting,  eight  to  fifteen 
leeches,  in  robust  persons,  with  very  good  results. 

If  the  signs  of  a  local  abscess-formation  appear,  we  may  replace  the  ice-bags 
by  warm  compresses  or  poultices.     We  do  not  take  the  useless  troiible  of  reducing 


422  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

the  fever  by  quinine,  but  we  try  to  keep  up  the  patient's  strength  as  much  as  pos- 
sible. If  there  is  fluctuation  externally,  we  should  open  the  abscess  and  treat  it 
antiseptically.     We  must  refer  to  tbe  text-books  on  surgery  for  all  tbe  details. 

[Tait  and  his  followers  deprecate  the  use  of  opium  in  peritonitis  of  this  as  well 
as  of  other  forms,  and  advocate  saline  laxatives  as  a  means  of  reducing  congestion. 
The  profession  at  large,  however,  in  this  country  and  in  England,  do  not  adopt 
his  views.  Absolute  rest  in  bed  is  to  be  secured  as  early  as  possible,  and  an  exclu- 
sively liquid  diet  is  to  be  enforced,  the  nourishment  being  given  in  such  quantities 
and  at  such  intervals  as  the  condition  of  the  stomach  and  other  features  of  the  case 
seem  to  indicate ;  but  four  to  six  ounces  every  two  hours  should  rarely  be  exceeded. 
It  should  be  remembered  that  grave  cases  of  this  affection  are  of  short  duration, 
and  that  death  from  simple  exhaustion  is  not  to  be  dreaded.  The  editor  has  of  late 
followed  a  plan  of  treatment  suggested  to  him  by  Dr.  Sabine,  of  Brookline,  Mass., 
whose  experience  with  it  has  been  fairly  large.  No  food  whatever  is  given  until 
the  temperature  is  normal,  even  if  this  period  extend  to  a  fortnight.  Water  is 
freely  allowed,  and  small  quantities  of  stimulants  may  be  administered  if  desirable. 
Morphine  is  given  in  small  doses,  not  exceeding  one  eighth  of  a  grain,  if  there  is 
pain  or  restlessness,  however  slight.  Peristalsis  is  thus  discouraged,  the  meta- 
morphosis of  tissue  is  delayed,  bodily  and  mental  rest  are  secured.  No  attempt  is 
made  to  move  the  bowels.    The  favorite  local  application  with  us  is  a  hot  poultice. 

In  fulminant  cases,  with  perforation  and  general  peritonitis  at  the  start,  the 
results  of  surgical  and  medical  treatment  are  alike  bad.  In  the  ordinary  run  of 
cases  the  peritonitis  is  at  first  local,  though  it  may  at  any  time  become  general 
from  rupture  of  the  limiting  adhesions,  and  herein  lies  one  of  the  main  dangers 
and  arises  the  necessity  of  the  greatest  watchfulness.  Abscess  formation  probably 
does  not  occur  unless  perforation  takes  place ;  but  we  have  at  present  no  certain 
criterion,  at  least  during  the  first  three  or  four  days,  by  which  we  can  determine 
the  existence  of  perforation.  Hence  springs  the  doubt  as  to  whether  to  operate, 
and  how  soon.  If  the  tumor  consists  only  of  faeces  and  simple  inflammatory 
exudation,  it  will  be  passed  along  and  absorbed  unless  perforation  takes  place. 
If  an  abscess  has  formed,  spontaneous  cure  is  highly  improbable  unless  the  pus  be 
discharged  into  the  intestine,  bladder,  or  vagina — avenues  which  are  far  less 
desirable  than  that  afforded  by  an  external  incision.  Fitz  advocates  waiting  for 
three  or  four  days  at  least,  and  then  being  guided  by  the  development  of  the 
general  and  local  symptoms  as  to  whether  to  operate  or  not.  It  may  be  stated  as 
a  general  rule  that  in  cases  where  the  existence  of  perforation  is  doubtful,  but  the 
symptoms  as  a  whole  are  grave  and  increasing,  it  is  wiser  not  to  postpone  incision, 
the  consequences  of  an  unnecessary  but  properly  performed  operation  being  less 
serious  than  those  of  overmuch  delay. 

In  mild  cases,  and  those  in  which  delay  is  decided  on,  opium  in  some  form 
should  be  given  in  sufficient  amount  to  relieve  pain  and  allay  restlessness ;  but 
anything  like  narcotism  is  to  be  avoided,  lest  the  effects  of  the  opium  lead  the 
attendant  into  a  feeling  of  false  security.  In  recurrent  cases  it  is  probably  wiser  to 
excise  the  appendix  between  attacks,  unless  the  patient  is  so  situated  that  he  can 
put  himself  under  skilled  treatment  on  the  first  threatenings  of  an  attack.  The 
necessity  of  so  doing  should  be  carefully  explained  to  him.  As  to  methods  of 
operation,  the  reader  is  referred  to  works  on  surgery.] 


TUBERCULOSIS  OF  THE  INTESTINES.  423 

CHAPTER  V. 
PERFORATING  ULCER   OF   THE   DUODENUM. 

There  is  a  form  of  ulcer  of  the  duodenum,  especially  of  its  upper,  horizontal 
portion,  which  is  precisely  analogous  to  the  round  gastric  ulcer  in  regard  to  aeti- 
ology, pathological  anatomy,  and,  very  largely,  symptomatology.  The  ulcer  is 
probably  also  due  in  most  cases  to  the  action  of  the  acid  gastric  juice  on  the  duo- 
denal mucous  membrane,  under  conditions  which  have  been  mentioned  more  fully 
in  the  aetiology  of  gastric  ulcer.  We  must  mention  here  the  noteworthy  fact  that, 
after  extensive  burns  of  the  external  skin,  ulceration  of  the  duodenum,  rarely  of 
the  stomach  also,  has  been  repeatedly  observed.  This  is  probably  due  to  the 
plugging  of  a  duodenal  vessel  by  an  embolus  from  decomposed  masses  of  blood. 

Ulcer  of  the  duodenum  is  much  rarer  than  the  round  gastric  ulcer,  and,  in  dis- 
tinction from  the  latter,  it  has  been  found  decidedly  offener  in  men  than  in  women. 

Many  cases  of  ulcer  of  the  duodenum  run  their  course  entirely  without  symp- 
toms, or  they  cause  symptoms  when  sudden  haemorrhage  appears,  from  erosion  of 
the  pancreatico-duodenalis,  gastro-duodenalis,  etc.,  with  haematemesis  and  bloody 
stools,  or  the  sudden  signs  of  peritonitis  from  perforation.  In  many  cases  a  type 
of  disease  exists  for  a  long  time  whose  symptoms,  as  we  have  said,  are  so  like  the 
clinical  symptoms  of  gastric  ulcer  that  we  can  very  rarely  distinguish  the  two 
forms  with  certainty  during  life.  We  notice  especially  continuous  or  neuralgic 
pain,  which,  in  ulcer  of  the  duodenum,  has  its  chief  seat  in  the  right  hypochon- 
drium.  Severe  gastric  symptoms,  especially  vomiting,  are  not  as  common  as  in 
gastric  ulcer.  The  general  health  and  general  nutrition  may  remain  quite  undis- 
turbed for  a  long  time. 

Ulcer  of  the  duodenum  ends  by  cicatrization  and  recovery,  or  by  cicatrization 
and  the  formation  of  stenosis,  with  secondary  dilatation» of  the  upper  portion  of 
the  duodenum  and  of  the  stomach.  In  regard  to  the  different  adhesions  and  per- 
forations of  the  ulcer  into  neighboring  organs,  we  may  refer  to  what  has  been 
said  of  gastric  ulcer. 

The  treatment  must  be  governed  by  the  same  principles  which  were  laid  down 
in  the  treatment  of  gastric  ulcer,  especially  as  the  diagnosis  is  usually  doubtful. 


CHAPTER  VI. 
TUBERCULOSIS   OF   THE   INTESTINES. 

Tuberculosis  of  the  intestines  is  in  most  cases  a  secondary  disease,  and  is  one 
symptom  of  a  more  extensive  general  tuberculosis.  It  develops  most  frequently 
in  the  course  of  chronic  pulmonary  tuberculosis,  and  depends  here,  as  we  have 
seen,  upon  an  infection  of  the  intestines  by  the  tubercular  sputum  that  has  been 
swallowed. 

Intestinal  tuberculosis,  however,  may  also  be  a  primary  disease,  and  the  source 
of  further  extension  of  tuberculosis  over  the  body.  >(  Tuberculosis  of  the  abdomi- 
nal organs,"  which  usually  comes  from  the  intestines,  has  a  clinical  significance, 
especially  in  children.  It  is  not  improbable  that  in  such  cases  the  first  infection 
of  the  intestine  comes  from  without,  and  that  the  tubercular  poison  is  taken  into 
the  body  with  the  food.  Here  we  must  suspect  especially  the  milk  from  cows 
with  pearly  distemper — that  is,  with  tubercular  disease. 

The  anatomical  changes  in  intestinal  tuberculosis  are  precisely  analogous  to  the 


424  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

tubercular  changes  in  other  mucous  membranes.  The  tubercular  new  growth  has 
its  origin  usually  in  the  lymph-apparatus  of  the  intestine,  in  the  solitary  follicles, 
and  in  Peyer's  patcbes.  The  first  miliary  tubercles  form  beneath  the  epithelium, 
and  soon  fuse  with  one  another  into  a  diffuse  infiltration.  In  its  further  course 
the  infiltration  on  one  side  extends  deeper  into  the  surrounding  tissue,  so  that  it 
attacks  the  siibmucous  and  muscular  coats  even  to  the  serous  coat,  and  on  the 
other  side,  by  the  destruction  of  the  new  growth  which  begins  at  the  surface  and 
constantly  spreads,  tubercular  ulcers  are  formed.  We  can  often  make  out  with 
the  naked  eye  single  miliary  tubercles  or  groups  of  them  at  the  base  or  in  the  in- 
filtrated edges  of  the  ulcer.  This  is  especially  plain  in  deep-seated  ulcers  on  the 
corresponding  portion  of  the  serous  coat.  The  form  of  the  larger  tubercular 
ulcers  is  often  irregular.  In  many  cases  the  long  diameter  of  the  ulcer  is  parallel 
to  the  circumference  of  the  intestine,  so  that  the  girdle-like  ulcers,  wdiich  are  espe- 
cially characteristic  of  tuberculosis,  are  formed. 

Tubercular  ulcers  are  situated  both  in  the  large  and  in  the  small  intestines. 
They  are  usually  most  marked  in  the  vicinity  of  the  ileo-csecal  valve.  Tubercular 
ulcers  in  the  stomach  are  extremely  rare.  Besides  the  intestinal  tuberculosis  there 
is  very  often  tuberculosis  of  the  mesenteric  lymph-glands,  and  also  frequently 
tuberculosis  of  the  peritoneum. 

The  symptoms  of  intestinal  tuberculosis  are  usually  quite  subordinate  to  the 
symptoms  caused  by  other  co-existing  tubercular  affections.  There  may  often  be 
quite  extensive  tubercular  ulcers  without  any  marked  symptoms,  but,  as  a  rule, 
the  onset  of  diarrhoea  turns  the  attention  to  the  intestinal  complication  (see  the 
chapter  on  pulmonary  tuberculosis). 

Primary  tuberculosis  of  the  abdominal  organs  sometimes  presents  quite  a  char- 
acteristic type  of  disease,  especially  in  children.  This  was  termed  by  the  older 
physicians  tabes  mesenterica.  The  chief  featm^e  of  this  type  of  disease  consists  in 
a  progressive  general  emaciation  and  anaemia,  which  is  usually  associated  with  a 
persistent  hectic  fever,  which  obstinately  resists  all  the  remedies  employed.  The 
abdomen  is  usually  swollen  by  meteorism,  but  it  is  sometimes  flat  or  sunken.  In 
some  cases,  but  less  frequently  than  was  formerly  believed,  we  can  feel  the  swollen 
mesenteric  lymph-glands  through  the  abdominal  wall  during  life.  The  liver  may 
be  enlarged  and  its  lower  border  can  often  be  felt.  The  bowels  are  irregular, 
and  there  is  usually  a  moderate  diarrhoea,  persisting  in  spite  of  all  remedies. 
The  invariably  fatal  termination  is  due  to  an  increase  of  the  general  marasmus, 
or  to  a  final  acute  tubercular  affection,  like  miliary  tuberculosis  or  tubercu- 
lar meningitis.  The  autopsy  shows  tuberculosis  of  the  intestines,  peritoneum, 
lymph-glands,  liver,  etc.,  to  a  greater  or  less  extent.  The  lungs  may  be  quite  free 
from  tuberculosis.  We  will  return  to  this  affection  in  the  description  of  tubercu- 
losis of  the  peritoneum. 

The  treatment  of  intestinal  tuberculosis  can  be  only  symptomatic.  Besides  the 
general  dietetic  treatment  which  seeks  to  keep  up  the  patient's  strength  as  far  as 
possible,  medical  interference  is  demanded  by  the  abdominal  pain  and  diarrhoea. 
The  chief  remedy  is  opium,  which,  alone  or  in  combination  Avith  tannin,  acetate 
of  lead,  etc.,  acts  most  rapidly  in  relieving  the  intestinal  symptoms.  Warm  poul- 
tices and  wet  compresses  give  the  best  service  for  local  applications. 

In  other  respects  the  treatment  coincides  with  the  general  treatment  of  tuber- 
culosis (vide  supra). 


SYPHILIS  OF  THE  RECTUM.  425 

CHAPTER  VII. 
SYPHILIS   OF   THE   RECTUM. 

In  not  very  rare  cases  we  see  in  the  rectum,  especially  in  its  lower  portions, 
extensive  syphilitic  ulcerations,  which  produce  a  severe  and  practically  important 
type  of  disease.  The  more  intimate  relation  between  syphilis  of  the  rectum  and 
the  general  syphilitic  process  is  not  perfectly  clear.  According  to  quite  a  wide- 
spread opinion,  the  infection  of  the  rectum  comes  from  the  secretion  trickling 
down  from  the  ulcers  of  the  genitals.  The  facts  seem  to  support  this  view,  since 
syphilis  of  the  rectum  is  seen  much  more  frequently  in  women  than  in  men. 
Some  authors  have  even  asserted  that  all  the  so-called  "  syphilitic  "  ulcers  in  the 
rectum  have  no  connection  at  all  with  genuine  syphilis,  but  are  chancroids.  It  is 
in  fact  striking,  even  if  it  by  no  means  proves  such  a  hypothesis,  that,  at  the 
autopsy  of  people  who  have  died  of  "  syphilis  of  the  rectum,"  we  rarely  find 
definite  syphilitic  changes  in  other  internal  organs — a  fact  which  we  also  can 
confirm. 

The  most  characteristic  mark  of  syphilitic  ulcers  in  the  rectum  is  their  tendency 
to  form  cicatrices  and  stenoses.  This  result  of  the  ulcer  is  also  important  in  its 
clinical  relations,  since  the  chief  symptoms  of  the  disease  usually  begin  with  the 
development  of  the  stenosis.  The  seat  of  the  stenosis  is  usually  so  low  down  that 
we  can  conveniently  reach  it  with  the  finger,  on  a  digital  examination  of  the  rec- 
tum during  the  patient's  life.  The  rectum  narrows  like  a  funnel  upward,  and  we 
can  feel  the  quite  sharp  edge  of  the  ring-like  cicatrix  with  the  point  of  the  finger. 
This  funnel-shaped  stenosis  of  the  rectum  is  so  characteristic  of  syphilis  of  that 
organ  that,  in  almost  all  cases,  we  can  make  the  diagnosis  with  perfect  certainty 
from  this  alone. 

The  rectum  and  the  descending  colon  are  usually  dilated  above  the  stenosis, 
and  here  extensive,  iiregular  ulcerations,  with  undermined  edges,  are  usually 
found  in  the  mucous  membrane.  These  are  partly  of  a  specific  nature,  and  partly 
diphtheritic  ulcers  caused  by  the  pressure  of  the  accumulated  fsecal  masses. 

The  symptoms  of  syphilis  of  the  rectum  usually  develop  quite  gradually.  At 
first  the  bowels  are  irregular,  and  there  are  disturbances  of  defecation  which  stub- 
bornly resist  the  ordinary  remedies  employed.  There  are  sometimes,  in  the  first 
stage  of  the  disease,  frequent  and  severe  haemorrhages  with  the  dejections,  as  we 
have  seen,  and  for  a  long  time  these  may  falsely  be  considered  to  be"  bleeding 
from  haemorrhoids. "  The  symptoms  become  more  marked  as  cicatrization  of  the 
ulcer  increases  and  as  stenosis  of  the  rectum  develops.  There  is  usually  a  decided 
catarrh  of  the  rectum,  so  that  the  thin  stools  contain  a  large  admixture  of  mucus 
and  pus.  The  patient's  condition  is  extremely  distressing,  from  the  pains  with  the 
frequent  but  always  scanty  dejections,  and  from  the  severe  tenesmus.  Nodular 
thickenings  and  prolapse  of  the  mucous  membrane,  and  sometimes  true  haemor- 
rhoids, form  about  the  anus.  The  patient's  strength  constantly  diminishes  from 
the  pain  and  the  continual  diarrhoea.  He  finally  becomes  emaciated,  looks  very 
pale  and  wretched,  and  has  fever  toward  night.  Death  ensues  from  increasing 
general  weakness,  or  rarely  from  a  terminal  peritonitis  due  to  perforation,  after 
the  whole  disease  has  lasted  one  and  a  half  to  two  and  a  half  years. 

This  unfavorable  termination  unfortunately  seems  to  be  the  rule  in  all  the 
cases  described;  hence  the  prognosis  is  to  be  regarded  as  very  serious  in  all  cases 
of  syphilis  of  the  rectum.  Improvement  worthy  of  mention,  or  even  perhaps 
recovery,  is  possible  only  when  the  disease  is  recognized  at  the  outset  and  properly 
treated. 

At  the  outset  of  the  disease  the  treatment,  of  course,  must  consist  chief!  v  in  an 


426  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

energetic  general  attack  upon  the  syphilis  hy  mercurial  inunction  and  iodide  of 
potassium ;  hut,  as  soon  as  the  characteristic  funnel-shaped  stenosis  of  the  rectum 
has  formed,  we  can  not  expect  much  from  anti-syphilitic  medication,  since  this 
can  no  longer  exert  any  influence  on  the  cicatrices  and  their  results.  Improve- 
ment is  now  to  be  obtained  only  by  mechanical  dilatation  of  the  stenosis  by 
bougies,  or,  if  this  is  not  enough,  by  a  surgical  operation.  A  suitable  local  treat- 
ment by  irrigation  is  also  of  benefit  to  the  catarrh  and  to  the  ulcers  that  still  exist 
in  the  rectum.     Internally,  we  may  continue  to  use  iodide  of  potassium. 


CHAPTER  VIII. 
CANCER  OF   THE   INTESTINES. 

The  development  of  cancer  is  far  more  rare  in  the  intestine  than  in  the 
stomach.  Carcinoma  is  seen  with  any  frequency  only  at  the  lower  end  of  the 
intestine,  in  the  rectum.  In  other  parts  the  points  of  election  for  the  develop- 
ment of  carcinoma  are  the  colon,  especially  at  its  bends,  the  cascum  and  vermi- 
form appendix,  and  the  small  intestine,  especially  in  the  region  of  the  papilla 
duodenalis. 

Most  cancers  of  the  intestine  appear  in  the  form  of  ring-like  swellings  that 
take  in  the  whole  circumference  of  the  intestine.  More  rarely  we  find  a  more 
diffuse  papillary  proliferation,  extending  over  a  larger  surface  of  the  intestine. 
There  is  often  quite  an  extensive  destruction  of  the  new  growth  on  the  surface 
of  the  cancer,  from  which  deep  ulcerations  arise.  We  sometimes  find  metas- 
tases in  other  organs ;  for  example,  the  lymph-glands,  the  abdominal  cavity,  or 
the  liver.  In  its  histological  structure,  cancer  of  the  intestine  is  to  be  regarded  as 
invariably  a  cylindrical- celled  carcinoma,  which  sometimes  shows  a  plainly 
glandular  structure — adeno-carcinoma — and  sometimes  that  of  the  other  forms 
of  cancer — scirrhus,  medullary,  or  colloid. 

Cancer  of  the  intestines,  like  all  cancers,  occurs  chiefly,  if  not  invariably,  in 
advanced  life. 

The  clinical  symptoms  of  cancer  of  the  intestines  are  only  in  a  part  of  the 
cases  so  pronounced  that  we  can  make  a  sure  diagnosis  of  the  disease.  Cancer 
of  the  rectum,  however,  presents  a  characteristic  picture. 

Cancer  of  the  rectum  begins  usually  with  distress  at  stool  and  pain  in  the 
rectum,  which  at  first  comes  only  with  defecation,  but  later  becomes  almost 
continuous.  The  pains  often  shoot  into  the  neighboring  parts — the  thighs,  the 
genitals,  etc.  The  local  symptoms  gradually  increase,  the  stools  often  contain 
some  mucus  and  blood,  and  diarrhoea  alternates  with  obstinate  constipation. 
The  patient  also  becomes  emaciated,  and  constantly  grows  weaker  and  more 
miserable.  Finally,  we  often  find  a  complete  paralysis  of  the  sphincter  ani,  so 
that  a  mucous,  bloody  fluid  constantly  comes  from  the  half-open  anus.  The 
diagnosis  can  almost  always  be  easily  and  surely  made  by  digital  examination 
of  the  rectum.  We  feel  the  firm,  nodulated  proliferations  of  cancer,  and  we  can 
usually  make  out  with  approximate  accuracy  its  extent  and  its  invasion  of 
neighboring  organs,  like  the  vagina  and  bladder.  Examination  with  the  rectal 
speculum  makes  the  diagnosis  more  accurate.  In  some  cases  the  destruction  of 
the  new  growth  may  cause  perforation  into  the  organs  mentioned,  and  we  can 
easily  understand  the  results  of  this,  such  as  cystitis,  purulent  discharges  from  the 
vagina,  etc.     We  may  also  have  peritonitis  from  perforation.     Secondary  cancer 


CANCER  OF  THE  INTESTINES.  '  427 

appears  with  especial  frequency  in  the  liver,  also  in  the  peritoneum  and  else- 
where. 

Carcinoma  of  the  colon  causes,  as  a  rule,  only  very  indefinite  symptoms,  which 
for  a  long1  time  are  hard  to  interpret.  These  symptoms  consist  chiefly  of  distress 
at  stool,  obstinate  constipation,  dull  pains  in  the  abdomen,  and  the  signs  of  slowly 
increasing  general  weakness  and  emaciation.  In  many  cases  the  stools  consist  of 
peculiar,  flat,  compressed  little  lumps,  which  have  a  certain  resemblance  to  sheep's 
dung.  A  similar  appearance  may  also  be  seen  in  cancer  of  the  small  intestines. 
In  many  cases  examination  of  the  abdomen  gives  a  negative  result,  but  we  can 
sometimes  feel  the  new  growth  as  an  evident  tumor  through  the  abdominal  wall. 
In  such  cases,  however,  it  is  almost  always  difficult  to  decide  upon  the  seat  of  the 
tumor  with  certainty.  It  may  be  very  easy  to  confuse  this  form  with  cancers 
arising  from  the  stomach,  the  omentum,  the  mesenteric  lymph-glands,  etc.  We 
may  also  be  deceived  as  to  the  location  of  the  tumor  by  the  fact  that  sometimes 
the  tumor  which  is  felt  in  intestinal  cancer  is  not  the  new  growth  itself,  but 
corresponds  to  the  faecal  masses  collected  above  it.  Carcinoma  of  the  caecum  can 
often  not  be  distinguished  for  a  long  time  from  the  tumors  caused  by  chronic 
typhlitis  and  perityphlitis.  The  patient's  age,  the  tedious  com*se  and  increasing 
severity  of  the  disease,  and  sometimes  the  swelling  of  the  inguinal  glands,  are  the 
only  things  that  make  us  think  of  a  cancer.  In  a  case  seen  at  the  surgical  clinique 
in  Leipsic,  a  cancer  arising  from  the  vermiform  appendix  ruptured  externally 
through  the  skin.  The  rare  instances  of  cancer  of  the  small  intestines  cause  still 
greater  difficulties  in  diagnosis.  In  cases  where  the  tumor  can  be  felt  externally 
we  can  sometimes  make  out  a  marked  mobility  of  the  swelling,  corresponding  to 
the  different  positions  of  the  affected  loop  of  intestine.  Cancer  of  the  duodenum 
in  many  of  its  relations  resembles  cancer  of  the  stomach,  especially  of  the  pylorus. 
It  also  leads  finally  to  dilatation  of  the  stomach  with  its  well-known  results, 
as  well  as  to  dilatation  of  the  part  of  the  duodenum  above  the  new  growth. 
Cancers  situated  in  the  region  of  the  papilla  duodenalis  usually  cause  intense 
and  protracted  jaundice. 

The  prognosis  of  all  intestinal  carcinomata  is  absolutely  unfavorable.  The 
disease  may  sometimes  last  quite  a  long  time,  some  two  or  three  years,  but  in  some 
cases  the  duration  of  the  special  symptoms  is  brief,  a  few  months  or  even  weeks, 
apparently  because  the  tumor  has  previously  existed  for  a  long  time  without 
symptoms.  Intestinal  cancer  terminates  with  the  signs  of  increasing  loss  of 
strength,  or  it  perforates,  causing  a  terminal  purulent  peritonitis.  Extensive 
ichorous  processes  in  the  surrounding  connective  tissue,  phlebitis,  and  pyaemia, 
may  follow  intestinal  cancer.  A  number  of  cases  die  with  the  signs  of  a  slowly 
or  rapidly  developing  intestinal  stenosis  (vide  infra),  but  in  some  cases,  upon 
ulceration  of  the  cancer,  the  already  pronounced  symptoms  of  stenosis  may  disap- 
pear for  a  time. 

The  treatment  must  be  confined  to  relieving  the  patient's  symptoms  as  far  as 
possible.  We  must  provide  for  easy  dejections  by  a  suitable  diet  and  cathartics. 
Pain,  if  it  is  present,  must  be  lessened  by  narcotics.  Surgical  treatment  of  intesti- 
nal cancer  has  shown  good  results  as  yet  only  in  cancer  of  the  rectum.  The  pal- 
liation which  lasts  for  a  long  time  after  scraping  out  the  rectum  is  often  quite 
marked,  even  in  advanced  cases.  In  early  cases,  permanent  relief  may  be  given 
by  extirpation  of  the  rectum.  If  the  cancer  has  advanced  too  far  for  this,  scrap- 
ing out  the  rectum  with  a  sharp  spoon  may  lessen  the  discomfort  at  least  for  a 
a  time.     All  the  details  are  to  be  found  in  the  text-books  on  surgery. 


428  DISEASES   OF  THE  DIGESTIVE  ORGANS. 

CHAPTER  IX. 
HEMORRHOIDS. 

By  the  name  "  haemorrhoids  "  we  mean  diffuse  or  varicose  dilatations  of  the 
haemorrhoidal  veins,  especially  of  the  venous  plexuses  at  the  lower  end  of  the 
rectum.  Haemorrhoids  are  single  large  varices,  which  usually  rise  from  the  sub- 
mucous layer,  and  push  the  mucous  membrane  out  before  them.  If  they  are  situ- 
ated outside  of  the  sphincter  ani  we  speak  of  external  haemorrhoids,  in  distinction 
from  internal  haemorrhoids,  which  lie  above  the  sphincter.  The  size  of  the  nod- 
ules varies  with  the  fullness  of  the  dilated  veins;  but  haemorrhoids,  as  a  rule,  do 
not  consist  exclusively  of  dilated  vessels,  for  we  often  find,  at  the  same  time,  quite 
a  considerable  thickening  of  the  surrounding  connective  tissue,  so  that  the  whole 
mucous  membrane  has  a  swollen  appearance,  with  a  polypoid  proliferation  in 
parts.  The  haemorrhoids  usually  present  themselves  as  bluish  tumors,  from  the 
size  of  a  pea  to  that  of  a  walnut,  which  surround  the  anus  like  a  garland.  Many 
of  them  have  a  broad  base,  while  others  are  pedunculated. 

The  cause  of  haemorrhoids  is,  chiefly,  frequently-repeated  stasis  in  the  veins 
affected.  The  hindrance  to  the  venous  blood  return  has  sometimes  a  purely  local 
cause.  Thus  haemorrhoids  quite  frequently  develop  in  persons  with  habitual  con- 
stipation, and  hence  in  those  who  lead  a  sedentary  life.  Haemorrhoids  also  occur 
as  a  result  of  stasis  in  the  portal  system,  in  cirrhosis  of  the  liver,  etc.,  and  finally 
in  general  disturbance  of  the  circulation,  as  in  diseases  of  the  heart  and  lungs. 
Quite  often,  however,  we  can  discover  no  sufficient  cause  for  the  development  of 
the  disease,  and  we  are  then  forced  to  the  hypothesis  of  a  local  disease  of  the 
affected  venous  plexus,  which  is  probably  often  connected  with  an  individual,  and 
apparently  sometimes  hereditary,  predisposition.  We  most  frequently  see  haemor- 
rhoids in  men  in  middle  life. 

Haemorrhoids  sometimes  cause  only  slight  symptoms,  or  none  at  all,  but  in 
other  cases  they  are  a  tedious,  burdensome,  and  even  distressing  evil.  The  chief 
symptom  is  pain,  which  is  felt  as  a  constant  burning  at  the  anus,  but  which  in- 
creases to  great  severity  at  each  dejection.  There  is  much  pain  when  the  haemor- 
rhoids and  the  surrounding  tissue  gradually  get  into  an  inflamed  condition.  In 
the  skin  about  the  anus,  erythema,  excoriations,  and  sometimes  little  but  very 
painful  fissures  are  formed.  The  mucous  membrane  at  the  lower  end  of  the 
rectum  is  often  found  in  a  catarrhal  state,  which  gives  rise  to  the  presence  of  pus 
and  mucus  in  the  dejections — "mucous  haemorrhoids."  Sometimes  there  is  a 
genuine  phlebitis  in  individual  haemorrhoids,  which  ends  by  forming  an  abscess. 
There  is  very  severe  pain  if  an  internal  haemorrhoid  is  pushed  out  by  the  strain 
and  pressure  at  stool  and  is  strangulated  by  the  sphincter.  Since  all  the  condi- 
tions mentioned — marked  temporary  filling,  inflammation,  and  strangulation  of  a 
haemorrhoid — must  at  times  give  rise  to  a  great  increase  of  the  disturbance,  we 
can  understand  why  we  often  hear  such  troubles  spoken  of  as  "  attacks  of  haemor- 
rhoids." 

Haemorrhoidal  bleeding  is  a  frequent  and  familiar  symptom,  which  rises  from 
a  rupture  of  the  dilated  veins,  and  usually  comes  on  at  stool.  The  haemorrhage  is 
seldom  very  large,  so  that  the  loss  of  blood  is  in  itself  very  rarely  dangerous. 
The  swelling  of  the  varices  after  the  haemorrhages  have  ceased  explains  why  the 
haemorrhoidal  symptoms  are  apt  to  be  less  marked  as  long  as  there  are  haemor- 
rhages than  when  there  are  none.  Hence  the  old  term  of  the  "  golden  vein  "  for 
haemorrhoidal  bleeding. 

Besides  the  local  symptoms  mentioned,  in  the  anus,  there  are  sometimes  other 
symptoms  which  are  due  to  an  implication  of  the  neighboring  venous  plexuses, 


HAEMORRHOIDS.  420 

the  vesical,  prostatic,  and  sacral  plexuses.  There  is  often  pain  in  the  sacral 
region,  difficulty  in  micturition,  and  sometimes  even  blood  in  the  urine — "  vesical 
haemorrhoids  " — and  in  women  vaginal  catarrh,  anomalies  of  menstruation,  etc. 
Since  the  symptoms  of  some  primary  disease  in  the  liver,  or  heart,  or  of  other 
co-existing  morbid  conditions,  like  abnormal  corpulency,  or  chronic  gastrointesti- 
nal catarrh,  may  be  added  to  the  general  picture,  we  can  comprehend  why  medi- 
cal superstition  has  found  in  haemorrhoids  an  excuse  for  the  strangest  ideas,  like 
that  of  "  transposed  haemorrhoids  "  ! 

The  treatment  of  haemorrhoids  is  usually  no  easy  task,  since  the  disease  often 
has  causal  factors  which  can  not  be  removed.  In  all  cases  where  there  are  large 
haemorrhoids  causing  severe  symptoms,  there  is  only  one  radical  cure — removal  by 
operation — which  is  not  dangerous  and  not  hard  to  perform.  It  is  best  done  by 
squeezing  the  nodule  with  a  clamp  and  burning  it  with  the  thermo-cautery.  De- 
tails in  regard  to  it  may  be  found  in  the  text-books  of  surgery. 

If  single  nodules  are  inflamed,  we  may  apply  ice  locally,  or  under  some  circum- 
stances local  blood-letting  is  to  be  preferred.  If  an  abscess  forms  it  must  be 
opened.  We  try  to  replace  strangulated  haemorrhoids  carefully  and  slowly  with 
the  oiled  finger. 

The  treatment  of  chronic  haemorrhoidal  symptoms  consists  chiefly  in  looking 
out  for  regular  and  easy  movements  of  the  bowels,  because  the  local  discomfort 
can  thus  be  best  relieved.  We  must  also  attend  to  any  underlying  trouble,  like 
disease  of  the  liver  or  heart.  The  food  to  be  prescribed  depends  upon  the  patient's 
physical  condition.  It  is  usually  wise  to  limit  the  supply  of  meat,  and  to  recom- 
mend instead  fruit,  vegetables,  light  farinaceous  food,  and  rice.  It  is  well  to  pre- 
scribe sufficient  physical  exercise,  cool  baths,  under  some  circumstances  sitz-baths, 
and  rubbing.  We  must  also  consider  cathartics,  especially  the  bitter  waters,  the 
springs  at  Marienbad  and  Kissingen,  and  the  regular  use  of  cold  enemata,  rhu- 
barb, aloes,  etc.  Sulphur  is  a  remedy  very  often  used  in  the  treatment  of  haemor- 
rhoids, the  chief  ingredient  of  most  of  the  "pile  powders"  for  internal  use.  It 
may  be  ordered  thus : 

B  Sulphuris  loti,  )  ää   §ss.  (grm.15); 

Potassn  bitartratis,  S 

Sacchari  albi,  )  .._...  .As       ,T 

™,  ,      •■*•*?■■••' aa   3  ijss.  (grm.  10).      M. 

Elaeosacchan  citri,*  ) 

Haemorrhoidal  bleedings,  as  has  been  said,  are  only  exceptionally  so  severe  as 
to  require  interference.  We  may  use  ice,  chloride  of  iron,  or  tamponing  the 
rectum. 

[Persistent  and  intelligent  treatment  will  often  bring  about  very  great  relief,  or 
even  complete  cure,  in  chronic  cases.  There  are  many  local  applications,  each  of 
which  has  its  warm  advocates — so  many  that  it  is  not  possible  here  to  go  into 
details.  Suffice  it  to  say  that  an  astringent  with  or  without  an  anodyne  may  be 
used  as  an  enema,  in  suppository  or  in  ointment.  The  fluid  extract  of  hamamelis, 
glycerine,  and  some  other  remedies  given  by  the  mouth,  are  reported  to  have 
afforded  good  results.] 

*  Powdered  sugar,  3  j  ;  volatile  oil,  gtt.  ij.    M. 


430  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

CHAPTER  X. 
HABITUAL   CONSTIPATION. 

A  persistent  tendency  to  constipation  is  a  frequent  symptom  in  many  different 
diseases,  where  it  is  almost  always  due  to  a  diminution  of  the  normal  peristaltic 
movements  of  the  intestines.  In  many  conditions  this  diminished  energy  of  peri- 
stalsis is  only  one  symptom  of  general  weakness  of  the  hocly.  Thus  we  see  in  all 
possible  forms  of  chronic  disease,  which  are  associated  with  loss  of  flesh  and 
strength,  that  the  intestinal  movements  become  sluggish,  and  hence  the  dejections 
are  delayed;  yet  many  other  causes  have  a  similar  action.  The  small  amount  of 
food  taken,  and  its  quality,  as  it  is  often  composed  largely  of  fluids  and  "  non-irri- 
tating "  substances,  and  also  the  rest  in  bed,  or  at  least  the  slight  amount  of  phys- 
ical exercise  taken — all  these  conditions  play  a  part  in  the  constipation  frequently 
seen  in  patients  with  chronic  disease. 

In  other  cases  we  have  to  do  with  disease  of  the  intestine  itself,  as  the  cause  of 
the  habitual  constipation.  In  chronic  primary  and  secondary  intestinal  catarrh 
we  often  observe  a  persistent  tendency  to  constipation,  which  is  only  occasionally 
interrupted  by  diarrhoea.  Many  factors  also  act  here  simultaneously.  The  chron- 
ically inflamed  membrane,  which  is  often  covered  with  mucus,  is  less  irritable,  and 
hence  it  is  more  difficult  to  excite  the  intestinal  movements  by  reflex  action  than 
if  the  intestinal  mucous  membrane  is  normal.  The  muscular  coat  itself  often 
takes  part  in  the  morbid  changes,  and  atrophy  of  it  has  been  repeatedly  observed 
as  a  result  of  chronic  intestinal  catarrh.  The  habitual  constipation  in  chronic 
affections  of  the  peritoneum  is  explained  in  a  similar  way,  as  the  muscular  coat  is 
also  directly  affected  by  collateral  oedema,  etc.  We  must  mention  here  the  con- 
stipation in  all  forms  of  chronic  jaundice,  which  depends  in  part  at  least  upon  the 
absence  of  the  irritation  which  the  bile  normally  exerts  upon  the  intestinal  wall. 

We  very  often  see  chronic  constipation  in  the  different  diseases  of  the  nervous 
system,  especially  of  the  brain  and  spinal  cord.  Here  we  have  to  do  with  abnor- 
mal inhibition  or  direct  disturbance  of  the  nervous  stimulus,  which  is  necessary 
to  cause  the  intestinal  movements.  Abnormal  mental  conditions  are  also  of  great 
influence.  In  many  psychoses,  especially  in  hypochondriasis,  melancholia,  and 
many  forms  of  hysteria  and  neurasthenia,  we  very  often  see  habitual  constipation. 

While  constipation,  in  the  diseases  thus  far  described,  is  a  symptom  which  is 
more  or  less  subordinate  to  the  other  symptoms  of  the  disease,  thei'e  is  a  form  of 
habitual  constipation,  extremely  important  practically,  where  the  constipation  is 
the  chief  or  almost  the  sole  symptom,  and  accordingly  it  may  be  regarded  to  a 
certain  extent  as  a  disease  sui  generis.  Patients  very  often  come  to  the  physician 
who  look  perfectly  well,  and  are  entirely  able  to  attend  to  their  business,  but  who 
are  constantly  troubled  because  they  can  not  have  a  movement  of  the  bowels  every 
day,  like  other  people,  but  only  every  three  or  four  days,  or  even  less  frequently. 
In  some  cases  of  this  sort  the  patient's  complaint  is  limited  to  the  delay  in  the 
stools,  but  more  often  a  number  of  other  abnormal  subjective  sensations  and  dis- 
turbances are  added  to  the  habitual  constipation,  and  these  are  regarded  as  a  result 
of  the  constipation  by  the  patient  himself,  and  are  usually  observed  with  great  care 
and  excessive  accuracy.  These  are  the  cases  which  may  lead  to  the  highest  degree 
of  hypochondriasis.  The  patient's  whole  thought  and  consciousness  are  busied 
almost  exclusively  with  his  own  morbid  condition,  through  which  he  has  lost  all 
energy  and  joy  in  life.  He  seeks  aid  from  different  physicians  and  from  quacks, 
usually  without  any  real  confidence,  and  without  having  the  perseverance  to  fol- 
low out  the  directions  given.  Besides  the  trouble  with  the  bowels,  such  patients 
complain  chiefly  of  dizziness,  of  pressure,  coldness,  and  other  abnormal  sensations 


HABITUAL  CONSTIPATION.  43 1 

in  the  extremities,  very  often  of  cold  sweaty  hands,  of  a  feeling  of  oppression  in 
the  chest,  of  disturbed  sleep,  etc. 

It  is  not  always  easy  to  interpret  these  cases  correctly.  The  nervous  affection, 
like  hypochondriasis  or  neurasthenia,  is  often  the  primary  disease,  which  is  fol- 
lowed by  constipation,  while  in  other  cases  the  habitual  constipation  leads  sec- 
ondarily to  the  nervous  depression.  The  two  conditions  usually  form  a  vicious 
circle,  since  each  of  them  is  apt  to  keep  up  and  to  increase  the  other.  The  cause 
of  primary  habitual  constipation  can  not  usually  be  discovered.  Probably  we 
often  have  to  do  with  a  congenital  weakness  of  the  muscles  or  of  the  innervation 
of  the  intestines,  since  many  cases  date  from  early  youth. 

The  treatment  of  habitual  constipation  is  a  difficult  and  often  a  thankless  task, 
and  it  demands  patience  and  professional  tact.  It  goes  without  saying  that  we 
must  first  of  all  look  for  the  causal  factors.  If  we  succeed  in  improving  the  un- 
derlying disease— as,  for  instance,  the  chronic  gastro-intestinal  catarrh,  the  chronic 
affections  of  the  heart  or  lungs,  the  anaemic  conditions,  or  certain  nervous  troubles 
— a  regulation  of  the  bowels  often  follows  of  itself.  In  ordinary  habitual  consti- 
pation we  must  first  attend  to  the  patient's  diet.  Since  most  of  these  patients  also 
suffer  from  symptoms  of  nervous  dyspepsia,  they  are  usually  very  careful  in  their 
diet,  and  take  only  a  little,  easily  digestible,  and  chiefly  liquid  food.  It  is  no  won- 
der that  no  good  dejections  follow  such  food.  Improvement  can  be  obtained  only 
by  eating  plenty  of  food  which  can  mechanically  stimulate  the  intestine.  Hence 
we  must  try  to  bring  the  patient  back  to  ordinary  "  household  fare  " — to  take,  be- 
sides plenty  of  meat,  a  sufficient  amount  of  bread,  vegetables,  etc.  It  is  a  very  good 
thing  to  recommend  especially  certain  kinds  of  bread,  like  Graham-bread  or  rye- 
bread,  and  also  larger  amounts  of  butter,  besides  fruit,  prunes,  grapes,  dates,  figs, 
almonds,  nuts,  and  honey.  The  well-known  remedy  of  drinking  a  glass  of  cold  wa- 
ter in  the  morning  before  breakfast  is  deservedly  popular.  We  should  be  very 
guarded  in  giving  special  cathartics,  since  the  patient  easily  gets  accustomed  to 
them,  and  then  must  take  them  in  larger  doses.  Of  the  milder  laxatives,  the  dif- 
ferent bitter  waters  like  Friedrichshall,  do  the  best  service.  We  usually  prescribe 
one  or  two  wine-glassfuls.  The  other  cathartics,  like  tamarinds,  rhubarb,  aloes, 
gamboge,  or  jalap,  which  may  sometimes  be  used  regularly  for  a  long  time,  are 
prescribed  in  various  combinations,  as  pills  and  powders.  We  may  often  have  to 
change  our  remedies  and  our  doses  a  number  of  times  until  we  find  the  right  ones. 

In  the  treatment  of  habitual  constipation  associated  with  hypochondriasis,  the 
first  rule  is  to  treat  the  patient's  mental  condition.  We  should  not  make  merry 
over  his  trouble,  nor  should  we  rudely  let  him  feel  that  we  do  not  consider  his 
complaints  so  important  as  he  himself  imagines.  The  patient  does  not  deserve 
to  be  scoffed  at,  since  his  subjective  symptoms  are  to  him  of  the  most  urgent 
nature ;  but  it  is  extremely  important  to  divert  his  thoughts  from  his  trouble. 
As  in  many  other  reflex  processes,  so  in  defecation,  the  voluntary  attention 
abnormally  directed  to  it  has  an  inhibitory  action.  Hence  we  admonish  the 
patient  to  think  of  his  trouble  as  little  as  possible  and  to  begin  his  regular 
activities  again,  and  we  try  to  convince  him  of  the  groundlessness  of  his  fears. 
The  cathartics,  which  most  patients  have  already  taken  freely  without  the 
desired  action,  are  usually  of  no  advantage  at  all.  On  the  contrary,  it  is  almost 
always  necessary  to  forbid  the  patient  to  use  cathartics  at  all.  Except  by  a 
proper  diet  {vide  supra),  we  try  to  regulate  the  peristalsis  by  external  remedies 
alone.  Methodical  massage  of  the  abdomen  is  most  employed  for  this,  and  also 
electrical  treatment,  faradization  of  the  abdominal  walls,  and  faradization  and  gal- 
vanization transversely  through  the  abdomen.  To  be  sure,  a  good  part  of  the 
benefit  of  these  methods  depends  upon  their  moral  effect  upon  the  patient.  We 
must  not  omit  a  proper  general  treatment:  cold  sponging,  baths,  a  country  resi- 


432  DISEASES  OP  THE  DIGESTiyE  ORGANS. 

dence,  and  sufficient  physical  exercise.  Finally,  it  is  often  very  useful  to  cause 
the  patient  to  go  to  the  closet  at  a  fixed  hour  daily,  even  if  there  be  no  special 
desire  for  a  stool,  and  to  try  to  have  a  movement  of  the  bowels.  Thus  a  sort  of 
training  and  education  of  the  bowels  is  achieved,  even  where  the  patient  at  first 
believes  it  impossible. 

By  these  means  only  do  we  succeed  in  giving  the  patient  renewed  courage,  and 
sometimes  finally  in  attaining  recovery  even  in  severe  and  persistent  cases.  (Com- 
pare the  chapters  on  nervous  dyspepsia  and  on  neurasthenia.) 


CHAPTER  XL 
STRICTURE   AND   OBSTRUCTION   OF   THE   INTESTINES. 

iEtiology  and  Pathological  Anatomy. — Different  pathological  processes  may 
lead  to  stricture  or  complete  obstruction  of  the  intestinal  tube  in  different  parts. 
Since  in  this  affection  the  purely  mechanical  effect  of  the  intestinal  stenosis  is  the 
chief  cause  of  the  clinical  symptoms,  the  type  of  the  disease  is  very  similar  in  all 
the  cases  of  this  class,  in  spite  of  the  manifold  anatomical  causes.  Hence,  after 
enumerating  the  individual  affections  which  may  lead  to  stricture  of  the  intestines, 
we  can  describe  their  symptoms  in  common. 

The  anatomical  causes  of  stricture  or  obstruction  of  the  intestines  are  as  follows : 

1.  Congenital  closure  of  the  intestines  is  found  at  the  anus,  atresia  ani,  and 
much  less  frequently  in  the  colon  or  small  intestines.  The  form  first  mentioned 
is  the  only  one  of  clinical  interest,  since  it  may  be  relieved,  at  least  in  some  cases, 
by  operation.  All  the  other  forms  of  congenital  closure  of  the  intestines  are 
incompatible  with  a  long  duration  of  life. 

2.  Tumors  and  Cicatricial  Strictures. — Cancer  of  the  intestine  is  the  only 
tumor  that  has  any  clinical  significance.  We  have  already  described  its  most 
important  anatomical  relations  and  the  possibility  of  intestinal  stenosis  as  a  re- 
sult of  it. 

We  see  cicatricial  strictures  most  frequently  in  the  large  intestine  after  recov- 
ery from  dysenteric  ulcers.  The  syphilitic  stenosis  of  the  rectum,  which  we  have 
already  described,  is  also  of  practical  importance.  Typhoid  ulcers  very  rarely  lead 
to  cicatricial  stenosis.  Strictures  as  a  result  of  tubercular  ulcers  of  the  intestines 
are  also  extremely  rare.  Stenosis  of  the  duodenum  after  the  healing  of  a  duodenal 
ulcer  (vide  supra)  resembles,  in  its  clinical  symptoms,  stenosis  of  the  pylorus,  and 
not  stenosis  of  the  intestines. 

3.  Intestinal  Obstruction. — The  most  frequent  form  of  intestinal  obstruction 
comes  from  the  impaction  of  fasces.  From  the  different  conditions  which  cause 
enfeeblement  of  the  peristaltic  movements,  an  accumulation  of  faeces  (copro- 
stasis)  may  arise,  especially  in  the  colon,  and  gradually  increase,  and  finally  lead 
to  the  fully  developed  symptoms  of  intestinal  stenosis.  Since  in  such  cases  a 
paralysis  of  the  muscular  coat  has  been  supposed  to  be  the  first  cause  of  the  con- 
stipation, the  occasional  stercoraceous  vomiting  which  finally  sets  in  has  been 
termed  "  ileus  paralyticus."  We  must  also  mention  that,  in  intestinal  stenosis 
from  other  anatomical  causes,  coprostasis  is  often  an  important  factor  in  increas- 
ing the  stenosis. 

We  see  obstruction  of  the  intestines  from  other  causes  much  less  frequently 
than  from  impaction  of  fasces.  In  some  cases  impacted  gall-stones  have  been 
found,  especially  in  the  lower  part  of  the  ileum,  almost  completely  stopping  up 
the  lumen  of  the  intestine.     Genuine  intestinal  calculi  may  exceptionally  lead  to 


STRICTURE  AND   OBSTRUCTION  OF  THE  INTESTINES.         433 

obstruction.  We  must  also  mention  here  the  very  rare  cases  where  a  large  foreign 
body  has  been  swallowed  and  wedged  itself  into  some  part  of  the  intestine,  öuch 
a  thing  has  been  seen,  especially  in  children  and  among  the  insane. 

4.  Intestinal  Constriction. — Although  the  mechanism  of  intestinal  constriction 
in  external  herniae  lies  in  the  domain  of  surgery,  we  must  mention  here  the  chief 
causes  of  the  so-called  internal  intestinal  constriction,  internal  incarceration,  or 
strangulation.  In  the  abdominal  cavity  itself  pouches  and  diverticula  are  found, 
either  as  normal  or  abnormal  formations,  in  which  single  loops  of  intestine  may 
be  caught  and  constricted.  The  duodeno-jejunal  hernia — the  so-called  Treitz's 
retro-peritoneal  hernia — is  worthy  of  special  mention,  and  comes  from  the  entrance 
of  a  loop  of  intestine  into  the  duodeno-jejunal  fossa.  This  hernia  may  become 
very  large.  It  is  sometimes  found  by  accident  in  the  cadaver,  not  having  caused 
any  symptoms  during  life,  but  in  rare  cases  it  may  be  the  cause  of  acute  internal 
constriction.  We  must  also  mention  the  hernia  of  the  omental  bursa — where  a 
loop  of  intestine  passes  through  the  foramen  of  Winslow — the  intersigmoid 
hernia,  the  subcaecal  hernia,  etc.  Diaphragmatic  hernia  is  of  greater  practical 
significance  because  it  is  somewhat  commoner.  By  this  name  we  designate  both 
genuine  protrusions  into  the  diaphragm,  and  also  the  passage  of  abdominal  viscera 
through  congenital  or  acquired  (traumatic)  defects  in  the  diaphragm.  These  her- 
nias may  exist  without  symptoms,  or  at  least  without  causing  any  signs  of  severe 
disease,  but  in  some  cases  they  cause  obstruction  by  constricting  or  twisting  a  dis- 
located loop  of  intestine. 

Those  cases  in  which  abnormal  slits  and  holes  in  the  omentum  or  mesentery 
give  rise  to  internal  constriction  are  to  be  added  to  the  list  of  the  internal  herniae. 

Finally,  abnormal  fibers,  membranes,  and  false  ligaments  in  the  abdominal 
cavity  are  a  comparatively  frequent  cause  of  internal  constriction.  Such  cords 
and  bands  are  sometimes  left  as  the  results  of  a  former  peritonitis,  and  may  cause 
actual  constriction  or  bending  of  single  loops  of  intestine.  One  such  false  liga- 
ment, which  must  be  specially  mentioned,  and  wThich  may  cause  intestinal  con- 
striction, is  found  as  a  prolongation  of  Meckel's  diverticulum.  By  this  we  mean 
that  diverticulum  which  must  be  regarded  as  the  remains  of  the  omphalomes- 
enteric duct,  still  persisting,  which  has  its  seat,  corresponding  to  the  duct,  from 
half  a  metre  to  a  metre  above  the  ileo-caecal  valve.  A  firm  cord  sometimes  arises 
from  the  free  end  of  this  diverticulum,  the  obliterated  omphalo-mesenteric  vein, 
which  adheres  to  some  part  of  the  internal  abdominal  wall  and  may  cause  con- 
striction of  the  intestine.  Adhesion  of  the  free  end  of  the  vermiform  appendix 
has  been  the  cause  of  internal  constriction  in  some  cases. 

5.  Twists  (volvulus)  and  Knots  of  the  Intestine. — Twists  about  the  mesenteric 
axis,  and  complete  constriction  of  a  portion  of  intestine  from  this  cause,  are  seen 
most  frequently  in  the  sigmoid  flexure,  especially  if  the  mesentery  of  the  flexure 
is  unusually  narrow  congenitally.  The  spontaneous  correction  of  this  abnormal 
condition  is  hindered  by  the  weight  of  the  loops  of  intestine  filled  with  gas  and 
masses  of  faeces,  and  by  other  portions  of  intestine  lying  on  the  place  of  twist- 
ing. Sometimes  other  portions  of  intestine  wind  themselves  several  times  about 
the  pedicle  of  the  twisted  loop  so  as  to  form  a  regular  knot.  Such  twistings  have 
been  seen  especially  between  the  sigmoid  flexure  and  a  portion  of  the  ileum.  Ex- 
ternal injury  sometimes  gives  rise  to  the  formation  of  a  knot.  In  some  cases  abnor- 
mally great  peristalsis,  severe  diarrhoea,  precedes  the  appearance  of  obstruction. 
We  have  ourselves  seen  a  case  of  volvulus  in  the  upper  part  of  the  small  intes- 
tines, äs  a  result  of  very  severe  vomiting  caused  by  a  remedy  for  tape  worm  given 
by  a  quack ! 

6.  Invagination  of  the  Intestine  (Intussusception). — If  a  portion  of  intestine 
is  pushed  into  the  lumen  of  the  portion  that  lies  next  below,  w7e  term  the  process 

28 


434  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

invagination.  The  cause  of  this  is  probably  to  be  looked  for  in  a  diminution  or  a 
complete  absence  of  peristalsis  in  a  circumscribed  portion  of  intestine.  If  now  there 
are  energetic  movements  in  the  portion  immediately  above,  they  push  this  into  the 
paralyzed  portion.  In  other  cases  we  may,  perhaps,  suspect  a  spasmodic  state  of 
the  muscular  coat.  We  find  invagination  of  the  ileum  most  frequently  in  the 
bodies  of  atrophic  children.  In  such  cases  it  is  an  ante-mortem  symptom,  due  to  the 
different  periods  of  cessation  of  peristalsis  in  the  different  parts  of  the  intestines. 

Besides  this  invagination,  which  has  only  an  anatomical  interest,  sudden  intus- 
susceptions are  seen,  especially  often  in  children  up  to  ten  years  of  age,  for  which 
we  can  usually  discover  no  certain  cause,  and  which  in  a  short  time  lead  to  the 
severest  symptoms  of  intestinal  stenosis.  Such  intussusceptions,  which  often 
involve  quite  long  portions  of  the  intestine,  may  have  their  seat  in  almost  any  part 
of  the  intestine.  The  invagination  of  the  caecum  and  a  portion  of  the  lower  part 
of  the  ileum  into  the  colon  (ileo-caecal  invagination)  is  relatively  the  most  fre- 
quent. These  intussusceptions  may  sometimes  reach  such  an  extent  in  children 
that  the  invaginated  portion  of  the  ileum  may  finally  reach  the  rectum,  and  some- 
times even  project  externally.  Inflammation  and  adhesions  usually  appear  in  the 
part  invaginated.  Gangrene  of  the  internal  portion,  from  the  constriction  of  the 
afferent  vessels,  is  also  common.  The  necrotic  portion  may  be  cast  off  and  passed 
with  the  dejections,  a  process  which,  in  some  cases,  has  led  to  a  spontaneous  heal- 
ing of  the  intussusception  and  to  a  cure  of  the  intestinal  obstruction  caused  by  it. 

We  must  mention  intestinal  polypi  as  a  special  cause  of  intussusception,  as  they 
gradually  pull  that  portion  of  the  intestine  in  which  they  are  situated  into  the  neigh- 
boring portion  next  below  by  their  weight.     This  has  been  repeatedly  observed. 

7.  Compression  of  the  Intestine  from  without,  by  tumors  of  the  uterus,  ovarian 
cysts,  pelvic  abscesses,  omental  tumors,  etc.,  has  been  met  with  in  rare  cases  as  a 
cause  of  intestinal  stenosis.  The  symptoms  of  stricture  in  such  cases  develop 
either  very  gradually  or  sometimes  rather  suddenly. 

We  must  now  mention  certain  pathological  changes  which  may  follow  every 
obstruction,  from  whatever  causes  it  may  arise. 

The  further  changes  in  the  intestine  deserve  the  chief  attention.  Above  the  con- 
stricted point  it  is  usually  greatly  swollen  from  gas  and  the  accumulation  of  fasces. 
The  whole  intestinal  wall  is  found  in  an  inflamed  condition,  which  is  due  in  part 
to  mechanical  action,  and  in  part  to  the  inflammatory  germs  which  are  abun- 
dantly developed  in  the  abnormally  situated  intestinal  contents.  A  severe  diphthe- 
ritic process  often  develops  in  the  intestine,  with  ulceration,  above  the  stenosis.  In 
the  inflamed,  softened  intestinal  wall,  thin  from  its  abnormal  distention,  a  little 
tear  easily  occurs  in  some  spot,  or  more  rarely  a  genuine  perforation  following  an 
ulcer.  Some  of  the  putrefying  contents  of  the  intestine  thus  enter  the  abdominal 
cavity,  and  an  intense  purulent  or  ichorous  peritonitis  is  unavoidable.  This 
is  why  acute  peritonitis  is  so  frequent  a  lesion  in  persons  who  die  of  intestinal 
obstruction.  If  the  intestinal  stenosis  has  lasted  a  long  time,  we  usually  find  in  the 
upper  portion  of  the  intestine,  besides  the  signs  of  inflammation,  a  manifest  hyper- 
trophy of  the  muscular  coat,  the  result  of  the  abnormally  active  peristalsis  by  which 
the  muscle  has  tried  to  overcome  the  obstacle.  The  intestine  below  the  constric- 
tion, in  contrast  to  the  part  just  described,  appears  narrow,  contracted,  and  empty. 

The  changes  in  the  other  organs  correspond  to  the  general  inanition.  The 
frequent  development  of  inhalation-pneumonia  is  easily  explained,  if  severe 
vomiting  has  preceded  (vide  infra). 

Clinical  History. — In  regard  to  the  clinical  symptoms  we  must  distinguish  the 
cases  with  a  rapid,  complete  obstruction  of  the  intestine  from  those  in  which  the 
condition  develops  gradually,  and  where  there  is,  therefore,  merely  a  constriction 
of  the  intestine,  at  least  for  a  time. 


STRICTURE  AND  OBSTRUCTION  OF  THE  INTESTINES.         435 

The  first  symptom  of  the  partial  intestinal  constrictions,  which  arise  from  cica- 
tricial strictures  and  new  growths,  from  partial  blocking  up  of  the  lumen,  from  intus- 
susceptions, etc.,  is  usually  a  disturbance  in  defecation.  The  bowels  are  costive;, 
they  move  only  at  long  intervals,  and  their  motion  is  often  associated  with  pain  and 
tenesmus.  In  the  description  of  cancer  of  the  intestines  we  have  already  mentioned 
that  the  faeces  passed  sometimes  have  a  peculiar,  flat,  compressed,  or  scybalous 
form.  Blood  and  mucus  are  often  mixed  with  the  dejections  and  are  due  to  the 
character  of  the  primary  disease.  In  some  cases  there  is  no  constipation,  and 
there  may  be  even  constant  diarrhoea.  We  can  easily  understand  from  the  physi- 
ological conditions  that  in  stenosis  of  the  small  intestines,  whose  contents  have  an 
approximately  fluid  consistency,  disturbances  of  defecation  are  less  apt  to  take 
place  than  in  stenosis  of  the  large  intestine,  where  the  faecal  masses  have  already 
assumed  a  more  firm  consistency. 

Physical  examination  of  the  abdomen  often  gives  important  and  valuable 
information.  The  abdomen  is  usually  swollen  by  meteorism,  which  arises  from 
the  accumulation  of  gas  above  the  constricted  portion.  The  intensity  of  the 
meteorism  varies  very  much  in  different  cases  and  at  different  times  in  the  same 
patient.  Meteorism  is  sometimes  absent,  especially  in  stenosis  at  the  beginning  of 
the  intestine.  There  may  then  be  gasti'ectasis.  The  marked  peristaltic  movements, 
plainly  visible  through  the  abdominal  walls,  are  very  characteristic  of  most  intes- 
tinal constrictions.  The  contour  of  single  loops  of  intestine  is  often  marked,  at 
times  quite  sharply,  and  then  we  can  sometimes  feel  the  thickened  intestinal  walls 
through  the  lax  abdominal  wall.  We  may  often  decide  upon  the  seat  of  the  ste- 
nosis from  the  location  and  course  of  the  visible  peristaltic  movements.  In  gen- 
eral, it  is  true  that  peristalsis  is  much  more  noticeable  when  the  stenosis  is  in  the 
small  intestine  than  when  it  is  in  the  colon.  We  must  finally  state  that  we  have 
been  repeatedly  struck  by  the  great  extent  and  strength  with  which  we  could  feel 
the  pulsation  of  the  aorta  through  the  swollen  loops  of  intestine.  If  we  put  our 
ear  to  the  anterior  abdominal  wall  we  can  often  hear  many  gurgling  and  splashing 
noises,  which  sometimes  have  a  distinct  metallic  quality.  Eructations  are  fre- 
quent, and  in  some  cases  there  is  occasional  vomiting. 

The  duration  of  all  these  symptoms  differs  with  the  form  of  the  primary  dis- 
ease. Either  gradually  or  sometimes  quite  suddenly  the  symptoms  of  intestinal 
constriction  pass  into  those  of  obstruction.  Then  the  same  type  of  disease  develops 
as  is  seen  in  all  acute  internal  strangulations. 

The  symptoms  of  intestinal  obstruction  form  one  of  the  severest  and  most 
frightful  conditions  known  to  pathology.  The  patient's  general  condition  in  a 
short  time  undergoes  a  threatening  change  for  the  worse.  The  signs  of  collapse 
rapidly  develop;  the  face  sinks  in  and  assumes  a  wasted  and  sharp  expression, 
the  extremities  become  cool  and  livid,  the  pulse  is  frequent  and  can  scarcely 
be  felt,  the  voice  is  weak  and  obscure.  The  temperature  usually  falls,  but  it 
occasionally  rises.  The  abdomen  is  much  swollen  from  meteorism,  and  is  usually 
very  tender  on  pressure  from  beginning  peritonitis.  The  passage  of  faeces  and 
the  escape  of  flatus  cease  entirely.  We  often  see  the  peristaltic  motions  of  the 
intestines  above  the  obstruction  through  the  abdominal  walls,  but  in  some  cases 
the  muscular  coat  is  so  paretic  that  it  is  no  longer  capable  of  marked  peristalsis. 

The  most  characteristic  symptom  of  intestinal  obstruction  is  the  vomiting  of 
feculent-smelling  masses,  the  so-called  stercoraceous  vomiting  {ileus,  miserere). 
There  is  often  frequent  eructation  at  the  beginning  of  the  attack,  which  alter- 
nates with  real  vomiting.  The  vomitus  at  first  is  of  the  usual  character,  but  it 
soon  acquires  a  manifestly  putrid,  faecal  odor.  The  old  opinion  is  false  that  in 
this  vomiting  real  faecal  masses  were  forced  backward  from  the  large  intestine 
into  the  stomach   by  an  antiperistaltic  action  of  the  intestine.      Stercoraceous 


436  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

vomiting'  occurs,  not  only  when  the  obstruction  is  in  the  large  intestine,  but  also 
in  obstruction  of  the  small  intestines.  In  this  case  we  have  to  do  with  a  putrid 
decomposition  of  the  contents  of  the  intestine  stagnating  above  the  obstruction. 
Part  of  this  putrid  mass  reaches  the  stomach  during  vomiting,  since  the  pylorus 
gradually  yields  to  the  increasing  swelling  of  the  small  intestines.  The  vomit- 
ing itself  is  probably  caused  in  large  part  by  the  pulling  on  the  peritoneum,  and 
perhaps  by  the  irritation  of  the  abnormal  matter  which  has  entered  the  stomach. 

We  must  mention,  finally,  certain  facts  observed  in  the  different  forms  of  in- 
testinal stenosis,  which  are  of  theoretical  interest  and  also  of  diagnostic  impor- 
tance. In  the  contents  of  the  intestine  stagnating  above  the  stenosis,  large  amounts 
of  indol  and  phenol  are  formed,  chiefly  from  the  decomposition  of  the  albumi- 
nous substances,  and  also  from  the  other  products  of  putrefaction.  These  are  in 
part  absorbed  and  exci*eted  with  the  urine.  Hence,  in  stenosis  of  the  small  in- 
testines we  often  find  that  the  urine  contains  an  increased  amount  of  indican* 
(Jaffe)  and  phenol  (Brieger),  but  in  stenosis  of  the  large  intestine  the  amount  of 
indican  in  the  urine  is  not  increased,  because  the  albuminous  substances  capable  of 
decomposition  are  no  longer  present  in  the  contents  of  the  large  intestine  to  cause  it. 

The  course  of  intestinal  obstruction  differs  according  to  the  anatomical  causes 
which  exist  in  different  cases.  In  many  cases  of  acute  internal  strangulation  the 
severe  type  of  general  disease  above  described  develops  in  a  very  short  time,  and 
may  lead  to  death  in  a  day  or  two,  but  usually  the  course  is  somewhat  longer  and 
lasts  a  week.  In  intestinal  obstruction  which  develops  gradually  from  intestinal 
constriction,  the  disease  may  go  on  longer  and  show  many  variations  in  its  inten- 
sity. In  mere  intestinal  constriction  we  can  make  fewer  definite  statements  as  to 
the  duration  and  course  of  the  affection,  since  the  symptoms  of  the  disease  depend 
entirely  upon  the  form  of  the  primary  disorder. 

In  a  great  majority  of  cases  iutestinal  obstruction  terminates  unfavorably. 
Death  results  either  from  increasing  collapse  or  from  secondary  peritonitis  {vide 
supra),  or  in  rare  cases  from  further  complications,  like  pyaemic  conditions  or 
pneumonia.  Recovery  may  occur  even  after  the  severest  symptoms,  but  it  is  very 
rare.  The  obstructions  from  impactions  are  most  hopeful  for  recovery.  Impacted 
gall-stones,  faecal  accumulations,  etc.,  may  be  evacuated,  after  which  the  severe 
symptoms  disappear.  The  possibility  of  recovery  in  intussusception,  by  throwing 
off  the  gangrenous  internal  portion  of  intestine,  has  been  mentioned  above.  We 
can  not  wholly  deny  that  internal  strangulations  are  capable  of  restoration, 
although  the  prognosis  must  almost  always  remain  doubtful  on  account  of  the 
uncertainty  of  the  diagnosis  in  any  individual  case. 

In  the  partial  intestinal  constrictions,  too,  the  nature  of  the  trouble  causes  an  un- 
favorable termination  in  most  cases,  either  from  the  primary  disease  itself  or  from 
the  complete  obstruction  that  finally  follows,  but  the  possibility  of  recovery  can  not 
ba  wholly  excluded  in  certain  conditions,  like  impaction  or  external  compression. 

To  go  into  details  as  to  the  clinical  symptoms  of  the  separate  forms  of  intestinal 
constriction  and  obstruction  would  lead  merely  to  repetitions.  In  most  of  the 
acute  and  many  chronic  cases  the  diagnosis  can  generally  be  made  only  as  to  the 
presence  of  a  mechanical  obstacle  in  the  intestine,  but  the  nature  of  the  obstruc- 
tion can  at  best  be  merely  surmised.  Individual  factors  in  reference  to  this,  and 
in  regard  to  the  question  of  the  seat  of  the  stenosis,  are  contained  in  the  account 
given  above  of  the  aetiology  and  symptomatology. 

*  The  indican  test  is  performed  in  the  following  way  :  We  mix  equal  volumes  of  urine  and  officinal 
hydrochloric  acid  (P.  G.),  and  then  add,  drop  by  drop,  a  concentrated  solution  of  chloride  of  lime, 
shaking  it  after  each  drop.  If  now  chloroform  is  added,  upon  shaking  again,  the  chloroform  will  take 
on  a  striking  blue  color,  if  the  urine  contains  any  considerable  amount  of  indican. 


STRICTURE  AND  OBSTRUCTION  OF  THE  INTESTINES.         4:; 7 

[The  diagnosis  of  the  nature  of  an  intestinal  obstruction  is  so  difficult  in  many 
cases,  and  yet  so  important  with  reference  to  treatment,  that  the  editor  ventures 
to  introduce  tables  of  differential  diagnosis  of  the  more  common  lorms  of  the 
condition.  These  tables  are  based  upon  the  masterly  prize-essay  of  Treves,  of 
London. 

ACUTE  INTESTINAL   OBSTRUCTION. 

Chief  Common  Symptoms.— Sudden  pain,  intermittent  or  constant,  with  exacerbations  ;  tends  to  become 
constant  with  time.  Vomiting,  early,  severe,  becoming  feculent.  Constipation,  more  or  less  abso- 
lute.    Abdominal  distention.     Shock. 


Age  and  Sex  . 
History , 

Onset 

Pain 

Local  Ten- 
derness . , 

Vomiting 

Constipation. 


Prostration 

Tenesmus 

Abdominal 

Wall.... 
Tumor 

Meteorism  . . 


Strangulation  by  Bands  or 
through  Apertures  (25 
per  cent,  of  all  cases  of 
acute  obstruction). 


Young  adults;  rare  after  40. 

Previous  peritonitis  in  68  per 
cent.;  previous  attacks  of 
obstruction  in  12  per  cent. 

Sudden  in  70  per  cent. 

Early,  severe,  continuous, 
with  exacerbations. 

Absent  at  first,  appears  later. 

Early,  marked ;  in  60  per  cent. 

becomes  feculent  ;  affords 

no  relief. 
Continuous  and  absolute;  no 

blood. 

Marked. 

Absent. 

Flaccid  unless  peritonitis. 
Very  rare. 

Slight,  appears  about  third 
day. 


Volvulus  of  Colon. 


Males  as  4  :  1 ;  40  to  60. 
Previous  constipation. 


Sudden. 

Early,  less  severe,  intermit- 
tent at  first,  becoming  con- 
stant with  exacerbations. 

Early  over  distended  coil, 
and  constant. 

Less  early,  severe,  and  con- 
stant ;  often  affords  relief. 

Early  and  absolute ;  no 
blood. 

Rather  less  marked;  maybe 

dyspnoea. 
In  15  per  cent. 

Rigid  from  early  peritonitis. 
Absent. 

Early,  rapid,  increases,  and 
is  extreme. 


Acute  Intussusception. 


More  than  50  per  cent,  under 

10  years. 
Usually  negative. 


Sudden  in  75  per  cent. 

Early  and  severe  ;  increasing 

and  later  subsiding;  at  first 

paroxysmal. 
Common  about  a  tumor. 

Still  less  early  and  severe  ;  in 
25  per  cent,  becomes  fecu- 
lent. 

Absolute  rare  ;  diarrhoea  not 
uncommon  ;  blood  in  80  per 
cent. 

Marked. 

In  55  per  cent.,  and  often  early. 

Flaccid  unless  peritonitis. 

In  50  per  cent. ;  invagination 
sometimes  felt  in  rectum. 

Rare,  unless  marked  consti- 
pation. 


N.  B.— No  trustworthy  conclusions  can  be  drawn  from  the  seat  of  the  pain  as  to  the  seat  of  the  obstruc- 
tion unless  local  peritonitis  comes  on.  The  pain  is  usually  referred  in  all  forms  to  the  region  of  the  navel. 
In  complete  obstruction  the  pain  is  constant,  though  with  exacerbations  ;  intermittent  pain  shows  that 
the  obstruction  is  partial.    Coils  of  intestine  are  not  visible  through  the  abdominal  wall  in  acute  cases. 

CHRONIC  INTESTINAL  OBSTRUCTION. 


Stricture  of  the  Small  Gut. 

Stricture  of  the  Large  Gut. 

F.ECAL  Accumulation. 

Age  and  Sex  . 

Adults. 

Adults. 

Adults  ;  more  common  in  fe- 
males; the  hysterical,  luna- 
tics, hypochondriacs. 

Cancer,   trauma,   tuberculo- 

Cancer,  trauma,   tuberculo- 

Previous constipation. 

sis;  disordered,  imperfect, 

sis,  dysentery;  disordered, 

irregular  action  of  bowels 

imperfect,  irregular  action 

from    time    to  time,  with 

of    bowels    from    time   to 

intervals   of    comparative 

time,    with     intervals     of 

ease. 

comparative  ease. 

Gradual. 

Gradual. 

Gradual. 

Intermittent. 

Intermittent. 

Less  prominent. 

Vomiting 

Late,  scanty,  feculent  only  to- 

Less prominent,  rarely  fecu- 

Late, scanty,  rarely  feculent, 

ward  end  of  acute  attack ; 

lent  or  provoked  by  food. 

often  absent. 

may  be  provoked  by  food. 

Constipation. 

May    alternate    with     diar- 

Form of  faeces  may  be  al- 

Gradually increasing:;  may  be 

rhoea;  blood  points  to  can- 

tered; blood  points  to  can- 

spurious diarrhoea ;  no  blood. 

cer. 

cer. 

Tenesmus 

Absent. 

Often  present. 

Absent. 

Meteorism  . . . 

Not  marked,  unless  acute  at- 

Often marked. 

Late:  generally  increases  with 

tack. 

obstruction. 

Tumor 

Only  in  cancer,  and  then  in 

Only  in  cancer,  and  then  in 

Common  and  distinctive:  most 

30  per  cent. 

40  per  cent. ;  may  be  felt 

easily  felt  in  cjecum  ;  little 

in  rectum. 

or  no  tenderness  :  some- 
times movable,  and  can  be 

Coils  of  In- 

changed in  shape. 

testine  . . . 

Marked     in    proportion    to 

Marked     in     proportion    to 

Rarely  seen. 

emaciation. 

emaciation. 

N.  B.— In  any  form  of  chronic  obstruction,  the  symptoms  of  acute  occlusion  may  suddenly  supervene.] 


43S  DISEASES   OF  THE  DIGESTIVE  ORGANS. 

We  would  here  make  special  brief  mention  of  only  one  frequent  form  of  in- 
testinal obstruction,  on  account  of  its  practical  importance.  We  mean  that  form 
which  is  caused  by  the  accumulation  of  large  masses  of  old  fasces  in  the  rectum. 
We  sometimes  find  monstrous  accumulations  of  faeces  in  the  rectum,  especially 
in  old  women  who  have  previously  suffered  from  habitual  constipation,  or  in 
whom  constipation  is  due  to  some  other  affection.  Severe  symptoms  usually 
come  on  quite  suddenly,  after  long-continued  mild  prodromal  symptoms,  and 
these  severe  symptoms  are  much  like  the  picture  of  internal  strangulation — severe, 
sometimes  colicky,  abdominal  pain,  great  tenderness  of  the  abdomen,  which  is  usu- 
ally swollen,  marked  general  collapse,  loss  of  strength,  a  small  pulse,  an  outbreak 
of  cold  sweat,  vomiting,  etc.  If  we  try  to  give  an  enema  in  such  cases,  very  little 
fluid  runs  into  the  rectum.  On  introducing  the. finger,  it  usually  strikes  solidly  on 
old,  hard,  faecal  masses  above  the  sphincter,  and  there  is  often  nothing  left  but  to 
uudertake  the  dirty  task  of  removing  at  least  a  part  of  the  scybala  with  our  own 
hands.  We  may  then  succeed,  by  repeated  enemata  and  by  giving  cathartics 
internally,  in  removing  sometimes  quite  an  incredible  amount  of  accumulated 
faeces,  and  in  obtaining  thus  a  rapid  recovery  from  the  condition. 

Treatment. — As  soon  as  the  dangerous  signs  of  intestinal  obstruction  are 
recognized  by  the  physician,  he  must  decide  in  the  first  place  whether  the  stenosis 
is  not  accessible  to  direct  treatment.  Hence  we  first  examine  in  the  most  careful 
manner  the  external  points  for  hernia,  that  we  may  not  overlook  a  strangulated 
hernia.  Then  we  make  a  digital  examination  of  the  rectum  in  order  to  decide 
whether  the  stenosis  may  not  have  its  seat  here,  as  from  coprostasis,  rectal  tumors, 
or  perceptible  intussusception.  Besides  that,  we  of  course  examine  the  res^t.  of  the 
abdomen,  as  far  as  the  patient's  condition  permits,  in  order  by  this,  and  by  any 
facts  in  the  history,  to  decide  as  to  the  form  of  the  stenosis,  from  obliteration  or 
compression. 

Definite  therapeutic  measures  sometimes  follow  from  the  conditions  thus  indi- 
cated. Strangulated  external  hernias  require  operative  treatment  as  taught  by  sur- 
gery. We  may  obtain  aid,  in  some  cases  of  stenosis  from  impaction,  by  the  prudent 
use  of  cathartics.  The  treatment  of  faecal  impaction  is  of  special  importance.  We 
have  described  the  most  frequent  form  of  this  in  detail  above.  As  has  already 
been  said,  it  is  usually  necessary  to  remove  at  least  a  part  of  the  faeces  with  the 
fingers,  or  some  instrument  like  dressing-forceps  or  a  spoon.  In  the  second 
place,  we  may  use  large  enemata  of  pure  water  or  soap-suds,  which  must  often  be 
repeated  four  or  five  times  a  day,  until  they  have  a  satisfactory  result.  These 
are  best  given  by  a  funnel  and  an  oesophageal  tube  ("  intestinal  tube  ")  introduced 
as  high  as  possible  into  the  intestine.  Cathartics  administered  internally  serve  as 
aids,  especially  castor-oil  and  rhubarb. 

In  stenosis  of  the  rectum  from  cicatrices  and  new  growths  we  can  also  some- 
times employ  a  local  surgical  treatment,  like  dilatation  or  scraping.  The  treat- 
ment of  faecal  accumulations  usually  plays  an  important  part  here.  Finally,  the 
cases  of  ileo-caecal  invagination,  in  which  the  lower  end  of  the  invaginated  ileum 
reaches  the  rectum,  may  yield  to  local  treatment.  We  may  try  a  partial  replace- 
ment by  a  "  sponge-sound  "  (an  elastic  oesophageal  tube  to  the  end  of  which  a 
sponge  is  fastened).  Blowing  in  air  by  the  bellows  was  also  recommended  for 
this  purpose  by  the  old  physicians.  As  a  rule,  however,  we  use  here  large 
enemata  of  warm  water,  which  sometimes  seem  to  exert  a  favorable  mechanical 
action. 

Very  often  we  can  not  decide  with  certainty  as  to  the  anatomical  cause  and  the 
seat  of  the  obstruction  at  the  bedside.  In  these  cases  nothing  but  a  symptomatic 
treatment  is  left  for  the  physician  to  employ.  With  constipation  we  usually  try 
first  cathartics,  first  the  weaker,  then  the  stronger,  and  finally,  as  a  "  last  resort," 


STRICTURE  AND   OBSTRUCTION  OF  THE  INTESTINES.         439 

reguline  quicksilver,  pure  mercury  in  doses  of  five  to  ten  ounces  (grm.  150-300;, 
which  is  sometimes  claimed  to  act  mechanically  in  u  doubtful  cases  "  by  its  weight. 
Except  among  some  defenders  of  mercury,  the  present  opinion  among  physicians 
tends  far  more  to  the  belief  that  cathartics  are  usually  of  no  service,  but  are  often 
directly  injurious  by  increasing  the  resistance.  Hence  we  have  at  present  gone 
over  to  the  treatment  of  severe  internal  incarcerations  with  large  doses  of  opium. 
Opium  acts  favorably  on  the  patient's  pain,  the  vomiting  is  diminished,  and,  by 
quieting  the  peristalsis,  the  danger  of  inci'easing  the  stenosis  and  tearing  the  intes- 
tine is  also  lessened.  In  fact,  the  opium  treatment  has  some  favorable  results  on 
record.    Sometimes  the  first  dejection  appears  during  the  administration  of  opium. 

Since,  therefore,  there  are  many  objections  against  the  internal  use  of  cathar- 
tics, we  may  try  large  enemata  in  those  cases  where  the  seat  of  the  stenosis  is  not 
known  to  be  in  the  large  intestine.  They  must  be  given  with  caution,  but  persist- 
ently, and  they  must  often  be  repeated ;  then  they  sometimes  give  good  results, 
even  in  severe  cases.  In  numerous  instances  of  faecal  vomiting  great  benefit  is 
also  derived  from  methodical  washing  of  the  stomach  as  recommended  by  Kuss- 
maul, Cohn,  and  others.  Large  amounts  of  feculent  liquid  are  frequently  re- 
moved through  the  tube  from  the  stomach ;  and  indeed  it  is  easy  to  see  that  free- 
ing the  stomach  of  its  accumulations  may  favor  a  more  vigorous  peristalsis.  Even 
when  the  nature  of  the  intestinal  obstruction  precludes  definitive  recovery, 
lavage  usually  gives  no  inconsiderable  relief. 

We  need  not  enter  into  details  as  to  the  general  treatment.  It  goes  without 
saying  that  the  patient's  strength  must  be  kept  up  as  much  as  possible,  and  that 
in  severe  states  of  collapse  all  possible  stimulants  must  be  used,  like  hot,  strong 
coffee,  camphor,  and  ether.  Local  applications  to  the  abdomen  are  usually  ill 
borne  on  account  of  the  tenderness,  still  we  may  try  ice  poultices  or  wet  com- 
presses. Opium  is  the  best  remedy  for  pain  and  vomiting,  but  it  must  often  be 
replaced  by  subcutaneous  injections  of  morphine.  In  cases  of  extreme  gaseous 
distention  the  intestinal  coils  may  be  punctured  with  the  needle  of  a  subcutane- 
ous syringe  and  the  gas  in  part  evacuated.  This  sometimes  proves  very  bene- 
ficial. 

Finally,  it  must  be  noted  that  in  severe  cases  we  are  justified  in  proposing 
laparotomy.  Sometimes  the  existing  obstruction  may  be  thus  detected  and  re- 
moved.    (For  particulars,  see  text-books  on  surgery.) 

[The  safety  with  which  laparotomy  is  now  performed  has  stimulated  the  study 
of  all  affections  on  which  the  operation  has  any  bearing.  Internal  strangula- 
tions and  invaginations  may  be  relieved,  and  the  portion  of  intestine  containing 
a  non-cancerous  stricture  can  be  excised.  An  early  operation  offers  much  better 
chances,  of  course.  In  these  days  persons  should  not  be  allowed  to  die  directly 
from  intestinal  occlusion  without  an  attempt  being  made  to  restore  the  permea- 
bility of  the  canal  by  surgical  means.] 


440 


DISEASES  OF  THE  DIGESTIVE  ORGANS. 


CHAPTER  XII. 

INTESTINAL  PARASITES. 

{Helminthiasis. ) 

1.  Tape-worms. 

Natural  History  of  the  Tape-worm.— Three  of  the  tape-worms  (cestodes)  which 
are  found  in  the  intestines  have  a  clinical  significance:  the  tcenia  solium,  the 
taenia  mediocanellata,  and  the  bothriocephalus  latus. 

1.  The  tamia  solium  is,  when  fully  developed,  two  or  three  metres  long.  Its 
head  (Figs.  37  and  38)  is  about  the  size  of  that  of  a  pin,  and  has  four  projecting 
cup-like  suckers,  and  in  front  a  beak  with  about  twenty-six  hooks.  The  top  of  the 
head  is,  as  a   rule,  plainly  pigmented.      A  small  neck,  about  an  inch  long,  is 


Fis.  37.— (From  Heller  ) 
Head  of  taenia  solium. 


Fig 


38.— (From  Heller.)    Head  of  Cysticercus  of 
the  brain. 


attached  to  the  head,  and  then  follow  the  single  "  joints  "  (proglottides)  of  the 
tape-worm,  of  which  the  youngest,  lying  near  the  head,  are  still  very  small  and 
short.  They  gradually  increase  in  length  and  breadth,  and  at  about  a  metre  from 
the  head  they  have  an  approximately  quadrilateral  shape. 
The  segments  which  lie  farther  down,  and  which  have  already 
reached  puberty,  have  the  form  of  pumpkin  seeds,  and  are 
nine  or  ten  millimetres  long  and  six  or  seven  wide.  The 
matrix  or  uterus  runs  through  the  middle  of  each  mature 
segment  (see  Fig.  39),  and  from  it,  on  each  side,  go  seven  or 
eight  side  branches,  which  ramify  like  a  tree.  On  one  side, 
a  little  below  the  middle,  lies  the  sexual  orifice  (Fig.  39,  a). 
The  male  sexual  organs  consist  of  a  number  of  little  clear 
vesicles  in  the  anterior  portion  of  the  segments.  The  thick- 
shelled  eggs  (Fig.  40,  3)  develop  in  the  uterus,  and  contain  an 
embryo  with  six  hooklets. 

The  taenia  solium  inhabits  the  small  intestines  of  man. 
Its  head  clings  to  the  mucous  membi^ane  so  tightly,  usually 
at  some  point  in  the  upper  third  of  the  small  intestine,  that 
the  neck  is  often  torn  off  in  trying  to  loosen  the  worm  from  the  intestinal  wall. 
The  rest  of  the  worm,  which  is  in  part  in  many  coils,  extends  to  the  lower  part  of 
the  ileum,  but  only  exceptionally  into  the  caecum.  From  the  lower  end  long 
chains,  or  single  mature  segments,  are  often  detached,  mix  with  the  contents  of  the 


Fig.  39. — (From  Heller.) 
Taenia  solium.  Ma- 
ture segment. 


INTESTINAL  PARASITES. 


441 


intestine,  and  are  passed  with  the  faeces,  together  with  some  of  the  eggs  from  the 
uterus. 

The  further  development  of  the  eggs  of  the  taenia  solium  takes  place  in  another 
"  host,"  almost  always  in  the  hog.  Hogs  are  infected  by  eating  faeces,  offal, 
etc.,  containing  taenia  eggs.  The  thick  shell  of  the  eggs  is  dissolved  in  the  hog's 
stomach,  and  the  free  embryos  pierce  the  walls  of  the  stomach  and  intestines  and 
travel  with  the  blood-current,  or  through  the  tissues,  into  the  different  organs, 
especially  into  the  muscles.  Here  they  develop,  in  two  or  three  months,  into 
cysts  something  larger  than  a  pea,  from  whose  walls  a  newly  developed  taenia- 
head  arises,  a  so-called  scolex  (nurse).  These  cysts  are  termed  worm-cysts, 
measles,  or  cysticerci  cellulosce.  They  live  from  three  to  six  years ;  then  they  die 
and  become  calcified.  If  a  Cysticercus  gets  into  a  man's  stomach  from  his  eating 
raw  or  imperfectly  cooked  ham  or  pork,  a  new  and  complete  taenia  sprouts  from 
the  scolex,  which  forms  mature  segments  in  three  or  four  months. 

We  usually  find  only  one  tape- worm  in  a  man,  but  several  specimens  have  been 
seen  at  the  same  time  in  the  same  intestine.  The  length  of  a  tape-worm's  life  is 
not  certainly  known,  but  it  has  happened  that  some  persons  have  lodged  the  same 
tape- worm  for  ten  or  fifteen  years. 

Although  the  fully  developed  taenia  solium  is  seen  only  in  man,  as  we  have 
said,  the  Cysticercus  cellulosae  has  been  found,  in  rare  cases,  in  dogs,  rats,  and  mon- 
keys, as  well  as  in  hogs.     It  is  a  particularly  important  fact  that  the  Cysticercus 


Fig.  40. — Comparative  view  of  the  eggs  of  some  of  the  commoner  intestinal  parasites.  1.  Eg?  of  dis- 
toma  hepaticum.  2  Distomum  lanceolatum.  3.  Taenia  solium.  4.  Taenia  mediocanellata.  5. 
Bothriocephalus  latus.  C.  Oxyuris  vermicularis.  7.  Trichocephalus  dispar.  8.  Ascaris  lumbri- 
coides. 


cellulosae  itself  may  also  occur,  as  such,  in  man.  If  tape-worms  or  mature  seg- 
ments get  into  a  man's  stomach  in  any  way,  probably  by  auto-infection,  by  the 
finger,  etc.,  the  embryos  travel  into  other  organs.  Cysticerci  are  often  found  in 
men,  singly  or  in  groups,  especially  in  the  skin,  the  brain,  the  eye,  and  the  mus- 
cles. There  is  a  special  form  of  Cysticercus  of  the  brain,  in  which  we  find  a  whole 
chain  of  cysts,  like  a  cluster  of  grapes,  but  sterile,  the  so-called  Cysticercus  race- 
mosus. 

2.  The  tcenia  mediocanellata,  or  taenia  saginata  (from  saginare,  to  fatten),  is 
even  more  common  than  the  taenia  solium  in  many  parts  of  Germany.  It  is  longer 
than  the  taenia  solium,  being  about  three  or  four  metres  long,  and  its  individual 


442 


DISEASES  OF  THE  DIGESTIVE  ORGANS. 


Fig.  41.— (From  Heller). 
Head  of  teenia  medio- 
canellata. 


Fig.  42.- (From  Heller.) 
Tsenia  mediocanellata. 
Mature  segment. 


joints  are,  on  the  whole,  broader  and  thicker.  The  head  (Fig.  41)  has  also  four 
prominent  cup-like  suckers,  but  it  has  no  crown  of  hooklels.  The  mature  seg- 
ments differ  from  the  proglottides  of  taenia  solium,  in  that 
the  central  uterus  sends  off  many  more  (twenty  to  thirty) 
side  branches,  which  divide  dichotomously,  and  not  like  a 
tree.  The  sexual  opening  is  also  on 
the  side  (Fig.  42,  a). 

The  life-history  of  the  taenia  medio- 
canellata is,  on  the  whole,  like  that 
of  the  taenia  solium.  The  taenia  medio- 
canellata, however,  throws  off  single 
mature  segments  much  more  frequent- 
ly than  the  taenia  solium.  These  seg- 
ments are  found  in  the  faeces,  and  here 
they  often  exhibit  a  crawling  motion. 
The  Cysticercus  of  taenia  mediocanella- 
ta does  not  inhabit  pork,  but  beef,  so 
that  the  infection  of  man  by  this  tape- 
worm comes  from  eating  raw  beef.  In 
man  the  Cysticercus  of  taenia  medio- 
canellata, which  is  somewhat  smaller  than  the  Cysticercus  cellulosae,  has  never 
yet  been  observed. 

3.  The  bothriocephalus  latus  occurs  in  Holland,  Switzerland  (Geneva),  Pome- 
rania,  East  Prussia,  Hamburg,  and  Russia  (the  German  Baltic  provinces).  It  has 
not  yet  been  observed  in  middle  Germany.  It  is  the  largest  tape-worm ;  it  may  be 
six  or  eight  metres  long,  and  sometimes  has  over  four  thousand  joints.  The  head 
of  the  bothriocephalus  (Fig.  43)  consists  of  a  little  club-shaped  swelling,  with  two 
u  slit-like  depressed  suckers  on  the  sides.     A  long,  thread-like  neck 

joins  the  head  to  the  youngest  segments.  The  full-grown  segments 
(Fig.  44)  are  short,  but  are  distinguished  by  their  great  breadth.  The 
largest  segments  measure  in  length  about  three  or  four  millimetres, 
and  in  breadth  ten  or  twelve,  but  the  last  joints  are  longer  and  are 
not  so  broad,  so  that  they  have  an  approximately  quadrilateral  form. 
The  uterus  consists  of  a  very  tortuous  canal  in 
the  center.  The  sexual  orifice  does  not  lie  on 
one  side,  as  in  the  taenia,  but  in  the  middle  of 
the  abdominal  surface,  nearer  the  anterior  bor- 
der of  the  segment  than  the  posterior.  The 
eggs  (vide  supra,  Fig.  40,  5)  are  of  an  oval 
form,  and  have  a  hood-shaped  lid  at  one  end. 
They  are  to  be  found  in  almost  every  dejection 
of  persons  affected  with  a  bothriocephalus. 
Single  joints  of  the  tape- worm  are  not  passed 
with  the  stools,  but  portions  of  the  worm,  several  feet  long,  come  away  from  time 
to  time,  especially  in  the  spring  and  autumn. 

The  noteworthy  life- history  of  the  bothriocephalus  has  been  made  perfectly  clear 
by  Braun,  of  Dorpat.  The  eggs  develop  only  in  fresh  water.  The  embryo  (Fig. 
45),  which  is  formed  in  them  in  a  few  months,  and  is  provided  with  six  hooklets 
and  with  vibrating  cilia,  is  swallowed  by  fishes,  especially  by  pike  and  eel-pouts, 
and  develops  in  their  muscles  and  internal  organs  into  cysticerci.  The  infec- 
tion of  man  with  bothriocephalus  comes  from  eating  such  fish  containing  cysti- 
cerci. 

Symptoms  and  Diagnosis.— In  many  cases  tape- worms  are  lodged  in  the  intes- 


Figs.  43  and  44.— (From  Heller.) 
Fig.   43.—  Head  of    bothriocephalus  latus. 

a,  Lateral  view,  enlarged,    b.  Natural 

size. 
Fig.  44.— Bothriocephalus    latus.      Mature 

segment. 


INTESTINAL  PARASITES. 


Uli 


tines  without  causing  any  morbid  symptoms.     We  can  recognize  their  presence 
only  by  occasionally  finding  the  joints  in  the  dejections. 

In  other  cases,  however,  tape- worms  cause  a  list  of  disturbances  which  are  of  ten 
exaggerated  by  anxious,  hypochondriacal,  and  nervous  persons,  but  which  ought 
not  to  be  too  little  regarded.  The  symptoms  are 
referred  chiefly  to  the  intestinal  canal.  Sometimes 
there  is  quite  severe  abdominal  pain,  which  may 
assume  a  colicky  character.  The  patient  also  fre- 
quently complains  of  irregularity  of  the  bowels, 
and  of  occasional  diarrhoea,  which  alternates  with 
constipation.  Many  general  symptoms  are  also 
added  to  those  mentioned — loss  of  appetite,  or  at 
times  marked  voracity,  general  languor,  disinclina- 
tion to  work,  mental  disturbance,  depression,  etc. 
We  can  see  that,  under  such  circumstances,  the 
general  health  may  suffer  considerably. 

We  must  also  mention  a  number  of  symptoms 
which  probably  owe  their  origin  to  abnormal  reflex  Fig.  45.— Embryo  of  bothriocephaius 
processes.  Among  these  we  sometimes  see  marked  (Lbuckart.)  '  S  °  'atX  °J&t" 
salivation,  tickling  in  the  nose,  dilatation  of  the  pu- 
pils, palpitation,  vomiting,  headache  (migraine),  etc.  In  some  cases  even  severe 
spasms,  and  choreic  conditions,  have  been  referred  to  the  presence  of  tape-worms 
in  the  intestinal  canal,  but  it  is  hard  to  decide  how  far  such  a  supposed  connec- 
tion can  really  be  regarded  as  justified. 

Although  many  of  the  symptoms  mentioned  may  arouse  suspicion  as  to  the 
presence  of  a  tape-worm,  the  diagnosis  can  be  made  only  by  finding  the  joints  or 
eggs  of  the  tape-worm  in  the  dejections.  In  many  cases  the  patient  himself 
brings  some  of  the  segments  found  by  him  in  the  dejections  to  the  physician,  but 
in  judging  of  them  a  certain  caution  is  always  necessary,  since  shreds  of  mucus, 
remains  of  food,  etc.,  are  quite  frequently  presented  to  the  physician,  under  the 
idea  that  they  are  segments  of  tape-worm.  If  possible,  we  should  take  pains  to 
decide  definitely,  from  the  segments  laid  before  us,  the  species  of  tape-worm, 
which  is  usually  not  a  difficult  task  if  we  follow  the  anatomical  description  given 
above.  If  we  spread  out  the  pieces  of  tape-worm  on  a  microscope  slide,  the  thicker, 
fatter  segments  of  the  taenia  mediocanellata,  with  its  many-branched  uterus,  may 
usually  be  distinguished  without  difficulty  from  the  more  tender  and  more  trans- 
lucent segments  of  the  taenia  solium,  with  a  smaller  number  of  lateral  branches 
to  its  sexual  apparatus.  The  statement  of  many  patients  that  single  segments  of 
tape-worm  come  from  them  at  other  times  than  when  at  stool,  and  that  they  find 
them  on  their  underclothing,  almost  always  points  to  the  presence  of  a  taenia 
mediocanellata  in  the  intestine. 

If  we  suspect  a  tape-worm,  without  having  secured  the  certain  evidence  of  seg- 
ments in  the  dejections,  it  is  a  good  plan  to  give  the  patient  a  mild  cathartic,  like 
castor-oil,  or  a  dose  of  boiled  pumpkin -seeds,  since  after  this,  if  the  intestine  har- 
bors a  tape-worm,  single  portions  of  it  almost  always  come  away. 

Treatment. — The  "  tape-worm  cures,"  which  are  recommended  in  so  great  a 
number  that  we  can  by  no  means  mention  all  of  them  here,  but  only  the  most 
important  and  the  most  serviceable,  aim  at  killing  or  benumbing  the  worm,  and 
then  at  removing  it  from  the  intestine  in  toto  by  cathartics. 

We  usually  begin  with  a  so-called  "preparatory  treatment,"  This  is  to  cleanse 
the  intestine,  especially  the  large  intestine,  from  old  faecal  masses,  in  order  to  pre- 
pare as  free  a  passage  as  possible  for  the  worm.  For  this  purpose  we  give  the 
patient  a  mild  laxative,  or,  better  still,  a  large  enema  of  cold  water.    We  also  forbid 


444  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

for  a  day  or  two  the  use  of  vegetables,  black  bread,  etc.,  and  prescribe  instead  a 
limited  diet  of  white  bread,  some  meat,  milk,  and  coffee.  It  is  a  wide-spread  prac- 
tice to  take  during  the  preparatory  treatment  certain  articles  of  food  to  "  make  the 
worm  ill."  Among  tbese  a  salad  of  finely  chopped  and  very  salt  herring  with 
onions  and  garlic  is  especially  recommended.  A  similar  action  is  also  ascribed  to 
strawberries,  cranberries,  and  bilberries.  Hence,  on  the  day,  and  especially  on 
the  afternoon,  before  treatment,  we  have  the  patient  take  a  large  amount  of  the 
articles  of  food  mentioned,  such  as  herring  salad. 

On  the  next  morning,  after  everything  has  been  prepared,  after  the  bowels 
have  moved  the  night  before,  etc.,  the  patient  takes  no  breakfast,  or  only  some 
strong  sweet  cafe  noir.  Then  he  takes  the  special  anthelmintic,  and  in  one  or 
two  hours,  if  he  feels  a  great  pressure  in  the  abdomen,  he  also  takes  a  few  spoon- 
fuls of  castor-oil  or  rhubarb. 

The  number  of  tsenicides  recommended  is,  as  we  have  said,  very  great.  At 
present  the  following  are  most  in  use : 

The  bark  of  pomegranate-root  (cortex  radicis  Punicce  granati)  is  one  of  the 
most  efficient  remedies.  We  usually  prescribe  it  in  combination  with  the  ethereal 
extract  of  male  fern,  in  the  following  prescription: 

^    Granati  radicis  corticis 1  iv-v  (grm.  120-150) ; 

Aquge O  ij  (grm.  1,000). 

Macerate  for  twenty-four  hours,  and  boil  until  it  is  reduced  to  §  v  (grm.  150). 
Add:  Oleoresinse  filicis gr.  lxxv  (grm.  5). 

The  whole  amount  is  to  be  taken  in  three  or  four  doses  as  near  together  as 
possible.  In  order  to  obviate  the  bad  taste  of  the  remedy  and  to  increase  the 
action  by  introducing  a  larger  amount  at  once,  it  has  been  recommended  to  intro- 
duce the  whole  amount  of  a  still  stronger  decoction  of  pomegranate-root  at  once 
into  the  stomach  by  means  of  an  oesophageal  tube.  As  "a  rule,  it  is  well  to  avoid 
this  procedure. — To  be  recommended  is  also  the  tannate  of  pelletierine,  prepared 
from  the  pomegranate-root.  It  is  almost  tasteless,  and  in  doses  of  8-25  grains 
(grm.  0'5-l"5)  is  said  to  be  a  very  certain  taenicide.  Usually  one  obtains  excellent 
results  with  male  fern.  Two  to  two  and  a  half  drachms  (grm.  8-10)  of  the  extractum 
filicis  (P.  G.)  must  be  given  [or  one  and  a  half  to  two  fluidrachms  of  the 
oleo resin].     It  may  be  put  in  gelatine  capsules  on  account  of  its  bad  taste. 

Another  remedy,  which  has  often  proved  successful,  is  kousso-flowers.  We 
give  three  or  four  powders,  each  containing  seventy-five  grains  (grm.  5)  of  powdered 
kousso-flowers,  in  white  wine,  giving' a  glass  of  wine  containing  one  powder  about 
every  half-hour.  Rosenthal's  "  kousso  tablets "  are  more  agreeable  to  take  and 
are  very  good,  but  they  are  more  expensive.  Twenty  of  these,  of  fifteen  grains 
each  (grm.  1),  may  be  taken  without  danger  within  an  hour  with  cafe  noir  or 
lemonade.  During  the  period  of  treatment  the  patient  must  lie  as  quiet  as  pos- 
sible in  order  to  avoid  vomiting.  Up  to  the  present  time  we  have  not  had  suf- 
ficient experience  of  the  koussine  or  kosseine,  prepared  from  the  alcoholic  extract 
of  kousso-leaves,  which  is  said  to  be  very  efficient  in  doses  of  thirty  to  forty-five 
grains  (grm.  2-3). 

Of  the  other  remedies  we  may  mention  kamala,  one  to  three  drachms  (grm. 
5-10)  of  the  powder  in  wine  or  water,  and  oil  of  turpentine,  one  or  two  ounces 
(grm.  40-60)  in  two  doses  in  milk — an  efficient  but  rather  dangerous  remedy  in 
these  doses — and  picro-nitrate  of  potassium.  We  may  also  prescribe  male  fern 
in  powders  of  a  drachm  (grm.  4)  each,  taking  three  or  four  powders  within 
an  hour. 

The  treatment  is  to  be  regarded  as  absolutely  successful  only  when  we  find  the 


INTESTINAL  PARA  SITES. 


445 


head  of  the  tape-worm,  as  well  as  its  joints,  in  the  patient's  dejections.  "We  may 
best  search  for  the  head  in  the  faeces  by  diluting-  the  dejection  with  water,  stirring 
it  repeatedly,  and  pouring  off  the  water.  The  tape-worm  then  remains  at  the 
bottom  of  the  vessel. 

Every  tape-worm  treatment  is  rather  drastic,  and  hence  it  is  well,  after  the 
treatment  is  over,  to  recommend  the  patient  to  be  prudent  in  his  diet,  and  to 
be  careful  about  his  digestive  tract  for  some  time. 
In  persons  who  are  very  weak,  or  who  have  some 
other  disease,  we  do  not  willingly  undertake  to  remove 
a  tape-worm  without  urgent  reasons;  but  in  people 
who  are  otherwise  healthy  it  is  always  well  to  get  rid 
of  a  tape-worm,  even  if  it  causes  no  severe  symptoms. 
Of  course  only  the  taenia  solium  is  attended  with  the 
serious  danger  of  the  cysticerci  invading  the  brain  (see 
diseases  of  the  brain).  The  best  time  for  undertaking 
a'treatment  is  when  joints  or  large  pieces  of  the  worm 
come  away  quite  frequently  of  their  own  accord.  We 
should  never  prescribe  a  treatment  on  the  mere  state- 
ments or  suspicions  of  the  patient.  We  must  always 
convince  ourselves  with  complete  certainty  of  the 
presence  of  a  tape-worm  in  the  intestine. 

We  must  finally  mention  that  the  only  efficient 
prophylaxis  against  acquiring  a  tape- worm  lies  in  en- 
tirely avoiding  the  use  of  raw  or  half -cooked  beef  or 
pork.  The  more  widely  spread  the  taking  of  raw  meat 
is,  as  in  Abyssinia,  the  more  common  are  tape-worms 
in  man.  Certain  callings,  like  those  of  cooks  and 
butchers,  are  also  especially  exposed  to  infection. 

2.  Round-worms. 

(Ascaris  lunibricoides.) 

Natural  History. — Ascarides  are  pale-reddish,  cyl- 
indrical worms,  pointed  at  both  ends,  with  the  sexes 
in  different  individuals.  The  females  are  thirty  or 
forty  centimetres  long,  the  males  about  twenty-five. 
At  the  cephalic  end  of  the  worm  are  found  three  lips 
furnished  with  fine  teeth.  The  tail  is  straight  in  the 
females  and  curved  in  the  males.  In  the  female  sex- 
ual organs  (Fig.  46)  sixty  millions  of  eggs  may  develop, 
at  a  rough  estimate.  These  eggs  are  often  found  in 
the  faeces  of  people  who  have  round- worms  in  their 
intestines  (see  Fig.  40,  8).  They  have  a  great  capacity 
of  resisting  external  influences,  and  a  worm-like  em- 
bryo develops  in  them  in  a  few  months.  Their  further 
fate,  and  the  form  and  manner  in  which  infection  usu- 
ally takes  place  in  man,  are  not  yet  accurately  known. 
It  is  probable  the  parasites  are. spread  without  any  in- 
termediate host  by  direct  ingestion  of  the  eggs  which 
contain  the  embryos. 

The  round-worms  inhabit  chiefly  the  small  intes- 
tine.    In  severe  vomiting  they  often  reach  the  stomach  and  are  vomited  up.     In 
individual  cases  they  have  been  found  in  the  bile-ducts,  in  the  air-passages,  and, 


Fig.  46. — (From  Heller.  1—Asca- 
ris  lunibricoides.  Female.  143 
millimetres  long.  a.  Vagina. 
b.  Intestine,  c.  Boundary  be- 
tween the  uterus  and  oviducts. 
d.  Longitudinal  bands,  e.  Coil 
of  oviducts  and  ovaries. 


U6  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

after  perforation  of  the  intestine,  in  the  abdominal  cavity.  The  number  of  round- 
worms existing  at  the  same  time  in  the  intestines  may  be  very  considerable.  "We 
find  them  most  commonly  in  children  and  in  adults  from  tbe  lower  classes. 
Round-worms  have  been  repeatedly  observed  to  crawl  out  of  the  anus,  the  mouth, 
or  the  nose  of  children  during  sleep. 

The  round-worm  is  also  common  in  hogs  and  cattle  as  well  as  in  man. 

Symptoms. — In '  general,  the  round-worms  are  innocent  parasites,  which  may 
exist  in  large  numbers  in  the  intestines  without  any  bad  results.  Exceptionally 
they  cause  symptoms  similar  to  those  ascribed  to  taeniae — abdominal  pain,  languor, 
itching  of  the  nose,  burning  in  the  eyes,  etc. — symptoms  which  are  all  ambiguous, 
and  whose  definite  connection  with  the  presence  of  round-worms  it  is  hard  to 
make  out.  The  cases  recorded  in  literature  are  quite  numerous  in  which  severe 
nervous  symptoms  have  been  caused  by  round  worms  and  have  disappeared  after 
the  removal  of  the  parasites.  However  cautious  we  may  be  in  accepting  such 
statements,  nevertheless  their  credibility  can  not  be  wholly  denied.  We  would 
mention  especially  convulsions,  epileptiform  seizures,  choreic  and  cataleptic  con- 
ditions, contractures,  and  temporary  mental  disturbances,  which  are  claimed  to 
be  excited  by  ascarides.  Milder  nervous  attacks — like  headache,  vertigo,  dilated 
pupils,  and  chills— are  quite  frequently  seen  in  children  with  ascarides. 

In  some  cases  the  presence  of  ascarides  may  excite  much  more  severe  symp- 
toms by  unfortunate  accidents,  as,  for  example,  sudden  suffocation  from  the 
entrance  of  a  round-worm  into  the  larynx.  When  a  very  large  number  of  round- 
worms have  been  present  in  the  intestine,  severe  symptoms  of  intestinal  stenosis 
have  been  observed  from  their  rolling  together  into  a  bail.  If  a  round- worm 
crawls  into  the  bile-ducts,  it  may  give  rise  to  jaundice,  and  even  to  the  develop- 
ment of  an  abscess  of  the  liver.  In  the  abscesses  of  the  anterior  abdominal  wall, 
usually  termed  "  worm  abscesses,"  the  round-worms  probably  play  a  purely  acci- 
dental part.  "We  have  to  do  in  such  cases  with  perityphlitic  abscesses  or  with 
inflamed  herniae,  which  have  perforated  externally,  by  which  the  round-worms 
which  are  accidentally  found  in  the  intestines  pass  out,  without  having  any  causal 
relation  to  the  abscess. 

Treatment. — The  oldest  and  most  approved  remedy  against  ascarides  is  worm- 
seed — santonica.  This  is  best  given  in  the  form  of  an  electuary — santonica,  a 
drachm  (grm.  5);  jalap,  fifteen  grains  (grm.  1);  and  syrup,  an  ounce  (grm.  30),  to 
be  taken  in  three  doses — in  combination  with  a  cathartic.  Of  late,  worm-seed,  on 
account  of  its  bad  taste,  has  been  almost  wholly  replaced  by  santonin,  which  is 
derived  from  it.  This  is  prescribed  in  one-  or  two-grain  (grm.  0"05-0'10)  powders, 
or  still  more  frequently  in  the  form  of  santonin  troches  ("  worm-tablets  "),  which 
may  be  had  of  any  apothecary.  It  is  wTell  to  give  santonin  also  in  connection 
with  a  cathartic,  like  calomel.  We  let  the  patient  take  one  or  two  doses  of  san- 
tonin in  the  morning  for  three  days,  and  on  the  fourth  we  give  a  cathartic.  Severe 
symptoms  of  poisoning — spasms — have  been  seen  only  occasionally  from  the 
careless  use  of  it.  Milder  symptoms,  like  a  yellowness  of  the  urine  and  conjunc- 
tivae, and  xanthopsia,  or  seeing  everything  as  yellow,  are  somewhat  more  fre- 
quent. 

3.  Oxyuris  vermicularis. 

(Seat-worms.     Pin-ivorms.) 

Natural  History. — The  oxyures  are  little  round  worms,  the  females  ten  or 
twelve  millimetres  long,  the  males  only  three  or  four  (see  Figs.  47  and  48).  The 
eggs,  when  they  reach  the  human  stomach,  develop  very  rapidly.  The  embryos, 
set  free,  collect  in  the  small  intestine  and  later  in  the  caecum,  where  they  soon 


INTESTINAL  PARASITE«. 


447 


become  mature.  The  impregnated  female  usually  crawls  down  into  the  rectum, 
deposits  her  eggs  there,  and  either  crawls  out  of  the  anus  herself,  or,  like  the 
male,  is  evacuated  with  the  faeces.  The  whole  devel- 
opment of  the  oxyuris  occupies  about  a  fortnight. 
The  total  number  of  oxyures  present  in  the  intestine 
at  the  same  time  may  be  very  considerable,  so  that 
"  the  whole  mucous  membrane  of  the  large  intestine 
is  covered  with  them  like  fur." 

The  infection  by  the  eggs  of  the  oxyuris  probably 
takes  place,  as  a  rule,  from  one  man  to  another,  since 
the  eggs  stick  to  the  hands  (in  scratching  the  anus), 
and  are  thus  communicated  to  food,  bread,  fruit,  etc. 
In  children  and  dirty  adults  auto-infection  may  often 
be  repeated  in  an  analogous  manner. 

Symptoms  and  Treatment.— The  oxyures  found  in 
the  upper  portions  of  the  intestine  and  in  the  caecum 
cause  no  symptoms  whatever,  but  in  the  lower  part 
of  the  rectum  their  presence  causes  local  symptoms, 
especially  a  very  severe  feeling  of  itching  and  burn- 
ing in  the  anus,  which  makes  the  child  constantly 
scratch  and  dig  with  his  fingers.  This  itching  of  the 
anus  is  most  severe  at  night  in  bed.  In  girls  the 
oxyures  frequently  travel  into  the  vagina,  by  which 
an  intense  itching  is  also  set  up  there,  which  some- 
times leads  to  masturbation.  In  some  cases  in  boys 
and  men  oxyures  have  been  found  to  be  the  cause 
of  abnormal  sexual  irritation. 

The  diagnosis  of  oxyures  is  not  difficult.  Our  at- 
tention is  called  to  the  itching  of  the  anus,  and  we 
look  for  worms.  Single  worms  are  easily  found  in 
the  dejections,  and  often  on  the  skin  about  the  anus. 
The  diagnosis  is  made  more  certain  by  finding  the 
eggs  (Fig.  40,  6)  in  the  faeces  under  the  microscope. 

Treatment  can  remove  the  oxyures  from  the  rec- 
tum with  ease,  but  only  with  difficulty  from  the  up- 
per portions  of  the  intestine,  especially  from  the  cae- 
cum and  the  vermiform  appendix.  Santonin  is  gen- 
erally tised,  but  we  must  also  prescribe  large  enemata 
of  cold  water  and  cathartics  internally.  Instead  of 
ordinary  water  we  may  use  soap-suds,  vinegar- water, 
and,  in  severe  cases,  a  weak  solution  of  corrosive  sub- 
limate (1  to  10,000)  in  the  enemata.     The  itching  of 


Fig. 


Fig.  48. 
4~.  —  Oxyuris     vermicularis. 
1.   Female.     2. 


Natural  size. 
Two  males. 

the  anus  is  relieved  by  rubbing  on  a  little  mercurial   Fig.  48.— (From  Heller.")  Oxyuris 

nintmmit  vermicularis,      enlarged.        a. 

<    ?mem.  Mature    female,    not   yet    im- 

pregnated,  b.  Male.    c.  Female 
containing  eggs. 


[Enemas    containing  infusion   of   quassia,   alum, 
eucalyptol,  tannin,  etc.,  are  much  in  use.     A  plain 
enema  should  be  given  first,  to  unload  the  rectum  and  clean  the  membrane  as 
far  as  possible,  so  that  the  anthelmintic  may  reach  the  worms  when  introduced.] 


448 


DISEASES  OF  THE  DIGESTIVE  ORGANS. 


Fig.  49. 


4.  Anchylostomum  duodenale. 

(Dockmius  seu  Strongylus  duodenalis.) 

The  anchylostomum  duodenale  is  a  worm  first  observed  in  upper  Italy  and  in 
Egypt,  which,  singly  or  in  large  numbers,  inhabits  the  upper  portion  of  the  small 
intestine,  especially  the  duodenum,  but  also  the  jejunum  and  ileum.  The  male 
is  six  to  ten  millimetres  long,  the  female  ten  to  eighteen.  At  the  cephalic  end 
(Figs.  49,  50)  is  found  a  bell-shaped  mouth-capsule,  which  is  provided  with  two 
small  teeth  on  its  dorsal  edge,  and  four  larger  curved  teeth  on 
its  ventral  edge.  With  this  sucking  and  biting  apparatus  the 
worm  fixes  itself  firmly,  like  a  wet  cup,  on  the  intestinal  mu- 
cous membrane,  and  is  nourished  by  the  blood  which  it  sucks 
out.  The  places  in  the  intestine  to  which  an  anchylostomum 
has  fastened  may  be  recognized  in  the  cadaver  as  little  ecchy- 
moses.  The  worms  sometimes  bore  completely  into  the  inner 
part  of  the  mucous  coat. 

If  the  intestine  harbors  many  anchylostoma,  the  small  but 
constant  loss  of  blood  caused  by  them  is  not  without  influence 
on  the  organism.  The  symptoms  of  a  severe  anaemia  gradu- 
ally develop.  Griesinger  first  made  the  discovery,  in  the  year 
1854,  that  the  disease  long  known  by  the  name  of  "  Egyptian 
chlorosis "  was  caused  by  the  anchylostomum  duodenale. 
Since  then  confirmatory  observations  have  been  made  in 
many  parts  of  the  tropics.  Of  late  years  the  anchylostoma  dis- 
ease has  become  well  known,  because  it  occurred  with  great 
frequency  among  the  Italian  laborers  employed  in  building 
the  St.  Gothard  tunnel.  In  Germany,  too,  cases  have  repeat- 
edly been  detected,  especially  among  brick-makers  in  the 
Rhineland  and  elsewhere,  who  work  in  wet  clay-pits.  The 
infection  probably  takes  place  chiefly  from  drinking  impulse, 
muddy  water,  in  which  the  eggs  of  the  anchylostomum  are 
found. 

The  symptoms  of  the  disease  consist  of  a  gradually  increas- 
ing general  anaemia,  for  which  no  special  organic  lesion  can 
be  made  out  objectively  as  a  cause.     The  patient  also  suffers 
from  very  great  general  weakness  and  languor,  constraint  in 
breathing,  palpitation,  headache,  oedema,  etc.      The  changes 
in  the  blood  (oligocythemia,  poikilocytosis)  are  precisely  similar  to  those  seen  in 
pernicious  anaemia.     The  disease  may  last  for  months,  or  even  years,  and  it  often 
ends  fatally,  if  it  be  not  recognized  and  treated  in  time. 

Leichtenstern  has  made  numerous  and  accurate  observations  with  regard  to 
the  brickmakers  of  Cologne.  He  states  that  no  symptoms  are  observed  for  three 
or  four  weeks  after  infection  with  the  embryos  of  the  anchylostomum.  Some  five 
or  six  weeks  after  infection,  when  the  parasites  become  sexually  mature  and  breed, 
there  appear  bloody  diarrhoea,  intestinal  colic,  and  accompanying  progressive 
anaemia.  At  this  time  there  is  probably  more  shifting  about  of  the  parasites  in 
the  intestine,  while  they  later  become  more  fixed.  This  explains  why  the  dis- 
ease evinces  a  more  acute  and  severe  character  at  first,  and  then  takes  on  the 
form  of  a  chronic  anaemia,  with  great  diminution  or  cessation  of  the  bloody 
stools. 

The  diagnosis  is  easy  if  we  only  think  of  the  possibility  of  anchylostoma. 
Many  eggs  may  be  found  in  the  faeces,  without  great  trouble;  these  are  quite  like 
the  eggs  of  ascaris  lumbricoides,  only  they  are  a  little  smaller.      After  using 


Fig.  50. 

Fig.  40.  —  Anchylosto- 
mum duodenale. 
Natural  size.  a 
Male.    b.  Female. 

Fig.  50.— (From  Hel- 
ler. )  Anchylosto- 
mum duodenale,  en- 
larged. Head  with 
bell-like  mouth. 


ACUTE  PERITONITIS.  IK, 

cathartics,  the  full-grown  worms  have  often  been  found  in  large  numbers  in  the 
patient's  dejections. 

If  the  trouble  is  correctly  diagnosticated,  treatment  will  usually  give  good  re- 
sults. We  prescribe  the  same  anthelmintics  as  for  the  other  intestinal  parasites, 
especially  male  fern  in  large  doses,  and  also  cathartics  and  enemata.  In  this  way 
we  often  succeed  in  removing  the  parasites  entirely  from  the  intestinal  canal,  and 
thus  bring  about  a  complete  cure,  even  in  severe  cases.  Less  certain  in  its  effecis 
is  doliarina  (made  from  ficus  doliaria),  of  which  the  dose  is  one  drachm  (grm.  4  0j 
three  times  a  day. 

5.  Trichocephalus  dispar. 

(  Whip-worm.} 

The  trichocephalus  dispar  is  a  worm  four  or 
five  centimetres  long,  whose  anterior  part  is  very 
thin,  but  whose  posterior  part  is  decidedly  thick 
(Fig.  51).   _ 

The  chief  dwelling-place  of  the  trichocepha- 
lus is  the  caecum,  where  it  is  often  found  singly 
or  in  large  numbers.      It  seems  to  have  no  clini-    Fig- 51.— (From  Heller.)   Trichocephalus 
cal  significance.     At  the  most,  if  present  in  very 

large  numbers,  it  may  give  rise  to  faecal  impaction,  typhlitis,  etc.,  but  up  to  the 
present  time  no  such  occurrence  has  been  actually  demonstrated. 


SECTION  VI. 
Diseases  of  the  Peritoneum. 

CHAPTER  I. 
ACUTE   PERITONITIS. 


JEtiology. — There  are  two  ways  by  which  inflammatory  agents  most  frequently 
reach  the  peritoneum:  one  is  from  the  gastro-intestinal  tract,  and  the  other — in 
women — is  from  the  genitals. 

All  the  diverse  forms  of  ulceration  which  attack  the  digestive  canal  may  in- 
volve the  serous  layer.  In  such  a  case  an  inflammation  arises  which  is  at  first 
limited,  but  may  under  certain  circumstances  become  more  extensive.  This  in- 
flammation may  be  regarded  as  analogous  to  that  of  the  pleura  in  pneumonia ;  but 
the  anatomy  of  the  stomach  and  intestine  is  such  that  very  often  an  ulcer  in 
their  walls  ends  in  a  complete  perforation.  If  this  occurs,  the  inflammatory 
germs  contained  in  the  primae  viae  at  once  escape  into  the  peritoneal  cavity  and 
there  excite  an  inflammation;  which,  from  the  specific  character  of  its  cause,  is 
invariably  purulent,  and  very  frequently  is  at  the  same  time  septic  or  ichorous. 
The  possibility  of  a  peritonitis  due  to  perforation,  as  a  result  of  the  various  ulcera- 
tive processes  of  the  stomach  and  intestines,  has  been  frequently  i*ef erred  to  in  the 
previous  sections  of  this  work.  Thus,  it  may  occur  in  simple  ulcer  and  in  ulcerat- 
ing cancer  of  the  stomach ;  in  typhoid,  tubercular,  or  dysenteric  ulceration  of  the 
intestine ;  in  ulceration  of  the  intestine  above  intestinal  stenoses  of  many  varie- 
ties; and  in  the  small  ulcers  of  the  vermiform  appendix  due  to  the  pressure  of 
hard  substances. 
29 


450  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

The  female  organs  of  genei'ation  are  the  other  frequent  source  of  peritonitis. 
In  labor  and  premature  delivery  the  genital  tract  is  often  directly  infected.  The 
infection  may  also  occur,  although  much  less  frequently,  at  other  times;  for  exam- 
ple, during  menstruation.  The  various  forms  of  inflammation  which  are  thus  set 
up,  including  endometritis,  metritis,  and  parametritis,  may  in  several  different 
ways  reach  the  peritoneum  and  excite  peritonitis.  A  septic  inflammation  of  the 
endometrium  may  involve  the  peritoneum  by  direct  extension  up  the  Fallopian 
tubes.  In  other  cases  it  is  through  the  lymph-vessels  that  a  purulent  metritis  or 
parametritis  spreads  to  the  peritoneum.  The  larger  parametritic  abscesses  may 
break  into  the  peritoneal  cavity.  It  is  to  be  particularly  noticed,  however,  that  in 
many  cases  of  septic  puerperal  peritonitis  the  uterus  and  its  appendages  are  in  a 
perfectly  normal  condition,  having  served  merely  as  a  gateway  to  the  inflamma- 
tory agents  without  suffering  any  harm  themselves. 

Besides  these  two  chief  soui-ces  of  peritonitis,  numerous  others  are  possible, 
although  much  less  frequent. 

Sometimes  peritonitis  is  due  to  an  extension  of  inflammation  from  other 
abdominal  viscera.  Hepatic  abscess,  suppurating  hydatid  cysts  of  the  liver,  ulcer 
of  the  biliary  ducts,  splenic  abscess  or  infarction,  purulent  nephritis  or  pyelitis, 
abscess  near  the  bladder  or  in  the  prostate,  suppurating  ovariau  cysts,  tubal  preg- 
nancy, psoas  abscess,  and  Pott's  disease— all  these  may  produce  peritonitis,  either 
by  direct  extension  or  by  perforation. 

It  is  worthy  of  note  that  peritonitis  may  occur  as  a  sequel  of  pleurisy.  The 
pleural  and  peritoneal  cavities  are  directly  connected  by  the  lymph-vessels  of  the 
diaphragm ;  and  empyema  as  well  as  tubercular  pleurisy  (see  next  chapter)  may 
spread  to  the  peritoneum. 

Penetrating  wounds  of  the  abdomen  are  a  fruitful  source  of  acute  peritonitis. 
Surgical  operations  upon  abdominal  organs  come  under  the  same  head.  A  large 
number  of  laparotomies  proved  fatal  before  Listerism  was  introduced,  because  the 
inflammatory  germs  thus  admitted  excited  a  diffuse  septic  peritonitis.  Even  tap- 
ping the  abdomen  for  ascites  may  cause  acute  peritonitis  if  the  trocar  is  not  asep- 
tic. Abdominal  injuries,  in  which  the  walls  are  not  penetrated,  very  rarely,  if 
ever,  give  rise  to  peritonitis.  One  way  in  which  they  have  been  said  to  produce 
it  is  by  exciting  internal  haemorrhage.  In  the  new-born,  peritonitis  sometimes 
results  from  infection  through  the  navel. 

Two  diseases  still  remain  to  be  mentioned,  in  the  course  of  which  acute  peri 
tonitis  may  be  developed,  although  the  occurrence  is  a  rare  one — acute  articular 
rheumatism  and  nephritis.  It  may  either  be  one  of  the  symptoms  of  these  dis- 
eases or  an  independent  complication.  We  are  somewhat  in  doubt  as  to  how  it 
arises.  In  acute  articular  rheumatism  it  must  be  regarded  as  analogous  to  the 
pleurisy  and  pericarditis  which  occur  in  the  course  of  this  disease,  for  they  also 
involve  serous  membranes.  We  should  likewise  bear  in  mind  the  possibility  that 
the  inflammation  may  extend  from  the  pleura  to  the  peritoneum  through  the 
lymphatics.  Acute  peritonitis  has  now  and  then  been  observed  in  the  various 
forms  of  nephritis,  both  acute  and  chronic,  inclusive  of  amyloid  disease.  It  usu- 
ally proves  fatal  in  these  cases.  Possibly  the  retention  of  urinary  impurities  in 
the  blood  plays  some  part  in  the  development  of  this  form  of  peritonitis. 

Pathology. — Like  the  analogous  inflammations  of  the  pleura  and  pericardium, 
peritonitis  is  divided  into  different  varieties  according  to  the  character  of  the 
inflammatory  exudation.  The  nature  of  the  exciting  cause  of  most  cases  of  peri- 
tonitis is  such  that  by  far  the  most  frequent  variety  is  the  flbrino-purulent.  If  the 
process  involves  the  entire  peritoneum — that  is,  if  there  is  a  "  diffuse  general  peri- 
tonitis"— we  generally  find  upon  opening  the  abdomen  that  the  parietal  layer  of 
the  peritoneum  and  the  outer  surface  of  the  intestinal  coils  are  distinctly  reddened, 


ACUTE  PERITONITIS.  451 

from  marked  vascular  injection.  There  may  even  be  small  ecchymoses  here  and 
there.  The  serous  membrane  is  clouded,  a  result  partly  of  desquamation  of  its 
endothelium,  and  partly  of  the  more  or  less  abundant  fibrinous  exudation  which 
covers  the  peritoneum  with  a  sheet  of  coagulated  fibrin.  Very  often  the  coils  of 
intestine  have  formed  numerous  adhesions  with  one  another  (compare  pleurit'c 
adhesions).  In  cases  of  brief  duration  these  can  still  be  easily  broken  up,  but  after 
a  prolonged  illness  they  are  extremely  firm.  There  is  usually  also  some  free,  fluid, 
fibrino-purulent  exudation  in  the  abdominal  cavity.  Its  amount  varies  greatly. 
Sometimes  there  is  only  a  small  quantity  of  opaque  fluid  in  the  dependent  por- 
tions of  the  cavity;  sometimes  there  are  many  quarts,  causing  great  distention  of 
the  abdomen.  The  exudation  seldom  inclines  to  a  sero-purulent  character.  It  is 
usually  predominantly  purulent.  Very  often  the  purulent  exudation  undergoes 
decomposition  into  the  offensive  sanious  fluid  of  septic  peritonitis.  This  is  par- 
ticularly apt  to  occur  when  the  disease  originates  from  an  intestinal  perforation 
or  from  puerpei*al  poisoning.  The  perforation  through  the  walls  of  the  intestine 
is  sometimes  so  large  as  to  admit  considerable  amounts  of  intestinal  gases  and 
faeces  into  the  peritoneal  cavity.  It  is  also  possible  that  the  putrefaction  of  peri- 
toneal exudations  may  generate  offensive  gases.  In  rare  instances  the  exudation 
is  hemorrhagic ;  but  most  cases  of  hemorrhagic  peritonitis  do  not  belong  here, 
but  come  rather  under  the  tubercular  form  {vide  infra). 

In  severe  and  protracted  cases  of  peritonitis  the  intestine  is  involved  to  a  cer- 
tain extent.  There  is  a  collateral  inflammatory  oedema  of  its  walls,  causing  some- 
times a  considerable  increase  in  thickness,  while  at  the  same  time  they  may  be 
non-resistant  and  easily  torn.  The  weakness  of  the  muscular  layer  of  the  intes- 
tine may  amount  to  complete  paralysis,  and  thus  permit  excessive  intestinal  tym- 
panites, either  diffuse  or  local. 

Milder  forms  of  general  peritonitis  with  sero-fibrinous,  or  chiefly  serous,  exuda- 
tion are  relative^  infrequent.  Under  this  head  would  come  certain  apparently 
primary  and  usually  chronic  cases  with  favorable  issue,  and  also  the  peritonitis  which 
sometimes  occurs  as  a  sequel  of  an  ascites  which  has  existed  for  some  time  (see  next 
chapter).  Probably  also  in  those  rare  cases  where  a  peritonitis  arising  in  the  course 
of  acute  rheumatism  has  ended  in  recovery,  the  exudation  has  been  sero-fibrinous. 

We  have  spoken  thus  far  of  diffuse  general  peritonitis,  but  cases  are  not 
rarely  seen  of  circumscribed  or  "  encapsulated  "  pei-itonitis.  Here,  also,  we  have 
mild  varieties  with  fibrinous  exudations  on  the  one  hand,  and  on  the  other  puru- 
lent inflammation.  The  milder  inflammation  is  a  result  of  the  extension  of  the 
most  varied  forms  of  inflammation  in  neighboring  organs.  Thus,  deep  intestinal 
ulcers,  for  example,  give  rise  to  a  mild  circumscribed  inflammation  of  the  corre- 
sponding portion  of  the  serous  layer.  A  similar  condition  results  from  superficial 
splenic  infarctions ;  from  various  hepatic  diseases,  when  they  i*each  the  surface 
of  the  liver ;  and  from  numerous  pathological  conditions  of  the  female  genitals. 
In  many  of  these  cases  the  peritonitis  takes  a  chronic  course  and  leads  to  adhe- 
sions, and  hence  is  called  adhesive  peritonitis. 

Circumscribed  purulent  peritonitis  has  precisely  the  same  astiology  as  the 
general  form,  with  this  single  difference,  that  firm  adhesions  are  quickly  formed 
around  the  spot  whence  the  inflammation  proceeds,  limiting  it  and  preventing  it 
from  involving  the  entire  peritoneum.  It  occurs  most  frequently  as  a  purulent 
perityphlitis  (q.  v.)  consequent  upon  perforation  of  the  vermiform  appendix ;  and 
also  as  pelvic  peritonitis,  which  is  a  possible  sequel  of  most  of  the  forms  of  puer- 
peral inflammation  to  which  the  uterus  and  its  appendages  are  liable.  It  may 
also  follow  perforative  gastric  or  intestinal  ulcer,  hepatic  abscess  with  perforation, 
and  analogous  affections.  So-called  sub-diaphragmatic  abscess  is  a  form  of  encap- 
sulated purulent  peritonitis. 


452  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

Histologically  considered,  acute  peritonitis  is  perfectly  analogous  to  the  in- 
flammatory processes  which  attack  other  serous  membranes.  The  endothelium 
becomes  degenerated,  and,  for  the  most  part,  is  cast  off.  There  is  an  exudation 
from  the  blood-vessels  of  a  fibrinous  fluid,  which  is  partly  coagulable,  and  with 
this  exudation  round  cells  escape  in  greater  or  less  abundance.  In  the  further 
progress  of  the  disease  there  is  an  inflammatory  new  growth  of  vascular  connect- 
ive tissue,  which  probably  originates  chiefly  from  the  endothelium  and  the  perma- 
nent tissue-cells,  but,  according  to  some,  starts  in  part  also  from  the  wandering 
cells.  The  new  formation  of  blood-vessels  certainly  seems  to  be  chiefly  due  to 
budding  from  the  capillaries  of  the  serosa.  Thus  arise  the  adhesions  of  connective 
tissue  and  the  false  membranes  found  in  chronic  cases  between  the  different  coils 
of  intestine.  They  lead  in  process  of  time  to  marked  thickening  and  retraction 
of  the  omentum  and  mesentery  {peritonitis  deformans).  Most  cases  of  purulent 
peritonitis  prove  fatal  in  the  early  acute  stage.  If  a  case  recovers,  the  exudation 
undergoes  fatty  degeneration,  and  its  cellular  constituents  are  thus  disintegrated 
and  then  are  absorbed. 

The  results  of  circumscribed  purulent  peritonitis  are  detailed  in  connection 
with  the  clinical  history. 

Clinical  History. — 1.  Acute  General  Peritonitis. — The  following  description 
applies  chiefly  to  the  severe  purulent  form,  the  one  by  far  most  frequently  met  with. 
It  occurs  in  most  instances  after  perforation,  in  puerperal  cases,  and  after  external 
injuries,  such  as  surgical  operations.  In  most  of  these  cases  the  peritonitis  is  a 
secondary  disease,  so  that  it  must  obviously  be  greatly  modified  in  its  general 
characteristics  and  behavior  by  the  original  trouble.  In  the  first  place,  the  on- 
set is  modified.  Many  cases  of  peritonitis  due  to  perforation  begin  abruptly,  the 
patient  having  been  previously  in  perfect  health.  Thus,  as  already  mentioned, 
the  first  indication  of  a  gastric  or  duodenal  ulcer  may  be  given  by  perforation. 
Most  cases  of  perforation  of  the  vermiform  appendix  present  equally  sudden  and 
unexpected  symptoms. 

There  are  many  other  cases  where  the  symptoms  of  peritonitis  supervene  upon 
those  of  some  grave  disease  already  existing.  For  example,  typhoid  fever, 
intestinal  tuberculosis  or  intestinal  stenosis,  may,  by  causing  perforation,  excite 
a  peritonitis.  Here  the  symptoms  of  this  secondary  disease  may  be  more  or  less 
completely  veiled  by  the  other  grave  local  and  constitutional  disturbances. 

Again,  an  acute  general  peritonitis  may,  as  we  have  already  said,  be  the  sequel 
to  a  local  and  circumscribed  inflammation  of  the  peritoneum.  Thus,  a  purulent 
perityphlitis,  or  a  purulent  puerperal  pelvic  peritonitis,  may  finally  become  uni- 
versal. In  such  unfortunate  cases  the  change  in  symptoms  is  often  gradual,  and 
is  not  clearly  pronounced. 

We  have  now  indicated  certain  variations  from  the  general  course  of  the  dis- 
ease; but,  with  these  exceptions,  almost  every  case  of  acute  general  peritonitis, 
whatever  its  aetiology,  presents  clinical  symptoms  which  are  so  characteristic  and 
typical  that  a  general  description  of  the  disease  will  be  both  easy  and  advanta- 
geous. 

The  symptoms  of  acute  peritonitis  form  two  groups,  the  local  and  the  constitu- 
tional. The  latter  are  the  result  of  the  local  disturbance  acting  upon  the  general 
condition  of  the  patient. 

Of  the  local  symptoms,  pain  deserves  to  be  named  first.  It  is  usually  the 
earliest  symptom ;  and,  as  the  disease  progresses,  it  is  generally  the  excruciating 
abdominal  pain  which  attracts  most  attention.  The  localization  of  the  pain  in 
the  beginning  of  the  illness  may  be  of  diagnostic  value  in  doubtful  cases,  if  such 
as  to  indicate  the  possible  starting-point  of  the  inflammation,  for  example,  the 
vermiform  appendix  or  a  gastric  ulcer.     Later  the  pain  extends  over  the  whole 


ACUTE  PERITONITIS.  45:', 

abdomen.  As  a  rule,  there  are  brief  remissions  followed  by  fresh  exacerbations. 
The  pain  is  aggravated  by  voluntary  movements,  by  deep  inspirations,  and  prob- 
ably by  intestinal  peristalsis.  The  abdominal  tenderness  is  often  extreme  in 
peritonitis,  and  is  very  characteristic.  The  gentlest  palpation  is  torture,  and  often 
the  slightest  pressure  of  the  bed-clothes  is  almost  unbearable.  Frequently  the 
greatest  tenderness  is  in  the  umbilical  region. 

Acute  peritonitis  seldom  exists  without  pain.  The  exceptions  to  this  rule  are 
chiefly  seen  in  patients  who  are  extremely  prostrated,  and  whose  sensibility  and 
intelligence  are  much  impaired.     Here  the  peritonitis  itself  may  escape  notice. 

Physical  examination  of  the  abdomen  greatly  aids  the  diagnosis  in  many  ways. 

As  a  rule,  the  abdomen  is  distended.  This  is  an  early  symptom,  and  gradually 
becomes  more  and  more  pronounced.  It  is  due  mainly  to  the  intestinal  tympa- 
nites, which  we  have  already  mentioned,  and  which  sometimes  becomes  very 
great  if  the  muscular  fibers  of  the  intestine  are  paralyzed.  In  the  later  stages  the 
liquid  effusion  into  the  peritoneal  cavity  of  course  contributes  to  the  prominence 
of  the  abdomen,  but  even  then  the  distention  is  seldom  so  uniform  or  so  broad  as 
in  ascites.  In  peritonitis,  coils  of  distended  intestine  can  often  be  recognized  by 
their  characteristic  contour  through  the  abdominal  wall.  In  general,  if  the 
abdominal  wall  is  yielding  and  thin,  the  peritonitic  distention  will  be  greater,  so 
that  it  is  most  marked  in  puerperal  cases,  where  the  preceding  pregnancy  has  ren- 
dered the  walls  lax.  In  a  person  with  powerful  muscles  and  tense  abdominal 
walls  the  convexity  of  the  abdomen  is  seldom  great.  In  some  cases  there  is  no 
convexity  whatever.  The  walls  may  be  as  hard  as  a  board,  and  the  abdomen  flat 
or  slightly  concave.  In  such  cases  diagnosis  may  be  difficult.  Sometimes,  again, 
the  original  retraction  of  the  abdominal  walls  is  succeeded  by  more  or  less  disten- 
tion of  the  abdomen. 

Percussion  over  the  distended  intestinal  coils  yields  a  resonant  and  usually 
tympanitic  sound.  It  is  not  till  a  considerable  amount  of  liquid  effusion  has 
collected  that  there  is  dullness,  most  marked  in  the  dependent  portions  of  the 
abdomen.  If  there  is  much  tympanites,  however,  quite  a  large  effusion  may  exist 
without  being  detected  on  percussion.  Usually  there  is  too  much  pain  to  permit 
a  careful  examination  of  the  change  of  dullness  consequent  upon  change  of  decu- 
bitus. In  general,  the  numerous  adhesions  between  the  separate  coils  of  intestine 
not  infrequently  interfere  with  the  free  motion  of  the  peritonitic  exudations. 

Percussion  not  only  gives  information  about  the  existence  of  a  liquid,  puru- 
lent effusion,  but  is  also  of  value  in  determining  the  level  of  the  diaphragm,  as 
affected  by  abnormal  abdominal  distention.  The  upper  limit  of  hepatic  dullness  is 
raised  to  the  fifth  or  even  the  fourth  rib.  The  heart  is  also  pushed  up.  There  is 
a  tympanitic  resonance  above  the  margin  of  the  ribs  on  the  right  side.  The  area 
of  hepatic  dullness  is  not  only  displaced  upward,  but  is  also  evidently  diminished. 
This  is  due  in  part  to  coils  of  distended  intestine  overlapping  the  anterior  edge  of 
the  liver,  and  in  part  to  the  organ  being  tilted  upward  in  such  a  way  that  its 
area  of  contact  with  the  anterior  wall  of  the  body  is  less  than  normal.  Various 
authors  formerly  laid  great  stress  upon  the  total  disappearance  of  hepatic  dull- 
ness, regarding  it  as  a  sure  sign  that  gas  has  escaped  from  the  intestine  into  the 
abdominal  cavity.  The  inference  is  not  always  correct.  The  liver  may  be  dis- 
placed backward  by  coils  of  intestine,  and  hepatic  dullness  be  thus  abolished, 
although  there  is  no  air  free  in  the  peritoneal  cavity. 

If  there  is  a  considerable  effusion,  it  is  possible,  as  in  ascites  (q.  v.),  to  get  a 
sensation  of  fluctuation  by  gentle,  quick  palpation. 

As  a  rule,  auscultation  of  the  abdomen  does  not  throw  much  light  on  a  case 
of  peritonitis.  In  the  distended  coils  of  intestine  we  not  infrequently  hear  all 
sorts  of  gurgling  and  splashing  sounds.    Sometimes  we  hear  a  peritonitic  friction- 


454  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

sound,  coincident  with  the  movements  of  respiration  and  due  to  the  rubbing 
against  each  other  of  two  rough  surfaces  under  the  impulse  of  the  diaphragm. 
In  particular  this  friction-sound  has  been  repeatedly  heard  over  the  liver. 

In  almost  every  severe  case  of  peritonitis  there  are  gastro-intestinal  symp- 
toms. 

As  to  the  stomach,  vomiting  is  the  most  frequent  and  important  symptom. 
Vomiting  is  often  seen  early  in  the  disease,  and  recurs  frequently  as  the  illness 
progresses.  It  sometimes  is  spontaneous,  and  sometimes  follows  the  ingestion  of 
food.  If  spontaneous,  the  vomitus  consists  of  watery  mucus,  usually  of  a  green- 
ish tinge.  Why  vomiting  is  so  prominent  in  peritonitis  we  do  not  know  abso- 
lutely. Apparently  it  is  in  part  a  reflex  action,  excited  by  the  inflammation  of 
the  serous  membrane.  Possibly  the  external  pressure  of  the  exudation  also  affects 
the  stomach.  It  must  he  added  that  vomiting  may  he  absent  in  acute  peritonitis. 
This  is  seen  when  the  patient  is  comatose,  and  sometimes  also  when  the  perito- 
nitis has  developed  upon  perforation  of  a  gastric  ulcer,  because  the  contents  of 
the  stomach  are  thus  emptied  out  through  the  hole  in  its  walls.  The  vomiting  usu- 
ally is  accompanied  by  frequent  eructations. 

Of  the  intestinal  symptoms,  the  reader  has  already  become  acquainted  with 
the  tympanites,  and  also  with  the  fact  that  it  is  due  mainly  to  a  paresis  of  the 
muscular  fibers  of  the  intestine.  This  same  muscular  weakness  furnishes  an 
obvious  reason  for  the  persistent  constipation  usually  observed  in  peritonitis;  but 
we  may  have  diarrhoea  instead,  from  increased  peristalsis  and  secondary  intes- 
tinal catarrh. 

The  pushing  up  of  the  diaphragm  has  a  noteworthy  effect  upon  the  thoracic 
organs.  The  lower  lobes  of  the  lungs  are  compressed,  so  that  considerable  dysp- 
noea results.  The  heart  is  likewise  crowded  upward,  so  that  tbe  apex-beat  is  usu- 
ally to  be  felt  in  the  fourth  intercostal  space. 

Every  case  of  acute  peritonitis  that  is  at  all  extensive  has  mai^ked  constitutional 
effects.  These  are  in  part  the  result  of  the  wakefulness  due  to  pain,  and  the  rest- 
lessness and  fever.  But  in  all  probability  there  are  also  decided  reflex  inhibitory 
influences,  originating  in  the  irritation  of  the  peritoneal  nerves  and  affecting 
chiefly  the  heart,  just  as  Goltz  in  his  well-known  experiment  killed  a  frog  by 
blows  upon  the  abdomen.  There  is  no  other  disease,  except  internal  strangulated 
hernia — and  the  effect  of  that  is  perfectly  analogous — which  produces  general  col- 
lapse so  quickly  as  does  peritonitis.  The  countenance  is  rapidly  altered,  the  cheeks 
fall  in,  and  the  eyes  become  hollow.  The  nose  grows  sharp  and  cool,  the  lips  dry 
and  cyanotic.  The  skin  of  the  extremities  is  also  cool  and  bluish,  as  a  result  of 
impaired  circulation.  The  patient  is  extremely  feeble.  The  chief  cause  of  all 
these  symptoms  is  the  excessive  weakness  of  the  heart.  The  peritonitis  has  hardly 
begun  before  we  find  the  pulse  small  and  soft.  In  many  severe  cases  the  pulse 
finally  becomes  almost  imperceptible.  At  the  same  time  the  pulse-rate  increases, 
as  is  usual  in  collapse  from  any  cause,  so  that  120  to  140  beats  per  minute  is  not 
an  exceptional  rapidity. 

The  temperature  varies  greatly  in  different  cases.  It  may  be  high  in  the 
rectum,  although  the  skin  feels  cool.  Still,  very  high  fever  is  not  usual ;  and 
there  are  often  considerable  remissions.  We  even  frequently  observe  the  subnor- 
mal temperature  of  collapse.  The  number  of  respirations  per  minute  is  usually 
30  to  40.  This  increased  rate  is  due  not  only  to  the  compression  of  the  lower 
lobes  of  the  lungs,  but  also  to  the  pain  caused  by  full  inspirations  and  to  the  im- 
peded circulation. 

The  intellect  remains  in  most  cases  almost  unimpaired  to  the  end.  There  may 
exceptionally  be  mild  delirium,  or  an  approach  to  stupor,  toward  the  close. 

The  course  of  acute  general  peritonitis  in  the  great  majority  of  cases  is  unfa- 


ACUTE  PERITONITIS.  455 

vorable.  With  the  appearance  of  the  grave  symptoms  just  depicted  the  prognosis 
becomes  almost  hopeless.  The  course  of  the  disease  is  also  comparatively  rapid. 
Marked  variations  in  the  intensity  of  the  symptoms  are  infrequent.  The  grave 
local  and  constitutional  symptoms  persist,  and,  as  a  rule,  the  patient  dies  at  the 
end  of  a  few  (two  to  six)  days.  Still,  it  is  not  well  to  make  general  dogmatic 
statements  as  to  the  clinical  history,  for  the  aetiology  of  each  individual  case  im- 
presses upon  it  individual  characteristics.  A  peritonitis  resulting  from  gastric 
or  intestinal  perforation  is  usually  quickly  fatal.  The  same  is  true  of  almost  all 
cases  of  puerperal  septic  peritonitis.  In  a  few  cases,  however,  the  inflammation 
is  limited,  by  the  encapsulation  of  the  exudation.  These  may  finally  end  in 
recovery  through  perforation  of  the  abdominal  walls  or  perforation  into  the  in- 
testinal canal.  Now  and  then  an  acute  general  peritonitis  may  assume  a  chronic 
form.  The  effusion  is  mostly  reabsorbed,  and  the  newly-formed  adhesions  and 
false  membranes  contract  into  firm  bands  of  connective  tissue.  The  liver,  spleen, 
and  other  abdominal  viscera  acquire  a  tough  coating  of  connective  tissue.  The 
omentum  and  mesentery  are  shortened  and  thickened.  Indeed,  the  omentum 
may  roll  itself  almost  completely  up.  Although  the  clinical  symptoms  become 
less  severe,  weakness  usually  persists,  with  gradual  exhaustion  and  death.  Often 
the  intestine  is  so  bent  or  pinched  as  to  give  rise  to  grave  symptoms  from  ste- 
nosis. 

Recovery  from  acute  general  peritonitis  is  very  exceptioal.  If  seen,  it  is  usu- 
ally in  mild  cases,  such  as  sometimes  occur  after  menstruation,  abortion,  or  labor. 
Peritonitis  as  a  complication  of  acute  articular  rheumatism  is  a  very  rare  event. 
Its  termination  is  generally  favorable.  In  all  cases  of  this  kind  the  inflammation 
is  probably  not  purulent,  but  sero-fibrinous. 

2.  Acute  Circumscribed  Peritonitis. — The  local  symptoms  of  this  are  essen- 
tially the  same  as  we  have  just  ascribed  to  the  general  form ;  except  that,  a  smaller 
extent  of  tissue  being  involved,  they  are  correspondingly  limited.  The  pain  and 
tenderness  are  confined  mainly  to  one  region,  but  its  boundaries  are  never  sharply 
defined.  On  palpation  of  this  region,  we  find  an  increased  resistance  which  is 
sometimes  almost  like  that  produced  by  a  tumor.  If  there  is  an  encapsulated 
effusion,  we  may  detect  fluctuation,  particularly  if  the  abscess  is  going  to  point 
outward.  On  percussion  over  the  affected  spot,  there  is  either  dullness  or  a  muffled 
tympanitic  resonance. 

The  constitutional  symptoms  are  likewise  those  of  general  peritonitis,  only  usu- 
ally less  severe.  Reflex  vomiting  does  occur,  but  is  seldom  so  persistent  as  in  the 
diffuse  inflammation.  The  physical  weakness  and  symptoms  of  collapse  are 
decided,  but  do  not  usually  become  extreme.  There  is  generally  an  irregular  fever, 
which  may  now  and  then  assume  an  intermittent,  pyaemic  character.  Most 
cases  run  a  chronic  course.  If  the  illness  be  very  much  prolonged,  death  may 
finally  ensue  from  general  debility.  Recovery  is  possible  if  the  pus  can  be  let  out. 
This  may  be  accomplished  either  by  the  surgeon  or  by  Nature.  Spontaneous  dis- 
charge of  the  abscess  m  ay  take  place  through  the  abdominal  walls,  into  the  in- 
testine, or  even,  in  rare  instances,  through  the  pleura  into  the  lungs.  But  if  the 
pus  finds  its  way  into  the  general  peritoneal  cavity,  the  peritonitis  becomes  diffuse 
and  causes  death. 

To  describe  in  detail  each  separate  variety  of  circumscribed  peritonitis  would 
occupy  too  much  space,  and  would  also  lead  to  useless  repetitions.  We  have 
already  spoken  at  some  length  of  one  especially  important  form — namely,  peri- 
typhlitis. Perimetritis  and  pelvic  peritonitis  are  chiefly  puerperal  affections,  and 
are  fully  discussed  by  writers  on  gynaecology. 

Abscesses  which  are  very  deeply  situated — as,  for  instance,  behind  the  stomach 
or  in  front  of  the  spinal  column — may  prove  very  difficult  to  diagnosticate,  being 


456  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

so  far  out  of  reach.  Sub-diaphragmatic  abscesses  containing  air  deserve  a  brief 
mention  (pyo-pneumothorax  subphrenicus) .  They  are  sometimes  observed  as  a 
result  of  perforation  of  the  stomach  or  transverse  colon.  Lying  between  the  liver 
and  the  diaphragm,  they  crowd  the  latter  upward,  and  are  liable  to  be  mistaken 
for  pyo-pneumothorax.  Sub-diaphragmatic  abscesses  containing  no  air  also  occur, 
originating  in  the  liver  or  spleen.  Finally,  there  is  a  rare  form  of  circumscribed 
purulent  peritonitis  to  be  noted,  to  which  children  seem  especially  exposed.  It 
declares  its  presence  by  a  painful  fluctuating  tumor  above  the  left  groin,  which 
usually  points  into  the  rectum  and  ends  in  recovery. 

Diagnosis.— The  diagnosis  of  peritonitis  is  in  many  cases  an  easy  matter,  when 
we  have  the  characteristic  symptoms  of  tenderness  and  tympanites,  vomiting,  and 
collapse.  Often  the  starting-point  of  the  inflammation  is  equally  obvious,  in  cases 
of  secondary  peritonitis  supervening  upon  some  disease  which  we  have  already 
clearly  recognized,  such  as  typhoid  fever,  gastric  ulcer,  or  puerperal  diseases.  But 
where  the  peritonitis  is  apparently  primary,  we  must  inquire  carefully  into  the 
previous  history  and  the  earliest  symptoms  of  the  attack,  in  order  to  form  even  a 
surmise  as  to  aetiology. 

The  diagnosis  is  sometimes  greatly  obscured  by  the  fact  that  under  certain  cir- 
cumstances very  similar  symptoms  may  be  excited  by  other  disorders  affecting 
the  intestines.  Thus,  in  typhoid  fever  there  may  be  great  tympanites  and  grave 
constitutional  symptoms,  with  abdominal  pain,  so  that  peritonitis  may  be  diagnos- 
ticated, while  the  autopsy,  if  there  be  one,  discloses  no  signs  of  it.  Deep  ulcers  of 
the  intestine,  however  produced,  may  give  rise  to  so  great  abdominal  tenderness 
as  likewise  to  simulate  peritonitis.  The  grave  symptoms  of  acute  intestinal 
obstruction  are  often  of  such  a  character  that  it  is  impossible  to  determine  whether 
the  intestinal  disorder  has  already  induced  a  peritonitis  or  not.  On  the  other 
hand,  we  have  mentioned  before  that  peritonitis  attended  by  stupor  and  general 
depression  may  hide  itself  from  the  keenest  eye,  because  the  abdominal  distention, 
tenderness,  and  other  chief  symptoms  are  absent. 

It  is  not  always  easy  to  diagnosticate  circumscribed  peritonitis,  even  where  the 
trouble  is  not  deep-seated  and  therefore  inaccessible.  It  is  not  infrequently  mis- 
taken for  a  new  growth.  In  doubtful  cases,  a  careful  use  of  the  aspirating  needle 
is  the  more  necessary,  because  the  presence  of  an  encapsulated  peritonitic  exuda- 
tion in  almost  all  cases  demands  operative  interference.  As  to  aetiology,  it  should 
be  added  that  localized  suppurative  peritonitis,  and  less  frequently  chronic  diffuse 
deforming  peritonitis,  may  be  due  to  actinomycosis  (vide  p.  274). 

It  is  well  to  remember  that  a  pregnant  uterus  and  a  distended  and  therefore 
painful  bladder  have  each  repeatedly  been  mistaken  for  peritonitis ! 

Treatment. — Although  sevens  cases  are  generally  almost  hopeless,  yet  we  must 
try  to  meet  the  symptomatic  indications,  and  must  do  all  in  our  power  to  promote 
a  limitation  of  the  process,  if  it  be  possible. 

External  counter-irritants  or  "  revulsants  "  are  seldom  of  much  use.  Painting 
with  tincture  of  iodine  and  mercurial  inunctions  seem  so  utterly  purposeless  that 
they  may  be  discarded.  The  local  abstraction  of  blood  can  not  be  employed  in  an 
extensive  peritonitis  with  constitutional  prostration.  It  is  only  in  a  circumscribed 
peritonitis  which  is  very  painful,  and  where  the  general  condition  of  the  patient 
remains  comparatively  favorable,  that  local  bleeding  is  to  be  considered.  Under 
these  circumstances,  the  application  of  eight  to  fifteen  leeches  sometimes  causes 
decided  abatement  of  the  pain.  The  local  application  of  ice  to  the  abdomen  is 
universally  in  vogue.  It  usually  moderates  the  pain,  and  it  may  also  have  a 
beneficial  influence  in  quieting  peristalsis.  Still,  some  patients  can  not  bear  ice, 
and  sometimes  hot  cloths  and  poultices  give  great  relief. 

Of  all  internal  remedies,  there  is  but  one  of  great  value,  namely,  opium.     This 


CHRONIC  PERITONITIS.     TUBERCULAR  PERITONITIS.         457 

in  large  doses  (a  grain — grm.  0"05 — of  extract  of  opium  every  hour)  almost  always 
proves  beneficial.  It  moderates  both  the  pain  and  the  vomiting  or  eructations; 
and  also,  by  diminishing  the  peristaltic  movements  of  the  intestine,  opium  contrib- 
utes in  another  way  to  assuage  the  suffering  and  possibly  to  limit  the  spread  of 
the  inflammation.  Experience  shows  that  almost  all  patients  bear  even  very 
large  doses  of  opium  remarkably  well  in  peritonitis.  Perhaps  this  is  because  the 
drug  is  only  slowly  absorbed.  To  substitute  injections  of  morphine  for  tbe  opium 
is  wise  only  in  cases  where  we  wish  to  produce  narcosis  as  rapidly  as  possible,  or 
where  the  vomiting  does  not  prove  amenable  to  the  ordinary  treatment. 

Sometimes  particular  symptoms  demand  special  attention.  For  vomiting  we 
may  employ,  besides  opium,  bits  of  ice,  or  small  quantities  of  "sherbet."  If  tym- 
panites is  excessive,  we  may  try  to  remove  some  of  the  gas  through  a  rectal  tube 
passed  as  high  up  as  possible.  Many  physicians  also  puncture  the  distended  intes- 
tinal coils  with  a  fine  trocar.  Collapse  and  cardiac  failure  require  the  exhibition 
of  stimulants,  such  as  champagne  or  other  alcoholic  liquors,  or  doses  of  ether  or 
camphor  given  subcutaneously.  It  is  generally  very  difficult  to  nourish  the 
patient.  As  a  rule,  small  quantities  of  ice-cold  milk  are  the  best  of  anything, 
as  food. 

The  treatment  of  circumscribed  peritonitis  should  conform  in  general  to  the 
above  indications.  In  suitable  cases  operative  interference  may  be  of  great  value ; 
but  upon  this  point  we  refer  to  works  on  surgery. 


CHAPTER  II. 
CHRONIC  PERITONITIS.     TUBERCULAR   PERITONITIS. 

iEtiology. — Chronic  peritonitis,  not  tubercular,  is  a  rather  rare  disease.  It  is 
found  most  frequently  in  post-mortem  examinations  of  patients  who  have  had  for 
a  long  while  ascites  due  to  venous  stasis — for  example,  in  chronic  cardiac  or 
hepatic  cases.  The  chronic  peritonitis,  however,  is  not,  as  a  rule,  the  direct  result 
of  the  passive  hyperemia  in  such  cases,  but  is,  as  already  hinted,  due  to  the  punc- 
turing of  the  abdomen  during  life  for  the  removal  of  the  ascitic  fluid.  Exception- 
ally, a  chronic  peritonitis  occurs  as  a  sequel  to  some  severe  intestinal  disorder, 
such  as  ulceration.  Thus,  chronic  peritonitis  is  sometimes  observed  to  follow 
typhoid  fever. 

Chronic  peritonitis  may  furthermore  be  the  result  of  an  acute  peritonitis.  The 
latter  seldom  terminates  in  this  way,  but  still  it  may,  when  rather  mild  and  not 
quickly  fatal.  The  encapsulated  exudations  of  peritonitis  usually  persist  a  long 
while,  as  was  implied  in  the  preceding  chapter. 

In  a  few  instances  we  can  find  no  satisfactory  cause  for  chronic  peritonitis.  It 
is  sometimes  ascribed  to  an  injury.  Alcoholic  excesses  are  also  said  to  predispose 
to  the  disease.  Many  of  the  apparently  spontaneous  cases,  however,  finally  turn 
out  to  be  tubercular. 

The  tubercular  is  the  most  frequent  form  of  chronic  peritonitis.  It  is  often 
merely  a  part  of  the  tuberculosis  of  serous  membranes  in  general  (vide  pages  261 
and  327),  of  which  mention  has  been  already  repeatedly  made.  In  these  cases  it  is 
usually  due  to  a  conveyance  of  the  process  from  the  pleura  through  the  diaphragm. 
Another  way  in  which  tubercular  peritonitis  may  arise  is  by  infection  from  neigh- 
boring tubercular  organs.  Tubercular  intestinal  ulcers  are  among  the  chief  causes 
of  this  kind,  the  ulcer  extending  to  the  peritoneum ;  or  the  peritonitis  may  be  ex- 
cited by  tubercular  retroperitoneal  or  mesenteric  lymph-glands.     In  women  a 


458  DISEASES  OF  THE  DIGESTIVE   ORGANS. 

tubercular  peritonitis  may  be  developed  in  consequence  of  tuberculosis  of  the 
genital  organs.  A  tuberculosis  of  the  uterus  sometimes  affects  tbe  Fallopian  tubes 
by  direct  extension,  and  tlience  tbe  virus  enters  tbe  abdominal  cavity  and  excites 
its  specific  inflammation.  In  conclusion,  we  bave  to  mention  tbat,  in  general 
miliary  tuberculosis,  the  peritoneum  also  may  be  tbe  seat  of  numerous  tubercles, 
although  these  do  not  as  a  l'ule  give  rise  to  important  symptoms. 

Pathology. — After  well-marked  cases  of  chronic  peritonitis,  the  peritoneum  is 
usually  found  to  be  considerably  thickened.  The  intestinal  coils  are  joined  to 
one  another  and  to  the  neighboring  organs  by  numerous  and  extensive  adhesions. 
It  is  often  a  hard  matter  to  disentangle  the  confused  mass  into  which  the  intes- 
tines have  been  rolled.  Sometimes  the  liver  and  spleen  are  covered  by  firm, 
tough  capsules.  The  omentum  and  mesentery  are  much  shrunken;  hence  the 
name  peritonitis  deformans.  The  mesentery  may  indeed  be  transformed  into  a 
single  thick  cord.  As  a  rule,  there  is  little  liquid  effusion,  and  perhaps  none.  In 
simple  chronic  peritonitis,  such  fluid  as  may  be  present  is  usually  a  cloudy  serum, 
pus  being  seldom  seen. 

The  milder  forms  of  simple  chronic  peritonitis  occur  oftenest,  as  we  have  said, 
in  cases  of  ascites  due  to  venous  stasis,  after  repeated  tappings.  It  is  frequently 
possible  to  detect  the  points  where  the  trocar  has  pierced  the  internal  layer  of  the 
abdominal  wall,  by  adhesions,  minute  haemorrhages,  or  other  lesions.  The  false 
membranes  which  exist  in  these  cases  are  often  very  numerous,  but  they  are  usu- 
ally not  dense  and  are  easily  separable.  The  serous  liquid  found  in  the  abdominal 
cavity  is  partly  a  transudation,  but  contains  clumps  of  fibrine  in  more  or  less 
abundance.  In  rare  instances  a  peculiar  form  of  chronic  peritonitis  has  been 
observed  as  a  sequel  to  punctures  for  ascites,  called  by  Friedreich  "  chronic  hemor- 
rhagic peritonitis  with  haematoma."  In  it  almost  the  entire  peritoneum  is  covered 
by  a  newly  formed  membrane  permeated  with  large  ecchymoses. 

Tubercular  disease  of  the  peritoneum  may  be  divided  into  two  forms:  tuber- 
culosis of  the  peritoneum,  which  may  be  acute  or  chronic ;  and  tubercular  peri- 
tonitis, which  is  usually  chronic.  In  tuberculosis  the  peritoneum  is  covered 
with  numerous  tubercular  nodules,  varying  in  size  from  a  millet-seed  up  to  a  pea; 
but  there  is  not  much  coincident  inflammatory  change.  In  genuine  tubercular 
peritonitis,  on  the  other  hand,  the  inflammatory  changes  above  described  are  well 
marked,  while  sometimes  it  requires  a  microscopic  examination  to  demonstrate  the 
tubercular  nature  of  the  inflammation,  by  the  detection  of  tubercles  and  cheesy 
degeneration  in  the  newly  formed  tissue.  Tubercular  peritonitis  is  usually  rather 
chronic,  so  that  the  adhesions  are  numerous  and  strong.  The  amount  of  liquid 
effusion  varies,  being  sometimes  considerable  and  sometimes  scanty.  Just  as  in 
tubercular  pleurisy,  it  is  not  rare  for  the  exudation  to  be  bloody.  Tubercular  peri- 
tonitis is  quite  often  accompanied  by  hepatic  cmhosis  (q.  v.). 

Clinical  History. — Diagnosis. — If  an  acute  peritonitis  becomes  chronic,  the 
violent  symptoms  gradually  abate,  while  another  group  of  symptoms  takes  their 
place.     In  other  cases  the  chronic  disease  develops  gradually  and  insidiously. 

The  sensitiveness  of  the  abdomen  is  never  so  extreme  as  in  the  acute  inflamma- 
tion. Sometimes,  tobe  sure,  the  patient  complains  of  dull  pains  and  a  sense  of 
abdominal  oppression,  but  quite  often  the  pain  is  either  constantly  or  at  times 
insignificant.  On  physical  examination,  we  usually  find  moderate  distention  of 
the  abdomen.  Frequently  this  is  not  perfectly  uniform,  certain  coils  of  intestine 
being  especially  prominent.  Occasionally  there  is  no  abdominal  distention  what- 
ever, the  belly  is  flat  or  concave,  and  the  walls  are  tense  and  unyielding. 

In  many  instances  palpation  furnishes  very  characteristic  signs;  for  sometimes 
the  thickening  of  the  omentum  and  the  numerous  fibrous  inter-intestinal  bands 
above  described  can  be  felt  through  the  abdominal  walls  as  peculiarly  resistant 


CHRONIC  PERITONITIS.     TUBERCULAR  PERITONITIS.  I.V.; 

masses  or  uneven  prominences.  Indeed,  if  the  omentum  is  rolled  up,  it  may 
closely  simulate  a  new  growth.  Not  infrequently,  particularly  in  tubercular  peri- 
tonitis, the  liver  is  enlarged  so  that  its  lower  edge  can  be  felt.  But  in  other  cases 
of  chronic  peritonitis  there  are  no  changes  discoverable  by  palpation  ;  or  they  may 
be  concealed  by  an  effusion  or  by  the  tenseness  of  the  abdominal  walls.  A  large 
exudation  can  be  demonstrated  by  the  great  distention,  or  by  its  causing  fluctua- 
tion, or  by  the  signs  yielded  on  percussion.  In  general,  uncomplicated  cases  do 
not  give  rise  to  great  accumulations  of  fluid.  Such  accumulations  are  almost 
invariably  present  when  tubercular  peritonitis  and  cirrhosis  of  the  liver  are  com- 
bined ;  and  here  there  are  usually  also  passive  congestion  and  enlargement  of  the 
spleen.  It  has  been  already  stated  that  the  distortions  and  flexions  which  the 
intestines  may  undergo  in  chronic  peritonitis  may  result  in  obstruction.  In  the 
same  way  the  duodenum  or  the  ductus  choledochus  maybe  so  occluded  as  to 
occasion  persistent  jaundice. 

The  objective  signs  of  both  the  simple  and  tubercular  forms  of  chronic  peri- 
tonitis have  been  embraced  in  one  description,  because  the  abdominal  signs  of  the 
two  are  identical.  To  differentiate  between  them,  other  factors  must  be  considered. 
We  regard  the  patient's  constitution  and  general  appearance,  and  inquire  into  his 
family  history,  or  discover  if  there  are  other  aetiological  factors,  such  as  previous 
tubercular  disease.  A  careful  thoracic  examination  is  extremely  important.  If 
we  find  the  signs  of  coincident  pulmonary  tuberculosis,  and  particularly  of  pleu- 
risy, then  it  is  almost  indubitable  that  the  peritonitis  is  tubercular.  The  character 
of  the  exudation  is  also  of  some  importance,  for  if  haemorrhagic,  as  already  stated 
the  peritonitis  is  probably  tubercular.  Tubercle  bacilli  are  not  usually  present  in 
the  exudation  of  tubercular  peritonitis. 

To  diagnosticate  simple  tuberculosis  of  the  peritoneum,  when  not  attended  by 
marked  inflammatory  changes,  is  generally  a  difficult  matter.  Often  it  is  abso- 
lutely impossible.  Frequently  there  is  no  abdominal  pain  or  tenderness  whatever. 
The  abdomen  is  usually  but  moderately  distended,  as  a  result  of  the  effusion 
present. 

Particular  notice  should  be  given  to  the  chronic  peritonitis  of  children.  The 
occurrence  of  ascites  in  children  between  the  ages  of  two  and  ten  years  has 
been  observed  repeatedly,  both  by  other  authors  and  by  ourselves.  The  ascites, 
which  may  be  quite  considerable,  can  not  be  traced  to  any  cause,  and  after  a 
few  months  completely  disappears.  The  child  during  this  time  is  usually  rather 
pale  and  languid,  but  not  much  emaciated,  nor  does  he  suffer  great  local  discom- 
fort. Since  the  cases  often  recover,  their  pathological  anatomy  remains  obscure. 
Probably  they  are  a  mild  form  of  simple  chronic  peritonitis.  Still,  of  course 
there  may  be  other  causes  for  the  ascites,  such  as  hereditary  syphilitic  disease  of 
the  liver. 

In  children,  tubercular  peritonitis  plays  an  important  part  in  general  tubercu- 
losis of  the  abdominal  organs,  a  condition  known  as  tabes  mesenterica.  In  these 
cases  the  tuberculosis  probably  originates,  as  we  have  already  said,  in  the  intes- 
tine, so  that  usually  we  find  the  intestine,  peritoneum,  liver,  and  abdominal  lymph- 
glands  all  simultaneously  involved.  The  clinical  symptoms  are  often  mainly  due 
to  the  peritonitis.  The  abdomen  is  distended  and  painful,  and  there  is  an  effusion. 
Often  there  is  also  obstinate  diarrhoea,  as  a  result  of  tubercular  intestinal  ulcers, 
with  persistent  fever  of  an  intermittent  character,  emaciation,  and  anaemia.  The 
tubercular  process  may  eventually  involve  the  lungs,  pleura,  meninges,  and  other 
organs,  or  it  may  never  extend  beyond  the  abdomen. 

As  to  the  course  of  chronic  peritonitis  we  have  little  to  say.  The  simple 
chronic  peritonitis  may  terminate  in  recovery,  although  on  account  of  other 
co-existing  lesions  this  event  is  rare,  except  in  the  special  form  which  children 


460  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

present.  Many  cases  of  tubercular  peritonitis  prove  fatal  in  a  few  months  01 
weeks.  In  some  instances,  however,  chronic  tubercular  peritonitis  has  a  favorable 
issue,  or  at  least  there  is  very  great  abatement  of  all  symptoms.  This  is  particu- 
larly apt  to  be  the  case  in  what  is  called  primary  tuberculosis  of  the  sei*ous  mem 
branes  in  general  {vide  supra).  If,  in  this  disease,  there  is  no  simultaneous 
tuberculosis  of  the  lungs,  intestines,  or  other  organs,  then  the  final  reabsorption 
of  the  exudation  is"  possible,  just  as  in  tubercular  pleurisy.  It  must  be  confessed 
that  often  the  recovery  is  not  permanent,  for  the  tubercles  may  appear  later  in 
some  other  part  of  the  body. 

Treatment.— The  means  by  which  we  can  exercise  a  favorable  influence  upon 
the  course  of  chronic  peritonitis  are  scanty.  Attention  to  nourishment  and 
hygienic  surroundings  is  very  important;  but,  beyond  this,  treatment  is  mainly 
symptomatic.  The  chief  local  applications  are  poultices  or  fomentations,  perse 
veringly  employed.  There  is  seldom  such  persistent  and  severe  pain  as  to  demand 
opiates,  but  they  may  be  required  for  the  diarrhoea  which  is  apt  to  occur.  Or, 
on  the  other  hand,  enemata  and  mild  laxatives  may  be  indicated.  Among  special 
remedies,  the  preparations  of  iodine  should  be  mentioned ;  iodide  of  potassium 
and  syrup  of  the  iodide  of  iron  sometimes  are  of  apparent  benefit.  Arsenic  may 
also  be  tried.  Iron  and  syrup  of  the  iodide  of  iron  are  also  employed  in  the 
chronic  peritonitis  of  children. 

[Of  recent  years  laparotomy  has  been  repeatedly  practiced  in  tubercular  peri- 
tonitis, and  has  been  held  by  some  to  be  distinctly  curative.  In  the  opinion  of 
the  editor,  what  surgery  has  done  for  us  in  this  affection  is  rather  to  demonstrate 
the  curability  of  many  cases  than  to  work  their  cure.  Formerly,  if  the  diagnosis 
of  tubercular  peritonitis  was  made  and  the  patient  recovered,  the  very  fact  of 
racovery  was  held  to  invalidate  the  diagnosis.  But  the  surgeon's  knife  has  laid 
bare  the  miliary  tubercles  to  the  eye,  given  an  exit  to  the  serous  exudation,  and 
recovery  has  ensued.  But  we  see  other  cases  get  well  after  simple  tapping,  and 
we  see  still  others  which  present  just  as  good  a  clinical  picture  of  the  affection 
and  recover  without  interference  of  any  kind.  Such  recovery  may  be  temporary, 
tuberculosis  breaking  out  afresh  in  the  peritoneum  or  elsewhere,  or  it  may  be 
permanent.  If,  in  spite  of  rest  and  appropriate  general  treatment,  considerable 
effusion  persists,  aspiration  or  siphonage  should  be  practiced.  Laparotomy  should 
probably  be  reserved  for  those  rather  rare  cases  which  seem  to  be  rapidly  getting 
worse,  and  those  in  which  the  fluid  reaccumulates  after  one  or  more  tappings. 

In  expressing  the  belief  that  tubercular  peritonitis  recovers,  the  editor  does  not 
lose  sight  of  the  fact  that  multiple  fibrous  nodules  occur  disseminated  over  the 
peritoneum,  indistinguishable  by  the  unaided  eye  from  tubercles.] 


CHAPTER  III. 

ASCITES. 

( Tlydroperiton  eum.) 

The  name  ascites  is  given  to  a  collection  of  transuded  serum  in  the  abdominal 
cavity,  due  to  venous  stasis.  The  peritoneal  veins  belong  to  the  portal  system,  so 
that  among  the  diseases  which  lead  to  ascites  those  which  impede  the  portal  cir- 
culation are  chief.  As  we  shall  see  in  the  next  section,  ascites  is,  therefore,  of  fre- 
quent occurrence  in  cirrhosis  of  the  liver,  syphilitic  disease  of  the  liver,  compres- 
sion of  the  portal  vein  by  tumors,  thrombosis  of  the  portal  vein,  and  similar 


ASCITES.  401 

disorders.  Ascites  is  also  frequently  present  as  one  of  the  dropsical  Symptoms  in 
general  circulatory  disturbances,  such  as  cardiac  disease  or  pulmonary  emphysema, 
and  in  the  various  acute  and  chronic  renal  affections. 

The  clinical  significance  of  ascites  is  due  partly  to  the  local  discomfort  occa- 
sioned by  the  presence  of  any  considerable  amount  of  fluid  within  the  abdominal 
cavity.  Small  quantities  of  serum  are  often  unnoticed  by  the  patient;  but,  where 
many  quarts  (fifteen  to  twenty,  or  even  more)  of  transudation  exist,  the  abdomi- 
nal walls  become  greatly  distended,  and  the  patient  has  a  very  troublesome  feeling 
of  pressure,  weight,  and  tension.  What  is  of  still  greater  importance  is  the  crowd- 
ing upward  of  the  diaphragm.  Kespiration  is  thereby  not  a  little  impeded.  If 
the  ascites  is  great,  the  lower  lobes  of  the  lungs  are  so  compressed  that  a  consider- 
able degree  of  atelectasis  is  produced. 

To  demonstrate  ascites  by  physical  examination  is  possible  only  when  a  con- 
siderable accumulation  exists.  Then  the  belly  is  prominent,  its  walls  are  tense 
and  shining,  and,  the  base  of  the  thorax  being  gradually  distended  by  the  pressure 
of  the  liquid,  the  lower  part  of  the  thorax  seems  much  broader  than  the  upper. 
Distended  veins  are  usually  visible  through  the  skin  of  the  abdomen,  like  blue 
lines,  here  and  there.  As  soon  as  the  abdominal  tension  has  attained  a  certain 
degree,  fluctuation  can  be  perceived,  by  laying  both  hands  upon  the  abdomen  and 
imparting  gentle  but  quick  impulses  to  the  fluid  thi'ough  the  walls.  Percussion 
gives  a  dull  sound  everywhere  that  the  fluid  is  in  contact  with  the  abdominal 
walls.  Gravity,  of  course,  leads  the  liquid  to  occupy  the  dependent  parts.  In  the 
dorsal  decubitus,  and  when  the  transudation  is  of  medium  amount,  the  dullness  is 
bounded  in  the  central  and  upper  parts  of  the  abdomen  from  a  region  of  tympa- 
nitic resonance  by  a  line  concave  toward  the  head  of  the  patient.  The  surface  of 
the  liquid  being  horizontal,  of  course  the  dullness  reaches  nearer  to  the  thorax 
along  the  sides  of  the  abdomen  than  in  the  central  line.  We  would  add,  that 
where  the  layer  of  ascitic  fluid  is  thin  we  can  obtain  dullness  only  by  light,  super- 
ficial percussion.  If  the  pleximeter  or  finger  is  pressed  deeply  in,  the  fluid  is 
crowded  to  one  side,  and  we  get  a  tympanitic  sound  from  the  underlying  coils  of 
intestine.  A  factor  of  great  diagnostic  value  is  the  change  of  dullness  on  change 
of  position  of  the  patient.  If  he  lies  upon  one  side,  the  fluid  seeks  the  dependent 
portions  of  the  cavity,  and  gives  rise  to  extensive  dullness  there,  while  the  oppo- 
site side  now  yields  a  tympanitic  resonance.  Or,  if  he  changes  to  the  other  side, 
it  in  turn  becomes  dull,  and  the  side  previously  dull  becomes  tympanitic.  Similar 
differences  are  found  between  the  results  of  percussion  in  a  horizontal  and  in  a 
sitting  posture.  It  is  only  when  the  accumulation  is  very  abundant  that  there  is 
dullness  over  the  entire  abdomen. 

The  signs  mentioned  enable  us  in  most  cases  to  make  a  diagnosis  of  ascites 
with  ease  and  certainty.  It  is,  indeed,  not  always  easy  to  distinguish  a  transuda- 
tion of  serum  from  the  exudation  of  chronic  peritonitis,  for,  of  course,  either  sort 
of  fluid  would  yield  the  same  physical  signs.  Only,  the  change  in  the  area  of 
dullness  consequent  upon  a  change  of  position  is  less  pronounced  in  case  of  an 
exudation,  because  the  peritonitic  adhesions  impede  the  movements  of  the  fluid ; 
and  we  have,  besides,  all  the  other  symptoms  to  guide  us;  there  maybe  pain, 
or  thickenings  of  the  peritoneum  discoverable  on  palpation,  or  signs  of  tuber- 
culosis; or,  on  the  other  hand,  there  may  be  some  cardiac  or  hepatic  disease, 
which  would  render  ascites  probable.  If  the  fluid  i  ■  drawn  off,  its  character  will 
sometimes  aid  us  in  diagnosis.  Ascites  yields  pure  serum,  containing  almost  no 
morphological  constituents.  Its  specific  gravity  is  usually  less  than  that  of  a 
peritonitic  exudation,  because  it  contains  less  albumen.  We  may  say  that  the 
specific  gravity  of  the  fluid  found  in  peritonitis  is  generally  above  1018,  and  that 
of  ascites  about  1012,  or  even  lowrer.     Hemorrhagic  ascites  sometimes  occurs  in 


462  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

anaemic,  patients  who  are  suffering-  from  marked  portal  obstruction,  as  we  have 
ourselves  seen,  for  example,  in  hepatic  syphilis. 

There  may  be  equal  difficulty  in  the  exclusion  of  ovarian  cysts,  particularly 
since  the  cysts  are  sometimes  so  large  as  to  fill  the  whole  abdominal  cavity.  We 
must  first  map  out  accurately  the  dullness  on  percussion,  and  also  see  if  it  varies 
with  changes  of  position.  In  cases  of  ovarian  tumor,  change  of  position  does  not 
make  much  difference.  The  resonance  on  percussion  of  the  deepest  and  most 
dependent  portions  of  the  abdomen  may  be  misleading,  in  this  way,  that  even  in 
ascites  a  narrow  zone  here  may  be  tympanitic.  This  should  be  remembered. 
Thus,  just  above  the  symphysis,  there  is  sometimes  a  tympanitic  resonance  in 
ascites  which  might  readily  be  mistaken  for  a  proof  of  the  existence  of  an  ovarian 
tumor.  The  explanation  is  that  in  the  places  indicated  a  coil  of  intestine  with  a 
short  mesenteric  attachment  may  remain  in  contact  with  the  abdominal  wall  in 
spite  of  ascitic  accumulations.  Further  aid  in  the  differential  diagnosis  is  to 
be  obtained  from  the  history  of  the  case  (place  where  the  swelling  began),  from  a 
consideration  of  possible  causative  diseases,  and  from  a  vaginal  examination.  In 
ascites  the  uterus  is  freely  movable,  while  in  case  of  ovarian  tumors  it  is  often 
bound  down  by  adhesions.  Further  particulars  may  be  sought  in  books  on 
gynaecology. 

The  treatment  of  ascites,  of  course,  depends  largely  upon  the  disease  of  which 
it  is  a  symptom.  As  to  the  symptomatic  treatment  of  ascites  itself,  we  will  con- 
fine ourselves  to  a  few  words  about  tapping.  This  operation  is  indicated  when 
the  local  disturbances  caused  by  the  ascites  are  great;  that  is,  if  there  is  an  unbear- 
able sensation  of  pressure  and  tension,  and,  above  all.  if  the  crowding  up  of  the 
diaphragm  causes  much  dyspnoea.  The  instrument  to  be  used  is  a  common  trocar 
of  medium  size.  Usually  the  patient  is  tapped  lying  on  his  side  in  bed,  at  the 
most  dependent  point  in  the  lateral  portion  of  the  abdominal  walls;  but  it  is  also 
a  good  way  to  make  the  puncture  in  the  median  line,  about  half-way  between 
the  umbilicus  and  the  pubes,  with  the  patient  in  a  chair.  The  operation  is 
easy,  and  almost  free  from  danger.  We  may  allow  large  amounts  of  liquid 
(five  or  ten  quarts,  or  more)  to  flow  slowly  away  at  one  tapping.  Over  the 
puncture  we  put  a  piece  of  sticking  plaster,  or,  if  great  caution  is  to  be  exercised, 
an  antiseptic  bandage.  Often  the  fluid  trickles  out  through  the  opening,  be- 
cause the  abdominal  walls  have  lost  their  elasticity  on  account  of  the  per- 
sistent distention.  We  may  then  employ  a  "  circumvoluted  suture  "  to  close  it. 
After  tapping,  the  laxness  of  the  walls  is  favorable  to  palpation  of  the  abdominal 
organs. 

Inasmuch  as  tapping  does  not  remove  the  cause,  there  is  in  most  cases  a  very 
rapid  reaccumulation  of  fluid.  Thus  the  system  is  deprived  of  much  albumen, 
and  nutrition  is  impaired,  so  that  not  infrequently  the  operation  is  followed  by 
decided  loss  of  strength.  Therefore,  we  should  not  tap  in  ascites,  as  a  rule,  unless 
the  indications  for  the  operation  are  urgent. 

[Before  puncture  the  precaution  should  always  be  observed  to  see  that  the 
bladder  is  empty. 

If,  as  is  very  frequently  the  case,  the  fluid  continues  to  drain  away  through  the 
puncture  after  the  trocar  is  withdrawn,  good  rather  than  harm  results,  provided 
the  danger  of  irritation  of  the  skin  and  of  bed-sores  is  kept  in  mind  and  guarded 
against,  and  an  instrument  of  moderate  size  is  used. 

Flint  advocates  early  and  repeated  tappings  if  the  fluid  causes  discomfort  and 
does  not  yield  to  diuretics  or  cathartics.  The  pressure  is  removed  in  a  measure 
from  the  abdominal  and  thoracic  organs,  and  nutrition  is  thus  promoted.  The 
fluid  is  likely  to  return,  but  does  not  always  do  so,  or  may  do  so  only  slowly.  He 
reports  cases  in  which,  after  repeated  removal,  the  fluid  ceased  to  return  and  the 


CANCER  OF  THE  PERITONEUM.  463 

patient  remained  apparently  well.     The  result  must  depend,  of  course,  chiefly  on 
the  underlying  cause,  which  is  sometimes  very  obscure. 

In  cases  of  cirrhosis  the  same  principles  govern  Flint's  treatment.] 


CHAPTER  IV. 
CANCER   OF   THE    PERITONEUM. 

Carcinoma  is  the  only  new  growth  of  any  practical  importance  to  which  the 
peritoneum  is  liable.  Primary  endothelial  cancer,  analogous  to  the  growth  which 
attacks  the  pleura,  is  very  rare.  Cancerous  growths  here  are  usually  secondary 
to  cancer  of  the  stomach,  intestine,  pancreas,  liver,  or  some  other  organ.  Often 
the  secondary  nodules  are  numerous,  and  almost  as  small  as  peas,  presenting  what 
is  called  miliary  carcinosis  of  the  peritoneum.  Separate  nodules  of  larger  size  are 
less  frequent.  These  may  be  found  in  the  omentum,  in  Douglas's  pouch,  around 
the  navel,  or  in  other  situations.  Colloid  cancer  attains  the  most  diffuse  and  exten- 
sive development  of  any  variety.  The  retroperitoneal  lymph -glands  may  also 
present  at  the  same  time  large  cancerous  growths.  Often  the  development  of 
cancer  in  the  peritoneum  is  attended  with  pronounced  inflammatory  disturbances 
— that  is,  we  have  a  cancerous  peritonitis. 

The  symptoms  of  peritoneal  cancer  resemble  in  many  points  those  of  chronic 
tubercular  peritonitis.  Simple  miliary  carcinosis  may  be  very  insidious  and  give 
rise  to  no  special  symptoms,  so  that  it  often  is  unsuspected.  In  many  cases  a 
moderate  amount  of  fluid  collects  in  the  abdomen,  and  this,  if  we  are  aware  of  the 
existence  of  a  primary  cancerous  growth,  may  lead  us  to  surmise  a  secondary  peri- 
tonea] carcinosis.  The  symptoms  are  much  more  pronounced  if  there  is  cancer- 
ous peritonitis.  In  that  case  there  is  usually  very  severe  pain,  marked  abdominal 
distention,  and  constipation.  We  may  sometimes  feel  the  larger  nodules  in  the 
omentum  or  upon  the  inner  surface  of  the  anterior  wall  of  the  abdomen,  or  even 
those  in  the  lowest  part  of  the  abdomen,  by  palpation  through  the  vagina.  If  the 
exuded  fluid  be  drawn  off,  it  is  sometimes  merely  serous,  but  it  may  be  haemor- 
rhagic.  When  the  new  growth  has  been  diffuse,  and  particularly  in  case  of  colloid 
cancer,  the  exudation  has  repeatedly  been  found  to  present  a  milky  opacity. 
Sometimes  this  fluid  also  has  been  tinged  with  blood.  The  opacity  is  due  to  fat, 
from  fatty-degenerated  and  disintegrated  cancer  cells.  Occasionally  the  micro- 
scope reveals  characteristic  cancerous  elements  in  the  fluid. 

The  diagnosis  can  not  be  made  with  any  positiveness  unless,  as  a  sequel  to  a 
primary  cancerous  growth  already  demonstrated,  we  observe  the  evident  tokens 
of  peritoneal  disturbance,  such  as  free  fluid  and  pain.  Other  points  are  the 
patient's  age,  cancerous  cachexia,  and  secondary  glandular  enlargements,  particu- 
larly in  the  groins. 

Treatment  must  be  confined  to  efforts  at  mitigaiion  of  the  suffering.  Warm 
applications,  morphine,  and  supporting  measures  are  chiefly  employed. 


464  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

SECTION    VII. 

Disk  asks   of  the  Liver,  Bile-ducts,  and   Portal   Vein. 

CHAPTER  I. 

CATARRHAL   JAUNDICE. 

{Icterus  catarrhalis.     G astro-duodenal  Catarrh  with  Jaundice.) 

iEtiology. — When  discussing  intestinal  catarrh,  we  mentioned  that  inflamma- 
tion of  the  duodenum  may  invade  the  secretory  ducts  of  the  liver,  and,  ahove  all, 
the  ductus  choledochus  communis.  This  complication  would  be  of  little  clinical 
importance  did  it  not  in  many  instances  prevent  the  flow  of  bile  into  the  intes- 
tine. Such  an  obstruction  at  once  gives  pathological  interest  to  a  catarrh  of  the 
bile-ducts,  because  it  entails  a  series  of  very  important  clinical  symptoms.  In  this 
case  the  cause  of  the  biliary  stasis  is  purely  mechanical,  and  any  closure  of  the 
hepatic  ducts,  however  produced,  gives  rise  to  identical  symptoms,  which  vary,  if 
at  all,  only  in  their  duration  and  intensity.  Catarrhal  jaundice  is  therefore  only 
one  form,  though  the  most  frequent  form,  of  what  is  called  hepatogenous  jaundice. 
Accordingly,  we  will  in  this  chapter  describe  in  detail  the  general  phenomena 
common  to  all  cases  of  hepatogenous  jaundice,  that  we  may  avoid  needless  repeti- 
tions hereafter. 

The  causes  which  lead  to  a  gastro-duodenal  catarrh,  with  consequent  jaundice, 
may  be  the  same  which  produce  ordinary  gastric  catarrh — such  as  errors  in  diet. 
But  we  must  emphasize  the  fact  that  we  see  catarrhal  jaundice  so  often  without 
any  striking  cause,  as  strongly  to  suggest  the  thought  of  some  specific  lesion, 
some  special  pathogenic  agent.  The  precise  facts  are  indeed  yet  to  be  learned ; 
still  it  has  been  often  observed  that  at  many  times  (particularly  in  spring  and 
autumn)  it  assumes  epidemic  proportions.  The  infectious  nature  of  the  jaundice 
is  still  more  probable  in  those  cases  where  the  disease  is  decidedly  endemic.  In 
barracks,  prisons,  and  single  houses  quite  important  endemics  of  jaundice  have 
been  seen,  the  only  explanation  for  which  could  be  found  in  assuming  the  exist- 
ence of  some  local  source  of  infection.  In  a  few  cases,  epidemics  of  catarrhal 
jaundice  have  followed  revaccination,  compelling  one  to  think  that  possibly  the 
pathogenic  agent  was  transferred  by  inoculation.  Patients  themselves  not  infre- 
quently refer  to  taking  cold,  or  to  mental  emotion  (particularly  anger),  as  circum- 
stances promoting  the  disease. 

Another  cause  is  the  rather  frequent  occurrence  of  duodenal  catarrh  as  a  result 
of  passive  congestion.  This  is  seldom  very  intense.  It  is  especially  frequent  in 
heart  disease.  Again,  the  slight  jaundice  quite  often  seen  in  the  course  of  many 
acute  diseases,  and  of  lobar  pneumonia  in  particular,  must  be  ascribed  to  catarrh. 

Pathology. — As  in  catarrhal  affections  of  most  other  mucous  membranes,  the 
post-mortem  signs  of  catarrh  of  the  bile-ducts  are  not  always  striking,  for  the 
swelling  and  injection  subside  considerably  after  death.  The  usual  method  of 
testing  the  patency  of  the  common  duct  is  by  pressing  upon  the  gall-bladder  to 
see  if  its  contents  can  be  squeezed  out  into  the  intestinal  canal.  If  a  catarrh  has 
closed  the  common  duct,  the  bile  is  not  discharged  at  once.  A  firmer  pressure 
drives  out  from  the  opening  of  the  duct  a  plug  of  tough,  white  mucus,  upon  which 
the  bile  follows;  but  such  a  plug  is  not  present  in  every  case,  by  any  means,  for 
even  a  simple  swelling  of  the  catarrhal  membrane  suffices  to  obstruct  the  flow 
of  bile. 

If  the  biliary  passages  are  slit  open,  the  common  duct  is  found  more  or  less 


CATARRHAL  JAUNDICE.  405 

filled  with,  tough,  white  mucus.  Usually  the  portion  which  lies  in  the  intestinal 
wall,  the  so-called  intestinal  portion,  is  most  affected.  Behind  the  occluded  part 
the  ducts  are  distended,  if  the  biliary  retention  has  been  chronic.  This  distention 
may  involve  even  the  smallest  ducts,  which  lie  in  the  liver  itself.  As  a  conse- 
quence, the  liver  is  somewhat  enlarged  and  has  a  diffuse  bilious  tinge.  If  the 
obstruction  persists  for  a  long  while,  which  is  very  exceptional  in  simple  catarrhal 
jaundice,  a  portion  of  the  hepatic  cells  are  destroyed  by  the  pernicious  influence 
of  the  retained  secretion.  The  lost  parenchyma  is  replaced  by  new-formed  con- 
nective tissue.     For  further  particulars,  see  the  chapter  on  biliary  cirrhosis. 

Clinical  History. — Inasmuch  as  catarrh  of  the  ductus  communis  is  almost 
always  consequent  upon  a  gastro-duodenal  catarrh,  the  first  symptoms  are  usually 
referable  to  the  latter  disease.  It  is  indeed  seldom  that  the  attack  begins  with 
marked  gastric  disturbances,  like  violent  vomiting  and  gastralgia,  but  almost  inva- 
riably the  jaundice  is  preceded  for  a  variable  period  by  indisposition,  as  shown  by 
malaise,  languor,  anorexia,  a  bad  taste  in  the  mouth,  nausea,  gastric  oppression, 
eructations,  and  sometimes  temporary  vomiting.  Then  comes  the  first  evidence 
that  the  catarrh  has  invaded  the  common  duct,  in  a  jaundiced  hue  of  the  skin  and 
of  the  visible  mucous  membranes.  In  many  cases,  however,  the  initiatory  gastric 
symptoms  are  almost  wholly  absent,  so  that  the  disease  begins  immediately  with 
the  appearance  of  the  jaundice. 

The  pressure  in  the  secretory  ducts  of  the  liver  is  extremely  low,  so  that  even 
the  catarrhal  swelling  of  the  mucous  membrane  and  the  collection  of  viscid  mucus 
in  the  common  duct  suffice  to  impede  in  a  marked  degree  the  further  outflow  of 
bile  into  the -intestinal  canal.  As  a  rule,  however,  the  retention  of  bile  is  not  com- 
plete, or,  if  so,  only  for  a  time.  Still  a  considerable  amount  of  bile  collects,  and 
distends  even  the  intra-hepatic  ducts.  As  soon  as  this  stasis  has  reached  a  certain 
point,  the  stagnant  bile  is  absorbed  by  the  hepatic  lymph-vessels.  Thus  the  bile 
and  all  its  constituents  are  poured  into  the  blood  by  way  of  the  thoracic  duct  and 
carried  to  all  parts  of  the  body. 

No  more  than  a  few  days  need  elapse  before  the  bile-pigments  are  absorbed 
into  the  tissues,  and  give  rise  to  the  evident  yellow  color  of  the  skin  and  mucous 
passages  which  we  call  jaundice.  Usually  the  yellowness  of  the  conjunctiva  is  the 
first  thing  to  attract  attention.  Later  the  entire  skin  becomes  yellow,  and  the  same 
color  is  plainly  visible  in  the  mucous  membrane  of  the  mouth  and  throat,  espe- 
cially after  we  have  produced  temporary  anaemia  by  pressure,  as  in  the  lips.  Of 
course,  the  internal  organs,  which  we  can  not  see,  are  likewise  stained.  Any 
abnormal  collection  of  liquid  will  also  have  a  marked  yellow  color.  The  cornea, 
the  peripheral  nerves,  and  the  cartilages  alone  escape  unstained.  In  other  parts 
we  may  not  only  find  this  diffuse  impregnation  with  the  biliary  pigments,  but 
even  solid  granules  of  the  latter. 

A  jaundiced  patient  often  presents  other  indications  of  the  presence  of  biliary 
coloring  matter  than  the  color  of  his  skin.  If  the  jaundice  is  at  all  chronic,  there 
is  almost  invariably  an  itching  of  the  skin,  which  may  be  very  troublesome.  It 
may  be  so  bad  at  night  as  to  disturb  sleep.  The  scratching  thus  induced  often 
causes  numerous  excoriations  and  fissures,  which  may  even  occasion  quite  large 
furuncles.  Urticaria  is  also  sometimes  observed.  A  peculiar  disease  of  the  skin, 
which  has  been  chiefly  described  by  English  authors  in  connection  with  jaundice, 
is  called  xanthelasma.  It  presents  bright-yellow  spots,  usually  somewhat  elevated, 
which  are  found  mainly  on  the  eyelids,  though  also  on  other  parts  of  the  body. 

The  remaining  symptoms  of  hepatogenous  jaundice  may  be  divided  into  two 
groups.  The  first  group  comprise  the  symptoms  excited  by  the  presence  of  the 
biliary  constituents,  and  particularly  of  the  biliary  acids,  in  the  blood,  while  the 
second  group  are  due  to  the  lack  of  bile  in  the  intestinal  canal. 


466  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

We  have  seen  that,  when  the  biliary  outlets  are  occluded  or  narro wed,  the  con- 
stituents of  the  bile  are  absorbed  by  the  lymphatics.  We  have  already  learned  in 
part  what  becomes  of  the  bile-pigments  thus  conveyed  into  the  blood-vessels.  The 
presence  of  the  bile-acids  in  the  blood  is  also  of  considerable  clinical  importance. 
Physiology  has  shown  that  these  acids  possess  certain  poisonous  properties,  and, 
among  others,  the  power  to  destroy  red  blood-corpuscles.  But  in  reality  few  if  any 
blood-corpuscles  are  destroyed  by  the  bile-acids  in  tbe  blood,  because  they  are  too 
much  diluted,  and,  besides,  seem  in  large  part  to  be  quickly  decomposed  after 
absorption.  These  acids  do  really,  however,  excite  certain  nervous  centres  in  a 
way  to  give  rise  to  decided  clinical  symptoms.  The  most  frequent  effect  is  that 
produced  by  the  cholate  of  sodium  upon  tbe  cardiac  ganglia,  or  possibly  also 
upon  the  center  for  the  vagus,  and  it  is  evinced  by  a  slowing  of  the  pulse.  This 
is  an  almost  invariable  phenomenon,  provided  there  be  no  fever  or  other  complica- 
tion, and  is  seen  not  only  in  simple  catarrhal  jaundice  but  in  all  cases  of  hepatoge- 
nous icterus.  The  pulse-rate  is  from  64  to  50,  or  even  less.  Slight  irregularity 
in  the  heart's  action  is  not  infrequent.  There  are  certain  other  nervous  disturb- 
ances often  seen  in  jaundice  and  referable  to  the  presence  in  the  blood  of  bil- 
iary constituents,  and  in  particular  of  biliary  acids.  Sometimes  there  is  a  strik- 
ing languor  and  muscular  weakness,  or  headache,  or  the  patient  is  "out  of 
sorts."  Grave  nervous  symptoms,  sometimes  seen  in  jaundice  and  grouped  under 
the  name  of  cholcemia,  are  discussed  in  another  chapter.  It  also  deserves  a 
brief  mention  here  that  many  cases  with  marked  jaundice  have  a  noticeable 
tendency  to  bleeding — that  is,  a  sort  of  "  hemorrhagic  diathesis."  Haemorrhages 
into  the  skin  and  in  the  viscera  are  quite  often  seen,  and  also  epistaxis  and 
analogous  occurrences. 

We  now  come  to  the  second  group  of  symptoms,  which  result  from  lack  of 
bile  in  the  intestinal  canal.  It  will  be  easy  to  understand  these  if  we  briefly 
review  the  physiological  functions  assigned  to  the  bile  which  is  poured  into  the 
alimentary  canal.  Bile  plays  an  important  part  in  the  digestion  of  fat,  emulsify- 
ing it,  and  promoting  its  absorption  into  the  chyle-ducts.  Now,  in  hepatogenous 
icterus  this  work  remains  undone,  as  is  shown  by  the  fatty  stools.  From  time 
immemorial  the  white  clay-colored  stools  of  jaundice  have  been  well  known, 
and  are  employed  as  the  best  measure  of  the  completeness  of  biliary  retention. 
The  light  color  of  the  stools  is  partly  due  to  the  lack  of  biliary  pigment,  for  it 
is  that  chiefly  which  imparts  to  normal  fasces  their  dark-brown  color;  but  the 
characteristic  white  clay  color  is  due  exclusively  to  the  presence  of  undigested 
fat  in  large  amounts.  We  have  ourselves  performed  the  experiment  of  putting 
a  patient  with  extreme  hepatogenous  icterus  upon  a  diet  containing  as  little  fat 
as  possible,  and  have  found  that  the  stools  then  became  light  brown,  and  not  at 
all  like  clay.  Upon  microscopic  examination  of  the  fasces  in  jaundice,  sheaf-like 
aggregations  of  crystals  are  not  infrequently  observed.  These  were  formerly 
supposed  to  be  tyrosine,  but  Oesterlein  has  shown  them  to  be  in  reality  magnesia- 
soap. 

The  retention  of  bile  has  some  further  effects  besides  retarding  the  digestion 
of  fat.  Bile  possesses  decided  antiseptic  properties,  and  thus,  to  a  certain  extent, 
protects  the  contents  of  the  primas  viae  from  putrefaction.  In  hepatogenous 
jaundice,  therefore,  the  processes  of  decay  are  abnormally  active ;  the  faeces  are 
unusually  offensive,  and  there  is  an  excessive  generation  of  gas,  often  leading 
to  flatulence  and  tympanites.  The  bile  also  undoubtedly  stimulates  peristalsis, 
and  so  in  jaundice  there  is  often  constipation. 

One  important  function  of  the  bile  remains  to  be  considered — namely,  that  by 
precipitating  pepsine  it  terminates  peptic  digestive  action.  Kühn  has  shown 
how  necessary  this  is  to  the  normal  processes,  because  pepsine  will  destroy  pan- 


CATARRHAL  JAUNDICE.  4G7 

creatine,  and  therefore  interferes  with  pancreatic  digestion.  Hence  we  are  justi- 
fied in  assuming  that  in  well-marked  jaundice  the  digestive  action  of  the  pan- 
creatic juice  on  fat  and  albumen  is  probably  disturbed,  even  though  the  pancreas 
itself  secretes  normally.  Often,  and  in  catarrhal  jaundice  probably  as  a  rule,  the 
pancreatic  duct  is  obstructed  as  well  as  the  biliary,  so  that  not  only  the  bile,  but 
also  the  pancreatic  juice  is  retained.  Just  how  far  the  digestive  disturbances  are 
to  be  ascribed  to  the  lack  of  each  of  these  secretions  we  are  of  course  unable  to 
determine. 

We  must  now  inquire  what  becomes  of  the  absorbed  bile.  As  to  the  biliary- 
acids,  we  have  already  said  that  they  probably  undergo  decomposition.  Of  the 
other  constituents,  including  the  taurine  and  Cholesterine  and  the  pigmentary 
matters,  we  know  the  fate  of  the  last-named  only — that  is,  we  have  learned  how 
Nature  seeks  to  rid  herself  of  this  foreign  substance.  As  soon  as  the  amount  of 
bile-pigment  in  the  blood  and  tissues  becomes  considerable,  excretory  efforts  are 
made,  in  which  the  kidneys  take  the  chief  share.  Certain  changes  take  place  in 
the  urine  almost  simultaneously  with  the  first  appearance  of  a  jaundiced  hue  in 
the  skin ;  and  these  changes  are  due  to  the  urine  containing  excreted  biliary  color- 
ing matter. 

The  urine  of  jaundice  is  generally  recognizable  from  its  color,  which  is  a  dark 
brown,  like  beer.  The  foam  caused  by  shaking  it  is  not  white,  but  distinctly 
yellow.  A  bit  of  white  filter-paper  dipped  in  the  urine  is  stained  yellow.  If  the 
urine  is  mixed  with  chloroform  in  a  test-tube,  the  chloroform  dissolves  the  pigment, 
and,  on  being  allowed  to  collect  at  the  bottom  of  the  tube,  displays  a  deep-yellow 
color.  This  is  known  as  the  "chloroform  test."  Another  reaction  which  usually 
gives  a  satisfactory  result,  but  not  always,  is  Gmelin's.  If  urine  containing  bile- 
pigment  is  slowly  poured  down  the  sides  of  a  test-tube  containing  some  fuming 
nitric  acid,  the  zone  between  these  two  liquids  exhibits  a  fine  play  of  colors.  The 
effect  of  the  acid  upon  the  biliary  pigment  is  to  produce  a  number  of  colored  rings, 
the  highest  and  most  characteristic  of  which  is  green ;  next  comes  blue,  then  violet 
and  red.  Gmelin's  test  often  shows  very  prettily  if  one  filters  the  urine  and  then 
adds  a  drop  of  nitric  acid  to  what  remains  upon  the  moist  filter-paper.  The  char- 
acteristic colored  rings  form  around  this  drop. 

The  biliary  acids  also  may  be  detected  in  the  urine  of  jaundice ;  but  the  process 
is  somewhat  tedious,  and  the  knowledge  gained  is  of  no  practical  importance. 

The  urine  very  often  contains  morphological  elements  which  are  characteristic. 
Nothnagel  was  the  first  to  describe  minutely  the  icteric  casts — that  is,  hyaline  casts 
which  usually  have  a  yellow  tinge  and  quite  often  are  completely  covered  with 
dark-yellow  granules.  The  urine  may  contain  a  little  albumen  also,  but  this  is 
not  constant. 

[The  presence  or  absence  of  albumen  depends  largely  on  the  amount  of  the 
biliary  constituents  and  on  the  length  of  time  they  continue  in  action  on  the  kid- 
neys; their  effect  on  these  organs  is  more  or  less  that  of  an  irritant.] 

The  sweat-glands  a^o  take  part  in  the  excretion  of  bile-pigment.  The  latter 
can  be  demonstrated  in  the  perspiration  of  jaundiced  persons,  as  well  as  in  their 
urine.  Not  infrequently  the  patient's  linen  is  colored  yellow  by  the  sweat.  On 
the  other  hand,  no  bile-pigment  is  found  in  the  tears,  saliva,  gastric  juice,  or  secre- 
tions other  than  those  mentioned. 

Having  now  considered  the  phenomena  common  to  all  cases  of  hepatogenous 
icterus  alike,  we  revert  to  the  subject  of  simple  catai'rhal  jaundice.  The  prodro- 
mal gastric  symptoms  usually  last  a  few  days,  more  rarely  a  week  or  two,  when 
the  skin  becomes  evidently  jaundiced  and  the  other  results  of  the  icterus  are  also 
seen.  The  urine  grows  dark  with  biliary  pigment,  the  stools  become  light -colored 
and  more  or  less  clay-colored.     The  nervous  system  is  not  usually  seriously  de- 


4:6$  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

ranged,  but  still  most  patients  feel  very  languid,  and  have  anorexia  and  a  tendency 
to  constipation.  The  pulse  becomes  somewhat  slower  than  normal,  and  some- 
times the  temperature  also  is  subnormal,  say  97°  or  98°  (36°-36"5°  C). 

In  most  cases  the  physical  examination  of  the  liver  is  of  interest,  the  organ 
being,  as  already  mentioned,  enlarged  from  tbe  retained  bile.  Accordingly  the 
lower  boundary  of  hepatic  dullness  usually  extends  two  or  three  finger-breadths 
below  the  edge  of  the  ribs,  and  not  infrequently  the  lower  margin  of  the  organ 
can  be  plainly  felt.  Often  the  gall-bladder  is  so  distended,  both  by  bile  and  by  the 
mucus  wThich  it  itself  secretes,  that  it  projects  from  under  the  edge  of  the  liver 
In  such  cases,  as  Gerhardt  tells  us,  we  may  sometimes  make  out  by  percussion  a 
convexity  in  the  lower  line  of  hepatic  dullness,  which  corresponds  to  the  gall- 
bladder. If  the  abdominal  walls  are  lax,  we  may  even  feel  the  distended  viscus. 
As  a  rule,  there  is  not  much  distress  in  the  hepatic  region,  although  now  and  then 
there  is  a  certain  sensation  of  pressure  or  tension. 

The  symptoms  depicted  seldom  last  longer  than  a  few  weeks.  Usually  a 
patient  who  takes  proper  care  of  himself  begins  to  feel  better  in  even  less  time. 
The  urine  grows  lighter  colored,  the  stools  darker,  and  the  pulse  more  i^apid.  The 
yellow  color  of  the  skin  often  remains  visible  for  quite  a  while,  although  gradu- 
ally diminishing,  even  after  the  patient  feels  perfectly  well ;  but  at  last  the  jaun- 
dice disappears  also  and  recovery  is  complete.  Relapses  are  indeed  possible,  par- 
ticularly after  errors  in  diet ;  but  they  are  rare. 

The  termination  of  catarrhal  jaundice  is,  therefore,  almost  invariably  favor- 
able. The  entire  course  of  the  disease  occupies  about  three  to  six  weeks,  rarely  a 
longer  period.  It  is  a  very  exceptional  occurrence,  but  one  which  we  must  always 
think  of  as  possible,  for  this  apparently  mild  and  secure  condition  to  be  suddenly 
merged  into  the  grave,  pernicious  variety  of  jaundice.  (See  the  chapter  on  acute 
yellow  atrophy  of  the  liver  and  pernicious  jaundice.) 

Diagnosis. — Catarrhal  jaundice  is  usually  easily  diagnosticated.  The  diagnosis 
is  made  chiefly  from  the  course  of  the  disease — the  development  of  jaundice,  pre- 
ceded by  gastric  symptoms,  in  a  previously  healthy  person,  and  generally  in  a 
youthful  individual.  It  is  very  important  to  exclude  other  conditions  which 
might  occasion  jaundice.  We  must  consider,  therefore,  whether  the  history  of 
the  case  suggests  the  presence  of  gall-stones  (hepatic  colic),  and  be  vigilant  in  our 
physical  examination  to  detect  a  possible  cirrhosis  or  new  growth.  In  the  case  of 
elderly  patients,  particularly,  it  is  not  rare  for  what  was  at  first  regarded  as  an 
attack  of  ordinary  catarrhal  jaundice  eventually  to  disclose  itself  as  a  grave 
chronic  disease.  We  should  not  make  a  diagnosis  of  catarrhal  jaundice  until  we 
have  carefully  weighed  all  the  rational  and  objective  signs. 

Treatment. — Most  cases  of  catarrhal  jaundice  terminate  favorably  and  require 
no  active  treatment.  Rest  and  prudence  are  indicated,  and  the  diet  should  be 
carefully  regulated,  that  the  gastro-duodenal  catarrh  may  not  be  aggravated.  Eat 
must  not  be  eaten,  for,  as  we  have  seen,  it  is  not  assimilated,  and  only  excites 
abnormal  processes  of  decomposition  in  the  intestinal  canal.  Lean  meat,  bread, 
soups,  if  not  too  rich,  vegetables,  preserves,  and  lemonade  or  tamarind-water  are 
allowable. 

We  should  also  employ  internal  remedies  to  mitigate  the  catarrh.  The  various 
stomachic  tonics  are  frequently  prescribed.  Rhubarb  is  a  favorite  drug.  A  very 
good  medicine  is  Carlsbad  water,  or  the  artificial  Carlsbad  salts,  of  which  latter 
the  dose  is  half  a  teaspoonful  to  a  teaspoonf ul,  in  a  tumbler  of  warm  water,  before 
breakfast.  The  alkalies  not  only  exert  a  direct  beneficial  influence  upon  the  gas- 
tric mucous  membrane,  but  are  also  useful  as  laxatives.  More  obstinate  constipa- 
tion may  call  for  castor-oil,  calomel,  or  rhubarb. 

Lately  much  enthusiasm  has  been  displayed  about  the  treatment  of  catarrhal 


ACUTE  FEBRILE  JAUNDICE.     WEIL'S  DISEASE.  409 

jaundice  by  large  enemata  of  cold  water.  The  injections  are  said  to  overcome  the 
biliary  retention  by  exciting  peristalsis,  and  possibly  by  also  promoting  the  secre- 
tion of  bile.  Once  a  day  a  quart  or  two  of  water,  at  60°  to  70°  (12°-18°  R.),  is 
injected,  and  is  retained  as  long  as  possible.  The  good  effect  is  said  to  be  observ- 
able in  a  few  days,  both  in  the  general  condition  of  the  patient  and  in  the  dimin- 
ished amount  of  bile-pigment  in  the  urine,  as  well  as  the  darker  color  of  the 
stools. 

The  effort  has  also  been  made  to  empty  the  gall-bladder  by  manipulation. 
Gerhardt  states  that  sometimes  the  distended  viscus  can  not  only  be  felt  through 
the  abdominal  walls  (vide  supra),  but  it  can  be  so  firmly  compressed  as  to  squeeze 
its  contents  into  the  duodenum.  Sometimes  the  obstruction  is  said  to  yield  sud- 
denly, as  if  a  plug  were  driven  out.  This  method  has  not  been  universally 
adopted.  It  seems  applicable  only  in  a  limited  number  of  cases,  and  is  probably 
not  free  from  danger.  Several  authorities  have  recommended  external  faradiza- 
tion as  a  means  to  stimulate  the  gall-bladder  to  contract  and  discharge  its  con- 
tents.    We  believe  that  few  will  adopt  the  suggestion. 

APPENDIX. 

ACUTE  FEBRILE  JAUNDICE.      WEIL'S  DISEASE. 

Within  a  few  years  an  acute  infectious  disease  has  become  known,  which 
invariably  causes  jaundice  and  may  therefore  be  properly  described  in  this  con- 
nection.    It  was  first  described  by  Weil,  then  by  Fiedler  and  others. 

The  disease  is  most  frequent  in  the  months  of  summer.  It  attacks  by  prefer- 
ence young  and  middle-aged  men.  Fiedler  was  struck  by  the  frequency  with 
which  butchers  suffered  from  it.  The  symptoms  usually  begin  suddenly.  Ex- 
treme chilliness,  fever,  headache,  and  malaise  are  almost  always  present  at  the 
onset.  Jaundice  usually  appears  on  the  second  day,  and  it  may  become  severe. 
Its  immediate  cause  is  doubtless  obstruction  of  bile,  for  the  stools  are  colorless,  and 
the  urine  contains  an  abundance  of  bile-pigment.  The  constitutional  symptoms 
remain  for  several  days  quite  severe.  The  patient  complains  of  violent  headache, 
wakefulness,  and  vertigo.  Sometimes  there  is  evident  stupor  or  mild  delirium. 
Upon  physical  examination  we  not  infrequently  notice  herpes  on  the  lips,  besides 
the  icterus.  The  tongue  is  coated.  There  is  nothing  unusual  about  the  lungs  or 
heart,  except  that  the  pulse  is  apt  to  be  quite  rapid.  The  abdomen  is  not  particu- 
larly distended.  The  liver  is  often  enlarged,  but  not  always.  An  acute  splenic 
tumor  is  very  often,  but  not  invariably,  present.  There  is  usually  diarrhoea.  Vom- 
iting may  occur.  There  is  genei^ally  albuminuria;  and  not  infrequently  the  exist- 
ence of  a  nephritis  is  shown  by  the  blood  and  casts  found  in  the  urine.  A  very 
characteristic  symptom  is  the  violent  pain  in  the  muscles,  particularly  in  the 
calves,  of  which  most  patients  complain. 

With  these  symptoms  the  disease  persists  for  from  five  to  eight  days,  during 
which  period  the  fever  is  often  very  considerable.  Temperatures  of  105°-106-8° 
(40°-41°  C.)  are  not  rare.  Then  the  fever  falls  by  lysis,  although  seldom  with  perfect 
regularity.  At  the  same  time  the  other  symptoms  abate  also,  and  convalescence 
ensues  after  an  illness  of  ten  to  fourteen  days  in  all.  Many  milder  cases  recover 
even  sooner.     An  unfavorable  termination  seems  to  be  quite  exceptional. 

It  is  highly  probable  that  this  perfectly  specific  disease,  the  most  important 
symptoms  of  which  are,  as  we  have  seen,  jaundice,  fever,  swelling  of  the  spleen, 
albuminuria,  and  pain  in  the  muscles,  is  an  acute  infectious  process ;  but  we  do 
not  yet  possess  any  precise  information  as  to  its  aetiology. 

The  treatment  must  be  purely  symptomatic.     In  the  beginning  calomel  is  use- 


470  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

ful.  Later  on,  hydrochloric  acid,  rhubarb,  and  the  like  are  prescribed.  The 
headache  is  relieved  by  an  ice-bag,  the  pain  in  the  muscles  by  rubbing  with  chloro- 
form liniment. 


CHAPTER  II. 

BILIARY  CALCULI. 

(Hepatic  Colic.     Cholelithiasis.) 

iEtiology. — Although  gall-stones  are  of  very  frequent  occurrence,  we  do  not 
yet  possess  much  information  as  to  their  causation.  It  is  only  possible  to  state  a 
few  factors  which  very  probably  promote  their  formation. 

Biliary  retention  certainly  acts  in  this  way,  both  directly  and  by  leading  to  an 
increased  consistency  and  increased  concentration  of  the  bile.  As  a  result,  certain 
constituents  which  were  before  held  in  solution  are  thrown  clown.  And  yet  this 
cause,  however  potent,  can  not  be  regarded  as  the  only  one.  The  chemical  exami- 
nation of  gall-stones  leads  plainly  to  the  conclusion  that  their  formation  must  be 
preceded  by  certain  abnormal  chemical  processes  of  decomposition  and  of  trans- 
formation. We  can  not  otherwise  explain  why  the  constituents  of  gall-stones 
should  differ,  as  they  do  in  many  ways,  from  the  matters  which  normal  bile  holds 
in  solution.  For  example,  the  pigment  in  gall-stones  is  never  found  unchanged, 
but  invariably  exists  in  composition  with  lime.  Now,  normal  bile  contains  only 
a  trace  of  lime,  so  that  long  ago  Frerichs  suggested  that  the  lime  comes  from  the 
mucous  membrane  of  the  gall-bladder.  It  is  an  important  fact  that  the  Choles- 
terine, and  probably  also  a  portion  of  the  pigmentary  matters,  are  held  in  solution 
in  normal  bile  by  the  combination  of  sodium  with  the  biliary  acids  which  it  con- 
tains. If  this  sodium  salt  were  decomposed  from  any  cause,  the  matters  named 
would  naturally  be  precipitated.  The  decomposition  of  the  salts  formed  by  the 
bile-acids  is  greatly  promoted  if  the  bile  acquires  an  acid  reaction;  but  of  the  cir- 
cumstances in  which  this  last-mentioned  change  occurs  we  do  not  yet  have  any 
accurate  knowledge.  Possibly  fermentation  may  have  something  to  do  with  it. 
The  idea  that  often  a  clump  of  mucus  forms  the  nucleus  of  a  biliary  concretion 
lacks  chemical  confirmation,  for  mucus  is  never  found  in  the  stones. 

We  have  rather  more  knowledge  as  to  predisposing  causes  than  about  the 
chemical  processes  involved  in  the  formation  of  gall-stones. 

Age  seems  to  be  an  important  factor.  The  great  majority  of  patients  are  over 
forty.  Gall-stones  are  much  less  frequent  between  twenty  and  forty  years  of  age ; 
and  in  children  they  are  very  rare,  although  they  have  been  observed  in  the  new- 
born. One  reason  why  elderly  people  are  so  liable  to  this  trouble  is  said  be  the 
senile  weakness  of  the  muscular  fibers  of  the  gall-bladder.  Thus  stagnation  and 
retention  of  bile  are  promoted.  It  has  also  been  suggested  that  in  old  age  the 
bile  may  contain  an  excessive  amount  of  Cholesterine  and  lime. 

Sex  also  has  a  decided  influence.  All  authors  agree  that  gall-stones  are  more 
frequent  in  females  than  in  males,  the  proportion  being  about  three  to  two.  An 
explanation  of  this  fact  has  been  sought  in  the  sedentary  life  of  women,  and  par- 
ticularly in  the  mechanical  effect  of  tight  lacing,  impeding  the  outflow  of  bile. 

Much  has  been  said  about  certain  peculiarities  of  bodily  temperament  in  rela- 
tion to  cholelithiasis.  Obesity,  gout,  and  chronic  endarteritis  are  said  to  favor  the 
formation  of  gall-stones.  A  like  influence  is  ascribed  to  excessive  indulgence  in 
meat  and  fat,  as  well  as  to  gluttony  in  general,  and  to  lack  of  exercise;  but  the 
real  importance  of  these  various  factors  is  not  at  all  definitely  determined. 


BILIARY  CALCULI.  471 

Diseases  of  the  liver  and  bile-ducts  do  undeniably  promote  cholelithiasis,  for 
they  interfere  in  many  ways  with  the  discharge  of  bile  from  the  ducts  and  from 
the  gall-bladder.  Thus  they  may  cause  compression  or  obstruction  of  a  duct,  or 
may  lead  to  degenerative  changes  in  the  tissues  of  the  gall-bladder.  The  view  is 
quite  generally  held,  but  is  apparently  incorrect,  that  even  a  simple  chronic 
catarrh  of  the  bile-ducts  tends  to  cause  gall-stones.  Gall-stones  and  catarrh  of  the 
ducts  are  indeed  often  found  to  co-exist,  but  it  is  probable  that  the  catarrh  is  not 
the  cause,  but  the  result,  of  the  presence  of  gall-stones. 

Occurrence,  and  Chemical  and  Physical  Properties  of  Gall-stones.— The  place 
where  gall-stones  are  most  frequently  found  is  the  gall-bladder.  We  may  find  in 
it  any  number,  from  one  or  two  up  to  a  hundred  and  more.  The  size  varies  from 
that  of  a  grain  of  sand  up  to  that  of  a  hen's  egg.  The  large  stones  may  completely 
fill  the  gall-bladder ;  and  sometimes  the  smaller  stones  are  numerous  enough  to 
fill  it  also.  The  stones  usually  lie  free  in  the  bladder,  although  exceptionally 
they  may  be  found  adherent  to  its  walls.  Rarely  the  bladder  presents  a  diverticu- 
lum, in  which  a  stone  has  been  formed.  The  lining  membrane  of  the  viscus  often 
suffers  such  mechanical  irritation  from  the  stones  as  to  present  quite  a  severe 
catarrhal  inflammation.  Sometimes  there  is  even  a  more  or  less  extensive  necrosis 
(vide  infra). 

Stones  which  are  found  in  the  larger  bile-ducts  were  not  formed  in  them,  but 
have  become  wedged  in  them  while  on  their  way  to  the  intestine.  This  condition 
is  described  as  an  impaction  of  gall-stones.  Gall-stones  are  quite  often  found  in 
the  liver  itself,  and  frequently  in  large  numbers.  These  concretions  may  meas- 
ure half  a  centimetre  to  a  centimetre  in  diameter.  In  such  cases  the  small  intra- 
hepatic bile-ducts  are  usually  a  good  deal  widened ;  or  occasionally  they  present 
niches  in  which  the  stones  lie.  As  a  rule,  the  hepatic  parenchyma  surrounding 
the  stone  is  in  a  state  of  chronic  or  acute  purulent  inflammation  (vide  infra). 

In  form,  gall-stones  vary  infinitely.  The  smallest  are  irregular  masses,  well 
described  by  the  name  of  "  gall-sand."  The  larger  stones  are  more  or  less  round, 
or  oval,  or  polyhedral.  The  polyhedi^a  are  usually  due  to  the  mutual  rubbing  and 
pressure  of  a  number  of  stones  upon  one  another.  In  color,  the  stones  vary  ac- 
cording to  the  amount  of  pigment  they  contain,  from  almost  black  or  dark  brown 
to  a  lighter  greenish  or  bright  yellow  shade.  A  fresh  gall-stone  always  sinks  in 
water;  but  when  dry,  gall-stones  contain  air  and  generally  float.  On  cross-sec- 
tion, they  are  found  to  be  either  homogeneous  or  composed  of  layers.  As  a  rule, 
there  is  a  nucleus,  darkly  pigmented,  which  is  surrounded  by  a  lighter-colored  en- 
velope, itself  either  made  up  of  concentric  layers  or  evidently  crystalline.  Often 
the  outermost  layers  are  still  distinguishable  as  peculiar  darker  and  harder  strata. 

As  to  chemical  composition,  gall-stones  are  usually  divided  into  several  groups. 
By  far  the  most  frequent  variety  is  made  up  of  Cholesterine  and  pigment  mixed 
together  in  greatly  varying  proportions.  The  pigment  is  part  of  it  in  its  natural 
state  and  part  of  it  combined  with  lime.  On  the  average,  stones  contain  about 
seventy  to  eighty  per  cent,  of  Cholesterine.  Besides  these  two  chief  ingredients, 
most  stones  also  contain  lime  and  magnesium.  In  color,  they  are  light  or  dark 
according  to  the  smaller  or  greater  proportion  of  coloring  matter  they  contain. 
Less  common  are  stones  of  pure  Cholesterine.  These  are  usually  found  singly,  are 
soft,  and  often  are  almost  transparent.  Most  Cholesterine  stones  have  a  nucleus 
of  pigment  and  lime  in  combination.  Pure  pigmentary  concretions  are  rare,  and 
are  generally  small,  like  coarse  sand.  A  still  greater  rarity  is  a  stone  made  up 
entirely  of  lime.     Such  a  stone  is  small  and  very  hard. 

It  should  also  be  added  that  just  as  is  the  case  with  renal  calculi,  an  organic 
cementing  substance  can  be  detected  by  the  microscope  in  gall-stones.  This  is  in 
part  itself  calcified,  in  part  it  unites  the  separate  crystals  (Posner). 


472  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

Pathological  and  Clinical  Consequences  of  Gall-Stones. — Gall-stones  may  remain 
for  a  long  while  in  the  gall-bladder,  and  even  in  the  liver,  without  causing  the 
slightest  unpleasant  symptom.  It  is  not  at  all  unusual  to  find  gall-stones  unex- 
pectedly at  an  autopsy. 

In  other  cases,  however,  gall-stones  occasion  severe  suffering,  and  sometimes 
even  death.  These  grave  phenomena  may  be  due  either  to  certain  mechanical 
conditions,  like  impaction,  or  occlusion  of  the  bile-ducts ;  or  to  secondary  inflam- 
mation resulting  from  their  presence.  These  two  kinds  of  disturbance  must  now 
be  discussed  in  detail. 

Gall-stones  not  infrequently  leave  the  place  where  they  were  formed.  Stones 
formed  in  the  liver  are  gradually  driven  onward  by  the  current  of  the  bile,  and 
pass  through  the  hepatic  duct  into  the  common  duct  and  the  intestine.  The  more 
numerous  concretions  formed  within  the  gall-bladder  also  often  change  their  loca- 
tion. What  should  make  them  move  is  not  perfectly  determined.  Probably  there 
are  various  factors;  in  the  first  place,  contraction  of  the  muscular  coat  of  the  gall- 
bladder; and  then  probably  the  weight  of  the  stone;  and  the  pressure  of  the  dia- 
phragm and  the  abdominal  walls,  as  in  breathing,  defecation,  and  vomiting. 
When  once  a  stone  has  entered  the  biliary  passages,  we  must  regard  the  secretion 
behind  it  as  the  chief  propulsive  power ;  for  neither  the  cystic  nor  the  common 
duct  possesses  muscular  fibers. 

Small  calculi  may  effect  their  escape  without  exciting  any  attention ;  but  the 
passage  of  larger  ones  produces  a  very  characteristic  set  of  symptoms,  known  un- 
der the  name  of  hepatic  colic.  Attacks  of  pain  are  frequently,  though  not  always, 
the  first  symptom  of  the  passage  of  gall-stones.  The  intensity  of  the  suffering 
varies  greatly  in  different  cases.  It  may  be  so  mild  and  ill-defined  as  not  to  sug- 
gest its  true  cause,  or  it  may  be  unbearable. 

A  typical  attack  of  hepatic  colic  either  begins  suddenly,  or  it  has  for  prodro- 
mata  nausea,  chilliness,  and  mild  constitutional  disturbance.  The  most  frequent 
time  for  its  occurrence  is  a  few  hours  after  dinner.  The  pain  may  be  violent  from 
the  start;  or,  if  at  first  less  severe,  it  quickly  reaches  an  extreme  degree.  It  is  usu- 
ally felt  chiefly  in  the  epigastrium  and  the  right  hypochondrium,  but  radiates 
thence  backward  and  toward  the  shoulders,  or  even  into  the  right  arm.  The  pain 
comes  in  paroxysms,  being  worse  each  time  till  it  becomes  extremely  severe. 
General  convulsions  have  been  repeatedly  observed  as  a  result  of  the  pain,  par- 
ticularly in  nervous  individuals.  Quite  often  there  is  a  severe  rigor.  Vomiting 
is  also  common.  Usually  there  is  constipation.  As  a  rule,  there  is  great  consti- 
tutional disturbance ;  there  are  extreme  languor  and  weakness,  with  an  appearance 
which  suggests  collapse.  The  pulse  is  small  and  somewhat  accelerated ;  less  fre- 
quently, it  is  slower  than  normal.  The  temperature  is  normal.  During  the 
rigor,  however,  it  may  be  elevated  to  104°  (40°  C.)  or  more.  On  physical  ex- 
amination, the  liver  is  more  or  less  enlarged;  and  sometimes  it  is  possible  to 
feel  a  full  and  distended  gall-bladder,  or  at  least  to  find  a  dullness  on  percussion 
corresponding  to  it.  Jaundice  often  appears  toward  the  end  of  the  attack,  but 
not  invariably.  Of  course  it  can  be  caused  by  a  calculus  only  when  it  blocks  up 
the  hepatic  or  common  ducts.     Occlusion  of  the  cystic  duct  would  not  produce  it. 

The  duration  of  an  attack  is,  in  mild  cases,  only  a  few  hours,  and  in  severer 
ones  seldom  more  than  one  or  two  days.  Probably  the  pain  ceases  the  instant 
the  stone  has  successfully  passed  the  final  narrow  portion  of  the  common  duct, 
just  above  its  opening  into  the  intestine.  Perhaps  relief  is  sometimes  due  to  the 
stone's  slipping  back  again  into  the  gall-bladder.  If  the  faeces  are  carefully  ex- 
amined after  an  attack  is  ended,  we  often  find  one  or  more  calculi.  The  best 
method  of  search  is  to  pour  the  fasces  upon  a  sieve,  after  adding  water  to  them. 
In  one  or  two  instances,  gall-stones  have  passed  into  the  stomach  and  been 


BILIARY  CALCULI.  473 

vomited  up.  The  interval  between  different  attacks  varies.  Sometimes  months 
or  years  intervene,  sometimes  only  a  little  while.  Not  infrequently  there  is  a 
quick  succession  of  attacks,  and  then  none  for  years  or  even  for  a  lifetime.  In 
the  intervals  the  patient  may  feel  perfectly  well,  hut  he  may  have  a  slight  jaun- 
dice or  an  enlarged  liver  or  chronic  digestive  disturbance. 

Permanent  impaction  of  a  stone  at  any  point  in  the  biliary  passages  gives  rise 
to  quite  different  phenomena.  Usually  the  violent  symptoms  of  hepatic  colic  per- 
sist for  some  days,  but  then  abate,  leaving  behind  only  a  dull  pain  subject  to  occa- 
sional exacerbations.  Sometimes  the  symptoms  almost  all  vanish,  in  case  the 
passage  is  not  entirely  occluded.  If,  however,  no  bile  whatever  can  pass,  further 
trouble  is  to  be  expected.  If  the  calculus  lies  in  the  cystic  duct,  mucus  collects  in 
the  gall-bladder  and  gradually  distends  it.  The  coloring  matter  of  the  retained 
bile  is  gradually  absorbed,  so  that  finally  the  contents  of  the  gall-bladder  is  an 
almost  colorless  mucous  fluid.  This  condition,  of  course,  arises  just  the  same 
from  occlusion  of  the  cystic  duct  due  to  any  other  cause.  It  is  termed  dropsy  of 
the  gall-bladder.  Sometimes  the  distended  viscus  can  be  felt  through  the  abdomi- 
nal walls.  If  a  gall-stone  lodges  in  the  hepatic  duct,  or,  as  is  much  offener  the 
case,  in  the  common  duct,  and  dams  tip  the  bile,  chronic  jaundice  is  inevitable. 

Another  seines  of  very  important  symptoms  is  due  to  the  secondary  inflamma- 
tion or  ulceration  resulting  from  the  impaction.  A  gall-stone  may  excite  a  sec- 
ondary inflammation,  no  matter  where  it  lodges,  whether  in  the  gall-bladder  or  the 
ducts,  or  in  the  liver  itself.  The  phenomena  are  quite  analogous  to  the  inflamma- 
tion which  a  faecal  calculus  excites  in  the  vermiform  appendix  (vide  supra).  The 
first  effect  of  the  stone  is  purely  mechanical.  Its  pressure  causes  a  simple  necrosis 
of  the  mucous  membrane.  The  inflammation  and  ulceration  are  developed  sec- 
ondarily around  the  necrosed  tissue;  but  once  started,  they  may  spread.  The 
germs  which  excite  the  inflammation  are  probably  in  all  cases  derived  from  the 
intestinal  canal.  As  long  as  the  ulcerative  process  is  confined  to  the  mucous 
membrane  there  are  no  special  symptoms ;  but  quite  often  it  gradually  involves 
the  deeper  tissues  or  invades  neighboring  organs.  In  such  cases  the  number  of 
possible  events  is  almost  infinite.  We  shall  mention  here  only  a  few  of  the  most 
frequent  and  important. 

If  the  gall-bladder  or  one  of  the  large  ducts  is  perforated,  the  bile  flows  into 
the  abdominal  cavity.  Gall-stones  also  have  more  than  once  escaped  in  the  same 
way.  Such  a  perforation  is  almost  invariably  followed  by  a  purulent  and  usually 
quickly  fatal  peritonitis.  This  is  not  excited  by  the  bile  itself,  for  normal  bile 
does  not  provoke  inflammation,  but  it  is  due  to  septic  matter  (or  decomposed  bile), 
which  also  gains  access  to  the  peritoneum.  Rarely  there  is  perforation  outward. 
The  inflamed  gall-blauder  forms  adhesions  to  the  abdominal  walls,  the  ulceration 
slowly  progresses,  and  finally  reaches  the  surface  of  the  body.  Thus  a  genuine 
"  external  fistula  of  the  gall-bladder  "  may  be  formed,  through  which  bile  and  cal- 
culi are  discharged.  More  frequent  than  either  of  these  occurrences  is  perfora- 
tion into  neighboring  organs,  and  into  the  duodenum  in  particular.  Virchow,  and 
more  lately  Fiedler,  have  pointed  out  that  we  can  not  explain  the  appearance  of 
large  gall-stones  in  the  faeces  on  any  other  supposition  than  that  of  duodenal  per- 
foration; for  it  is  hardly  supposable  that  calculi  the  size  of  a  walnut  or  even 
larger  should  pass  through  the  bile-ducts  if  in  anormal  state.  Of  course,  the  bile 
can  also  escape  through  this  same  abnormal  opening,  whereupon  the  symptoms 
of  biliary  retention  and  those  due  to  lack  of  bile  in  the  intestines  cease.  There 
have  been  a  few  cases  of  similar  perforation  into  the  stomach  and  the  colon,  and 
even  into  the  portal  vein  and  the  urinary  passages.     ■ 

The  clinical  symptoms  of  all  these  secondary  inflammatory  and  ulcerative  pro- 
cesses may,  of  course,  vary  greatly.     Sometimes  the  symptoms  are  for  a  long  time 


474  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

so  indefinite  that  no  diagnosis  can  be  made  with  any  degree  of  certainty.  There 
are  abdominal  pain,  occasional  febrile  attacks,  constitutional  derangement,  and 
anorexia — symptoms  which,  to  be  sure,  indicate  some  serious  trouble,  but  do  not 
reveal  its  nature.  The  case  is  different  if  there  be  a  previous  history  of  colic, 
jaundice,  the  appearance  of  gall-stones  in  the  stools,  or  similar  more  definite  indi- 
cations. If  perforation  into  the  abdominal  cavity  takes  place,  acute  and  severe 
peritonitis  is,  as  we  have  said,  almost  inevitable.  If  a  perforation  into  other 
organs  occurs,  the  only  sign  by  which  it  can  he  recognized  is  the  discharge  of 
gall-stones  through  some  unusual  channel — for  instance,  through  the  abdominal 
walls,  or  the  oesophagus,  or  the  urinary  organs.  The  "  biliary  abscesses  "  which 
may  be  produced  in  the  liver  by  gall-stones  will  be  considered  under  the  general 
head  of  hepatic  abscesses.  It  is  worth  while  to  mention,  that  in  rare  instances 
large  gall-stones  wbich  have  reached  the  intestinal  canal  cause  obstruction  of  the 
gut.  There  have  also  been  a  few  cases  of  secondary  inflammation  and  ulceration 
of  the  intestine  due  to  gall-stones. 

Diagnosis. — It  is  evident  from  what  has  been  already  said  that  often  the  diag- 
nosis of  cholelithiasis  is  easy  and  indubitable,  while  in  other  cases  the  symptoms 
and  course  of  the  disease  are  obscure  and  ambiguous.  The  attacks  of  colic  are 
certainly  the  most  characteristic  symptom.  We  should  therefore  make  it  a  rule, 
in  case  of  severe  paroxysmal  pain  in  the  region  of  the  stomach  or  liver,  to  think 
of  the  possibility  of  gall-stones.  Any  mild  jaundice  accompanying  such  an  attack 
mates  the  diagnosis  more  probable.  For  absolute  certainty,  however,  we  need 
to  find  the  stones  in  the  dejecta ;  hut  even  without  this,  in  most  of  the  typical 
cases,  the  disease  may  be  correctly  diagnosticated.  It  is  most  easily  confounded 
with  cardialgia,  intestinal  colic,  renal  colic,  and  attacks  of  pure  "  neuralgia  in  the 
distribution  of  the  hepatic  plexus."  Observation  of  the  patient  for  a  considerable 
time  may  often  be  required  in  order  to  reach  a  definite  conclusion. 

It  is  but  seldom  that  physical  examination  of  the  liver  in  this  disease  yields  de- 
cisive results.  Still  it  is  possible,  as  has  been  said,  that  a  gall-bladder  distended 
with  calculi  may  be  felt  through  the  abdominal  walls.  Sometimes  we  can  even 
hear  with  a  stethoscope  the  friction  of  the  stones  upon  each  other. 

Prognosis. — We  have  already  enumerated  the  manifold  dangers  which  are 
incident  to  cholelithiasis,  but  on  the  whole  these  untoward  results  seldom  occur. 
As  a  rule,  the  termination  is  favorable.  Either  the  calculi  escape  in  some  way, 
and  there  is  complete  recovery ;  or  at  least  the  symptoms  abate,  and  the  patient 
feels  as  well  as  ever,  although  the  possibility  of  a  relapse  hangs  over  him. 

As  to  the  separate  symptoms,  the  colic  itself  is  very  seldom  dangerous.  In  a 
very  few  cases  of  extreme  severity  there  has  been  a  fatal  collapse.  Permanent 
obstruction  of  the  common  duct  is  worse,  because  it  greatly  impairs  nutrition,  and 
also  leads  to  secondary  changes  in  the  liver  (vide  infra).  The  most  favorable 
direction  for  a  perforation  to  take  is  into  the  small  intestine.  It  would  seem  that 
the  fistula  thus  originated  may  even  heal  up  perfectly.  The  ulcerative  process  may 
cause  an  unfavorable  result  by  entailing  a  cicatricial  closure  of  the  common  duct. 

Treatment. — Our  first  efforts  must  be  directed  to  a  relief  of  the  symptoms 
excited  by  the  gall-stones.  We  must  further  endeavor  to  promote  their  discharge 
from  the  body  and  to  prevent  the  formation  of  new  ones. 

It  is  the  hepatic  colic  which  most  often  demands  therapeutic  interference.  The 
most  important  and  indispensable  remedy  is  opium  or  morphine.  If  there  is 
violent  pain,  a  grain  of  opium  (0"05  grm.)  is  usually  required  every  hour  or  two. 
If  there  is  vomiting,  or  if  immediate  relief  is  called  for,  a  sixth  to  a  third  of  a 
grain  (0 -01-0  02  grm.)  of  morphine  may  be  injected  subcutaneously.  Other  nar- 
cotics, like  chloral  and  belladonna,  are  seldom  needed.  In  the  way  of  external 
applications  to  the  hepatic  region,  warm  or  hot  poultices  serve  the  best  purpose. 


BILIARY  CALCULI.  475 

Some  few  patients  get  more  comfort  from  an  ice-bag.  Usually  some  relief  can  be 
obtained  from  a  mixture  of  equal  parts  of  chloroform  and  olive-oil  rubbed  gently 
in  over  the  liver.  Sometimes  relief  is  obtained  by  a  prolonged  warm  bath.  For 
violent  emesis,  opium,  potassic  bromide,  or  bits  of  ice  may  be  administered.  In 
collapse,  we  must  exhibit  such  stimulants  as  wine,  strong  black  coffee,  or  even 
ether  or  camphor  subcutaneously.  After  the  colic  is  over,  some  mild  laxative, 
such  as  a  mineral- water,  is  generally  given,  to  favor  the  evacuation  of  such  calculi 
as  may  have  entered  the  intestinal  canal. 

[When  giving  repeated  doses  of  opium  for  biliary  or  renal  colic,  it  sbould  be 
remembered  that  the  pain  will  cease  abruptly  as  soon  as  the  stone  ceases  to  obstruct 
the  passage,  and  that  severe  toxic  effects  of  the  drug  may  then  appear.  In  bilious 
colic  the  distance  to  be  traversed  by  the  stone  is  relatively  short,  and  in  that  affec- 
tion especially  the  inhalation  of  ether  or  chloroform  is  sometimes  the  Ijest,  and, 
indeed,  the  imperative  treatment. 

The  operation  of  cholecystotomy  has  now  won  for  itself  an  enviable  position 
in  surgery,  and  in  the  hands  of  a  skilled  surgeon  gives  permanent  relief  at  rela 
tively  small  risk  to  cases  of  recurrent  and  persistent  gall-stone  impaction  which 
are  quite  beyond  the  reach  of  internal  remedies.] 

The  second  indication,  namely,  to  prevent  the  formation  of  fresh  concretions, 
is  best  met  by  certain  alkaline  mineral  waters.  Just  how  they  act  is  uncertain, 
but  that  they  do  exert  a  favorable  influence  has  been  satisfactorily  established  by 
experience.  The  springs  of  Carlsbad  have  gained  the  highest  reputation  of  any. 
If  the  patient's  circumstances  permit,  it  is  always  best  to  send  him  to  Carlsbad. 
During  the  "  cure  "  there  it  often  happens  that  a  large  number  of  gall-stones  are 
passed  with  comparatively  little  discomfort,  and  the  patient  not  infrequently 
returns  home  to  enjoy  for  years,  or  even  for  life,  freedom  from  his  old  trouble. 
Vichy  is  good,  as  are  also  Kissingen,  Homburg,  Marienbad,  and  Ems.  If  the 
patient  can  not  travel,  he  must  drink  Carlsbad  water  at  home  for  a  month  or  six 
weeks. 

All  the  other  remedies  are  of  dubious  efficacy.  "  Durande's  remedy,"  which  is 
a  mixture  of  three  parts  of  ether  and  two  parts  of  oil  of  turpentine,  is  much  in 
vogue :  twenty  or  thirty  drops  are  to  be  given  two  or  three  times  daily  for  a  long 
while.  The  internal  use  of  chloroform  is  also  recommended.  Ten  or  fifteen 
drops  in  some  mucilaginous  vehicle  are  given  three  or  four  times  a  day.  Of 
newly  suggested  remedies,  salicylate  of  sodium  deserves  especial  mention.  It 
certainly  promotes  the  secretion  of  bile.  It  is  given  in  long-continued  small 
doses  (80  grains  to  1  drachm — 2'0-4-0  grm.— per  diem).  Italian  physicians  highly 
praise  the  free  use  of  olive-oil,  say  six  or  seven  ounces  (200*0  grm.)  daily  in  divided 
doses.  It  is  said  that  in  obstinate  and  severe  cases  of  hepatic  colic  the  oil  some- 
times causes  marked  improvement. 

[Most  of  the  oil  is  passed  in  lumps,  which  have  a  superficial  resemblance  to 
gall-stones,  and  are  sometimes  called  such.] 

If  perforation,  peritonitis,  or  any  other  special  complications  arise,  they  are  to 
be  treated  on  general  principles. 


476  DISEASES   OF   THE  DIGESTIVE  OBGANS. 


CHAPTER  III. 

SUPPURATIVE   HEPATITIS. 

{Hepatic  Abscess.) 

JEtiology. — Exclusive  of  traumatism  there  are  two  ways  by  which  bacteria 
may  penetrate  into  the  liver,  there  to  excite  a  suppurative  inflammation— namely, 
by  the  blood  and  through  the  bile-ducts.  In  the  circulatory  system  the  main  route 
is  by  way  of  the  portal  vein,  by  which  germs  from  the  intestines  reach  the  liver. 
This  explains  why  many  ulcerative  processes  in  the  intestine,  like  severe  dysen- 
tery, are  followed  by  hepatic  abscess;  and  why  purulent  pylephlebitis  (q.  v.)  and 
other  suppurative  processes  within  the  portal  system  may  have  a  similar  sequel. 
In  general  pyasruia,  the  germs  must  take  a  very  circuitous  route  in  order  to  reach 
the  liver.  They  must,  on  leaving  the  primary  abscesses,  first  enter  the  veins  and 
the  lungs,  and  then  gain  the  liver  by  way  of  the  hepatic  artery.  It  has  been  well 
known  for  a  long  time  that  suppurating  wounds  of  the  head  are  followed  by 
hepatic  abscess  with  comparative  frequency.  Perhaps  it  may  exceptionally  happen 
that  infectious  matter  enters  the  hepatic  veins  by  "  retrogressive  embolism  "  from 
the  vena  cava. 

The  germs  which  make  then'  way  into  the  liver  from  the  bile-ducts  invariably 
originate  in  the  intestine.  In  these  cases  the  hepatic  inflammation  is  almost 
invariably  preceded  by  disease  of  the  biliary  passages.  The  most  frequent  cause 
by  far  of  this  variety  of  hepatic  abscess  is  the  formation  of  gall-stones.  The  two 
most  essential  factors  are  the  mechanical  injury  caused  by  the  concretion — that  is, 
necrosis  from  pressure— and  the  decomposition  of  the  retained  bile. 

Among  us,  hepatic  abscesses  are  rarely  occasioned  in  other  ways  than  those 
indicated;  but  in  the  tropics  it  is  said  that  quite  a  large  number  of  apparently 
primary  hepatic  abscesses  are  met  with.  Their  origin  is  not  yet  explained, 
although  in  this  case  also  there  is  most  probably  an  invasion  of  pyogenic  bacteria 
from  the  intestine. 

Pathology. — The  smallest  and  as  yet  imperfectly  developed  abscesses  best  illus- 
trate the  mode  of  formation.  We  find  the  blood-vessels  choked  with  micrococci, 
and  the  cells  of  the  surrounding  parenchyma  void  of  nuclei  and  in  process  of  dis- 
integration. Along  the  course  of  the  blood-vessels  nuclei  are  very  abundant. 
These  are  due  to  wbite  corpuscles  which  have  escaped  through  the  vascular  walls. 
The  cells  and  the  liquid  exudation  rapidly  increase,  and  there  is  complete  destruc- 
tion of  the  hepatic  parenchyma,  and  the  formation  of  an  abscess  in  its  place.  This 
may  extend  indefinitely  in  all  directions.  Large  abscesses  may  at  last  involve 
an  entire  lobe.  In  other  cases  the  suppurative  process  is  limited  by  encapsula- 
tion. Sometimes  quite  large  portions  of  the  liver  become  necrotic  and  slough  off, 
under  the  influence  of  what  is  called  "sequestrating"  suppuration.  We  almost 
invariably  find  some  shreds  of  hepatic  tissue  in  the  pus  of  hepatic  abscesses. 
Where  the  abscess  is  due  to  gall-stones,  the  latter  are  found  in  the  pus. 

Small  abscesses  may  be  absorbed,  but  they  are  often  merely  symptomatic  of 
pyaemia  or  some  such  disease,  which  is  itself  incurable.  Larger  abscesses  may 
point  into  neighboring  organs.  If  they  are  discharged  into  the  abdominal  cavity, 
diffuse  peritonitis  follows.  The  most  favorable  termination,  and  one  repeatedly 
observed,  is  perforation  through  the  abdominal  walls,  after  these  walls  and  the 
liver  have  been  joined  by  adhesions.  They  may  also  break  into  the  pleural  cavity, 
the  pericardium,  the  intestine,  and  the  pelvis  of  the  right  kidney. 

Clinical  History.— An  absolutely  complete  clinical  description  of  hepatic 
abscess  is  impossible,  because,  as  we  have  seen,  it  may  be  a  symptom  of  such 


SUPPURATIVE  HEPATITIS.  477 

diverse  pathological  processes.  Hepatic  abscesses  are  often  found  post  mortem 
which  had  given  no  previous  indication  of  their  presence  ;  this  is  frequently 
true  in  pyaemia.  In  other  cases  there  are  symptoms,  in  part  directly  referable  to 
the  seat  of  inflammation,  and  in  part  due  to  its  influence  upon  neighboring 
organs. 

Enlargement  of  the  liver  can  often  be  made  out  by  percussion  or  even  by  pal- 
pation. It  is  the  result  of  swelling  and  hypersemia  involving  the  entire  organ. 
Extensive  abscesses  may  give  much  more  definite  signs  of  their  presence,  however, 
if  situated  near  the  anterior  edge  of  the  organ.  They  are  sometimes  felt  through 
the  abdominal  walls  as  hemispherical  and  actually  fluctuating  tumors.  It  is  not 
so  very  rare  for  tropical  hepatic  abscess  to  attain  these  dimensions. 

Pain  in  the  right  hypochondrium,  although  it  may  be  entirely  absent  when 
the  abscesses  are  small,  even  if  they  are  numerous,  is  often  violent  and  persistent 
when  the  abscess  is  large.  It  is  excited  by  the  tension  of  the  peritoneal  covei'ing 
of  the  liver,  or  by  a  perihepatitis.  The  pain  often  radiates, — and  with  especial 
frequency,  it  is  said,  into  the  neighborhood  of  the  right  shoulder. 

The  course  of  the  fever  may  prove  a  strong  diagnostic  point.  When  the  abscess 
is  chronic  and  encapsulated  there  may,  it  is  true,  be  no  fever  whatever ;  but,  as  a 
rule,  fever  does  exist,  and  often  presents  a  very  characteristic  intermittent  char- 
acter. There  are  great  elevations,  usually  ushered  in  by  a  chill,  and  succeeded 
by  deep  depressions  of  temperature  accompanied  by  perspiration.  If  the  hepatic 
trouble  is  merely  a  symptom  of  general  pyaemia,  then  the  fever  is  to  be  ascribed 
to  the  latter;  but  if  there  are  signs  of  a  severe  local  hepatic  disease,  such  as  pain, 
enlargement,  and  jaundice,  and  if  these  febrile  attacks  come  on  at  irregular  inter- 
vals, we  should  always  consider  the  possibility  of  abscess  of  the  liver.  In  the 
cases  of  large  tropical  abscess  this  sort  of  fever  is  the  rule.  It  is  most  frequent 
with  us  in  cases  of  purulent  pylephlebitis  and  of  abscess  excited  by  gall-stones. 
The  ufievre  intermittente  hepatique  "  of  the  French  is  in  most  instances  due  to 
the  presence  of  gall-stones  in  the  liver,  with  secondary  suppuration. 

Among  the  secondary  symptoms  of  hepatic  abscess  jaundice  is  prominent.  It 
is  not  invariably  present,  however,  occurring  only  when  the  abscess  has  com- 
pressed some  large  biliary  duct,  and  has  thus  given  occasion  to  the  absorption  of 
bile  by  the  lymphatics.  In  rare  instances  the  abscess  compresses  the  portal  vein 
and  thus  causes  ascites.  There  may  be  pulmonary  symptoms  of  considerable 
importance,  even  when  there  are  no  actual  pulmonary  complications.  This  is 
because  the  right  half  of  the  diaphragm  is  crowded  up  by  abscesses  projecting 
from  the  convex  surface  of  the  liver.  Hiccough  is  sometimes  a  source  of  distress, 
and  may  be  due  to  the  pressure  of  the  abscess  upon  the  stomach.  Vomiting  is 
also  a  rather  common  and  often  very  troublesome  symptom. 

There  is  almost  always  great  constitutional  disturbance.  The  patient  has  no 
appetite,  and  loses  flesh,  particularly  if  there  are  frequent  febrile  exacerbations. 
Often  there  are  severe  nervous  attacks.  Very  exceptionally,  the  disease  remains 
latent  for  a  long  while,  and  does  not  disturb  the  general  health  to  any  great 
extent. 

The  course  of  the  disease  depends  mainly  upon  the  nature  of  the  original  dis- 
turbance. Severe  pyaernic  cases,  in  the  course  of  which  hepatic  abscesses  develop, 
are  generally  brief,  and  are  almost  invariably  fatal.  Abscesses  due  to  gall-stones, 
and  the  large  abscesses  which  are  apparently  idiopathic,  are  generally  chronic, 
lasting  for  weeks,  or  even  for  many  months.  Cases  exhibit  manifold  diversities, 
according  to  the  position,  size,  number,  and  sequelae  of  the  abscesses.  Among  the 
possible  results,  we  would  once  more  call  attention  to  perforation  into  neighboring 
organs.  If  the  pus  is  discharged  externally,  recovery  may  ensue ;  as  also  if  the 
pus  reaches  the  intestinal  canal  or  the  bronchi,  which  seldom  happens.     Perfora- 


478  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

tion  into  the  abdominal  cavity  always  excites  a  fatal  acute  peritonitis.  As  a  gen- 
eral rule,  hepatic  abscess  finally  proves  fatal,  recovery  being  exceptional.  Death 
is  due  either  to  the  gradual  loss  of  strength  or  to  some  complication. 

Treatment. — Local  bleeding,  counter-irritation,  purgatives,  and  emetics  are 
among  the  remedies  which  are  advocated,  but  we  can  hardly  expect  them  to  exert 
much  influence  aipon  a  hepatic  abscess.  The  best  way  is  to  treat  the  case  pui'ely 
symptomatically,  seeking  to  keep  up  the  patient's  strength  and  mitigate  his  suf- 
fering until,  if  we  are  very  fortunate,  we  have  a  chance  for  operative  interference. 
When  once  the  other  symptoms  are  re-enforced  by  the  discovery  on  palpation  of 
a  fluctuating  tumor,  the  diagnosis  is  established,  and  the  pus  should  be  evacuated 
and  the  cavity  drained.  Particulars  about  the  operation  should  be  sought  in 
works  on  surgery.  More  than  one  case  of  the  large  tropical  abscess  has  been 
cured  in  this  way;  but  the  cases  which  are  most  common  among  us — namely, 
embolic  abscesses  and  those  excited  by  gall-stones — hardly  ever  afford  any  oppor- 
tunity for  surgical  interference. 


CHAPTER  IV. 


CIRRHOSIS   OF   THE   LIVER. 

{Chronic  Diffuse  Interstitial  Hepatitis.     Zaennec's  Cirrhosis.     Gin-drinker's  Liver.) 

iEtiology  and  Pathology.— Cirrhosis  of  the  liver  is  usually  defined  as  a  diffuse 
interstitial  inflammation,  chronic  in  duration,  and  resulting  in  a  secondary  atro- 
phy of  the  true  hepatic  parenchyma.  This  conception  makes  the  disease  perfectly 
analogous  to  "  chronic  interstitial  inflammation  ''  of  the  kidney  and  many  other 
organs.  Weigert's  careful  study  of  the  processes  of  "  chronic  interstitial  nephritis  " 
has  shown  that  at  least  a  large  part  of  the  changes  which  take  place  in  the  con- 
nective tissue  are  not  primary,  but  secondary,  and  the  consequence  of  a  primary 
destruction  of  the  genuine  renal  parenchyma.  The  question  naturally  suggests 
itself,  whether  the  same  may  not  be  true  of  the  apparently  closely  allied  phenom- 
ena of  hepatic  cirrhosis.  We  feel  justified,  therefore,  in  seeking  the  origin  of  the 
disease  in  a  primary  injury  and  consequent  partial  destruction  of  the  hepatic  cells, 
whereupon  follow  a  secondary  proliferation  and  final  contraction  of  the  interstitial 
tissue,  just  as  is  seen  in  lesions  of  the  parenchyma  of  the  kidneys,  spinal  cord,  and 
heart. 

Such  a  conception  would  be  extremely  compatible  with  one  fact  about  the  asti- 
ology  of  the  disease,  namely,  that  chronic  alcoholism  is  universally  regarded  as  a 
potent  predisposing  cause.  Hence  the  English  name,  "gin-drinker's  liver."  The 
harmful  influence  of  alcohol  can  be  appreciated,  if  we  remember  that  on  being 
absorbed  it  is  carried  directly  by  the  blood-vessels  to  the  liver.  The  stronger 
liquors  are  more  potent  for  evil  in  this  direction ;  wine  and  beer  are  not  harmless, 
however.  According  to  the  usual  view  of  the  disease,  the  poison  excites  a  chronic 
inflammation  of  the  connective  tissue ;  while,  according  to  the  new  view,  the  alco- 
hol exerts  a  specific  injurious  influence  upon  the  hepatic  cells  proper,  impairing 
their  nutrition,  and  finally  causing  their  destruction.  That  the  disease  attacks  the 
periphery  of  the  lobules  and  the  interlobular  connective  tissue  is  equally  conso- 
nant with  either  theory.  It  is  well  known  that  the  capillary  anastomoses  of  the 
portal  vein  are  situated  between  the  lobules. 

The  abuse  of  alcohol  is  by  no  means  the  only  cause  of  cirrhosis,  for  quite  often 
the  disease  attacks  persons  in  whose  case  no  such  aätiology  is  possible.     In  such 


CIRRHOSIS  OF  THE  LIVER.  479 

instances  we  are  seldom  able  to  demonstrate  the  real  cause.  The  excessive  use  of 
spices,  and  other  analogous  substances,  has  sometimes  been  regarded  as  causative. 
It  is  also  said  that  sometimes  malaria,  and  the  acute  infectious  diseases,  leave 
behind  them  a  tendency  to  cirrhosis.  The  form  of  cirrhosis  which  follows  dis- 
eases of  the  bile-ducts,  and  also  "  syphilitic  cirrhosis,"  will  receive  separate  consid- 
eration. 

Cirrhosis  of  the  liver  is  seen  much  oftener  in  men  than  in  women,  and  usually 
occurs  in  middle  life. 

The  anatomical  changes  are  generally  divided,  without  regard  to  the  way  in 
which  they  are  brought  about,  into  two  stages.  In  the  first  stage  the  liver  is 
uniformly  enlarged,  resistant,  with  its  edge  blunt,  and  its  surface  at  first  per- 
fectly smooth,  but  later  presenting  little  dimples.  On  section,  the  increased  con- 
sistency, or  "  interstitial  induration  "  of  the  liver,  can  be  readily  perceived.  The 
acini  are  separated  from  one  another  by  a  relatively  thick  band  of  grayish-red 
interstitial  tissue,  and  are  at  first  readily  distinguishable.  Later  on,  the  interstitial 
hyperplasia  invades  the  acini  themselves,  and  they  cease  to  be  discernible.  The 
microscope  shows  that  the  cause  of  this  increase  in  size  and  firmness  of  the  organ 
is  due  exclusively  to  the  abundant  cellular  infiltration  and  the  new  formation  of 
connective  tissue  between  the  individual  lobules.  The  neighboring  cells  of  the 
parenchyma  exhibit  signs  of  disintegration,  undergoing  either  simple  atrophy  or 
else  fatty  degeneration. 

The  second  stage  corresponds  with  the  process  of  contraction  of  the  newly 
formed  connective  tissue,  but  in  this  stage  the  destruction  of  the  proper  hepatic 
tissue  has  already  assumed  grave  proportions.  On  the  old  theory,  the  parenchyma 
perishes  because  of  the  great  disturbance  of  circulation  in  the  portal  capillaries, 
great  numbers  of  which  are  obliterated  by  the  shrinking  of  the  connective  tissue. 
Under  this  process  of  contraction  the  liver  undergoes  progressive  atrophy,  and  its 
surface  becomes  mammillated.  The  size  of  the  nodules  varies.  The  size  of  the 
whole  organ  may  be  reduced  one  half,  or  even  more.  Frequently  its  general  con- 
tour is  considerably  modified.  Upon  microscopic  examination,  we  now  find 
merely  vestiges  of  parenchyma,  embracing  which  are  wide,  firm  bands  of  connect- 
ive tissue.  Even  within  the  acini  there  is  decided  interstitial  hyperplasia  along 
the  blood-vessels.  Brown  masses  of  pigment  are  often  found  here  and  there, 
which  have  been  left  behind  by  the  hepatic  cells  now  destroyed.  Regenerative 
changes  can  also  be  detected  quite  frequently.  The  most  common  of  these  is 
the  formation  of  small  biliary  passages  in  the  broad  bands  of  interstitial  tissue. 

The  division  of  hepatic  cirrhosis  into  two  stages  is  somewhat  diagrammatic,  for 
there  is  really  no  sharp  dividing  line  between  them.  The  same  liver  may  in  dif- 
ferent places  illustrate  both  stages  simultaneously.  Thus,  the  surface  is  often  dis- 
tinctly granular,  while  the  liver  as  a  whole  remains  hypertrophic. 

Clinical  History. — The  onset  of  the  disease  is  usually  insidious.  At  autopsies, 
quite  an  advanced  stage  of  cirrhosis  is  sometimes  found,  to  which  not  a  single 
clinical  symptom  had  pointed;  and  it  is  often  observed  that  the  dilation  of 
unambiguous  symptoms  is  much  shorter  than  the  degree  of  anatomical  change 
discovered  post  mortem  would  have  led  us  to  expect. 

It  is,  however,  true  that  certain  prodromata  may  appear  long  before  the  genu- 
ine cirrhotic  symptoms ;  but  there  is  generally  room  for  doubt  whether  these  pro- 
dromata are  excited  by  the  incipient  hepatic  disease  or  whether  they  are  not  due 
to  other  coincident  affections,  such  as  the  chronic  gastric  or  intestinal  catarrh 
which  drunkards  so  often  have.  There  are  anorexia,  nausea,  epigastric  uneasiness, 
eructations,  constipation,  and  sometimes  vomiting.  There  is  evident  constitutional 
disturbance  in  many  cases,  but  in  others  the  strength  is  unimpaired.  The  severer 
symptoms  usually  date  from  the  time  when  disturbance  of  the  portal  circulation 


4S0  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

arises.  "We  have  already  stated  that  the  diseased  process  is  most  active  in  the 
interlobular  connective  tissue — that  is,  where  the  portal  capillaries  are  situated. 
When  the  contraction  of  the  connective  tissue  has  resulted  in  the  destruction  of  a 
large  number  of  these  portal  capillaries  and  the  minute  veins  from  which  they 
spring,  the  portal  circulation  is  inevitably  impeded,  and  there  arises  a  passive  con- 
gestion of  the  whole  portal  system.     The  signs  of  this  are  soon  manifest. 

The  stasis  in  the  veins  of  the  peritoneum  is,  as  a  rule,  the  first  to  attract  atten- 
tion, from  the  ascites  which  it  occasions.  The  distention  of  the  abdomen  and  the 
sensation  of  weight  and  pressure  due  to  this  effusion,  are  often  the  first  things 
which  excite  the  patient's  attention  and  lead  him  to  seek  medical  advice.  Later 
on,  the  ascites  sometimes  becomes  enormous,  causing  immense  swelling  and 
extreme  tension  of  the  abdominal  walls,  and,  of  course,  proportionate  discomfort. 
Proper  nursing  and  internal  treatment  may  diminish  the  ascitic  effusion,  but  they 
will  seldom  wholly  remove  it.  It  quite  often  remains  nearly  uniform,  until  final- 
ly, for  some  reason,  there  is  a  change  for  the  worse. 

Next  to  ascites,  the  most  important  symptom  of  portal  obstruction  is  enlarge- 
ment of  the  spleen,  which  is  due  both  to  the  increased  amount  of  blood  in  the 
organ  and  to  a  diffuse  hyperplasia  of  its  tissues.  As  a  rule,  the  increase  in  size  is 
considerable,  amounting  sometimes  to  two  or  three  times  the  normal  dimensions. 
The  demonstration  of  splenic  tumor  is  of  great  diagnostic  importance,  but  is  often 
a  difficult  matter.  Percussion  and  even  palpation  are  greatly  interfered  with  by 
the  co-existing  ascites.  On  the  whole,  however,  palpation  is  the  more  reliable. 
Pain  or  other  subjective  symptoms  are  rarely  observed.  Exceptionally,  there  is 
no  enlargement  of  the  spleen.  This  may  be  due  to  the  firmness  and  thickness 
of  its  capsule,  or  to  the  general  marantic  condition  of  the  patient. 

The  venous  congestion  of  the  stomach  and  intestine  excites  catarrh,  which  is 
evinced  by  anorexia,  nausea,  and  irregularity  of  the  bowels.  Usually  there  is  quite 
obstinate  constipation,  but  there  may  be  persistent  diarrhoea.  None  of  these  symp- 
toms occupy  the  foreground  of  the  clinical  picture,  however,  both  because  they 
are  frequent  in  all  grave  chronic  diseases  and  because  mauy  patients  have  had 
digestive  derangements  long  before  these  severer  troubles  began.  A  more  signifi- 
cant symptom,  if  it  occurs,  is  haemorrhage.  This  is  now  and  then  occasioned  by 
the  extreme  gastro-intestinal  congestion.  The  bleeding  may  be  from  either  the 
stomach  or  the  intestine,  and  is  sometimes  a  relatively  early  phenomenon.  Some- 
times there  is  a  capillary  oozing  sufficient  to  tinge  the  stools  day  after  day  for 
some  time.     Very  rarely  there  is  haemorrhage  from  the  oesophagus. 

The  patient  may  be  moderately  jaundiced  even  in  the  common  form,  of  cirrho- 
sis. This  is  sometimes  due  to  duodenal  catarrh.  Often  there  is  no  jaundice  what- 
ever; or  there  may  be  a  slight  yellowish  tinge  of  the  skin,  in  addition  to  the  dirty, 
grayish,  earthen  color  which  not  infrequently  characterizes  the  cirrhotic.  Per- 
haps the  jaundice  is  due  in  many  cases  to  stenosis  of  the  intra-hepatic  bile-ducts, 
involving  biliary  retention. 

The  above  signs  of  portal  obstruction  will  often  render  the  diagnosis  of  hepatic 
disease  extremely  probable,  but  we  should  always  endeavor  to  confirm  our  opin- 
ion by  physical  examination  of  the  liver.  In  the  later  stages  of  the  disease,  and 
particularly  if  there  be  great  ascites,  our  efforts  may  be  fruitless ;  but  at  first,  or 
after  paracentesis  has  been  performed,  percussion  and  palpation  may  yield  valua- 
ble information.  In  the  earliest  stages  the  liver  is  large.  Hepatic  dullness 
reaches  some  ways  below  the  edge  of  the  ribs,  and  we  can  often  feel  the  lower 
edge  and  anterior  surface  of  the  organ.  Later  on  we  find  the  surface  irregular 
and  rough.  If  we  can  feel  these  little  nodules  or  prominences  through  the  ab- 
dominal walls,  as  we  sometimes  can,  of  course  the  diagnosis  of  cirrhosis  of  the 
liver  is  nearly  certain.    As  already  mentioned,  it  often  happens  that  irregularities 


CIRRHOSIS  OF  THE  LIVER.  481 

are  already  to  be  felt  upon  the  surface  of  the  organ  while  it  still  remain:;  hyper- 
trophic. The  demonstration  of  atrophy  by  percussion  in  the  later  stages  of  the 
disease  is  less  reliable.  The  ascites  often  iuterferes  with  such  an  attempt.  Wo 
may  also  be  misled  by  coils  of  intestine  distended  with  gas  and  perhaps  lying  in 
front  of  the  liver.  If,  however,  after  guarding  against  error,  we  constantly  find 
the  area  of  hepatic  dullness  diminished,  the  sign  has  some  value. 

General  nutrition  is  usually  much  impaired  in  the  later  stages  of  the  disease. 
At  first  the  patient  may  retain  vestiges  of  his  former  corpulence,  but  finally  he 
grows  emaciated.  Anasarca  may  exceptionally  occur  toward  the  close;  but  there 
is  frequently  considerable  oedema  of  the  lower  extremities,  and  even  of  the  scro- 
tum and  the  dependent  portions  of  the  abdominal  walls.  The  cause  of  this  is  a 
purely  local  one— the  pressure  of  the  ascites  impedes  the  return  of  blood  from  the 
lower  limbs  to  the  heart. 

Occasionally  there  are  ecchymoses  into  the  skin,  the  mucous  membranes,  the 
retina,  and  other  parts.  These  are  probably  due  to  malnutrition  of  the  vascular 
walls. 

Unless  there  are  complications,  there  is  no  fever.  Respiration  may  be  impeded 
and  accelerated  on  account  of  the  upward  displacement  of  the  diaphragm.  The 
pulse  is  usually  small,  and  often  somewhat  more  rapid  than  normal. 

At  first  the  urine  presents  no  characteristic  changes.  When  the  ascites  has 
become  considerable  and  there  is  oedema,  the  urine  grows  scanty,  dark,  and  con- 
centrated, and  often  has  an  abundant  sediment  of  urates.  It  should  be  mentioned 
that  earlier  observers  found  a  diminished  excretion  of  urea.  This  is  perhaps  due 
to  a  disturbance  of  the  urea-generating  function  of  the  liver,  about  which  both 
earlier  and  more  recent  investigators  agree.  In  a  few  instances  the  urine  has 
been  found  to  contain  a  trace  of  sugar. 

It  remains  for  us  to  describe  Tjfriefly  the  collateral  circulation  which  may  be 
developed  in  cirrhosis,  so  as  to  enable  the  blood  of  the  portal  system  to  reach  the 
systemic  veins.  The  clinical  history  of  the  disease  does  not  indicate  that  this 
attempt  at  compensation  is  vei\v  successful.  We  may  have:  1.  Communications 
between  the  veins  of  the  mesentery  and  of  the  abdominal  walls.  2.  Communica- 
tions between  the  coronary  vein  of  the  stomach  and  the  veins  of  Glisson's  capsule 
on  the  one  hand,  and  the  phrenic  veins  on  the  other.  3.  Anastomoses  between 
the  internal  hseruorrhoiclal  and  the  hypogastric  veins.  4.  As  pointed  out  by 
Baumgarten,  enlargement  of  the  not  yet  completely  obliterated  umbilical  vein  in 
the  ligamentum  teres.  Through  all  these  the  blood  may  flow  from  the  portal 
system  into  the  veins  of  the  abdominal  walls — that  is,  in  the  reverse  of  the  normal 
direction.  In  cases  of  portal  obstruction  the  veins  of  the  abdominal  walls  are 
often  much  enlarged,  and  this  may  be  partly  due  to  the  changes  just  enumerated. 
In  some  instances  the  veins  around  the  umbilicus  have  been  strikingly  tortuous 
and  swollen;  this  condition  has  been  termed  " caput  Medusce.''' 

The  complications  which  sometimes  occur  are  probably  in  part  due  to  the  same 
injurious  influences  as  the  cirrhosis.  This  is  apparently  true,  for  example,  of  the 
cardiac  hypertrophy,  the  contracted  kidney,  and  the  chronic  pachymeningitis.  An 
interesting  combination  is  the  simultaneous  occurrence  of  cirrhosis  and  chronic 
tubercular  peritonitis.  Various  observers  as  well  as  ourselves  have  observed  this 
with  comparative  frequency.  The  explanation  is  unknown.  Probably  cirrhosis 
is  the  primary  lesion,  and  it  promotes  the  development  of  peritoneal  tuberculosis 
through  the  passive  congestion  of  the  portal  system.  Sometimes,  however,  the 
order  of  development  seems  to  be  reversed. 

As  to  the  general  course  of  the  disease,  its  duration  can  not  easily  be  deter- 
mined because  the  onset  is  usually  insidious.  As  a  rule,  the  disease  lasts  one  to 
three  years,  or  rarely  longer.  In  many  cases  the  symptoms  are  insignificant  for 
31 


482  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

the  first  six  to  eighteen  months.  Then  the  disorder  takes  on  a  severer  form,  per- 
haps rather  suddenly.  Ascites  appears,  for  example.  These  graver  symptoms 
persist,  till  after  a  few  months  the  patient  dies.  The  course  of  the  disease  reminds 
one  of  cardiac  cases,  where  for  a  long  while  the  compensatory  changes  avert  any 
distress,  till  on  a  sudden  the  circulatory  disturbances  become  pronounced  and 
persist  to  the  end. 

The  prognosis  is-  always  unfavorable,  at  least  when  the  symptoms  have  once 
become  well  marked.  It  may  be  that  in  the  earlier  stages  the  disease  can  be 
checked  or  even  permanently  cured;  but  even  this  is  open  to  doubt.  No  case 
recovers  in  which  the  diagnosis  of  cirrhosis  is  certain. 

Death  is  due  either  to  intercurrent  disease,  or  more  often  to  gradually  increas- 
ing exhaustion.  In  some  few  cases  severe  cerebral  symptoms  suddenly  appear: 
there  are  coma,  general  convulsions,  and  delirium ;  and  these  usually  are  soon 
fatal.  Just  how  these  nervous  phenomena  originate  we  do  not  certainly  know 
(see  the  chapter  on  acute  yellow  atrophy  of  the  liver). 

Diagnosis. — The  diagnosis  is  seldom  very  easily  made.  It  becomes  extremely 
probable  if  a  patient  who  is  known  to  have  been  addicted  to  alcohol  gradually 
develops  ascites  and  splenic  tumor,  and  has  a  liver  which  presents  distinct  evi- 
dences of  disease,  such  as  an  irregular  surface.  Often,  however,  we  are  left  in 
doubt,  because  one  or  another  of  these  more  characteristic  symptoms  can  not 
be  clearly  made  out.  Often  a  patient  does  not  come  under  observation  till  a  con- 
siderable ascitic  effusion  has  already  taken  place,  so  that  physical  examination  of 
the  liver  and  spleen  is  rendered  very  difficult.  Then  we  must  first  exclude  any 
general  disturbance  of  circulation  as  a  cause  of  the  ascites.  If  the  heart,  lungs, 
and  kidneys  are  found  to  be  normal,  and  if  there  is  no  oedema  in  the  upper  half  of 
the  body,  it  is  very  probable  that  there  is  a  local  derangement  of  the  portal  circu- 
lation ;  but  we  have  still  to  determine  whether  the  cause  of  this  derangement  is 
cirrhosis  of  the  liver.  This  may  be  assumed  to  be  the  case  if  the  whole  course  of 
the  disease  warrants  the  assumption,  and  if  the  history  furnishes  that  most  frequent 
of  all  aetiological  factors,  chronic  alcoholism.  Otherwise  we  must  be  cautious, 
for  portal  obstruction  with  precisely  similar  results  may  be  due  to  other  causes — 
like  the  external  pressure  of  tumors  or  portal  thrombosis.  Many  forms  of  hepatic 
syphilis  (q.  v.)  can  not  be  differentiated  from  cirrhosis  by  mere  clinical  observation 
of  the  hepatic  disorder.  Here  it  is  only  the  aetiology  and  the  demonstration  of 
other  signs  of  syphilis  that  can  justify  the  assumption  that  the  disease  in  hand  is 
of  specific  origin. 

It  is  also  very  difficult  in  many  instances  to  exclude  chronic  peritonitis.  The 
aetiology  may  aid  us.  Other  points  are,  that  in  chronic  peritonitis  there  may  be 
tenderness  on  pressure,  the  abdominal  distention  is  less  uniform,  and  there  is  no 
enlargement  of  the  spleen.  The  combination  of  cirrhosis  and  chronic  tubercular 
peritonitis  can  not  be  diagnosticated  with  any  approach  to  certainty  unless  we  find 
both  the  symptoms  of  cirrhosis  and  pronounced  indications  of  a  tubercular  affec- 
tion.    In  such  a  case  coincident  pleurisy  is  significant  of  tuberculosis. 

Treatment. — As  we  know  the  causes  which  sometime  excite  cirrhosis  of  the 
liver,  an  obvious  prophylaxis  consists  in  avoiding  them ;  and,  even  after  the  early 
symptoms  of  the  disease  have  appeared,  alcohol  should  be  forbidden,  as  well  as 
spices  and  other  similar  articles,  in  the  hope  that  we  may  thus  do  something  to 
prevent  the  extension  of  the  abnormal  process. 

If  the  disease  has  already  made  considerable  progress,  treatment  becomes 
purely  symptomatic.  Iodide  of  potassium  is  said  to  exert  a  favorable  influence 
upon  cirrhosis  of  the  liver,  but  its  powers  are  doubtful.  Probably  it  does  good 
only  in  syphilitic  hepatitis.  Of  the  individual  symptoms  the  results  of  portal  con- 
gestion deserve  the  most  consideration.     It  is  important  that  the  patient  should 


BILIARY  AND  HYPERTROPHIC   CIRRHOSES  OF  THE  LIVER,    is:; 

enjoy  complete  physical  rest,  and  that  his  bodily  vigor  should  be  promoted  in 
every  way  possible.  Even  by  tbese  means  we  are  sometimes  able  to  diminish,  or 
at  least  prevent  the  increase  of,  the  ascites  and  other  effects  of  portal  obstruction. 

Further  remedies  are  given  with  the  purpose  (1)  to  deplete  the  congested  por- 
tal system,  and  (2)  by  promoting  the  watery  excretions  to  cause  reabsorption  of 
the  ascitic  effusion.  Depletion  is  usually  attempted  with  purgatives,  the  action  of 
which  is  expected  to  diminish  the  high  tension  existing  in  the  portal  vein.  The 
custom  is  an  old  one.  In  the  milder  cases,  just  developing,  salines  are  recom- 
mended, usually  in  the  form  of  mineral  waters.  The  continued  use  of  small  doses 
of  calomel  (say  2  or  3  powders  a  day,  each  containing  one  half  to  one  grain — 0'03- 
0-05  grm.)  seems  to  be  sometimes  advantageous.  But  if  the  ascites  is  already 
great,  it  is  claimed  that  drastic  remedies  sometimes  prove  beneficial.  Gamboge  is 
reputed  to  be  particularly  appropriate  in  cirrhosis.  We  should  not  persist  in  the 
use  of  such  drugs,  however,  if  they  disturb  digestion. 

The  second  indication  of  promoting  watery  discharges  is  fulfilled  by  diuretics. 
Besides  the  usual  remedies  of  this  class,  like  potassic  acetate  and  squills,  copaiba 
and  its  resin  have  been  especially  recommended  for  the  various  forms  of  ascites 
by  English  authors.  The  dose  [of  the  resin]  is  about  fifteen  grains  (grm.  1)  daily, 
best  given  in  capsules.  In  some  cases  this  remedy  has  caused  a  rapid  increase  in 
the  amount  of  urine  and  an  accompanying  diminution  of  the  ascites.  The  im- 
provement is  not  permanent,  however.  Good  diuretic  effects  are  sometimes  ob- 
tained with  calomel  (vide  p.  306). 

If  the  ascites  is  so  excessive  as  to  occasion  much  local  discomfort  and  to  impede 
respiration,  the  removal  of  the  fluid  by  paracentesis  may  afford  relief.  The  details 
of  this  proceeding  were  given  in  the  last  section.  Many  physicians  recommended 
tapping  as  early  as  possible,  before  it  is  absolutely  necessary.  The  relief  is  said 
to  be  more  lasting  in  that  case;  but,  as  a  rule,  the  abdomen  generally  is  quickly 
filled  again.  Possibly  the  application  of  an  elastic  bandage  after  the  fluid  is  re- 
moved may  retard  its  reaccumulation  by  the  pressure  thus  exerted  upon  the  ab- 
dominal cavity. 

Special  symptoms  may  sometimes  demand  attention.  They  are  to  be  treated 
according  to  general  principles. 


CHAPTER  V. 
BILIARY  AND   HYPERTROPHIC    OIRRHOSES   OP  THE   LIVER. 

There  are  two  forms  of  cirrhosis  which  differ  in  many  respects  from  the  dis- 
ease just  described :  they  are  called  biliary  cirrhosis  and  hypertrophic  cirrhosis  of 
the  liver.  Charcot  and  other  French  investigators  were  the  first  to  call  attention 
to  them.  Since  then  the  literature  of  the  subject  has  become  quite  considerable, 
but  all  doubts  and  differences  of  opinion  are  not  yet  settled.  We  shall  try  to  state 
the  most  important  points  in  what  follows. 

Whenever  there  is  retention  of  bile  in  the  liver  for  any  length  of  time,  no 
matter  what  causes  it,  certain  changes  result.  The  small  and  the  medium-sized 
bile-ducts  become  distended,  and  granules  of  pigment  are  deposited,  both  in  the 
interlobular  connective  tissue  and  within  the  acini  themselves.  Besides  this,  how- 
ever, and  undoubtedly  because  of  the  noxious  influence  of  the  retained  bile,  the 
hepatic  cells  undergo  destructive  changes.  In  accordance  with  the  general  rule, 
connective  tissue  gradually  fills  the  gaps  thus  left  in  the  parenchyma,  and,  more 
than  this,  the  interstitial  hyperplasia  is  so  great  as  to  increase  the  size  of  the  organ. 


4Si  DISEASES  OP  THE  DIGESTIVE  ORGANS. 

If,  therefore,  thei^  is  persistent  obstruction  of  the  common  duct  by  a  gall-stone,  or 
a  cicatricial  stenosis,  or  a  tumor  pressing  from  without  upon  the  duct,  the  liver 
will,  in  all  such  cases,  be  found  to  be  larger,  firmer,  and  richer  in  fibrous  tissue 
than  normal— in  a  word,  "cirrhotic."  Hence  this  condition  does  not  represent  an 
independent  disease,  but  is  a  result  of  chronic  biliary  retention,  in  whatever  way 
occasioned.  It  is  appropriately  termed  "  secondary  biliary  cirrhosis."  That  reten- 
tion is  really  the  cause  of  this  change  has  been  proved  by  experiments,  for  it  has 
been  shown  that  ligature  of  the  common  duct  in  animals  causes  well-marked  bili- 
ary cirrhosis. 

This  secondary  cirrhosis  is  due  to  occlusion  of  the  large  bile-ducts.  There  is 
also  a  rare  primary  form  of  the  biliary  cirrhosis,  usually  known  as  hypertrophic 
cirrhosis.  French  authors  have  given  it  the  name  of  ucirrhose  hypertrophique 
avec  ictere,"  out  of  regard  to  its  most  important  clinical  symptom.  That  there  is 
an  essential  difference  between  this  form  and  the  ordinary  "atrophic"  cirrhosis 
of  Laennec  is  manifested  by  the  clinical  behavior  of  the  disease. 

Often  this  disorder  attacks  hard  drinkers,  but  they  are  not  its  only  victims. 
While,  in  the  common  form  of  cirrhosis,  ascites  is  usually  the  earliest  grave  symp- 
tom of  disease,  in  hypertrophic  cirrhosis  a  slight  jaundice  generally  appears  simul- 
taneously with  the  first  indefinite  symptoms  of  pressure  in  the  region  of  the  liver, 
languor,  and  anorexia.  This  jaundice  rapidly  increases,  and  persists  throughout 
the  illness.  In  ordinary  cirrhosis  there  may  be,  as  we  have  said,  hardly  any  jaun- 
dice, or,  at  any  rate,  it  is  a  rather  late  symptom,  and  even  then  it  is  seldom  extreme. 
On  the  other  hand,  ascites  may  be  slight  or  absent  in  hypertrophic  cirrhosis.  It 
is  true  that  there  have  been  cases  with  great  ascitic  effusion,  but  it  never  comes 
till  the  disease  is  quite  far  advanced. 

On  physical  examination  the  liver  is  usually  found  to  be  considerably  enlarged, 
and  its  surface  is  smooth,  as  a  rule,  or  rarely  rough.  In  general  there  is  said  to 
be  this  important  difference  between  the  ordinary  and  the  hypertrophic  forms, 
that  in  the  latter  the  newly  formed  connective  tissue  evinces  little  tendency  to 
contraction,  so  that  the  liver  remains  large,  even  late  in  the  course  of  the  disease, 
and  does  not  shrink.  Somewhat  too  much  stress  has  been  laid  upon  this  point. 
If,  in  many  cases  of  hypertrophic  cirrhosis,  the  live:'  has  remained  large  to  the 
end,  this  is  probably  in  part  due  to  an  early  death,  before  there  was  opportunity 
for  much  shrinkage.     Cases  that  lasted  longer  have  presented  a  contracted  liver. 

It  must  be  said  that  the  pathological  appearance  of  the  liver,  particularly  in 
the  later  stages  of  the  disease,  affords  no  certain  evidence  as  to  whether  the  cir- 
x'hosis  was  of  the  ordinary  or  of  the  "  primary  biliary  "  variety.  Clinically,  how- 
ever, the  two  forms  present  such  important  diversities  as  to  justify  the  distinction 
made.  Of  course,  the  clinical  peculiarities  of  primary  biliary  cirrhosis  must  be 
due  to  some  anatomical  lesion.  The  most  noticeable  peculiarity  of  this  sort  is, 
that  the  development  of  connective  tissue  in  hypertrophic  cirrhosis  is  more  active 
within  the  lobules  than  is  the  case  in  ordinary  cirrhosis.  Probably  the  hyper- 
plasia in  hypertrophic  cirrhosis  is  most  vigorous  at  first  around  the  small  biliary 
ducts,  and  thus  leads  to  a  retention  of  bile  within  the  minutest  biliary  passages, 
with  consequent  jaundice,  while  the  ramifications  of  the  portal  vein  are  not 
encroached  upon  till  the  process  is  far  advanced.  Whether  these  two  forms  of 
cirrhosis  are  merely  modifications  of  one  disease,  or  whether  they  are  two  inde- 
pendent disorders,  is  as  yet  unsettled.     Certainly  there  are  transitional  forms. 

As  to  the  other  clinical  symptoms  of  primary  biliary,  or  hypertrophic,  cirrhosis 
we  need  say  little.  The  most  noticeable  symptoms  besides  the  hepatic  enlarge- 
ment and  the  jaundice  are  the  effects  of  the  jaundice  itself — namely,  digestive  dis- 
turbances, slowness  of  the  pulse,  and  nervous  disorders.  Of  the  occasional  dis- 
turbances in  the  portal  system,  we  have  mentioned  the  ascites  already.      Still 


CUTE  YELLOW  ATROPHY  OF  THE  LIVER.  485 

more  frequent, and  usually  earlier  in  the  time  of  its  appearance,  is  chronic  passiv. 
congestion  of  the  spleen,  with  enlargement. 

The  entire  duration  of  the  disease  is  about  one  or  two  years ;  but  it  may  last 
much  longer.  The  prognosis  is  almost  always  bad.  Occasionally  a  case  will 
exhibit  marked  temporary  improvement  or  an  apparent  arrest  of  tbe  disease. 
Death  comes  as  a  result  of  gradual  exhaustion,  or  is  suddenly  ushered  in  by  coma, 
convulsions,  and  other  grave  nervous  symptoms,  usually  ascribed  to  cholaemia 
(vide  infra). 

The  diagnosis  of  hypertrophic  cirrhosis  can  sometimes  be  made  with  consider- 
able positiveness,  and  sometimes  can  merely  be  regarded  as  probable.  The  gradual 
development  and  persistence  of  jaundice  and  the  presence  of  an  enlarged  liver 
and  spleen,  but  usually  without  ascites,  would  suggest  the  disease  strongly;  but 
in  some  cases  it  is  often  impossible  to  exclude  the  existence  of  some  mechanical 
obstruction  in  the  larger  biliary  passages,  such  as  gall-stones  or  new  growths. 

The  treatment  should  conform  to  the  principles  laid  down  in  the  chapters  on 
jaundice  and  ordinary  cirrhosis  of  the  liver.  Sacharjin  has  lately  recommended 
the  frequent  use  of  small  doses  of  calomel— one  grain  (0'06)  several  times  a  day. 


CHAPTER  VI. 
ACUTE   YELLOW    ATROPHY   OF   THE   LIVER. 

iEtiology. — Acute  fatty  degeneration  of  the  liver  occurs  both  as  a  primary  dis- 
ease and  as  secondary  to  other  hepatic  disorders,  or  as  a  symptom  of  constitu- 
tional diseases.  Secondary  acute  fatty  degeneration  in  rare  instances  accompanies 
severe  acute  infectious  diseases,  like  typhoid  fever,  recurrent  fever,  septicaemia,  and 
puerperal  disease.  It  also  appears,  with  equal  rarity,  in  the  course  of  cirrhosis  of 
the  liver  or  of  persistent  biliary  retention ;  and  it  is  a  constant  phenomenon  in 
acute  phosphorus  poisoning.  Indeed,  the  effects  of  phosphorus  resemble  the 
symptoms  of  primary  acute  yellow  atrophy  in  many  ways  so  closely,  even  post 
mortem,  that  formerly  the  two  were  often  confounded. 

Primary  acute  yellow  atrophy  of  the  liver  is  an  extremely  severe  disease  which 
almost  invariably  leads  to  speedy  death.  There  is  generally  no  determinable 
cause,  and  its  victims  are  struck  down  in  blooming  health.  It  is  so  rare  that  not 
much  over  two  hundred  cases  have  thus  far  been  reported.  It  is  most  common  in 
young  adult  life,  say  between  the  fifteenth  and  thirty-fifth  year.  Children  and 
elderly  people  have  been  occasionally  attacked.  Females  are  much  more  liable 
to  the  disease  than  males ;  and  pregnancy  increases  the  predisposition  to  it. 

As  we  have  said,  we  can  not  as  a  rule  find  any  exciting  cause.  It  is  stated  that 
sometimes  the  onset  has  been  preceded  by  some  violent  emotional  excitement,  or 
excess  in  alcohol,  or  the  like;  but  how  important  these  factors  may  be  is  not  at 
all  clear. 

It  is  an  interesting  fact  that  sometimes  the  disease  becomes  rather  more  fre- 
quent than  usual,  and  endemic.  For  instance,  several  members  of  one  family 
will  be  attacked.  This  favors  a  view  as  to  the  nature  of  acute  yellow  atrophy 
which  a  majority  of  the  present  investigators  seem  inclined  to  adopt.  The  view 
referred  to  is  suggested  not  only  by  the  whole  course  of  the  disease,  but  by  the 
pathological  appearances,  and  places  it  in  the  category  of  acute  infectious  diseases. 
It  must  be  confessed  that  as  yet  we  know  nothiug  about  the  intimate  nature  of 
the  infection.  Klebs  maintains  that  he  has  discovered  micrococci  in  the  hepatic 
blood-vessels;  but  thus  far  the  observation  lacks  confirmation. 


4-86  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

Pathology. — The  chief  change  found  post  mortem  is  in  the  liver,  and  has 
determined  the  name  given  to  the  disease. 

The  liver  is  much  atrophied,  sometimes  being  only  one  half  or  one  third  its 
normal  size.  This  makes  its  capsule  often  seem  contracted  and  wrinkled.  The 
oro-an  is  usually  soft  and  flabby,  so  that  in  some  places  it  seems  as  if  the  finger 
could  be  pressed  into  it.  The  color  of  the  surface,  and  for  the  most  part  of  the 
cross-section  also,  is  yellow,  like  ochre  or  saffron;  but  the  cut  surface  may  be  parti- 
colored, having  red  and  yellow  spots  interspersed.  Hence  the  names  "  red  atro- 
phy" and  "yellow  atrophy."  The  arrangement  and  relative  extent  of  these 
patches  may  vary  exceedingly.  The  red  places  look  as  if  they  had  collapsed,  and 
seem  tougher  than  the  yellow.  They  correspond,  as  we  shall  soon  see,  to  the 
more  advanced  stages  of  the  affection,  while  the  yellow  spots  have  undergone 
less  change.  The  lobules  are,  as  a  rule,  no  longer  distinguishable  by  the  naked 
eye.  Such  lobules  as  can  still  be  made  out  seem  abnormally  small  and  have  a 
gray  periphery. 

On  microscopic  examination,  we  find  that  the  essential  change  is  an  intense 
and  uniform  fatty  degeneration  of  the  hepatic  cells,  affecting  the  entire  paren- 
chyma. But  few  cells  still  retain  their  normal  condition.  The  others  are  filled 
with  large  and  small  fat-globules,  and  many  are  already  suffering  evident  disin- 
tegration and  absorption.  Where  the  degeneration  is  furthest  advanced,  fat, 
detritus,  and  pigment  alone  remain.  Inasmuch  as  the  lymphatics  rapidly  absorb 
and  remove  the  fatty  and  albuminoid  granules,  there  is  finally  little  left  except  blood- 
vessels and  connective  tissue.  The  blood-vessels  are  frequently  quite  congested, 
and  thus  occasion  that  red  color  which  the  naked  eye  detects  in  the  more  ad- 
vanced, broken-down  portions.  Frerichs  made  an  interesting  discovery,  which 
deserves  mention,  of  the  existence  of  leucine  and  tyrosine  crystals  both  in  the 
parenchyma  and  in  the  blood-vessels.  Bilirubin  crystals  also  are  sometimes  found 
in  the  detritus,  and  more  rarely  in  the  interior  of  the  hepatic  cells. 

Not  only  the  liver,  but  many  other  organs  present  fatty  degeneration:  the 
heart  in  particular,  the  kidneys,  and  rarely  the  muscles ;  but  the  process  is  always 
most  intense  in  the  liver.  The  skin  (vide  infra)  and  most  of  the  viscera  are  evi- 
dently tinged  with  jaundice. 

Acute  splenic  tumor  is  invariably  present.  This  suggests  that  the  disease  may 
be  infectious.  That  the  disease  is  a  constitutional  one  is  also  to  be  inferred  from 
the  numerous  ecchymoses  in  the  skin  and  the  interior  of  the  body,  especially  in 
the  mucous  membrane  of  the  stomach  and  intestines,  in  the  serous  membranes, 
in  the  pelvis  of  the  kidneys,  and  the  kidneys  themselves,  and  more  rarely  in  the 
brain  and  heart.  This,  again,  is  like  the  grave  septic  diseases.  The  blood  itself  is 
dark,  with  few  clots.  Leucine  and  tyrosine  have  repeatedly  been  detected  in  it. 
The  peritoneum  and  other  serous  cavities  sometimes  contain  a  considerable  amount 
of  serum. 

Clinical  History.— The  disease  is  usually  divided  into  two  stages,  the  first  of 
which  corresponds  to  the  milder  prodromal  symptoms,  the  second  to  those  severe 
symptoms  which  are  alone  characteristic.  In  many  instances,  however,  the  first 
period  is  wanting,  or  is  so  brief  that  the  patient  is  plunged  almost  without  warn- 
ing into  the  gravest  condition. 

The  prodromata  in  most  cases  consist  of  constitutional  disturbances  and  mild 
gastro-intestinal  symptoms.  The  patient  is  languid,  without  appetite,  and  disin- 
clined to  exertion.  There  are  headache,  nausea,  vomiting,  and  sometimes  mod- 
erate fever.  In  a  few  days  jaundice  usually  appears.  This  is  almost  invariably 
taken  for  an  ordinary  catarrhal  attack. 

After  some  days,  or  it  may  be  weeks,  the  second  stage  begins.  The  chief 
characteristic  of  this  is  the  occurrence  of  grave  nervous  symptoms.     First  there 


ACUTE  YELLOW  ATROPHY  OF  THE  LIVER.      ■  487 

is  violent  headache,  with  sleeplessness  and  marked  restlessness.  The  intellect  is 
usually  somewhat  dulled  even  now,  and  articulation  is  slow  and  clumsy.  The 
mental  confusion  usually  advances  very  rapid] y  to  a  noisy  and  violent  delirium. 
The  excitement  becomes  at  time  maniacal.  The  patient  screams  and  storms,  and 
can  hardly  be  kept  in  bed.  Often  there  are  convulsive  twitchings  of  individual 
muscles;  and  there  may  be  typical  epileptiform  attacks,  but  this  is  not  common. 
After  one  or  two  days,  or  rarely  longer,  the  excitement  abates,  and  is  followed  by 
sopor,  which  soon  passes  into  deep  coma.  At  death  the  patient  is  usually  per- 
fectly unconscious.  It  is  exceptional  for  the  excited  stage  to  be  wanting;  in  such 
cases  the  first  nervous  symptom  is  sopor. 

The  cause  of  the  nervous  symptoms  has  not  yet  been  explained  in  a  way  to 
silence  discussion.  The  same  theories  which  have  been  set  up  to  account  for  the 
grave  form  of  jaundice  in  general  (see  appendix  to  this  chapter)  have  also  been 
employed  to. elucidate  the  nervous  phenomena  of  acute  yellow  atrophy.  Thus, 
some  refer  them  to  cholasmia,  some  to  acholia,  and  still  others  to  acute  cerebral 
anaemia.  It  seems  to  us  worth  considering  whether  the  cerebral  disturbance  in 
acute  yellow  atrophy  of  the  liver  may  not  be  due  to  the  constitutional  infection 
(or  intoxication)  which  we  have  seen  to  be  so  probable. 

The  jaundice,  which  is  present  even  in  the  first  stage,  afterward  usually  deep- 
ens. The  urine  contains  bile-pigment,  and  many  investigators  have  also  found 
bile-acids  in  it.  If  these  latter  are  present,  it  suggests  that  the  jaundice  is  not 
hematogenous — that  is,  the  result  of  a  destruction  of  red  blood-corpuscles  and  the 
transformation  of  their  pigment  into  biliary  coloring  matter — but  is  rather  due  to 
a  retention  of  bile.  Just  how  this  retention  arises  we  do  not  yet  know  for  certain. 
The  obstruction  can  not  be  in  the  large  bile-ducts,  for  the  gall-bladder  is  usually 
found  empty.  Hence  the  cause  of  the  retention  of  bile  and  of  the  jaundice  is  prob- 
ably a  derangement  of  the  smaller  biliary  passages  within  the  liver.  We  should 
add  that  in  a  few  rare  cases  there  has  been  little  or  no  jaundice. 

On  physical  examination  of  the  liver  during  the  last  stage  of  the  disease,  there 
is  usually  a  striking  diminution  of  hepatic  dullness,  corresponding  to  the  atrophy 
of  the  organ.  Generally  the  first  change  to  be  detected  is  a  contraction  of  the 
left  lobe,  as  shown  by  the  development  of  tympanitic  resonance  in  the  epigastrium. 
At  the  commencement  of  the  illness,  the  hepatic  dullness  is  normal  or  slightly 
increased  in  area.  If  the  disease  proves  very  rapidly  fatal,  the  organ  may  never 
become  very  small.  In  most  cases,  though  by  no  means  in  all,  there  are  pain  and 
tenderness  in  the  hepatic  region,  but  these  are  seldom  so  great  as  in  phosphorus 
poisoning. 

The  enlargement  of  the  spleen  has  been  already  mentioned  as  an  almost  con- 
stant symptom  of  the  disease.  Even  during  life  some  increase  of  the  area  of 
splenic  dullness  can  usually  be  made  out,  and  sometimes  the  spleen  can  be  felt 
under  the  edge  of  the  ribs. 

The  occurrence  of  the  haemorrhages,  which  have  already  been  referred  to 
under  the  pathological  lesions,  can  often  be  demonstrated  diiring  life.  The  cuta- 
neous ecchymoses  can,  of  course,  be  seen,  and  the  hasmorrhages  in  the  mucous 
membranes  may  give  rise  to  haematemesis,  bloody  stools,  bleeding  from  the 
female  genitals,  or  epistaxis.  The  haemorrhages  are  probably  due  to  the  impaired 
nutrition  and  diminished  resisting  power  of  the  vasctdar  walls  occasioned  by  the 
grave  constitutional  disturbance. 

The  condition  of  the  urine  in  acute  yellow  atrophy  is  very  interesting.  The 
amount  is  either  normal  or  slightly  diminished,  and  the  specific  gravity  is  some- 
what increased.  Often  there  is  a  trace  of  albumen.  We  have  already  mentioned 
the  presence  of  bile-pigment.  The  point  of  chief  interest,  however,  is  one  that 
Frerichs  discovered  and  various  others  have  since  confirmed,  and  is  the  great 


488  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

diminution  of  ui'ea  and  the  appearance  in  its  place  of  several  other  substances, 
which  are  likewise  the  products  of  the  decomposition  of  albuminoid  matter,  and 
represent,  in  all  probability,  the  first  steps  in  the  formation  of  urea.  Of  these  sub- 
stances, the  most  important  are  leucine  and  tyrosine.  Their  characteristic  crys- 
tals can  often  be  detected  by  the  microscope  in  the 
urinary  sediment  (see  Fig.  52).  The  crystals  may  also 
be  obtained  by  allowing  a  drop  of  the  fresh  urine  to 
evaporate  slowly  upon  an  object-glass.  There  is  a 
chemical  test  for  them  which  we  can  not  here  de- 
scribe. There  are  some  other  abnormal  constituents 
to  be  found  in  the  urine  besides  leucine  and  tyrosine ; 
but  what  their  significance  is  we  do  not  know. 
Among  these  are  sarcolactic  acid,  oxymandel  acid, 
peptonoid  substances,  and  large  amounts  of  kreatine. 
It  at  once  suggests  itself  that  this  disappearance 
Fig  52.-a ..Leucine  crystals,    b.     0f  urea  an(j  appearance  of  leucine  and  tyrosine,  which 

are  regarded  as  preparatory  stages  in  the  formation 
of  urea,  gives  valuable  support  to  Meissner's  and  Von  Schroder's  idea  that  this 
substance  is  manufactured  in  the  liver. 

As  to  the  other  organs  little  need  be  said.  Vomiting  is  very  frequent  in  the 
second  stage,  as  well  as  in  the  first.  It  usually  ushers  in  the  severe  cerebral  symp- 
toms. The  stools  are,  as  a  rule,  clay-colored,  as  is  usual  in  jaundice.  There  is 
generally  constipation.  The  pulse  is  rapid,  often  reaching  140  to  160  beats  per 
minute,  and  is  also  small  and  compressible.  It  is  this  acceleration  of  the  pulse, 
contrasting  with  its  usual  slowness  during  the  first  stage,  which,  along  with  the 
vomiting,  announces  the  onset  of  dangerous  symptoms.  The  pulmonary  signs 
are  seldom  marked,  although  there  may  be  bronchitis  or  a  pneumonia  due  to 
the  inhalation  of  foreign  substances.  During  the  coma  which  precedes  death 
respiration  is  usually  hurried,  and  often  deep  and  noisy.  Sometimes  it  is  irregu- 
lar. 

The  temperature  is  generally  approximately  normal.  Toward  the  fatal  termi- 
nation there  may  be  a  subnormal  temperature.  Still  more  frequently  the  tem- 
perature rises  before  death,  and  even  sometimes  grows  higher  after  death,  reaching 
107-5°  (42°  C.)  or  more. 

In  case  the  disease  attacks  a  pregnant  woman,  abortion  or  premature  delivery 
is  almost  certain  to  occur. 

The  entire  duration  of  the  disease  depends  mainly  upon  the  length  of  the  first 
stage.  This  may  be  entirely  absent,  or  may  be  brief,  or  may  occupy  several 
weeks.  The  duration  of  the  second  stage,  reckoning  from  the  occurrence  of  grave 
cerebral  symptoms,  is  generally  only  a  few  days  (two  to  four),  rarely  a  week. 
The  termination  is  invariably  fatal.  In  the  few  cases  of  recovery  reported  there 
is  doubt  about  the  correctness  of  the  diagnosis. 

The  diagnosis  can  not  be  made  till  the  second  stage.  The  symptoms  of  the 
first  stage  are  indistinguishable  from  those  of  simple  catarrhal  jaundice.  With 
the  development  of  the  grave  symptoms  all  doubt  usually  vanishes.  The  general 
course  of  the  disease,  the  deep  jaundice,  the  cerebral  disturbances,  the  cutaneous 
ecchymoses,  and  the  character  of  the  urine,  form  a  clinical  picture  resembling  no 
other  disease.  The  only  cases  where  there  can  be  any  uncertainty  about  the  diag- 
nosis are  the  exceptional  ones  in  which  there  is  no  jaundice.  Acute  phosphorus 
poisoning  (q.  v.)  is  in  many  respects  very  similar  in  its  phenomena,  but  can  gen- 
erally be  differentiated,  even  if  the  history  of  the  case  is  not  conclusive.  The 
chief  points  are  that  in  phosphorus  poisoning  the  liver  remains  of  large  size  for 
some  time,  and  is  very  painful ;  that  the  nervous  symptoms  much  less  frequently 


PERNICIOUS  JAUNDICE.     CHOLiEMIA   AND  ACHOLIA.  jsti 

assume  the  form  of  maniacal  excitement ;  and  that  in  but  few  cases  is  there  any 
large  amount  of  leucine  and  tyrosine  in  the  urine. 

After  what  has  been  said,  we  need  hardly  add  that  treatment  is  unavailing. 
Usually  laxatives  are  employed,  e.  g.,  calomel.     The  nervous  symptoms  are  com 
bated  by  an  ice-cap  and  baths  and  narcotics;  the  vomiting,  by  opium  and  bits  of 
ice;  and  the  cardiac  weakness,  by  stimulants. 


APPENDIX. 

PERNICIOUS  JAUNDICE.      CHOLJEM1A  AND  ACHOLIA. 

Reference  has  been  repeatedly  made  in  the  preceding  chapters  to  the  possibil- 
ity of  the  sudden  supervention  of  grave  nervous  derangements  in  the  course  of 
various  hepatic  diseases.  These  nervous  symptoms  resemble  one  another  so  much 
in  the  different  instances  of  their  occurrence  that  we  are  forced  to  believe  tbem 
always  due  to  the  same  cause. 

These  symptoms  are  relatively  most  frequent  where  there  is  chronic  biliary 
retention.  Whether  this  retention  be  the  result  of  obstruction  of  the  common  or 
the  hepatic  duct,  or  of  stenosis  of  the  biliary  passages  from  a  carcinoma  involving 
the  opening  of  the  common  duct  into  the  duodenum,  or  that  duct  itself,  the  patient 
may  quite  suddenly  fall  into  a  condition  which  in  many  respects  corresponds  to 
the  second  stage  of  acute  yellow  atrophy  just  described.  Grave  cerebral  disturb- 
ances declare  themselves,  with  delirium,  convulsions,  and  coma.  There  are  haem- 
orrhages  into  the  skin  and  into  the  mucous  membranes,  and  in  a  few  days  the 
patient  dies.  Usually  the  end  is  attended  with  high  fever.  We  have  ourselves 
seen  a  temperature  of  107'4°  (41 '9°  C.)  in  a  case  of  cancer  at  the  duodenal 
extremity  of  the  common  duct.  It  is  this  group  of  symptoms  which  is  usually 
termed  pernicious  jaundice ;  but  almost  precisely  similar  phenomena  may  sudden- 
ly appear  in  hepatic  cirrhosis,  when  there  is  no  great  degree  of  jaundice,  if  any. 

Just  what  produces  these  grave  results  in  acute  yellow  atrophy  and  the  other 
disorders  just  enumerated,  we  are  not  certain.  Three  theories  have  been  pro- 
pounded in  explanation.  The  first  theory,  the  latest  champion  of  which  is  Ley- 
den,  attributes  pernicious  jaundice  to  cholaemia — that  is,  to  the  accumulation  in 
the  blood  of  the  constituents  of  bile,  and  in  particular  of  the  biliary  acids,  as  a 
result  of  absorption.  This  accumulation,  it  is  said,  is  promoted  by  the  paralyziug 
effect  of  the  jaundice  upon  the  activity  of  the  kidneys.  Opposed  to  this  theory  is 
the  fact  that  these  same  symptoms  may  occur  where  there  is  no  marked  hepa- 
togenous jaundice. 

Traube  has  suggested  that  as  a  result  of  the  great  impairment  of  nutrition 
there  is  a  cerebral  anaemia,  which  in  its  turn  brings  on  the  nervous  attacks. 
Cohnheim  also  advocated  this  view,  with  some  modifications. 

The  view  which  we  are  most  inclined  to  accept  is  that  of  Frerichs.  He  has 
given  to  the  group  of  symptoms  under  discussion  the  name  of  acholia.  These 
symptoms  he  ascribes  to  the  pernicious  influence  of  those  substances  which  under 
normal  conditions  are  manufactured  by  the  liver  into  bile,  but  which  in  such  cases 
accumulate  in  the  blood  and  the  tissues.  As  Frerichs  himself  has  said,  and  we 
believe  very  justly,  this  view  should  be  extended  to  include  all  other  transforming 
functions  of  the  liver,  and  especially  the  production  of  urea.  It  is  also  very  pos- 
sible that  in  addition  to  the  acholia,  cholasmic  poisoning  may  sometimes  exert  a 
simultaneous  influence. 

The  termination  of  cholaemia  or  acholia  is  almost  always  as  unfavorable  as 
that  of  acute  yellow  atrophy.  In  cases  of  this  kind  there  is  usually  marked  fatty 
degeneration  of  the  hepatic  parenchyma  to  be  found  post  mortem. 


490  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

CHAPTER  VII. 

ICTERUS  NEONATORUM. 

{Jaundice  of  the  New-born.) 

Frequently  the  normal  red  color  of  the  skin  in  children  changes  on  the 
second,  third,  or  fourth  day  after  birth  to  a  distinctly  yellow,  jaundiced  hue.  The 
yellow  tinge  is  deeper  on  the  face  and  trunk  than  on  the  extremities.  There  are 
no  special  digestive  or  constitutional  disturbances.  Still  it  may  be  taken  for  the 
rule  that  weaklings  more  often  present  this  jaundice  than  do  vigorous  babes. 
The  abnormal  hue  is  almost  certain  to  vanish  in  a  week  or  two,  and  leave  no 
sequela?.  The  termination  is  unfavorable  in  those  instances  alone  where  there  is 
some  special  complication,  not  directly  connected  with  the  jaundice  as  such. 

The  eetiology  is  a  disputed  matter.  A  large  number  of  all  sorts  of  theories  have 
been  set  up,  no  one  of  which  to  this  day  has  gained  universal  acceptance.  For- 
merly there  was  considerable  tendency  to  regard  the  jaundice  as  hematogenous— 
that  is,  due  to  the  transformation  of  the  pigment  of  broken-down  blood-corpuscles 
into  bile-pigment.  Points  which  seemed  to  support  this  view  are  the  light  (not 
jaundiced)  color  of  the  urine  and  the  yellow  color  of  the  stools  (from  bile).  But 
more  accurate  examination  has  shown  that  the  urine  does  contain  biliary  pig- 
ment, as  do  also  the  kidneys  of  such  infants  as  happen  to  die  during  the  existence 
of  the  jaundice ;  and  the  biliary  acids  have  been  clearly  shown  to  be  present  in 
the  serous  transudations.  It  may  therefore  be  considered  certain  that  icterus 
neonatorum  is  hepatogenous;  hut  how  the  biliary  retention  and  consequent 
absorption  are  caused  we  do  not  know.  Perhaps  at  first  the  bile  is  not  ejected 
properly,  from  weakness,  or  the  ducts  may  be  narrow,  or  temporarily  plugged  by 
desquamated  epithelium.  Birch -Hirschfeld  has  called  attention  to  the  fact  that 
after  birth  there  is  a  tendency  to  considerable  passive  congestion  of  the  liver,  with 
resultant  oedema  of  Glisson's  capsule  and  pressure  upon  the  interlobular  bile- 
ducts.  We  should  also  consider,  as  Hofmeier  points  out,  that  probably  during 
the  first  few  days  of  extra-uterine  life  there  is  a  comparatively  large  amount  of 
bile  secreted,  occasioned  by  the  destruction  in  considerable  numbers  of  the  red 
blood-globules. 

It  is  well  to  mention  in  conclusion  that  in  very  rare  instances  there  is  complete 
congenital  stenosis,  or  even  entire  absence,  of  the  larger  bile-ducts.  Then  deep 
jaundice  comes  on  soon  after  birth,  and  is  persistent.  The  children  become 
extremely  emaciated,  and,  after  a  few  weeks,  inevitably  perish. 


CHAPTER  VIII. 
SYPHILIS  OP  THE   LIVER. 

iEtiology  and  Pathology. — Syphilitic  disease  of  the  liver  occurs  both  when  the 
syphilis  is  acquired  and  when  it  is  congenital.  Congenital  syphilitic  disease  of 
the  liver  may  be  diffuse  or  localized,  and  causes  a  cellular  infiltration  in  either 
case.  If  the  changes  are  extensive,  the  organ  is  hard  and  considerably  enlarged ; 
or,  if  the  newly  formed  connective  tissue  has  undergone  contraction,  the  liver  is 
smaller  than  normal,  and  its  surface  is  uneven.  In  some  cases  of  hereditary 
syphilis,  distinct  gummata  of  considerable  size  have  been  observed. 

In  acquired  syphilis,  hepatic  disease  is  one  of  the  so-called  tertiary  symptoms, 
and  does  not  usually  develop,  at  least  to  any  great  extent,  until  several  years  after 


SYPHILIS  OF  THE  LIVER.  491 

infection.  Indeed,  it  may  be  a  very  late  result.  It  may  take  the  form  either  of 
a  diffuse  syphilitic  hepatitis,  or  of  circumscribed  gummata  or  syphilomata.  The 
diffuse  hepatitis  does  not  present  essentially  different  anatomical  appearances  from 
those  of  ordinary  cirrhosis.  The  gummata  are  the  most  characteristic,  and  the 
most  important  clinically.  They  may  form  separate  tumors  the  size  of  an  apple 
or  even  larger.  The  convex  surface  of  the  organ,  particularly  that  portion  near 
the  suspensory  ligament,  seems  to  be  a  favorite  location  for  the  new  growth.  The 
same  is  true  of  the  porta  hepatis,  where  Glisson's  capsule  enters  the  liver.  At  the 
autopsy  the  gummata  have  in  most  cases  already  begun  to  undergo  contraction. 
If  so,  the  liver  is  usually  smaller  than  normal,  and  traversed  in  various  directions 
by  deep  furrows,  which  divide  it  into  lobes.  These  furrows  are  due  to  firm  cica- 
tricial bands,  among  the  fibers  of  which  we  may  sometimes  find  necrotic  and 
cheesy  vestiges  of  the  gumma  proper.  Often  there  is  evident  syphilitic  endarteri- 
tis in  the  smaller  and  sometimes  also  in  the  larger  branches  of  the  hepatic  artery 
and  portal  vein. 

Clinical  History. — Circumscribed  syphilitic  changes  in  the  liver  often  give  rise 
to  no  symptoms  whatever.  It  is  only  when  the  disease  comes  to  disturb  the  portal 
circulation  that  a  series  of  symptoms  result,  which,  for  evident  reasons,  may  be 
analogous  in  all  essential  points  to  the  effects  of  ordinary  cirrhosis.  Whenever 
the  syphilitic  growths  contract  so  as  to  obliterate  a  large  number  of  branches  of 
the  portal  vein,  or  whenever  a  gumma  happens  to  be  so  situated  as  to  compress 
the  trunk  of  the  portal  vein  itself,  then  the  well-known  results  of  portal  obstruc- 
tion are  inevitable,  the  chief  being  ascites  and  enlargement  of  the  spleen.  The 
disturbance  of  circulation  often  gives  rise  also  to  anorexia  and  digestive  disorders. 
Experience  shows  jaundice  to  be  rare  in  hepatic  syphilis,  but  it  may  appear  when 
the  lesions  involve  the  larger  bile-ducts  or  a  considerable  number  of  the  smaller 
biliary  passages. 

On  physical  examination,  the  results  vary  according  to  the  form  and  the  stage 
of  the  disorder.  Sometimes  the  larger  gummata  may  be  plainly  felt  through  the 
abdominal  walls,  usually  as  flattened  hemispheres.  Frequently,  also,  we  can  feel 
the  edge  of  the  enlarged  organ,  and  can  detect  that  the  edge  is  less  sharp  than  nor- 
mal. In  other  instances  the  separate  elevations  and  prominences  can  be  made  out. 
The  area  of  dullness  on  percussion  of  course  varies  in  different  cases. 

It  deserves  mention  that  hepatic  syphilis  quite  often  causes  severe  pain,  some- 
times over  the  entire  region  of  the  liver  and  sometimes  in  just  one  spot.  Pain  is 
by  no  means  felt  in  every  case.  With  the  pain  there  may  be  great  tenderness  on 
pressure. 

The  course  of  the  disease  is  usually  tedious,  and  may  occupy  many  years. 
Probably,  too,  lesions  exist  in  many  cases  long  befolge  there  are  any  symptoms. 
Just  as  in  cirrhosis,  ascites  is  usually  the  first  thing  to  attract  the  patient's  atten- 
tion. Improvement  and  temporary  arrest  of  the  disease  are  more  frequent  than 
in  ordinary  cirrhosis.  Still,  in  most  cases,  where  the  lesions  are  at  all  extensive, 
the  termination  is  unfavorable. 

The  diagnosis  is  not  always  easy.  Usually  the  objective  changes  in  the  liver, 
the  ascites,  and  the  enlarged  spleen,  indicate  hepatic  trouble,  but  we  are  often 
unable  to  determine  just  what  the  trouble  is.  Naturally,  the  getiological  factors 
are  of  great  importance.  In  a  toper  we  would  think  rather  of  the  common 
form  of  cirrhosis.  If  there  is  a  syphilitic  history,  or  if  we  find  scars  in  the 
throat,  irregularities  in  the  surface  of  the  bones,  or  other  signs  of  a  specific 
dyscrasia,  we  would  naturally  ascribe  the  hepatic  disorder  to  the  same  cause. 
As  to  special  signs,  if  the  prominences  on  the  liver  are  rather  large  in  contrast 
to  the  smaller  granulations  of  common  cirrhosis,  syphilis  is  somewhat  more 
pi'obable.     Severe  pain  in  the  right  hypochondrium  also  suggests  syphilis  rather 


492  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

than  cirrhosis.  It  should  also  be  considered  that  the  course  of  hepatic  syphilis 
is  usually  much  more  protracted  than  that  of  ordinary  hepatic  cirrhosis. 

Treatment. — Whether  we  feel  certain  that  syphilitic  hepatitis  exists,  or  merely 
suspect  it,  specific  treatment  should  be  tried.  Mercury  and  potassic  iodide  should 
both  be  given,  but  probably  the  iodide  is  the  more  valuable  of  the  two.  But 
these  remedies  can  be  successful  only  when  the  gummata  are  still  in  process 
of  formation.  Our.  therapeutic  efforts  produce  no  impression  upou  the  cicatri- 
cial bands,  the  contraction  of  which  is  the  main  cause  of  derangement.  Hence 
we  see  why  the  results  of  treatment  in  advanced  cases  are  seldom  very  favor- 
able. 

For  symptomatic  treatment,  the  reader  is  referred  to  cirrhosis  of  the  liver. 


CHAPTER   IX. 
CANCER   OP   THE    LIVER   AND   BILE-DUCTS. 

iEtiology  and  Pathology.— Primary  cancer  of  the  liver  is  very  rare,  but  sec- 
ondary or  metastatic  cancer  of  this  organ  is  met  with  comparatively  often.  The 
chief  explanation  of  this  latter  fact  is  the  slowness  of  the  blood-current  in  the 
liver,  which  favors  the  deposition  of  the  cancerous  germs  suspended  in  the  blood. 

Secondary  hepatic  cancer  may  be  a  sequel  to  primary  cancer  of  any  organ.  It 
is  most  often  seen,  however,  when  the  primary  growth  lies  within  the  portal  sys 
tem,  in  the  stomach,  intestines,  rectum,  oesophagus,  or  pancreas.  In  some  in- 
stances the  projection  of  the  primary  growth  into  the  lumen  of  a  branch  of  the 
portal  vein  has  been  directly  demonstrated,  thus  furnishing  an  obvious  source  for 
metastasis.  The  secondary  cancers  in  the  liver  may  be  very  numerous.  They  are 
found  both  within  the  organ  and  upon  its  surface.  If  superficial,  they  form  flat- 
tened protuberances,  which  are  often  dimpled  in  the  middle.  If  the  new  growth 
is  extensive,  the  liver  may  be  greatly  enlarged,  so  as  to  occupy  a  great  part  of  the 
abdominal  cavity. 

As  we  have  said,  primary  cancer  of  the  liver  is  very  unusual.  It  may  occur 
cither  in  the  form  of  separate  large  nodules,  or  as  a  more  diffuse  cancerous  infil- 
tration pervading  the  greater  part  of  the  organ.  Histologically  considered,  the 
primary  growths  are  of  cylindrical-cell  carcinoma,  apparently  originating  from 
the  epithelium  of  the  minute  bile-ducts,  but  also,  according  to  some  authors,  some- 
times starting  from  the  cells  of  the  parenchyma. 

Primary  cancer  of  the  larger  bile-ducts  is  of  more  frequent  occurrence  than 
genuine  primary  hepatic  cancer,  and  therefore  it  is  of  more  importance  clinically. 
The  gall-bladder  may  also  be  the  seat  of  primary  carcinoma.  From  these  sources 
may  proceed  abundant  metastatic  growths  in  the  liver  itself. 

As  to  the  aetiology  of  hepatic  cancer  we  can  be  brief.  The  disease  is  most  fre 
quent  in  advanced  life,  from  forty  to  sixty,  following  in  this  the  general  rule  for 
cancer.  Special  causes  are  not  known.  It  sometimes  seems  possible  to  trace  a 
hereditary  predisposition  to  it.  In  many  cases  gall-stones  seem  to  start  up  the 
development  of  carcinoma. 

Clinical  History — Diagnosis. — Many  small  nodules  of  cancer,  as  well  as  large 
masses  which  are  favorably  situated,  may  exist  in  the  liver  without  exciting  any 
symptoms.  If  there  is  an  undoubted  primary  cancer  in  another  organ,  such  as 
the  stomach,  we  must  always  remember  the  possibility  of  metastatic  growths  in 
the  liver ;  but  they  can  not  be  proved  to  exist,  unless  they  alter  appreciably  the 
size  or  shape  of  the  organ.     Sometimes  they  may  be  inferred,  when  we  observe 


CANCER  OF  THE  LIVER  AND  BILE-DUCTS.  493 

either  ascites  and  enlargement  of  the  splesu  from  pressure  on  the  portal  vein,  or 
jaundice  from  pressure  on  the  bile-ducts. 

On  palpation,  we  are  often  able  to  make  out  one  or  more  tumors  plainly  in 
hepatic  cancer.  These  tumors  are  in  the  region  of  the  liver,  and  they  are  directly 
connected  with  it,  as  we  can  prove  by  marking  out  its  limits  by  percussion  and 
palpation.  Another  characteristic  sign  is  that  almost  all  hepatic  tumors  can  he 
felt  to  move  with  respiration,  on  account  of  the  inspiratory  depression  of  the  dia- 
phragm pushing  down  the  liver  and  all  that  is  joined  to  it.  Percussion  over  a 
hepatic  tumor  almost  invariably  gives  flatness,  in  contrast  to  the  muffled  tym- 
panitic resonance  of  many  gastric  tumors. 

The  most  characteristic  condition  is  not  a  very  rare  one;  in  it  the  liver  is  the 
seat  of  a  very  large  number  of-  cancerous  nodules.  In  such  cases  the  organ  is 
usually  much  enlarged.  Often  we  can  detect  by  mere  inspection  a  great,  irregular 
prominence  in  the  hepatic  region,  pressing  forward  the  flabby,  atrophied  walls  of 
the  abdomen,  and  reaching  down  to  the  level  of  the  umbilicus,  or  even  lower. 
On  palpation,  we  can  feel  most  of  the  anterior  surface  of  the  liver,  and  the  sepa- 
rate cancerous  nodules  scattered  over  it.  These  usually  are  as  large  as  walnuts, 
or  even  apples.  The  lower  or  anterior  margin  of  the  liver  can  often  be  made  out 
plainly,  and  it  also  is  often  the  seat  of  nodules ;  aud  we  can  sometimes  feel  nodules 
on  the  lower  surface  of  the  organ. 

The  other  clinical  phenomena  in  hepatic  cancer  have  several  causes :  (1)  The 
primary  disease,  such  as  cancer  of  the  stomach ;  (2)  the  general  cancerous  cachexia, 
as  shown  by  languor,  emaciation,  and  possibly  a  slight  oedema  of  the  ankles;  and 
(3)  the  possible  compression  of  the  blood-vessels  or  bile-ducts.  This  compression  is 
not  infrequent,  and  produces  a  moderate  or  even  a  large  ascitic  effusion.  Even  in 
these  instances  the  spleen  is  seldom  much  enlarged  as  a  result  of  the  passive  con- 
gestion, because  the  universal  emaciation  and  anaemia  counteract  the  tendency  to 
increase  in  size.  Jaundice  is  relatively  more  frequent  in  cancer  of  the  liver  than 
is  ascites.  It  is  caused  by  compression  either  of  the  hepatic  duct  or  of  the  minuter 
bile-ducts.  On  the  other  hand,  however,  we  can  easily  see  that  hepatic  cancer 
may  exist  without  producing  either  icterus  or  ascites. 

The  differential  diagnosis  of  hepatic  cancer  from  cancer  in  other  organs  is 
sometimes  extremely  difficult.  This  is  particularly  true  of  pyloric  cancer,  and 
especially  so  when  the  pylorus  has  become  adherent  to  the  liver,  which  often  is  the 
case.  Cancers  of  the  omentum  and  of  the  colon  sometimes  simulate  hepatic 
cancer,  but  they  seldom  move  so  decidedly  in  respiration  as  do  hepatic  tumors. 
Given  a  new  growth  in  the  liver,  it  is  usually  comparatively  easy  to  distinguish 
between  carcinoma  and  other  tumors.  The  benign  growths,  like  adenoma,  are 
so  rarely  found  in  the  liver  that  they  can  actually  be  almost  disregarded.  If 
there  are  syphilitic  growths,  we  may  be  aided  by  the  history  of  the  case  and 
other  signs  of  syphilis,  or  by  the  eventual  contraction  and  atrophy  of  the  organ. 
Echinococci  have,  as  a  rule,  a  much  more  regular  shape,  like  a  flattened  sphere. 
Large  abscesses  are  rare  in  our  latitudes ;  and  if  they  occur,  usually  the  aetiology 
is  significant.  They  also  frequently  cause  fever  and  rigors,  which  cancer  does 
not. 

When  we  have  decided  that  cancer  of  the  liver  is  present,  the  question  arises, 
Is  it  primary  or  secondary?  In  the  first  place,  primary  cancer  here  is  so  rare  that 
the  probabilities  are  in  favor  of  a  secondaiy  growth.  Not  infrequently  the 
primary  tumor  can  not  be  detected  during  life.  Thus  a  small  cancer  of  the 
stomach,  or  a  flat  oesophageal  cancer,  or  carcinoma  of  the  pancreas,  are  all  easily 
overlooked.  If  we  find  many  nodules  in  the  liver  and  no  primary  trouble  else- 
where, then  there  comes  the  possibility  that  there  is  primary  cancer  in  the  gall- 
bladder or  the  bile  ducts.     In  rare  instances  palpation  may  discover  the  gall- 


494 


DISEASES  OF  THE  DIGESTIVE  ORGANS. 


bladder  in  a  state  of  cancerous  degeneration  close  underneath  the  liver;  hut 
usually  the  viscus  will  be  small  and  contracted,  and  the  flat  and  ulcerating 
growth  is  not  noticeable,  except  from  the  inside.  It  is  particularly  in  those  cases 
of  hepatic  cancer  where  there  is  great  and  persistent  icterus,  and  no  evidence  of 
carcinoma  in  any  other  organ,  that  we  should  be  most  apt  to  think  of  primary 
cancer  of  the  bile-ducts. 

The  duration  of  hepatic  cancer  is  usually  not  prolonged.  The  first  decided 
evidences  of  its  existence  no  sooner  present  themselves  than  marasmus  and 
cachexia  rapidly  develop.  The  fatal  end  comes  in  a  few  months,  or  at  latest 
within  a  year. 

The  prognosis  is  hopeless.  Treatment  can  avail  only  to  alleviate  somewhat 
the  patient's  sufferings. 


CHAPTER  X. 


ECHINOCOCCUS   OF   THE   LIVER. 

Natural  History  and  Pathology.— Inasmuch  as  it  is  the  liver  which  suffers 
most  frequently  from  invasions  of  the  echinococcus,  we  will  here  state  the  main 
general  points  relative  to  the  troubles  produced  by  this  parasite. 

The  tcenia  echinococcus  (see  Fig.  53)  is  a  small  tape-worm 
about  four  millimetres  long,  and  composed  of  three  or  four 
joints.  It  inhabits  the  intestinal  canal  of  the  dog.  Man 
\  becomes  infected  by  the  ingestion  of  the  eggs  of  this  tape- 
0  worm  into  the  stomach.  The  striking  prevalence  of  the  dis- 
ease in  Iceland  is  explained  by  the  fact  that  the  inhabitants 
live  in  constant  contact  with  their  numerous  canine  friends. 
Among  us  the  echinococcus  is  comparatively  rare. 

If  a  human  being  has  become  infected,  the  blood-current 
carries  the  embryo  into  some  organ.  In  a  great  majority  of 
cases  it  passes  through  a  branch  of  the  portal  vein  into  the 
liver  and  there  fastens  itself ;  but  the  echinococcus  may  be 
developed  in  other  organs — like  the  lungs  (vide  page  252), 
the  bones,  the  brain,  and  the  kidneys.  A  hydatid  cyst  de- 
velops from  the  embryo,  and  is  filled  with  a  non-albuminous 
fluid.  The  cyst  is  composed  of  an  external  cuticle  of  lamel- 
lated  structure,  and  an  inner,  parenchymatous  layer,  which 
contains  muscular  fibers  and  blood-vessels.  Surrounding 
the  cyst,  as  it  lies  in  the  infested  organ,  there  is  gradually 
developed  a  thick  capsule  of  connective  tissue. 

After  the  cyst  has  continued  its  growth  for  some  four  to 
six  months,  being  now  about  the  size  of  a  walnut,  there  are 
generated  upon  the  inner  surface  of  the  capsule,  from  the 
parenchymatous  layer,  so-called  breeding  capsules,  contain- 
ing numbers  of  echinococcus-heads,  or  "  scolices."  Each 
Fl°TffinTI(Fredlin^coccus!  scolex  has  four  suckers  and  a  circlet  of  hooks.  It  can  draw 
enlarged.     Above,  at   itself  into  the  breeding  capsule  and  also  produce  a  promin- 

the    right,    eehinoeoc-  ...  »  <.  n       i    JA        /         -rv  kj    kp- 

cua,  of  natural  size.  ence  upon  the  outer  surface  of  the  latter  (see  s  igs.  54,  55, 
and  56).  # 

Usually  the  primary  cyst  gives  rise  to  secondary  "  daughter  vesicles."  and  these 
to  "granddaughter  vesicles."  Some  of  these  are  formed  in  the  cuticle,  others 
from  the  breeding  capsules.     In  man  they  generally  grow  inward — that  is,  are 


ECHINOCOCCUS  OF  THE  LIVER.  495 

endogenous  (echinococcus  hydatidosus) — and  finally  become  detached.  Hundreds 
of  them  may  sometimes  he  found  free  in  the  liquid  contents  of  the  cyst.  In 
animals  the  daughter  vesicles  are  more  often  exogenous  (echinococcus  veterino- 
rum  sen  gramdosus).  A  peculiar  kind  of  echinococcus,  which  was  formerly 
regarded  as  a  kind  of  new  growth,  is  that  called  by  Virchow  echinococcus  mulli- 


^b 


Fig.  54.  Fig.  55.  Fig.  50. 

Figs.  54  and  55.— (From  Heller.)    Echinococcus  scolices,  free,  drawn  in  and  turned  outward. 
Fig.  56.— Echinococcus  hooklets. 

locidaris.  This  gives  rise  to  a  hard  tumor,  which  is  composed  of  vesicles  the  size 
of  a  pea,  and  which  seems  to  grow  along  the  lymph-vessels,  and  possibly  in  the 
blood-vessels  also. 

The  growth  of  a  hydatid  cyst  is  slow,  and  may  continue  for  years.  It  may 
finally  attain  the  size  of  a  child's  head.  At  last,  however,  the  echinococcus  dies. 
The  cyst  then  undergoes  considerable  though  gradual  contraction,  and  both  walls 
and  contents  become  calcified. 

Clinical  Phenomena. — As  long  as  the  cyst  in  the  liver  retains  moderate  dimen- 
sions, there  is  usually  no  discomfort.  Frequently  the  cysts  perish  and  become 
calcified,  without  having  ever  attracted  attention,  and  are  found  post-mortem 
merely  by  accident. 

If  the  cyst  becomes  very  large,  it  causes  a  sensation  of  pressure  and  pain  in  the 
hepatic  region.  In  rare  instances,  unusually  large  cysts,  if  situated  on  the  convex 
surface  of  the  liver  may  crowd  up  the  diaphragm  so  as  to  compress  the  lower 
portions  of  the  lung  and  induce  dyspnoea.  Again,  the  cyst  may  be  so  situated  as 
to  compress  the  portal  vein  or  a  large  bile-duct.  Then  appear  ascites  and  enlarge- 
ment of  the  spleen,  or  jaundice,  as  the  case  may  be. 

It  is  an  important  fact  that  sometimes  the  cyst  ruptures  and  discharges  its 
contents  into  neighboring  parts.  Thus  in  repeated  instances  the  pleural  cavity 
has  been  invaded ;  also  the  lungs,  as  evidenced  by  the  expectoration  of  vesicles ; 
the  intestinal  canal,  with  the  appearance  of  vesicles  in  the  stools;  the  bile  ducts, 
followed  by  jaundice  and  the  eventual  appearance  of  vesicles  in  the  intestine ;  and 
the  vena  cava  inferior,  causing  sudden  death  from  pulmonary  embolism.  Some- 
times the  cyst  pushes  outward  through  the  abdominal  walls,  and  terminates  in  re- 
covery. Exceptionally,  the  echinococcus  sac  undergoes  purulent  inflammation, 
with  all  the  symptoms  of  a  hepatic  abscess. 

A  multilocular  echinococcus  usually  excites  grave  disturbance.  The  liver  is 
decidedly  enlarged,  and  generally  is  firm  and  smooth,  not  uneven,  to  the  touch. 
As  a  rule,  there  are  jaundice,  swelling  of  the  spleen,  and  ascites,  and  accompany- 
ing these  a  gradual  loss  of  flesh  and  strength,  ending  fatally. 

A  diagnosis  is  sometimes  easily  reached  if  the  cysts  can  be  felt  upon  the  surface 
of  the  liver.  Usually  the  tumors  are  flat  or  globular,  and  of  firm  consistence, 
though  often  evidently  elastic.  A  peculiarly  characteristic  sign,  though  one  which 
is  seldom  obtainable,  is  the  "hydatid  thrill."  It  is  felt  upon  giving  the  tumor  a 
quick,  short  blow  with  the  flat  of  the  hand.  The  diagnosis  is  certain  if.  in  any 
way,  echinococcus  vesicles  are  discharged.     Aspiration  for  purposes  of  diagnosis 


496  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

has  been  repeatedly  performed.  The  fluid  thus  evacuated  is  light-yellow,  almost 
always  non-albuminous,  and,  upon  microscopic  examination,  sometimes  presents 
fragments  of  the  lamellated  membrane,  or  some  of  the  booklets.  But  if  we  do 
not  find  these  morphological  elements,  we  are  by  no  means  warranted  in  exclud- 
ing echinococcus.  Chemically,  the  fluid  should  yield  sugar  and  succinic  apid. 
This  fact  may  perhaps  aid  diagnosis. 

Frequently  it  is  difficult  to  distinguish  between  an  echinococcus  of  the  liver 
and  other  hepatic  disorders.  We  may  need  to  consider  all  the  circumstances — 
causation,  age,  fever,  shape  of  the  tumor,  or  perhaps  the  results  of  an  exploratory 
puncture.  Large  cysts,  which  crowd  themselves  upward  into  the  pleural  cavity 
may  simulate  a  pleuritic  effusion. 

Treatment. — The  administration  of  internal  remedies  is  extremely  unreliable. 
Iodide  of  potassium  and  mercury  are  especially  recommended.  It  is,  however, 
operative  interference  alone  that  holds  out  any  promise  of  success ;  but  this  has 
its  dangers,  and  should,  therefore,  be  held  in  reserve  till  the  symptoms  become 
grave  or  very  distressing.  For  details  of  the  numberless  methods  of  operation 
which  have  been  proposed,  we  would  refer  to  wTorks  on  surgery;  but  we  may 
mention  here  that  simple  aspiration  of  the  contents  of  the  cyst  sometimes  affords 
permanent  relief;  the  cyst  becomes  obliterated,  and  there  is  complete  recovery. 
In  a  few  cases,  after  the  sac  has  been  emptied,  tincture  of  iodine  has  been  injected. 
Most  of  the  other  methods  aim  (1)  to  bring  about  adhesion  of  the  sac  to  the  ab- 
dominal walls,  and  (2)  to  lay  it  open  and  evacuate  the  contents.  At  the  surgical 
clinique  in  Leipsic  the  favorite  and  a  very  satisfactory  method  is  to  employ  a 
caustic  paste,  made  with  chloride  of  zinc,  which  slowly  effects  an  opening  of  the 
cyst,  and,  by  the  adhesive  inflammation  it  excites  previously,  fixes  the  cyst  to  the 
abdominal  walls.  Simon's  method  is  to  thrust  in  several  trocars,  at  intervals  from 
one  another,  and  allow  them  to  remain  till  adhesions  are  formed.  Then  the 
points  of  puncture  are  united  by  an  incision,  the  sac  emptied,  syringed  out,  disin- 
fected, and  allowed  to  heal  gradually. 

[The  experience  of  Australian  surgeons  with  hydatid  disease  is  very  large, 
and  Thomas  believes  that  the  cure,  after  tapping,  is  often  illusory,  and  that  failure 
follows  in  at  least  forty  per  cent,  of  the  cases.  He  has  collected  sixty-eight  cases 
of  hydatid  diseases  treated  by  laparotomy,  with  only  seven  deaths.  In  twenty- 
one  cases  treated  as  in  Leipsic  (Volkmann's  method),  the  mortality  has  been  nine- 
teen per  cent.] 


CHAPTER  XL 
CIRCULATORY  DISTURBANCES  IN  THE   LIVER. 

1.  Hepatic  anaemia  is  seldom  extreme  except  in  cases  of  profound  general 
anaemia,  and  has  no  clinical  imj)ortance,  so  far  as  we  are  aware. 

2.  Passive  congestion  of  the  liver  is  of  frequent  occurrence  and  is  of  impor- 
tance. It  may  arise  in  any  disorder  which  disturbs  the  systemic  circulation.  It 
is  oftenest  seen  in  connection  with  heart  disease,  particularly  mitral  disease.  It 
also  follows  pulmonary  emphysema  and  chronic  processes  which  result  in  con- 
traction of  the  lungs.  The  liver  is  enlarged  and  engorged.  The  hepatic  veins 
being  situated  in  the  center  of  the  lobules,  this  central  portion  becomes  darkly 
pigmented,  while  the  periphery  of  the  lobules  seems  lighter  colored.  The  periph- 
eral cells  may  even  appear  distinctly  yellow,  from  a  fatty  infiltration  which  is  not 
infrequent.  In  this  way  the  cut  surface  comes  to  present  that  variegated  appear- 
ance which  has  led  to  the  name  of  "  nutmeg  liver."     If  the  venous  stasis  be  per- 


CIRCULATORY  DISTURBANCES  IN  THE  LIVER.  407 

sistent,  thei*e  is  considerable  atrophy  of  the  hepatic  parenchyma,  involving  espe- 
cially the  cells  near  the  center  of  each  lobule.  Thus  the  liver  atrophies,  and  its 
surface  may  become  slightly  granular.     This  is  the  "  atrophic  nutmeg  liver." 

The  clinical  phenomena  are  chiefly  those  due  to  the  hepatic  enlargement.  If 
chronic  cardiac  disease,  emphysema,  or  some  analogous  trouble  has  occasioned 
congestion  of  the  liver,  the  area  of  hepatic  dullness  is  increased,  and  frequently 
we  can  feel  the  edge  or  even  a  portion  of  the  anterior  surface.  In  pronounced 
cases  the  organ  may  extend  almost  a  hand's  breadth  below  the  ribs.  Often  there 
is  a  slight  jaundice.  Sometimes  it  is  quite  marked.  It  is  probably  due  to  the  dis- 
tended blood-vessels  compressing  the  smaller  bile-ducts.  We  have  already  men- 
tioned how  characteristic,  in  many  cardiac  cases,  is  a  complexion  presenting  both 
cyanosis  and  jaundice. 

Quite  often  the  congestion,  if  great,  produces  subjective  disturbances.  There 
is  a  feeling  of  pressure  and  weight  in  the  hepatic  region ;  and  if  the  capsule  of  the 
organ  is  tightly  stretched,  there  may  be  actual  pain. 

The  prognosis  and  treatment  depend,  of  course,  upon  the  primary  disorder. 

3.  About  active  hyperaemia  of  the  liver  we  have  little  definite  information. 
Formerly  there  was  a  great  deal  said  about  it,  as  one  of  the  conditions  in  "  ab- 
dominal plethora."  Active  hyperaeniia  is  most  frequently  assumed  to  exist  in 
case  of  those  who  are  good  livers  and  of  sedentary  habit.  In  such,  we  are  told, 
the  temporary  physiological  hyperaemia  which  attends  digestion  passes  on  into  a 
permanent  congestion  of  the  liver.  Thereby  the  organ  is  enlarged,  there  are  pain- 
ful sensations  in  the  right  hypochondriun,  digestive  disturbances,  and  occasional 
slight  jaundice.  The  abnormal  condition  just  described  is  certainly  often  met 
with  in  practice,  but  it  would  seem  hardly  possible  to  draw  a  clear  dividing-line 
between  active  hyperemia  of  the  liver  and  other  disturbances  which  give  rise  to 
similar  symptoms.  Such  are  chronic  gastric  and  intestinal  catarrhs;  cardiac 
hypertrophy  and  functional  cardiac  derangement,  with  passive  congestion  of  the 
liver ;  fatty  liver ;  and  incipient  cirrhosis. 

A  prominent  factor  in  the  production  of  active  hyperaemia  of  the  liver  is  also 
ascribed  to  the  ingestion  of  such  matters  as  are  said  to  "  irritate  "  the  liver,  like 
the  various  spices,  coffee,  and,  above  all,  alcohol. 

It  should  also  be  noted  that  the  liver  may  be  much  engorged  in  many  acute 
infectious  diseases,  particularly  in  pernicious  malarial  diseases  and  in  typhus  or 
typhoid  fever. 

It  is  also  maintained  that  the  hyperemia  may  result  from  the  cessation  of 
haemorrhages  elsewhere,  such  as  the  catamenia  or  bleeding  from  haemorrhoids. 
The  facts  that  have  been  brought  forward  to  sustain  this  view  are  none  of  them 
conclusive.  We  will  mention  that  the  "  menstrual  jaundice  "  which  occasionally 
appears  when  the  menses  are  scanty  or  absent  has  been  referred  to  a  vicarious 
hyperaemia  of  the  liver. 

It  is,  of  course,  impossible  to  make  general  statements  about  the  course  and 
duration  of  active  hyperaemia  of  the  liver.  The  treatment  of  the  first  variety 
mentioned — namely,  that  arising  from  an  improper  mode  of  life — demands  careful 
regulation  of  the  diet,  abundant  exercise  in  the  open  air,  like  horseback-riding, 
and  laxatives.  We  may  give  rhubarb,  aloes,  or  a  course  of  the  waters  at  Carls- 
bad, Marienbad,  Kissingen,  or  Homburg. 


32 


498  DISEASES  OE  THE  DIGESTIVE  ORGANS. 

CHAPTER  XII. 
ATROPHY,   HYPERTROPHY,   AND  DEGENERATIONS   OF   THE   LIVER. 

1.  Simple  Atrophy  of  the  Liver. — Simple  atrophy  is  not  of  rare  occurrence, 
being  seen  in  senile  marasmus,  and  in  malnutrition  from  almost  any  cause.  The 
degree  of  atrophy-  varies.  The  borders  of  the  organ  are  much  wrinkled.  The 
lobules  seem  decidedly  smaller  than  normal,  and  even  the  individual  cells  that 
still  remain  are  atrophied  and  also  usually  deeply  pigmented. 

The  condition  does  not  of  itself  give  rise  to  any  special  symptoms.  The  area 
of  hepatic  dullness  is  usually  lessened,  but  this  sign  is  too  ambiguous  ever  to  justify 
us  in  making  from  it  a  diagnosis  of  hepatic  atrophy.  Perhaps  there  is  some  value 
in  the  alleged  lighter  color  of  the  stools,  as  indicating  a  diminished  secretion  of 
bile. 

2.  Hypertrophy  of  the  Liver. — Even  under  normal  circumstances  the  liver 
undergoes  quite  marked  alterations  in  size.  The  exact  point,  therefore,  where  an 
abnormal  hypertrophy  begins  can  not  be  set.  Sometimes  the  autopsy  reveals  an 
unusually  large  liver,  of  which  there  had  been  no  indications  during  life,  and  for 
which  no  cause  can  be  made  out. 

There  are  certain  diseases  in  which  enlargement  of  the  liver  is  found  with 
comparative  frequency :  diabetes  mellitus,  chronic  malarial  poisoning,  leukaemia, 
and  sometimes  rachitis.  Topers  quite  often  have  enlarged  livers,  which  as  a  rule 
present  simple  hypertrophic  changes.  Occasionally  a  liver  has  been  reported  as 
showing  spots  of  localized  hyperplasia,  which  may  form  flattened  prominences 
upon  the  surface  of  the  organ. 

Hypertrophy  is  to  be  diagnosticated  only  when  palpation  and  percussion  give 
proof  of  an  enlargement,  and  yet  amyloid,  hypertrophic  cirrhosis,  and  other  dis- 
eases which  cause  an  increase  in  the  size  of  the  liver,  can  be  excluded.  The  aeti- 
ology of  the  case  should  also  be  considered. 

3.  Fatty  Liver.— This  name  is  applied  to  excessive,  diffuse,  fatty  infiltration  of 
the  hepatic  cells.  The  size  of  the  organ  is  increased.  It  is  firm,  anaemic,  and  of  a 
uniform  yellow  color,  both  externally  and  upon  section.  The  microscope  shows 
that  the  cells  of  the  parenchyma  are  filled  with  large  and  small  globules  of  fat. 
The  fat  is  most  abundant  toward  the  periphery  of  the  lobules. 

The  causes  of  fatty  liver  are  by  no  means  clear.  Sometimes  it  is  found  in 
cases  of  general  obesity,  where  we  may  assume  that  the  amount  of  fat  which  the 
liver  receives  as  nourishment  is  abnormally  great;  but  often  we  find  a  liver  that 
contains  comparatively  little  fat  in  those  who  have  a  well-developed  panniculus 
adiposus  and  much  fat  in  other  organs.  Topers  may  have  a  decidedly  fatty  liver. 
The  occurrence  of  fatty  liver  in  the  cachectic,  and  particularly  in  the  consumptive, 
is  remarkable;  and  individuals  suffering  from  cancer,  or  marantic  children,  may 
also  exhibit  the  same  change.  We  have  no  intimate  knowledge  of  the  conditions 
that  prevent,  in  such  cases,  the  oxygenation  of  the  fat  which  comes  to  the  liver 
from  the  ingesta  or  from  other  organs. 

We  do  not  know  that  the  fatty  liver  is  in  any  way  functionally  impaired.  The 
only  clinical  indication,  therefore,  of  its  existence  is  the  increased  bulk  of  the 
organ.  In  phthisis  we  may  sometimes  feel  pretty  certain  that  the  liver  is  fatty,  if 
an  increase  in  bulk  can  be  demonstrated,  and  if  other  causes  for  this  enlargement, 
like  amyloid,  appear  improbable.  If  the  anterior  edge  of  a  fatty  liver  can  be  felt, 
it  is  usually  found  to  be  noticeably  thick  and  blunt. 

The  treatment  of  fatty  liver  is  to  combat  the  original  disease. 

4.  Amyloid  Liver  (Waxy  Liver). — Amyloid  degeneration  of  the  liver  is  almost 
invariably  a  part  of  extensive  amyloid  disease,  involving  also  the  spleen,  kidneys, 


ANOMALIES  IN  THE  SHAPE  AND  POSITION  OF  THE  LIVER.    499 

intestine,  and  other  organs.  The  disease  occurs  chiefly  in  certain  cachectic  condi- 
tions, such  as  chronic  suppuration,  as  in  caries  and  persistent  empyema,  and  also 
in  chronic  pulmonary  tuberculosis,  and  constitutional  syphilis. 

The  amyloid  liver  is  usually  increased  in  bulk.  The  organ  may  even  become 
almost  double  its  normal  size.  It  feels  very  firm  and  hard,  its  surface  is  perfectly 
smooth,  and  its  edge  is  slightly  thickened.  The  cut  surface  presents  a  character- 
istic grayish-brown  u  waxy  "  appearance. 

The  microscope  shows  that  the  degenerative  process  attacks  chiefly  the  walls  of 
the  hepatic  capillaries,  the  hepatic  cells  proper  showing  infrequent  and  slight 
amyloid  changes.  Very  often  the  cells  of  the  parenchyma  are  atrophied  and 
somewhat  infiltrated  with  fat. 

The  diagnosis  of  amyloid  liver  requires  (1)  the  demonstration  by  palpation  and 
percussion  of  hepatic  enlargement.  We  can  often  feel  a  large  part  of  the  anterior 
surface  and  the  margin  of  the  hard  and  firm  organ.  The  liver  may  reach  as  low 
as  the  level  of  the  umbilicus.  The  diagnosis  further  demands  (2)  that  some  dis- 
ease which  predisposes  to  amyloid  be  present,  and  (3)  that  there  be  evidence  of  the 
degenerative  process  in  other  organs :  the  spleen  should  be  enlarged,  and  the  kid- 
neys secrete  albuminous  uriue. 

The  other  symptoms,  as  well  as  both  prognosis  and  treatment,  are  determined 
mainly  by  the  nature  of  the  causative  affection.  About  amyloid  disease  in  general 
see  the  chapter  on  amyloid  kidney  (page  864). 


CHAPTEE  XIII. 
ANOMALIES   IN  THE    SHAPE   AND   POSITION   OF   THE    LIVER. 

1.  Corset  Liver. — The  constant  pressure  of  the  lower  ribs  against  the  liver,  as  a 
result  of  tight  lacing,  often  produces  an  atrophy  of  the  hepatic  parenchyma  from 
pressure,  as  shown  by  a  deep  furrow  crossing  transversely  the  anterior  surface  of 
the  organ.  This  "  corset  furrow  "  lies  chiefly  in  the  right  lobe.  Its  usual  situation 
corresponds  to  the  margin  of  the  ribs,  and  the  atrophy  may  be  so  extreme  that  the 
liver  is  divided  into  a  large  upper  part  and  a  small,  usually  roundish,  lower  por- 
tion, connected  by  a  narrow  isthmus  of  tissue.  At  the  atrophic  place,  the  con- 
nective-tissue capsule  of  the  liver  is  almost  always  much  thickened.  Often  the 
lower  section  can  be  bent  upward  as  if  attached  by  a  hinge. 

This  deformity  of  the  liver  is  found  quite  often  in  elderly  females,  and  rarely 
in  men,  as  in  soldiers.  Unless  extreme,  it  can  not  be  detected  during  life,  and 
causes  no  discomfort.  Even  the  bad  cases  do  not,  as  a  rule,  occasion  any  special 
symptoms ;  but  they  can  be  clearly  made  out  if  the  abdominal  walls  are  lax.  The 
deep  transverse  furrow  can  be  felt,  and  also  the  lower  section,  with  its  usually 
blunt  edge.  Particularly  in  the  case  of  old  women  we  must  bear  this  condition 
in  mind,  else  we  might  easily  confound  it  with  some  enlargement  of  the  liver, 
like  amyloid  or  passive  congestion,  or  even  new  growths. 

In  not  rare  instances  there  are  clinical  symptoms.  A  constant  sensation  of 
pressure  and  pulling  is  felt  in  the  hepatic  region ;  and  sometimes,  as  a  result  of 
venous  stasis,  there  is  a  temporary  but  decided  swelling  of  the  isolated  portion, 
and  possibly  violent  pain  and  indications  of  irritation  of  the  peritoneum,  such  as 
vomiting  and  an  approach  to  collapse.  Usually  rest  in  bed  and  cold  applications 
give  speedy  relief ;  but  relapses  are  possible. 

2.  Movable  Liver A  movable  or  "wandering"  liver  is  of  very  rare  occur- 
rence, and  has  thus  far  been  seen  only  in  women.     Its  cause  is  not  perfectly  deter- 


500  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

mined.  Probably  the  suspensory  ligament  is  abnormally  long.  Tbe  liver  does 
not  occupy  its  usual  position,  but  lies  deep  in  tbe  lower  part  of  tbe  abdomen. 
Here  it  can  be  plainly  felt,  and,  by  external  pressure,  it  can  generally  be  brought 
back  iuto  its  normal  place  with  considerable  ease.  It  is  always  abnormally  mov- 
able, and  can  be  sbown  to  cbange  its  position  wben  the  patient  changes  from  one 
side  to  the  other. 

In  most  cases  a  movable  liver  causes  considerable  discomfort,  particularly  pain 
and  digestive  disturbances.  The  only  way  of  affording  relief  is  by  applying  a 
bandage  which  may  maintain  the  organ  in  its  proper  position. 


CHAPTER  XIV. 

SUPPURATIVE    PYLEPHLEBITIS. 

{Purulent  Inflammation  of  the  Portal  Vein  and  its  Branches.) 

JEtiology.— Purulent  pylephlebitis  is  seldom  a  primary,  idiopathic  disease.  In 
most  instances  it  is  due  to  the  propagation  of  a  suppurative  inflammation  of 
neighboring  tissues  to  the  walls  of  the  vein.  The  main  trunk  of  the  portal  vein 
is  rarely  directly  attacked.  Usually  the  process  originates  in  the  hepatic  branches 
of  the  vein  or  in  the  veins  of  the  portal  system,  and  thence  extends  to  the  larger 
vessel. 

Perityphlitic  abscess  is  the  most  frequent  source  of  suppurative  pylephlebitis. 
The  inflammation  involves  a  mesenteric  vein,  and  thence  extends  upward.  Other 
causes  are  gastric  ulcer,  intestinal  ulcers,  as  in  dysentery,  splenic  abscess,  and 
purulent  inflammation  at  the  porta  hepatis  or  within  the  liver  itself,  as  in  abscess 
due  to  gall-stones.  The  mode  of  production  in  these  cases  is  precisely  analogous 
to  that  in  perityphlitic  abscess ;  but  they  are  rare. 

A  special  form  of  pylephlebitis  is  observed  in  the  new-born.  Here  the  inflam- 
mation originates  in  the  umbilical  vein,  and  we  need  hardly  say  that  the  cause  is 
a  septic  infection  through  the  navel. 

In  rare  instances  it  has  been  found  that  pylephlebitis  has  resulted  from  the 
penetration  into  a  vein  of  some  foreign  body  that  had  been  swallowed,  such  as  a 
pin.  Here,  too,  the  true  factors  in  producing  the  inflammation  are,  of  course, 
the  bacteria  which  adhere  to  the  foreign  body. 

Pathology. — Where  the  inflammation  has  attacked  the  vascular  walls,  the  vein 
is  thickened,  and  often  the  surrounding  connective  tissue  is  infiltrated  with  pus- 
cells  and  mottled  with  minute  ecchymoses.  If  the  vein  is  cut  open,  the  intima 
is  seen  to  be  opaque  and  often  superficially  ulcerated.  The  lumen  of  the  vessel 
is  filled  with  a  thrombus,  which  is  usually  to  a  great  extent  in  a  state  of  purulent 
softening,  so  that  offensive  purulent  or  sanious  fluid  flows  out.  The  course  of 
events  is  as  follows:  First,  the  wall  of  the  vein  becomes  inflamed.  As  a  conse- 
quence of  this,  a  thrombus  forms  at  the  same  place.  The  bacteria  penetrate  this 
thrombus  and  occasion  its  purulent  softening. 

The  extent  of  a  pylephlebitis  naturally  varies  in  different  cases.  As  a  rule, 
little  fragments  become  detached  from  the  thrombus  and  enter  the  liver,  produc- 
ing metastatic  abscesses.  Secondary  suppuration  may  also  occur  in  the  lungs, 
kidneys,  brain,  and  joints,  so  that  we  have  all  the  anatomical  characteristics  of  a 
general  pyaemia. 

Clinical  History. — Inasmuch  as  the  primary,  causative  disease  may  be  very 
different  in  different  cases,  it  is  impossible  to  delineate  the  disease  comprehen- 


SUPPURATIVE  PYLEPHLEBITIS.  501 

sively.  It  is,  however,  frequently  ushered  in  by  a  number  of  symptoms,  which 
render  a  diagnosis  possible,  at  least  in  some  cases,  if  the  original  disease  has 
been  recognized. 

The  symptoms  of  suppurative  pylephlebitis  are  in  part  due  directly  to  the  local 
disease  itself,  and  in  part  are  occasioned  by  the  general  pyaemia.  One  of  the  local 
symptoms  is  pain  in  the  epigastrium.  This  is  rare.  It  may  radiate  downward  or 
laterally,  according  to  the  starting-place  and  extent  of  the  inflammation.  An 
inevitable  result  of  the  portal  thrombosis  is  portal  obstruction.  The  spleen  be- 
comes considerably  swollen,  and,  if  the  disease  be  not  too  quickly  fatal,  there 
is  an  evident  effusion  into  the  peritoneal  cavity.  The  splenic  enlargement  can 
not  be  regarded  as  due  merely  to  venous  stasis,  but  is  in  part  the  "  acute  splenic 
tumor  "  of  constitutional  septic  conditions.  If  the  inflammation  spreads  from  the 
branches  of  the  portal  vein  to  the  neighboring  bile-ducts,  jaundice  results.  This 
is  seen  quite  often.  Sometimes  it  is  also  due  to  the  hepatic  abscesses,  or  to  a  gall- 
stone which  happens  to  cause  trouble  simultaneously.  Now  and  then  there  is  no 
jaundice  whatever. 

Of  the  pyaemic  symptoms,  hepatic  abscesses  come  first.  They  are  due,  as  we 
have  said,  to  the  conveyance  of  septic  matter  directly  into  the  liver  by  emboli. 
The  one  almost  constant  sign  of  their  occurrence  is  a  decided  enlargement  of  the 
liver.  Where  there  are  no  hepatic  abscesses,  the  organ  usually  retains  its  normal 
bulk. 

The  course  of  the  fever  is  very  characteristic.  As  in  other  pyaemic  conditions, 
there  are  almost  invariably  great  elevations,  to  106°  (41°  C),  or  higher,  accom- 
panied by  rigors,  and  followed  by  marked  remissions,  with  profuse  perspiration. 
These  onsets  of  fever  occur  at  irregular  intervals,  either  daily,  or  every  two  or 
three  days: 

There  are  at  the  same  time  indications  of  constitutional  septic  infection,  which 
keep  increasing  in  severity.  The  pulse  grows  rapid  and  small.  Intelligence  is 
impaired.     Somnolence  and  delirium  come  on,  and  the  strength  rapidly  fails. 

There  are  other  symptoms.  Vomiting  is  frequently  seen.  The  bowels  are  sel- 
dom constipated,  but  usually  relaxed.  The  dejections  may  contain  blood,  because 
of  the  venous  stasis.  In  some  cases  the  inflammation  extends  so  as  to  produce  a 
fatal  general  peritonitis.  It  is  noticeable  that  the  urine  is  generally  scanty,  and 
the  amount  of  urea  is  strikingly  diminished. 

The  disease  usually  runs  a  rather  acute  course.  On  the  average,  it  lasts  about 
two  weeks,  but  may  occupy  three  or  four  weeks,  or  even  a  longer  period.  It  is 
invariably  fatal.     At  least,  no  cases  of  recovery  are  known. 

The  diagnosis  can  sometimes  be  made  with  considerable  positiveness.  In  other 
instances  it  is  impossible  to  exclude  other  pyaemic  conditions,  or  abscess  due  to 
gall-stones,  etc.  Important  factors  are  the  origin  of  the  trouble — if  it  can  be  made 
out — the  pyaemic  rigors,  the  enlargement  of  the  spleen  and  liver,  jaundice,  epi- 
gastric pain,  and  the  evidences  of  general  sepsis. 

Treatment  is  unfortunately  almost  entirely  useless.  The  fever  is  not  affected 
even  by  large  doses  of  quinine.  All  we  can  aim  at  is  to  support  and  relieve  the 
sufferer  as  far  as  possible. 


502  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

CHAPTER  XV. 

THROMBOSIS   OF   THE   PORTAL   VEIN. 

(  Chronic  Adhesive  Pylephlebitis.    PyLthrombosis.) 

iEtiology  and  Pathology.— Like  suppurative  pylephlebitis,  chronic  portal  throm- 
bosis is  not  an  independent  disease,  but  is  the  sequel  of  a  great  variety  of  pathologi- 
cal conditions.  Marantic  thrombosis  is  of  rare  occurrence,  and  is  usually  formed 
toward  the  close  of  life,  so  as  not  to  be  of  practical  interest.  Apart  from  this, 
almost  all  cases  of  thrombosis  of  the  portal  vein  are  due  to  a  compression  of  the 
trunk  of  that  vessel  or  one  of  its  main  branches.  This  most  often  occurs  in  cer- 
tain chronic  hepatic  diseases  which  involve  a  mechanical  stenosis,  either  of  the 
smaller  branches  of  the  portal  vein  within  the  liver,  or  of  the  vein  itself,  with 
resulting  coagulation  of  the  blood  within  it.  Chief  among  these  diseases  are  cirrho- 
sis and  syphilis  of  the  liver,  which  have  repeatedly  been  observed  to  entail  j)ortal 
thrombosis;  but  other  diseases  in  the  neighborhood  of  the  vein  may  produce  a 
similar  effect.  New  growths  of  various  kinds  may  press  upon  the  vessel,  or  chronic 
inflammatory  hyperplasia  of  the  connective  tissue  at  the  porta  hepatis  may  act  in 
the  same  way.  This  is  illustrated  in  chronic  peritonitis,  whether  circumscribed  or 
diffuse,  an  example  of  the  former  being  sometimes  seen  as  an  effect  of  duodenal 
ulcer. 

It  was  formerly  held  that  many  forms  of  so-called  "lobulated  liver"  were  due 
to  a  primary  adhesive  pylephlebitis.  This  is  erroneous.  These  cases  are  probably 
all  due  to  some  primary  hepatic  disease,  usually  syphilitic.  The  size  of  the  liver 
is  little  influenced  by  obstruction  of  the  portal  vein,  even  if  long  continued,  for 
the  hepatic  artery  suffices  to  supply  all  the  blood  required  by  the  organ: 

The  anatomical  changes  in  pylethrombosis  do  not  differ  essentially  from  those 
seen  in  thrombosis  of  any  other  vein.  If  fresh,  the  thrombus  is  still  red;  later 
it  grows  harder,  paler,  and  more  friable.  If  the  thrombosis  has  existed  a  long 
while,  the  clot  becomes  completely  organized.  We  have  observed  this  even  in  the 
main  trunk  of  the  portal  vein. 

Clinical  History. — The  symptoms  of  portal  thrombosis  are  those  occasioned  by 
the  obstruction,  and  therefore  such  as  we  have  already  repeatedly  met  with,  in 
connection  with  various  hepatic  diseases.  The  intensity  and  extent  of  these  results, 
as  well  as  the  time  occupied  in  their  development,  depend,  of  course,  upon  the 
place  and  size  of  the  clot.  If  it  is  the  portal  vein  itself  which  is  attacked,  and  if 
the  thrombus  is  extensive  enough  to  obstruct  the  flow  of  blood,  then  the  signs 
of  venous  stasis  are  evident  throughout  the  portal  system.  The  spleen  becomes 
much  enlarged,  as  can  be  easily  demonstrated  by  percussion  and  palpation.  Soon 
ascites  appears,  as  a  result  of  the  passive  congestion  of  the  peritoneal  veins ;  and 
from  a  similar  condition  of  the  gastro-intestinal  veins  arise  catarrhal  disorders, 
like  diarrhoea ;  or,  not  so  very  exceptionally,  there  is  repeated  gastric  and  intesti- 
nal haemorrhage. 

As  we  have  seen,  a  collateral  circulation  may  be  developed  {vide  page  481),  by 
which  the  venous  blood  of  the  portal  system  is  enabled  to  reach  the  systemic 
veins.  This  explains  why  some  of  the  symptoms  of  venous  stasis  may  tempora- 
rily (perhaps  permanently)  vanish.  We  saw  one  case  of  portal  thrombosis,  the 
sequel  to  what  was  apparently  a  syphilitic  disease  of  the  liver,  where  a  quite  large 
ascitic  effusion  appeared  some  six  or  seven  times  at  intervals  of  three  to  six  months, 
and  under  proper  treatment  as  often  abated.  The  patient  did  not  die  till  the  ill- 
ness had  lasted  six  years,  and  tapping  had  been  demanded  some  fifteen  times.  At 
the  autopsy  the  trunk  of  the  portal  vein  was  found  to  be  converted  into  a  fibrous 
cord,  with  a  lumen  which  barely  admitted  a  knitting-needle.     It  is  the  develop- 


DISEASES  OF  THE  PANCREAS.  503 

ment  of  a  collateral  circulation  which  causes  the  frequent  distention  of  the  veins 
in  the  abdominal  walls.  Sometimes  these  enlarged  veins  take  the  form  of  the 
"  caput  Mednsce  "  mentioned  above. 

In  simple  pylethrombosis  there  are  no  local  symptoms  such  as  pain.  The  con- 
dition of  the  liver  depends  upon  the  primary  disease.  It  is  possible  that  a  moder- 
ate atrophy  of  the  entire  organ  might  at  length  ensue  if  the  portal  blood  were 
permanently  cut  off  from  it.  But,  as  we  have  said,  any  cirrhotic  changes,  or  any 
"lobulation,"  are  not  to  be  regarded  as  the  result,  but  as  the  cause  of  the  throm- 
bosis, or  at  least  related  to  the  cause. 

The  course  and  duration  of  the  trouble  are  according  to  the  nature  of  the 
original,  causative  trouble.     No  general  statements  can  be  made. 

The  diagnosis  of  thrombosis  of  the  portal  vein  is  usually  extremely  difficult, 
and  can  really  hardly  ever  be  made  with  absolute  certainty.  We  may,  indeed, 
recognize  readily  that  there  is  some  decided  obstruction  to  the  portal  circulation ; 
but  whether  this  be  due  to  a  thrombus,  or  to  compression  of  the  portal  vein,  or  to 
the  obliteration  of  a  large  number  of  the  smaller  branches  of  that  vein  within  the 
liver,  we  can  very  seldom  determine.  Pylethrombosis  may  be  regarded  as  prob- 
able, if  no  other  possible  cause  of  the  portal  obstruction  seems  likely,  and  if 
we  are  able  to  discover  a  cause  for  thrombosis,  like  a  former  attack  of  circum- 
scribed peritonitis. 

The  prognosis  is  always  unfavorable,  although  there  may  be,  as  we  have  said, 
great  temporary  improvement.  Treatment  must  be  symptomatic,  and  follows  in 
the  main  the  principles  set  forth  under  cirrhosis  of  the  liver. 


APPENDIX. 

DISEASES  S   OF   THE   PANCREAS. 

The  few  facts  of  clinical  importance  that  are  known  about  the  pathology  of 
the  pancreas  are  given  below. 

1.  Haemorrhages  into  the  Pancreas  of  small  size  occur  as  one  symptom  of  a 
general  haemorrhagic  diathesis,  or  as  the  result  of  excessive  passive  congestion. 
They  are  of  no  special  importance.  Klebs  and  Zenker  have  described  a  few  cases, 
however,  where  there  was  extensive  haemorrhage  into  this  organ,  and  where  this 
was  the  only  discoverable  cause  of  death.  The  patients  had  been  previously  well 
and  vigorous,  although  decidedly  obese,  and  had  died  suddenly.  Perhaps  the 
speedy  termination  was  caused  by  the  influence  of  the  haemorrhage  upon  the 
semilunar  ganglion  or  solar  plexus.  The  cause  of  the  haemorrhage  could  not  be 
determined. 

2.  Atrophy  of  the  Pancreas. — The  organ  may  share  in  a  general  marasmus. 
There  is  also  extreme  atrophy  of  the  pancreas  in  those  who  have  died  of  diabetes 
mellitus  (q.  v.).     What  relation  this  change  bears  to  the  diabetes  is  not  known. 

3.  Pancreatitis. — A  few  cases  have  been  reported  of  what  would  seem  to  be  a 
primary  acute  pancreatitis.  The  disease  is  certainly  very  rare.  It  begins  with 
violent  colicky  pains  in  the  epigastrium.  Vomiting  and  collapse  soon  follow. 
The  pulse  grows  small,  the  extremities  become  cool,  and  death  is  speedy.  At  the 
autopsy  the  pancreas  is  found  to  be  much  enlarged,  and  mottled  with  ecchy- 
moses,  or  it  even  presents  scattered  foci  of  suppuration.  The  aetiology  is  unknown. 
Secondary  abscesses  of  the  pancreas  are  not  infrequent  in  pyaemia. 

[Fitz,  in  the  Middleton- Goldsmith  lecture  for  1889,  threw  much  light  on  the 
aetiology  and  diagnosis  of  acute  pancreatitis,  which  he  subdivides  into  three  anatom- 
ical forms — the  haemorrhagic,  the  suppurative,  and  the  gangrenous.     He  shows 


504  DISEASES  OF  THE  DIGESTIVE  ORGANS. 

that  the  affection  is  not  so  rare  as  has  been  supposed ;  that  its  victims  are  usually 
in  middle  life,  fat,  and  good  livers ;  that  it  commonly  originates  by  the  extension 
of  a  gastro-duodenal  inflammation  along  the  pancreatic  duct. 

"  If  the  case  does  not  end  fatally  in  the  course  of  a  few  days,  recovery  is  pos- 
sible, or  a  recurrence  of  the  symptoms  in  a  milder  form  takes  place,  and  the  char- 
acteristics of  a  subacute  peritonitis  are  developed." 

In  the  differential  diagnosis  irritant  poisoning,  perforation  of  the  digestive  or 
biliary  tracts,  and  acute  intestinal  obstruction  are  to  be  considered.  The  location 
of  peritonitic  symptoms,  their  suddenness  of  onset,  the  absence  of  apparently 
sufficient  cause,  and  the  age  and  habit  of  the  individual  are  important  points.] 

Chronic  interstitial  pancreatitis  sometimes  results  from  the  extension  of  chronic 
inflammatory  processes  affecting  neighboring  parts.  Friedreich  states  that  it 
sometimes  is  a  primary  disease  in  topers.  Syphilitic  lesions  of  the  pancreas  have 
been  observed,  occasioning  contraction  and  induration.  None  of  these  changes 
give  rise  to  special  clinical  symptoms;  or,  if  there  were  a  single  distinctive 
symptom,  it  would  be  one  common  to  all  sorts  of  grave  pancreatic  disorder — 
namely,  the  appearance  of  a  large  amount  of  fat  in  the  stools.  As  we  know,  the 
pancreatic  juice  is  an  important  factor  in  the  digestion  of  fat,  so  that  it  is  very 
natural  for  any  great  derangement  of  the  organ  to  have  this  result ;  and  yet  the 
bile  alone  may  render  the  ingested  fat  capable  of  absorption,  so  that  in  repeated 
instances  there  have  been  no  fatty  stools  when  the  pancreas  has  been  completely 
atrophied  or  degenerated. 

4.  Cysts  of  the  Pancreas. — After  closure  of  Wirsung's  duct  by  scars,  concre- 
tions, or  the  like,  cysts  of  the  pancreas  may  form,  as  a  result  of  the  damming  up  of 
the  secretion.  These  may  become  so  large  as  to  be  felt  as  great  tumors  through 
the  abdominal  walls.  In  some  instances  they  have  been  operated  upon  with 
success. 

5.  Cancer  of  the  Pancreas.— Primary  cancer  is  the  most  frequent,  and  there- 
fore clinically  the  most  important  disease  of  this  organ.  As  a  rule,  the  new 
growth  is  situated  in  the  head  of  the  pancreas.  It  is  usually  of  the  medullary 
variety,  though  occasionally  colloid.  It  may  involve  neighboring  parts  by  direct 
extension,  and  a  great  many  organs  by  metastasis;  for  example,  the  liver,  peri- 
toneum, and  lymph-glands. 

The  clinical  symptoms  of  cancer  of  the  pancreas  are  very  seldom  so  decided  as 
to  justify  a  positive  diagnosis.  Sometimes  the  secondary  nodules  can  be  detected 
in  the  liver,  peritoneum,  and  elsewhere.  Then  we  are  left  in  doubt  about  the  seat 
of  the  primary  growth.  Or  the  primary  tumor  may  be  plainly  felt  through  the 
abdominal  walls ;  but  then  we  can  hardly  ever  exclude  cancer  of  the  stomach  or 
of  the  omentum,  and  neighboring  parts. 

The  symptoms  of  pancreatic  cancer,  as  a  whole,  resemble  closely  those  occa- 
sioned by  most  cancers  of  abdominal  organs.  Usually  the  patient  is  elderly.  The 
first  symptoms  are  loss  of  flesh  and  strength,  or  are  the  result  of  compression. 
Often  there  is  complaint  of  a  persistent  dull  pain  in  the  epigastrium.  If  the  portal 
vein  is  pressed  upon  by  the  tumor,  ascites  appears.  If  the  common  duct  is  com- 
pressed, there  is  jaundice.  Marasmus  increases,  and  usually  at  the  end  of  six 
months  or  a  year  the  patient  dies. 

The  diagnosis  can  be  said  to  be  somewhat  probable  in  those  cases  only  where 
there  are  fatty  stools,  where  a  tumor  can  be  felt  in  a  position  corresponding  to  the 
pancreas,  and  where  primary  cancer  of  any  other  organ  is  unlikely;  but  usually, 
as  we  have  said,  the  symptoms  are  very  ambiguous.  There  have  been  no  fatty 
stools  in  a  number  of  cases,  even  where  the  cancer  was  extensive. 

The  prognosis  is  absolutely  bad.  The  treatment  is  merely  symptomatic,  with 
the  aim  of  lessening  the  patient's  suffering. 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


I. — The  Diseases  of  the  Peripheral  Nerves. 

SECTION   I. 
Diseases  of  the  Sensory  Nerves. 

CHAPTER  I. 
GENERAL   REMARKS    UPON    THE    DISTURBANCES    OF    SENSIBILITY, 

The  disturbances  of  sensibility,  like  all  otber  functions  of  tbe  nerves,  are  mani- 
fested in  two  directions.  Under  pathological  conditions  we  observe  either  an 
abnormal  diminution  or  a  complete  absence  of  sensibility — anaesthesia — or  a  morbid 
increase — hyperesthesia.  While,  in  anaesthesia,  the  ordinary  or  even  the  strongest 
irritations  which  excite  the  sensory  nerves  produce  only  a  weak  and  insignifi- 
caut  sensation,  or  even  no  corresponding  sensation  at  all,  in  hyperesthesia  very 
severe  and  painful  sensations  are  caused  by  weak  irritations.  The  "  symptoms  of 
sensory  irritation  "  are  to  be  distinguished  from  hyperaesthesia,  although  they  are 
often  present  along  with  it.  By  this  term  we  mean  sensations  which  cause  inter- 
nal irritation,  not  from  without,  but  from  certain  abnormal  morbid  conditions  in 
the  nerve  itself.  In  the  region  of  cutaneous  sensibility,  with  which  we  shall 
chiefly  concern  ourselves  in  what  follows,  these  symptoms  of  sensory  irritation 
show  themselves  partly  as  actual  pain  and  partly  as  the  so-called  paraesthesiae — 
that  is,  abnormal  sensations  in  the  skin,  which  are  termed  "  formication "  (the 
crawling  of  ants),  "prickling,"  "numbness,"  "a  furry  feeling,"  etc. 

The  Different  Varieties  of  Cutaneous  Sensibility  and  the  Methods  of  testing 
them. — As  is  known  from  physiology,  the  irritation  of  the  sensory  cutaneous 
nerves  produces  in  lis  a  number  of  sensations,  differing  in  quality  according  to 
the  manner  of  action  of  the  irritation.  If,  therefore,  we  would  obtain  an  accurate 
estimate  of  the  condition  of  the  patient's  cutaneous  sensibility,  we  must  make  a 
special  test  of  all  the  different  forms  of  sensation,  for  we  often  see  that  the  disturb- 
ances of  sensibility  do  not  involve  all  the  forms  mentioned  alike,  but  that  one 
kind  of  irritation  is  followed  by  perfectly  normal  sensations,  while  there  is  more 
or  less  complete  anaesthesia  for  another  kind.  We  term  such  partial  anaesthesias 
of  the  skin,  which  are  manifest  toward  only  one  form  of  irritation,  "  partial  paraly- 
ses of  sensation."  Such  partial  paralyses  will  be  much  more  easily  understood  if 
the  remarkable  statements  of  Blix,  Goldscheider,  and  others  are  confirmed. 
According  to  these  statements,  the  different  qualities  of  cutaneous  sensation  are 
transmitted  to  the  consciousness  by  special  nerve-fibers,  so  that  there  are  in  the 
skin  special  nerves  for  the  tactile  sense,  for  the  sense  of  cold,  for  the  sense  of  heat, 
etc.  Such  a  condition  is  analogous  to  the  well-known  specific  energy  of  the 
different  fibers  of  the  optic  nerve  to  colors,  assumed  by  many  physiologists.     The 

(505) 


506  DISEASES  OF  THE    NERVOUS  SYSTEM. 

separate  varieties  of  cutaneous  sensibility,  and  the  methods  of  testing-  them,  are 
as  follows: 

1.  Tactile  Sensibility. — The  examination  of  the  tactile  sensibility — that  is,  of 
the  sensibility  of  the  skin  to  simple  contact — is  usually  performed  by  repeatedly 
touching  or  stroking  the  part  of  tbe  skin  to  be  tested  with  the  finger,  a  fine  brush, 
or  some  other  blunt  object  (not  of  metal,  iu  order  to  exclude  sensations  of  cold) 
while  the  patient's' eyes  are  shut,  and  making  the  patient  say  whether  he  has  felt 
the  touch  or  not.  When  it  is  necessary  to  call  the  patient's  attention  to  the  inves- 
tigation, it  is  always  best  to  do  so  afresh  by  asking  "  Now  ? "  and  then  either  really 
touching  the  skin  or  else  asking  the  question  when  only  pretending  to  do  so.  In 
this  way  we  are  safest  from  error,  which  is  otherwise  easily  produced  by  a  lack  of 
attention  or  of  practice  on  the  part  of  the  patient.  All  accurate  tests  of  sensibility 
must  be  repeatedly  performed  and  controlled  in  order  to  obtain  accurate  objective 
results. 

If,  as  in  most  cases,  we  have  to  do  with  disturbances  of  sensibility  which  affect 
only  a  part  of  the  skin,  we  must  make  comparative  tests  of  sensibility  on  the 
healthy  and,  if  possible,  symmetrical  portions  of  the  skin.  Slight  disturbances  of 
sensibility  are  then  often  shown  in  this  way,  that  the  patient  feels  almost  every 
touch  on  the  affected  part;  but  the  sensation  always  seems  to  him  more  indefinite, 
blunter — in  short,  "  different "  from  that  on  the  corresponding  normal  portion  of 
the  body. 

Besides  simply  touching  the  skin,  we  also  try  how  far  the  patient  is  able  to  dis- 
tinguish the  form  and  certain  external  peculiarities  of  objects  by  the  aid  of  his 
tactile  sense.  We  touch  the  skin  with  smooth  and  rough  (woolly)  or  round  and 
angular  objects,  and  see  whether  the  patient  can  distinguish  them  respectively 
with  his  eyes  shut,  and  also  whether  he  can  distinguish  between  the  head  and  the 
point  of  a  pin,  etc.  If  we  are  testing  the  sensibility  of  the  fingers,  we  may  put 
different  well-known  objects— like  coins,  rings,  or  keys — into  his  hands,  and  let 
him  name  them  with  his  eyes  shut.  We  may  also  try  the  last  method  of  testing 
by  the  aid  of  a  number  of  wooden  geometrical  objects,  cubes,  octahedra,  or  cones. 

2.  Sense  of  Locality. — Under  normal  conditions,  as  we  know,  not  only  do  we 
feel  the  touch  of  an  object,  but  we  can  tell. with  a  good  deal  of  accuracy  the  place 
on  our  skin  which  was  touched.  This  power  we  term  the  ability  to  localize  our 
sensation.  In  nervous  patients  we  often  see  that,  while  cutaneous  sensibility  is 
still  present  (we  refer  not  only  to  tactile  sensibility  but  also  to  the  other  forms),  it 
is  localized  more  poorly  and  with  less  accuracy  than  is  the  case  under  normal 
conditions. 

In  the  simple  test  of  the  tactile  sense  we  may  also  examine,  at  least  roughly, 
the  power  of  localization  if  wTe  make  the  patient  also  state  where  the  touch  is  felt, 
or  if  we  ask  him  to  designate  with  his  hand  as  accurately  as  possible  the  part  of  the 
skin  touched.  A  more  accurate  method,  much  used  in  nervous  pathology,  was 
proposed  by  E.  H.  Weber.  It  consists  in  determining  the  smallest  distance  which 
must  separate  two  simultaneous  cutaneous  irritants  from  each  othei',  in  order  that 
they  may  be  perceived  as  two  locally  distinct  sensations.  Weber  has  found  that 
this  distauce  differs  very  much  in  different  parts  of  the  body,  and  from  this  he  has 
divided  the  whole  surface  of  the  skin  into  so-called  tactile  circles.  As  data  for  the 
examination  of  patients,  some  of  the  figures  obtained  by  Weber  in  healthy  indi- 
viduals may  here  be  given:  The  smallest  distance  at  which  the  two  points  of  a 
pair  of  compasses  *  applied  at  the  same  time  to  the  skin  may  plainly  be  distin- 
guished from  each  other  is  11  to  15  millimetres  on  the  cheeks,  6  mm.  at  the  tip  of 
the  nose,  22  mm.  on  the  forehead,  1'2  mm.  at  the  tip  of  the  tongue,  4  to  5  mm.  at 


*  There  are  special  "tactile  compasses"  with  blunt  ivory  points  and  graduated  quadrants. 


REMARKS  UPON  THE  DISTURBANCES  OP  SENSIBILITY.      507 

the  back  of  the  tongue  and  on  the  lips,  34  mm.  on  the  neck,  77  mm.  on  the  upp<  r 
arm,  40  mm.  on  the  forearm,  31  mm.  on  the  backs  of  the  hands,  11  to  16  mm.  on 
the  backs  of  the  fingers,  2  to  3  mm.  at  the  tips  of  the  fingers,  55  to  77  mm.  on  the 
back,  45  mm.  on  the  chest,  77  mm.  on  the  thigh,  40  mm.  on  the  leg,  40  mm.  on  the 
instep;  but  these  figures  show  certain  variations  in  different  individuals,  so  that 
they  are  to  be  regarded  as  only  average  values. 

Testing  the  sense  of  locality  according  to  Weber's  method  takes  a  great  deal  of 
time,  and  demands  much  patience  and  good  will  on  the  part  of  the  patient.  The 
influence  of  practice  is  manifested  in  a  very  remarkable  way,  since  the  perceptible 
difference  becomes  considerably  less  if  the  examinations  are  often  repeated.  On 
the  other  hand,  a  single  examination,  as  in  testing  any  form  of  sensibility,  must 
not  be  too  long  protracted,  for  otherwise  the  patient  may  easily  become  fatigued, 
and  the  data  obtained  will  be  entirely  contradictory.  If  we  test  the  sense  of 
locality  by  bringing  down  the  two  points  not  at  the  same  time  but  one  after  the 
other,  and  vary  it  by  touching  the  same  place  twice,  or  a  different  place  each  time, 
we  obtain  from  the  outset,  as  we  have  repeatedly  proved,  smaller  numbers  than 
if  we  touch  the  skin  with  the  two  points  of  the  compasses  at  the  same  time.  We 
also  obtain  some  different  values  for  the  fineness  of  the  sense  of  locality  if  we  test 
the  so-called  sensations  of  motion  (Leube) — that  is,  the  distinction  between  a  simple 
circumscribed  touch  of  the  skin,  and  a  very  short  line  drawn  with  a  stick  on  the 
skin.  In  this  way  we  can  also  determine  whether  the  patient  can  distinguish 
accurately  the  direction  of  transverse  and  longitudinal  lines. 

We  may  also  mention  here  the  peculiar  symptom  termed  by  Fischer  poly- 
aesthesia,  which  is  that  certain  patients,  especially  ataxics,  when  the  skin  is  touched 
with  only  one  point  of  the  compasses,  have  a  sensation  as  if  they  felt  two  or  even 
more  points.  The  cause  of  this  remarkable  anomaly  of  sensation  is  not  yet 
adequately  explained. 

3.  Sense  of  Pressure. — Since  E.  H.  Weber's  investigations  we  know  that  we 
estimate  the  difference  in  the  intensity  of  our  sensations  of  pressure,  not  according 
to  the  absolute,  but  according  to  the  relative  increase  in  the  pressure.  If,  for 
instance,  a  place  in  the  skin  has  a  weight  of  nineteen  grammes  on  it,  and  we 
perceive  the  first  manifest  increase  in  our  sensation  of  pressure  when  a  weight  of 
one  gramme  is  added  to  it ;  when  the  skin  has  a  weight  of  one  hundred  and  ninety 
grammes  on  it,  we  first  perceive  the  increase  of  pressure  not  when  one  gramme  is 
added,  but  when  we  add  ten  grammes.  If  this  law,  on  more  accurate  testing,  is 
not  as  simply  proved  as  it  seems  according  to  the  results  of  Weber's  first  investi- 
gations, still  it  is  generally  a  fact  that  under  normal  conditions  an  increase  of 
pressure  of  about  one  twentieth  to  one  thirtieth  of  the  original  pressure  may  be 
plainly  perceived  in  the  different  parts  of  the  body. 

Different  methods  and  instruments,  like  Eulenburg's  "  bargesthesiometer,"  have 
been  devised  for  testing  accurately  the  sense  of  pressure  in  patients,  but  they  have 
entered  but  little  into  practice  on  account  of  their  elaborate  character.  We 
usually  content  ourselves  with  testing  the  sense  of  pressure  by  applying  different 
weights,  or  coins.  We  must  mention  here  that  the  part  of  the  body  to  be  tested 
must  be  fully  supported,  that  we  must  also  exclude  sensations  of  temperature  at  the 
same  time  by  putting  something  beneath  the  weights,  and  that  we  must  apply  the 
separate  weights  to  the  same  place  on  the  skin  at  equal  intervals  of  time,  which 
must  not  be  too  long  after  one  another.  There  are  cases  where  the  patient  does  not 
feel  even  the  doubling  or  tripling  of  the  weights.  We  can  easily  conhrm  a  con- 
siderable loss  of  the  sense  of  pressure  by  means  of  simply  varying  pressure  with 
the  hand  or  any  object,  such  as  a  pencil  applied  to  the  skin. 

Partial  paralyses  of  the  sense  of  pressure  are  by  no  means  rare.  We  find  quite 
often,  especially  in  spinal  diseases,  like  locomotor  ataxia,  that  the  patient  feels  a 


508  DISEASES  OF  THE  NEEVOUS  SYSTEM. 

light  touch,  on  the  skin,  hut  that  he  can  not  distinguish  a  marked  pressure  at  all, 
or  only  obscurely. 

4.  Sense  of  Temperature. — As  we  have  already  said  (p.  505),  we  have  lately 
been  led  by  physiological  investigations  (Goldscheider,  etc.)  to  believe  more  and 
more  strongly  that  sensations  of  heat  and  cold  are  to  be  regarded  as  due  to  two 
wholly  distinct  functions  of  the  cutaneous  nerves.  These  functions  are  probably 
performed  by  distinct  nerve  terminations  and  nerve-fibers.  From  repeated  per- 
sonal observation  we  can  state  that  pathological  symptoms  agree  completely  with 
this  theory,  for  we  see  that  changes  in  the  temperature  sense  in  the  skin  by  no 
means  affect  the  heat  sense  and  the  cold  sense  equally.  It  is  therefore  always 
necessary  to  test  both  forms  of  the  temperature  sense  separately.  We  often  find 
that  while  one  form  of  temperature  sense  is  in  normal  activity,  the  other  is  much 
altered — a  pronounced  partial  anaesthesia  to  heat  or  cold.  The  affected  sense  may 
be  wholly  lost  or  merely  blunted,  so  that  hot  water  is  felt  merely  as  tepid,  or  ice 
as  cool.  If  the  temperature  sense  be  lost,  the  application  of  a  hot  or  cold  object 
will  cause  only  a  sensation  of  touch,  and  not  of  temperature. 

If  anaesthesia  to  cold  be  present,  patients  often  speak  of  having  a  distinct 
sensation  of  warmth  when  the  skin  is  touched  with  a  bit  of  ice.  This  symptom, 
which  we  discovered  and  called  "  perverted  temperature  sense,"  may  be  explained 
most  readily  by  supposing  that  the  heat  nerves  are  excited  by  the  severe  irritation 
from  cold.  The  contrary  symptom,  that  heat  excites  a  distinct  sensation  of  cold, 
is  very  much  less  common. 

Besides  the  sensations  of  temperature  we  usually  test  also  the  patient's  capacity 
to  distinguish  differences  of  temperature.  Within  the  moderate  degrees  of  tem- 
perature, 80°  to  100°  (25°-35°  C),  differences  of  a  degree  Fahrenheit  (0"5  C.)  are 
easily  distinguishable  under  normal  conditions,  and  even  half  a  degree  (0-2  C.) 
can  be  distinguished  on  the  face  and  fingers,  but  only  about  two  degrees  (1°  C.)  on 
the  back. 

Variations  in  the  temperature  sense  are  very  common,  especially  in  spinal  dis- 
eases. The  test  of  the  sensibility  to  heat  and  cold  should  therefore  never  be 
omitted  in  testing  the  sensibility.  It  can  be  done  with  sufficient  accuracy  for  all 
ordinary  purposes  simply  by  touching  the  skin  with  test-tubes  filled  with  ice  or 
hot  water.  The  various  thermaesthesiometers  that  have  been  devised  are  too  com- 
plicated for  practical  purposes.  For  a  hasty  test  it  is  sometimes  quite  serviceable 
to  try  whether  the  patient  can  distinguish  warm  breathing  upon  a  given  portion 
of  the  skin  from  cool  blowing  upon  it. 

5.  Sensation  of  Pain. — The  fact  is  of  great  theoretical  interest  that  the  cuta- 
neous sensibility  for  touch  and  pain  do  not  always,  under  pathological  conditions, 
run  parallel  with  each  other.  We  sometimes  see  that  a  patient  does  not  feel  a 
simple  touch  on  the  skin,  when  sticking  a  needle  into  it  is  immediately  painful ; 
while,  on  the  other  hand,  we  often  find  that  a  patient  feels  quite  a  light  touch  on 
the  skin,  but  that  the  most  marked  irritation,  like  pinching  or  pricking  it,  does  not 
excite  the  slightest  pain,  but  is  felt  only  as  a  simple  touch,  or  at  most  as  a  slight 
pressure  on  it.  This  latter  condition  of  sensibility,  the  loss  of  cutaneous  sensibility 
to  pain  with  retained  tactile  sensibility,  is  termed  analgesia.  Both  in  peripheral 
and  in  central  nervous  diseases  analgesia  is  a  symptom  that  may  be  quite  fre- 
quently observed. 

The  test  of  sensibility  to  pain  may  be  made  most  simply  by  the  point  of  a  pin, 
and  also  by  pinching  or  severe  pressure  on  the  skin,  by  painful  thermal  irritants, 
by  strong  electrical  currents,  etc. 

6.  Electro-cutaneous  Sensibility. — The  test  of  cutaneous  sensibility  by 
means  of  the  electric  current  has  been  proposed  from  various  quarters.  The 
advantage  of  it  is  that  in  this  way  the  intensity  of  the  irritation  can  be  very 


REMARKS  UPON  THE  DISTUEBANCES  OF  SENSIBILITY.      509 

easily  and  accurately  graded  and  expressed  in  numbers,  by  the  position  of  the 
cylinder  in  using  the  faradic  current,  or  by  the  galvanometer  in  using  the  con- 
stant current.  The  faradic  current  is  usually  sufficient  in  testing  the  sensibility, 
and  we  designate  it  by  the  position  of  the  cylinder  when  the  first  sensation  is  felt 
and  the  position  when  the  first  pain  is  felt.  In  general,  the  differences  of  the 
farado-cutaneous  sensibility  are  not  very  marked.  Pathological  deviations  are 
given  by  comparison  with  normal  portions  of  the  skin  (testing,  if  possible,  sym- 
metrical parts)  or  with  healthy  people.  For  practical  purposes,  the  test  of  electro- 
cutaneous  sensibility  is  unnecessary,  since  its  results  are  the  same  as  in  testing  the 
sensibility  to  touch  and  to  pain. 

7.  Delayed  Conduction  op  Sensation  and  After-sensations. — In  diseases  of 
the  spinal  cord,  especially  in  locomotor  ataxia  (q.  v.)  we  quite  frequently  see  a 
marked  delay  in  sensation  after  the  action  of  an  irritant;  this  is  also  seen,  but 
more  rarely,  in  peripheral  lesions.  This  delay  of  conduction  affects  chiefly  the 
sensibility  to  pain.  If  in  such  a  case  we  stick  a  pin  into  the  sole  of  a  patient's  foot, 
several  seconds  elapse,  even  ten  or  twenty,  it  is  said,  before  the  pain  is  felt.  As 
was  first  observed  by  Naunyn  and  E.  Remak  in  ataxics,  and  as  has  often  been  con- 
firmed since,  after  sticking  a  pin  into  the  foot  there  is  first  a  sensation  of  touch, 
and  some  seconds  later  the  peculiar  sensation  of  pain,  so  that  the  patient  at  once 
responds  to  the  prick  with  "  Now,"  and  a  little  later  with  "  Ow!  "  as  an  expression 
of  pain. 

This  latter  phenomenon  has  a  certain  relation  to  the  abnormal  after-sensations 
which  are  often  observed  under  pathological  conditions.  After  a  simple  pin-prick 
a  feeling  of  burning  lasts  for  an  extraordinarily  long  time,  or  else  the  first  pain  dis- 
appears quite  soon,  and  then  a  new  sudden  sense  of  pain  appears  several  times  in 
the  same  part  of  the  skin,  just  as  if  the  patient  were  pricked  again.  There  is  also 
a  delayed  conduction  of  the  sensations  of  touch  and  temperature,  but  it  is  rarer, 
and  can  be  made  out  only  by  the  aid  of  more  accurate  methods  of  measuring 
time. 

The  Sensibility  of  the  Muscles  and  Joints.— A  number  of  sensations  are  classed 
together  under  the  names  of  "  muscular  sense  "  or  "  muscular  sensibility."  They 
are  not  all  wholly  of  the  same  value,  and,  under  pathological  conditions,  they 
must  be  tested  separately. 

Ordinarily  we  call  our  power  to  be  informed  of  the  position  of  any  of  our  limbs 
without  the  help  of  our  eyes,  and  of  the  extent  of  any  motion  made  by  them,  the 
"  muscular  sense.''  If  we  put  a  healthy  person's  arm  into  a  given  position  when  his 
eyes  are  closed,  and  tell  him  to  put  the  other  arm  into  the  same  position,  he  can  do 
it  with  considerable  accui'acy.  If  we  make  passive  movements  in  any  of  the  joints 
of  the  extremities,  a  healthy  person  whose  eyes  are  closed  can  easily  and  coiTectly 
state  the  form  and  direction  of  these  movements,  even  if  they  be  very  slight.  In 
nervous  patients,  however,  this  power  may  be  diminished  or  lost,  and  we  often 
speak  of  "  disturbances  of  the  muscular  sense  " ;  but  we  must  note  that  the  judg- 
ment as  to  the  position  of  the  limbs  and  the  passive  movements  executed  with 
them  is  not  chiefly,  much  less  exclusively,  clue  to  the  sensibility  of  the  muscles. 
In  all  probability  it  depends  much  more  upon  the  sensibility  of  the  articular  sur- 
faces, the  ligaments  and  tendons,  and  in  part  even  of  the  skin,  all  which  tissues 
are  relaxed  or  made  tense  in  the  different  movements.  It  would  therefore  be 
more  correct  to  speak  simply  of  the  seuse  of  position  of  the  limbs  and  the  sense  of 
passive  movements  instead  of  the  muscular  sense.  The  sense  of  passive  move- 
ments can  also  be  conveniently  tested  by  describing  in  the  ah'  different  letters  or 
figures  with  the  affected  extremities  of  the  patient,  and  requiring  him  to  recognize 
them  with  his  eyes  closed.  Another  convenient  way  to  test  the  muscular  sense  is 
to  have  the  patient  make  a  definite  movement — pointing  to  or  taking  hold  of  some 


510  DISEASES  OF  THE  NERVOUS  SYSTEM. 

object — with  the  eyes  open,  end  then  to  make  him  repeat  the  act  with  the  eyes 
shut. 

We  also  include  in  the  muscular  sense  the  power  of  estimating  the  amount  of 
work  done  by  muscular  contraction.  This  is  the  so-called  u  sense  of  power. "  In 
raising  weights  we  can  distinguish  with  considerable  accuracy  the  lighter  from  the 
heavier,  when  the  pressure  on  the  skin  is  excluded  as  far  as  possible.  In  such 
cases,  also,  we  donot  deal  with  the  absolute,  but  with  the  relative  differences  in 
weight ;  we  can  usually  tell  quite  plainly  when  one  fortieth  of  the  original  weight 
has  been  added  or  taken  away.  The  sense  of  power,  then,  is  somewhat  finer  than 
the  sense  of  pressure.  In  order  to  exclude  the  latter  in  the  test  we  have  the  pa- 
tient lift  the  weight,  suspended  in  a  towel,  with  his  hand  or  foot,  but  in  the  lower 
extremities  it  is  scarcely  possible  to  exclude  entirely  the  co-existing  sensations  of 
pressure. 

We  must  mention,  in  conclusion,  that  muscular  contraction  is  in  itself  ac- 
companied by  a  sensatiou,  as  may  be  proved,  for  example,  in  irritating  the  muscles 
by  faradism — electro-muscular  sensibility  ;  but  we  have  not  yet  found  any  real 
practical  value  in  testing  the  feeling  of  contraction  in  muscles.  We  must  state, 
however,  that  in  certain  forms  of  spasm  the  muscular  contraction  becomes  so 
strong  that  it  causes  a  decided  pain,  which  is  probably  due  to  irritation  of  the  sen- 
sory muscular  nerves  discovered  by  C.  Sachs. 

Disturbances  of  the  muscular  sense,  or,  to  speak  more  correctly,  disturbances 
in  the  sensibility  of  the  deeper  parts,  are  seen  chiefly  in  locomotor  ataxia,  some- 
times in  paralysis  of  cerebral  origin,  and  quite  frequently  in  severe  hysterical 
affections. 


CHAPTER  II. 
ANESTHESIA   OF   THE    SKIN. 

iEtiology  and  Pathogenesis.— In  every  tract  of  the  conducting  path,  which 
runs  from  the  terminal  apparatus  of  the  sensory  cutaneous  nerves  to  the  centers 
for  the  perception  of  sensation  in  the  cerebral  cortex,  we  may  have,  under  patho- 
logical conditions,  a  break  in  the  conduction,  and,  as  a  result  of  it,  a  complete 
or  partial  anaesthesia  of  the  corresponding  part  of  the  skin.  We  speak  of  a 
peripheral,  spinal,  or  cerebral  anaesthesia,  according  to  the  place  where  this 
break  in  the  conduction  occurs.  The  precise  anatomical  course  of  the  sensory 
fibers  is,  however,  very  imperfectly  known,  so  that  we  can  only  approximately 
determine  the  location  of  the  sensory  fibers  in  the  different  portions  of  the 
nervous  system. 

We  know  this,  however,  of  the  mixed  peripheral  nerves  before  their  entrance 
into  the  spinal  cord,  that  all  their  sensory  fibers  enter  the  cord  through  the 
posterior  roots.  A  part  of  the  posterior  root-fibers  pass  directly  into  the  sub- 
stance of  the  posterior  gray  cornua,  while  another  part  enter  toward  the  median 
line  into  the  external  (in  the  lumbar  cord,  more  correctly  the  median)  portion 
of  the  posterior  columns — that  is,  into  the  region  of  the  "  root-zones,"  or  the  so- 
called  "elementary  bundles  of  the  posterior  columns."  Since  new  fibers  from 
the  posterior  roots  constantly  enter  the  posterior  columns  of  the  cord,  going 
upward  from  the  lumbar  region,  the  fibers  which  have  entered  in  the  lower 
portions  must  gradually  be  more  and  more  crowded  inward- toward  the  median 
line.  Hence  it  follows  that  the  fibers  entering  the  lumbar  region,  belonging 
to  the  sciatic,  the  crural,  etc.,  must  in  the  upper  dorsal  and  cervical  region  occupy 
that  internal  portion  of  the  posterior  columns  which  is  called  the  "  columns  of 


ANAESTHESIA  OF  THE  SKIN.  511 

Goll "  (Fig1.  88,  G).  We  can  not,  however,  state  definitely  at  present  which  of 
the  different  prolongations  of  the  posterior  roots  is  the  special  path  for  sensory 
conduction.  We  are  ourselves  very  much  inclined  to  the  opinion  that  the  special 
sensory  fibers  of  the  posterior  roots  for  the  most  part  enter  directly  into  the 
gray  matter  of  the  posterior  cornua,  and  that  the  elementary  bundles  of  the 
posterior  columns — the  continuation  of  the  fibers  which  enter  directly  into  the 
posterior  columns — accordingly  serve  chiefly  for  other  functions.  We  are  led 
to  this  opinion  especially  by  observations  of  quite  severe  disease  of  the  columns 
of  Goll,  which  occasioned  no  perceptible  disturbance  of  sensation  in  the  lower 
extremities  during  the  patients'  life.  Disease  of  the  posterior  cornua  of  the  gray 
matter,  however,  is  always  associated  with  disturbances  of  sensibility.  It  is  not 
probable,  according  to  our  present  experience,  that  there  is  a  sensory  tract  in  the 
lateral  columns  also  in  man.  The  fact  is  certainly  proved,  and  is  of  importance, 
that  all,  or  at  least  the  greater  part,  of  the  sensory  fibers  undergo  a  decussation 
after  their  entrance  into  the  spinal  cord,  so  that  the  fibers  from  the  right  half 
of  the  body  pass  upward  in  the  left  half  of  the  cord,  and  vice  versa.  We  know 
absolutely  nothing  definite  as  to  the  further  course  of  the  sensory  fibers  through 
the  medulla  oblongata  and  the  pons,  or  as  to  their  relations  to  the  gray  matter 
there,  but  it  seems  to  be  certain  that  the  sensory  tract  continues  on  to  the  cerebral 
hemispheres,  not  through  the  crusta,  but  through  the  tegmentum.  From  this 
point  the  sensory  fibers  pass  to  the  internal  capsule,  and  a  number  of  experiments 
show  that  they  lie  in  the  posterior  third  of  the  posterior  limb  of  the  internal  cap- 
sule behind  the  pyramidal  tracts  (see  Fig.  64),  a  place  where  the  cutaneous  and 
muscular  sensory  fibers  are  probably  near  the  fibers  for  the  impressions  for  the 
special  senses  of  vision,  hearing,  etc.  Nothing  certain  is  known  as  to  the  central 
termination  of  the  sensory  fibers.  Perhaps  the  posterior  central  convolution  and 
the  portions  of  the  parietal  lobe  behind  it  may  be  regarded  as  the  special  places 
of  termination  for  the  sensory  tract.  We  do  not  know  whether  tracts  of  conduc- 
tion go  to  the  brain  which  are  distinguished  from  one  another  according  to  the 
different  forms  of  cutaneous  sensibility. 

Eegarding  the  separate  causes  of  anaesthesia,  we  see,  in  the  first  place,  periph- 
eral anaesthesia  under  conditions  where  the  terminal  organs  of  the  sensory  cutane- 
ous nerves  have  lost  their  direct  irritability.  After  chilling  the  skin,  after  the  local 
action  of  ether  and  similar  substances,  after  the  corrosive  action  of  acids  and  alka- 
lies, carbolic  acid,  etc.,  as  well  as  after  the  use  of  certain  narcotics,  such  as  cocaine, 
morphine,  or  atropine,  we  see  an  anaesthesia  of  the  skin,  which  is  due  to  injury 
of  the  terminal  sensory  organs.  We  may  probably  put  the  frequent  anaesthesia 
of  washerwomen  in  this  class,  for  their  hands  and  forearms  are  exposed  all  day 
to  the  action  of  cold,  lye,  etc.  The  anaesthesias  which  develop  in  circulatory  dis- 
turbances of  the  skin  also  have  the  same  peripheral  origin,  especially  the  "  spastic 
anaemia"  which  sometimes  comes  in  the  hands  and  is  due  to  a  spasm  of  the  small 
arteries. 

We  distinguish  the  peripheral  anaesthesia  of  conduction,  which  may  be  pro- 
duced by  all  forms  of  lesion  of  the  nerve-trunks,  from  the  peripheral  anaesthesia 
in  the  strict  sense  of  the  term.  Traumatic  influences,  compression  from  new 
growths,  and  inflammation  and  degeneration  of  the  peripheral  nerves,  as  in  neuri- 
tis, are  the  most  frequent  causes  of  this  form  of  anaesthesia,  which  is  often  limited 
to  the  region  of  distribution  of  one  or  more  definite  nerves. 

Spinal  anaesthesia  is  very  often  seen  in  the  different  diseases  of  the  spinal  cord, 
most  frequently  in  locomotor  ataxia,  because  this,  as  we  shall  see  later,  attacks 
chiefly  the  posterior  roots,  the  posterior  columns,  and  the  posterior  cornua  of  the 
cord;  but  spinal  anaesthesia  is  not  infrequent  in  diffuse  acute  and  chronic  inflam- 
mation of  the  cord  and  in  compression  and  new  growths.     As  a  rule,  it  is  bilateral, 


512  DISEASES  OF  THE  NERVOUS  SYSTEM. 

para-anaesthesia.  The  hypothesis  advanced  by  Schiff  is  quite  widespread,  hut  is 
by  no  means  certainly  proven,  that  the  gray  matter  of  the  cord  conducts  chiefly 
the  impressions  of  pain,  and  the  white  matter  of  the  posterior  columns  the  sensa- 
tions of  touch.  According'  to  this,  in  spinal  analgesia  we  must  assume  chiefly  an 
impairment  of  the  gray  matter. 

Cerebral  anaesthesia  is  seen  especially  in  haemorrhages,  foci  of  softening,  and 
tumors,  which  affect  the  posterior  portion  of  the  internal  capsule ;  but  of  course 
the  break  may  occur  in  any  other  part  of  the  tract  of  sensory  conduction  in  the 
brain.  If  the  cerebral  anaesthesia,  as  is  often  the  case,  affects  the  half  of  the  body 
opposite  the  lesion  in  the  brain,  we  term  it  hemianaesthesia.  Very  extensive 
cerebral  anaesthesia  of  a  marked  degree  is  quite  frequently  found  in  severe  cases 
of  hysteria.  We  also  know  that  the  anaesthetic  action  of  the  remedies  termed 
anaesthetics  and  narcotics,  such  as  chloroform,  morphine,  ether,  alcohol,  bromide  of 
potassium,  etc.,  must  be  explained  by  their  influence  on  the  central  nervous 
system. 

Among  other  aetiological  factors  we  must  also  mention  that  we  sometimes  see 
more  or  less  extensive  anaesthesia  as  a  result  of  acute  diseases,  such  as  typhoid,  diph- 
theria, and  other  acute  infectious  diseases,  the  origin  of  the  anaesthesia,  whether 
peripheral  or  spinal,  being  as  yet  uncertain.  Peculiar  insular  and,  rarely,  diffuse 
anaesthesia,  showing  itself  chiefly  on  the  backs  of  the  hands  and  the  chest,  is  found 
in  the  secondary  stages  of  syphilis,  according  to  Fournier;  but  there  has  been  no 
further  confirmation  of  this  statement  so  far  as  we  know. 

Symptoms. — In  many  cases  the  patient  himself  notices  the  existence  of  anaes- 
thesia. He  finds  that  in  certain  parts  of  the  body  he  no  longer  feels  the  pressure 
of  his  clothing  or  the  bedclothes  in  the  usual  way.  Anaesthesia  of  the  hands  is 
soonest  noticed,  because  this  can  affect  the  patient's  occupation  in  diverse  ways,  so 
that,  for  example,  he  readily  lets  fine  objects,  such  as  needles,  drop  from  his  hands. 
In  other  cases,  of  course,  the  anaesthesia  is  first  found  on  a  physical  examination, 
which  alone  can  give  definite  disclosures  as  to  the  extent  and  intensity  of  the 
affection.  For  this  purpose  the  skin  must  be  carefully  examined  by  the  methods 
given  in  the  preceding  chapter.  It  is  worthy  of  note  that  hysterical  anaesthesia 
especially,  even  if  it  be  very  marked  and  extensive,  may  often  be  wholly  over- 
looked by  the  patients  themselves. 

Anaesthesia  is  very  often  combined  with  abnormal  subjective  sensations,  pares- 
thesia?, in  the  affected  portions  of  the  skin.  The  patient  has  a  feeling  there  of 
"  numbness,"  or  a  "  furry  feeling,"  or  complains  of  prickling  or  formication.  The 
anaesthetic  parts  may  even  be  the  seat  of  very  decided  pain  (anazsthesia  dolorosa), 
if  there  is  abnormal  irritation  of  the  sensory  nerves  from  the  break  in  the  con- 
duction toward  the  center.  The  most  diverse  forms  of  anomalies  of  motility  and 
of  the  reflexes,  and  vaso-motor  disturbances,  may  of  course  be  present  in  addition 
to  the  anaesthesia.  Special  mention  must  be  made  of  trophic  disturbances  which 
are  often  seen  in  anaesthetic  regions.  We  shall  return  to  the  peculiar  characteris- 
tics of  these  repeatedly  in  subsequent  chapters;  therefore  we  need  state  here  only 
that  the  trophic  disturbances  have  nothing  to  do  with  the  anaesthesia  itself.  They 
depend  either  upon  a  co-existing  lesion  of  special  trophic  or  vaso-motor  nerves,  or 
upon  the  fact  that  external  irritants,  which  act  upon  any  anaesthetic  portion  of 
the  skin,  are  not  felt  normally  by  the  patient,  and  hence  are  often  not  avoided.  In 
anaesthetic  regions  we  often  find  large  external  wounds,  burns,  bed-sores,  inflam- 
mations, etc.,  which  were  not  noticed  by  the  patient  in  time  to  prevent  them,  and 
hence  they  often  attain  an  unusual  extent. 

Voluntary  motion  is  not  disturbed  by  anaesthesia  in  itself,  of  however  great  a 
degree,  as  long  as  the  motions  can  be  controlled  by  the  eyes,  but  finer  movements 
are  often  considerably  impaired  by  cutaneous  anaesthesia;    thus   patients  with 


ANESTHESIA  OF  THE  SKIN. 


5 1  3 


diminished  sensibility  in  the  fingers  can  usually  no  longer  sew,  because  they  lose 
the  needle  every  minute.  With  the  eyes  shut,  however,  the  motions  of  the  anaes- 
thetic parts  become  very  uncertain,  both  in  anaesthesia  of  the  skin  and  of  the 
deeper  parts,  the  muscles  and  joints,  since  then  the  patient  loses,  to  a  great  degree, 
his  power  of  judging  of  the  extent  and  of  the  precise  direction  of  his  movements. 
Very  extensive  anaesthesia  of  the  skin,  associated  at  the  same  time  with  anaesthesia 
of  tbe  organs  of  special  sense,  is  sometimes  not  without  influence  upon  conscious- 
ness. We  have  for  several  years  had  under  observation  a  very  remarkable  case 
of  total  anaesthesia  of  the  whole  body  associated  with  unilateral  blindness  and 
deafness.  If  we  entirely  exclude  this  patient  from  all  external  impressions  of 
sense  by  closing  his  still  serviceable  eye  and  ear,  we  can  at  once  in  this  way  put 
him  into  a  deep  sleep ! 

We  can  not  here  go  into  details  of  the  different  forms  and  distributions  of 
anaesthesia,  since  they  will  be  spoken  of  under  the  different  diseases  which  lie  at 
the  basis  of  the  anaesthesia.  The  course,  the  duration,  and  the  prognosis  of  the 
affection  depend,  in  the  first  place,  of  course,  upon  the  form  of  the  primary  disease. 
We  will  add  here  merely  a  few  remarks  upon  anaesthesia  of  one  nerve,  namely, 
anaesthesia  in  the  distribution  of  the  trigeminus. 

Anaesthesia  of  the  trigeminus  is  observed  in  tumors,  syphilitic  new  growths, 
chronic  inflammations,  and  analogous  processes  at  the  base  of  the  skull,  which 
compress  the  trunk,  the  Gasserian  ganglion,  or  one  of  the  three  branches  of  the 
trigeminus,  or  directly  involve  the  nerves.  Traumatic  lesions  of  the  trigeminus 
are  also  not  very  uncommon.  The  distribution  of  the  anaesthesia,  according  as 
the  affection  involves  the  whole  trigeminus,  or  only  one  branch  of  it,  may  be  seen 
in  Figs.  57  and  58.     In  total  anaesthesia  of  the  trigeminus,  the  conjunctiva  and 


Fig.  57.  Fig.  58. 

Figs.  57  and  58.— Distribution  of  the  sensory  cutaneous  nerves  in  the  head  :  oma  and  ami.  Occipitalis 
major  and  minor,  am.  Auricularis  magnus.  cs.  Superficial  cervical.  V1,  F2,  F3.  First,  second,  and 
third  branches  of  the  fifth  (V).  so.  Supraorbital,  st.  Supratrochlear,  it.  Infratrochlear.  e.  Eth- 
moidal. I.  Lachrymal,  sm.  Subcutaneus  mala?,  or  zygomatic,  at.  Auriculotemporal,  b.  Buccinator, 
m.  Mental.    B.  Posterior  branches  of  the  third  cervical. 


cornea,  the  mucous  membrane  of  the  nose,  the  cavity  of  the  mouth,  and  the 
tongue  are  anaesthetic  on  the  affected  side.  Hence  we  often  find  ulcers  on  the 
tongue  and  the  mucous  membrane,  which  come  from  being  bitten.  The  "  neuro- 
paralytic ophthalmia  "  not  infrequently  seen  in  anaesthesia  of  the  trigeminus  is  of 
special  interest,  and  has  been  much  studied  by  physicians  and  physiologists.  This 
33 


514 


DISEASES   OF  THE  NERVOUS  SYSTEM. 


is  an  ulcerative  keratitis,  almost  always  beginning  in  the  lower  segment  of  the 
cornea,  and  sometimes  passing  over  into  a  purulent  inflammation  of  the  whole 
eyeball.  This  affection  is  regarded  in  many  quarters  as  an  immediate  result  of 
the  disturbance  of  special  "  trophic  "  functions,  but,  after  careful  experiments 
(Senftleben),  it  seems  most  probable  that  external  traumatic  influences  always 
occasion  the  first  trouble,  and  render  the  intrusion  of  inflammatory  agents  pos- 
sible. It  is  still  uncertain  whether  we  must  also  assume  a  specially  diminished 
power  of  resistance  on  the  part  of  the  tissues  as  a  result  of  the  nervous  lesion. 

The  skin  of  the  face  is  often  somewhat  bloated  in  anaesthesia  of  the  trigeminus, 
and  it  is  cyanotic  and  feels  cool.  The  reflexes  are  lost  in  peripheral  anaesthesia, 
and  the  lacbrymal  secretion  is  diminished.  The  taste  is  almost  always  decidedly 
diminished  on  the  anterior  two  thirds  of  the  tongue  on  the  affected  side,  the  terri- 
tory supplied  by  the  lingual  nerve. 


Fig.  61. 


Fig.  59.  Fig    60. 

Figs.  59  and  60.*-Distribution  of  the  sensory  cutaneous  nerves  in  the  trunk  and  upper  extremities: 
Fig.  59.  Posterior  aspect.  Fig.  60.  Anterior  aspect.  The  shaded  portion  in  Fig.  59  designates  the 
territory  supplied  by  the  radial  nerve.  (From  Henle.)  sc.  Supraclavicular  nerves  (from  the  cer- 
vical plexus),  ax.  Cutaneous  branch  of  the  axillary  nerve,  cps  and  cpi.  Superior  and  interior  pos- 
terior cutaneous  nerves  from  the  radial  <ra).  cmd,  cm,  and  cl.  Median  cutaneous,  median,  and  lateral 
nerves,  me.  Median  nerve,  u.  Ulnar  nerve,  du.  Second  dorsal  nerve,  dxn.  Twelfth  dorsal  nerve. 
ih.  Ileo-hypogastric  nerve,  ii.  Ileo-insruinal  nerve,  il.  Lateral  perforating  branches,  and  la,  anterior 
perforating  branches  of  the  intercostal  nerves. 

Fig.  61.— Detailed  distribution  of  the  nerves  to  the  dorsal  surface  of  the  fingers.  (From  Krause.) 
r.  Radial  nerve,    m.  Median  nerve,    u.  Ulnar  nerve. 

Treatment. — Since  anaesthesia  in  most  cases  is  only  a  symptom,  treatment,  of 
course,  must  always  first  be  directed  against  the  underlying  disease.  Therefore 
we  will  mention  here  only  those  measures  which  are  to  be  used  symptom atically 


*  Henlc's  nomenclature  of  the  peripheral  nerves  has  been  adopted. — Trans. 


NEURALGIA  IN  GENERAL. 


515 


N 


IS? 


Cl 


against  anaesthesia,  and  which  must  be  tried  when  the  special  cause  can  not  he 
discovered,  or  when  it  is  inaccessible  to  treatment. 

The  chief  remedy  is,  without  doubt,  the 
electric  current.  We  treat  the  anaesthetic 
part  of  the  skin  with  the  faradic  current, 
using  ordinary  electrodes,  or,  better  still, 
the  wire  brush,  or  with  the  galvanic  cur- 
rent, stroking  the  skin  slowly  back  and 
forth  with  the  cathode  for  three  or  four 
minutes.  Sometimes  we  can  see  a  result 
immediately  after  the  sitting.  Hysterical 
anaesthesia  may  often  be  removed  in  this  \  CP  i  i 
way  in  a  very  short  time.  |  \  j     J  \       cr 

Besides  electricity  we  usually  prescribe 
embrocations  to  irritate  the  skin,  such  as 
spirits  of  camphor,  spirits  of  mustard,  for- 
mic acid,  spirits  of  thyme,  etc.,  and  also 
baths,  and  cold  or  hot  local  douches,  com- 
bined with  rubbing  the  skin.  The  action 
of  internal  remedies  is  extremely  doubtful. 
Nux  vomica  or  strychnine,  tincture  of 
valerian,  etc.,  have  been  recommended. 

It  is  very  important  to  protect  the  an- 
aesthetic part  against  external  injuries. 
In  anaesthesia  of  the  trigeminus,  particu- 
larly, we  guard  the  eye  as  far  as  possible 
from  the  development  of  a  n euro-paralytic 
keratitis,  by  a  carefully  applied  occlusive 
bandage. 


icpm 


\cpett 


cti 


As  an  appendix,  we  will  add  here  some 
illustrations  (Figs.  59  to  63)  to  represent, 
in  a  diagrammatic  fashion,  the  distribution 
of  the  sensory  cutaneous  nerves.  These 
diagrams  will  be  of  service,  both  in  the 
consideration  of  anaesthesia  and  in  the 
diagnosis  of  the  neuralgias  to  be  described 
in  the  following  chapters. 


Fig.  62.  Fig.  63. 

Figs.  62  and  63.— Distribution  of  the  sensory  cuta.- 
neous  nerves  to  the  lower  extremities.  Fig. 
62.  Posterior  aspect.  Fig.  63.  Anterior  aspect. 
(From  Henle.)  ii.  Ileo-inguinal  nerve,  li. 
Lumbo-inguinal  nerve,  se.  External  spermat- 
ic, cp.  Posterior  cutaneous,  cl.  Lateral  cu- 
taneous, cr.  Crural,  obt.  Obturator,  sa. 
Saphenous,  cpe.  Peroneal  communicating 
nerve,  cti.  Tibial  communicating  nerve. 
per'.  Superficial  branch  of  the  peroneal 
nerve,  per".  Deep  peroneal  nerve,  cpm. 
Posterior  median  cutaneous  nerve,  cpp.  Cu- 
taneous plantar  nerve. 


CHAPTER  III. 

NEURALGIA  IN  GENERAL. 

Although  every  pain  is,  of  course,  excited  by  abnormal  irritation  of  the  nerves, 
still  we  are  justified  in  giving  a  certain  special  variety  of  pain  the  name  of  neu- 
ralgia. The  characteristics  of  this  particular  "  nervous  pain  "  are  as  follows :  1,  it 
is  felt  exactly  in  the  course  or  in  the  distribution  of  one  or  more  special  nervous 
trunks  or  nervous  branches ;  2,  it  is  usually  of  very  considerable  intensity ;  and, 
3,  as  a  rule,  it  is  not  present  continuously,  but  it  shows  manifest  remissions  and 
intermissions.     It  often  comes  on  in  single  pronounced  paroxysms  of  pain,  which 


516  DISEASES  OF  THE  NERVOUS  SYSTEM. 

are  due  to  definite  causes,  or  which  can  not  be  referred  to  any  evident  external 
irritation. 

Pathogenesis  and  iEtiology. — In  many  cases  the  cause  of  neuralgia  is  entirely 
unknown,  hut  in  other  cases  we  can  discover  factors  which  may  be  regarded  either 
as  more  or  less  direct  exciting  causes,  or  at  least  as  pi'edisposing  causes,  for  the  ap- 
pearance of  neuralgia ;  but  in  all  these  cases  the  precise  form  of  action,  and  the  pe- 
culiar nature  of  the  disturbance  produced  in  the  nerves,  are  almost  wholly  unknown 
to  us.  At  best  we  may  suspect  that  perhaps  sometimes  we  have  to  do  with  slight 
inflammatory  changes  in  the  nerve-trunks,  with  hyperemia,  exudation,  oedema,  etc. 

We  may  mention  the  following  as  predisposing  factors,  which  clinical  observa- 
tion has  taught  us:  1.  Age.  Neuralgia  comes  on  most  frequently  in  middle  life, 
but  it  is  also  found  in  older  people,  and  more  rarely  in  children.  2.  Sex  exerts  an 
influence  so  far  that  certain  forms,  such  as  trigeminal  neuralgia,  are  seen  more  fre- 
quently in  women,  and  other  forms,  such  as  sciatica  and  brachial  neuralgia,  are  more 
common  in  men.  Certain  phases  of  sexual  life,  too,  such  as  puberty,  pregnancy, 
childbed,  and  the  climacteric,  favor  the  disposition  to  neuralgia.  3.  The  general 
neuropathic  predisposition,  which  is  hereditary  in  the  majority  of  cases,  is  of  great 
significance.  Neuralgia  often  appears  in  people  who  suffer  from  other  neuroses, 
or  in  whose  families  other  nervous  diseases,  such  as  the  psychoses,  epilepsy,  hys- 
teria, or  neurasthenia  have  repeatedly  occurred.  4.  The  physical  constitution  also 
seems  to  be  of  influence.  We  often  see  neuralgia  in  anaemic  people,  or  in  those 
whose  constitution  has  been  impaired  by  physical  and  mental  strain,  by  imprudent 
living,  or  by  mental  excitement. 

We  may  mention,  as  exciting  causes  of  neuralgia:  1.  Cold,  the  action  of 
draughts,  wind,  or  wet — the  so-called  "rheumatic  neuralgias."  It  is  not  per- 
fectly clear  how  the  cold  acts  in  such  cases.  We  usually  assume  that  by  its  action 
slight  anatomical  (inflammatory  ?)  changes  arise  directly  or  in  a  reflex  manner  in 
the  nerves  themselves.  2.  Mechanical  and  traumatic  action.  Among  these  are, 
first,  wounds  and  contusions  which  directly  involve  the  nerves.  Thus,  for  exam- 
ple, extremely  severe  neuralgia  sometimes  arises  from  the  pressure  of  foreign 
bodies,  such  as  splinters  of  wood  or  of  bones  in  wounds,  on  the  branch  of  a  nerve. 
We  may  also  mention  here  the  very  severe  neuralgia  sometimes  met  with  after 
amputations,  which  develops  as  a  result  of  the  so-called  amputation  neuromata. 
To  this  class,  too,  belong  diseases  in  the  neighborhood  of  nerves  which  act  as 
mechanical  irritants.  Diseases  of  the  bones  or  periosteum  often  lead  to  neuralgia 
in  those  nerves  which  run  through  bony  canals  or  grooves.  Lastly,  tumors, 
aneurisms,  herniee,  or  the  gravid  uterus,  may  lead  to  neuralgia  by  pressure  on  the 
neighboring  nerves;  but  we  must  call  to  mind  that  every  pressure  on  a  nerve 
does  not  lead  to  neuralgia  in  the  same  way,  so  that  we  must  assume  a  special  con- 
sequent change  in  the  nerve  in  "  neuralgia  from  compression." 

The  relation  which  certain  infections  and  poisons  have  to  the  development  of 
neuralgia  is  very  important.  In  the  first  place,  it  is  not  impossible  that  many  of 
the  apparently  "  idiopathic  "  neuralgias  are  to  be  referred  to  infectious  causes — an 
assumption  which  may  be  made,  for  instance,  in  intercostal  neuralgia  associated 
with  an  eruption  of  zoster  (q.  v.),  or  in  many  acute  trigeminal  neuralgias.  Many 
neuralgias,  however,  also  have  a  definite  relation  to  other  infectious  diseases.  We 
may  mention  in  particular  the  malarial  neuralgias,  which  are  directly  dependent 
upon  the  malarial  infection,  often  come  on  at  regular  intervals,  and  are  cured  by 
specific  treatment,  namely,  quinine.  Neuralgia  is  often  seen  during  the  course, 
or  as  a  result,  of  typhoid,  small-pox,  and  similar  acute  infectious  diseases,  and  in 
the  secondary  stage  of  syphilis.  Among  toxic  substances  we  may  mention  espe- 
cially lead,  copper,  mercury,  and  also  alcohol  and  nicotine,  as  those  which  have  a 
special  relation  to  the  development  of  neuralgia. 


NEURALGIA  IN  GENERAL.  517 

Neuralgia  is  also  found  in  many  constitutional  diseases,  in  gout,  and  quite  often 
in  diabetes  mellitus,  and  seems  to  bear  a  direct  relation  to  the  general  disease ; 
and  hence,  like  many  of  the  other  neuralgias  mentioned  as  symptomatic,  it  may 
be  contrasted  with  the  idiopathic  neuralgia  due  to  some  direct  affection  of  the 
nerves  themselves.  Finally,  neuralgia  is  met  with  sometimes  in  distant  nerves  in 
diseases  of  other  than  nervous  organs,  like  the  sexual  organs,  and  is  termed  "  reflex 
neuralgia";  but  we  must  be  very  cautious  in  accepting  the  theory  of  reflex  neu- 
ralgias, since  in  most  of  these  cases  we  have  to  do  with  other  affections,  such  as 
hysteria,  etc. 

General  Symptomatology  of  Neuralgia. — The  neuralgic  paroxysm  begins  either 
quite  suddenly,  or,  more  frequently,  after  certain  prodromata,  such  as  cold  feelings, 
prickling,  slight  painful  sensations,  etc.,  have  preceded  it  for  some  time.  The 
pain  during  the  attack  is  usually  of  the  greatest  severity,  and  is  described  as  either 
burning  and  boring,  or  as  shooting  and  tearing  like  lightning.  There  are  fre- 
quently short  temporary  remissions  of  the  pain.  The  location  of  the  pain  usually 
corresponds  precisely  to  the  distribution  of  the  affected  nerve,  so  that  the  patient 
can  often  point  out  quite  definitely  the  anatomical  course  of  the  nerve.  At  the 
height  of  the  attack  there  is  often  an  "  irradiation  "  or  shooting  of  the  pain  into 
the  territory  of  neighboring  nerves.  External  irritants,  such  as  cold  air,  mental 
excitement,  and  especially  movements  of  the  affected  part,  often  produce  an 
increase  of  the  pain. 

On  physical  examination,  we  notice,  first,  certain  disturbances  of  sensibility. 
The  skin  in  the  neuralgic  part  often  shows  more  or  less  anaesthesia,  which  is  most 
apparent  in  the  intervals  between  the  separate  attacks  and  immediately  after 
them.  Much  more  frequently,  however,  both  during  the  attack  and  during  the 
time  when  the  patient  is  free  from  pain,  there  is  hypersesthesia  of  the  skin  and 
the  parts  beneath.  There  are  certain  definite  points  which  are  often  very  sensi- 
tive and  tender  even  to  light  pressure.  These  are  called  painful  points  (points 
douloureux).  They  were  first  fully  described  by  Valleix,  in  1841,  for  the  different 
forms  of  neuralgia,  and  they  have  considerable  diagnostic  importance,  since  they 
may  often  be  found,  not  only  during  the  attack  itself,  but  also  during  the  free 
intervals,  although  in  a  lesser  degree.  The  painful  points  always  correspond  to 
certain  places  in  the  course  of  the  trunk  or  the  larger  branches  of  the  affected 
nerve,  and  are  found  especially  where,  in  marked  and  deep  pressure  on  the  nerve, 
we  can  press  on  some  firm  part  beneath.  They  are  probably  always  due  to  an 
abnormal  sensitiveness  to  pressure  in  the  affected  nerve  itself.  In  many  cases  of 
neuralgia  they  may  of  course  be  wholly  wanting. 

Motor  symptoms  as  well  as  sensory  are  not  infrequent  in  neuralgia.  Co-exist- 
ing symptoms  of  paralysis  must  always  be  regarded  as  a  complication  caused  by 
some  coarse  lesion  of  the  motor  nerves ;  hence  in  ordinary  idiopathic  neuralgia 
they  are  entirely  absent.  The  co-existing  symptoms  of  motor  irritation,  which 
are  often  seen,  are  usually  directly  dependent  upon  the  neuralgia,  however,  and 
hence  are  to  be  regarded  as  reflex  contractions,  set  up  in  the  muscles  by  the  great 
irritation  of  the  sensory  nerves. 

Vaso-motor  symptoms  are  often  seen  in  neuralgia.  In  the  face  especially,  in 
trigeminal  neuralgia,  we  often  see  a  marked  pallor  or  a  decided  reddening  of  the 
skin  and  conjunctiva.  Abnormal  secretions,  of  tears  or  sweat,  may  also  be  seen 
during  the  attack  or  at  the  end  of  it.  We  do  not  know  whether  all  these  symp- 
toms arise  from  direct  or  reflex  nervous  irritation.  Trophic  disturbances  are 
noticed  in  various  ways.  During  the  attack  we  see  eruptions  of  urticaria,  or  siill 
more  frequently  of  herpes  vesicles,  along  the  coui'se  of  the  affected  nerves,  as  in 
herpes  zoster.  In  severe  and  protracted  neuralgias  permanent  changes  in  the 
tissues  have  been  repeatedly  seen  in  the  parts  supplied  by  the  affected  nerves. 


518  DISEASES  OF  THE  NERVOUS  SYSTEM. 

Among  these  are  a  falling  out  or  a  whitening  of  the  hair,  or  more  rarely  an 
abnormally  great  growth  of  hair,  thickening  or  atrophy  of  the  skin,  staining  or 
pigmentation  of  the  skin.  etc.  Lastly  we  may  mention  that  during  the  neuralgic- 
attack  we  sometimes  find  a  diminished  frequency  of  the  pulse. 

The  general  nutrition  of  the  body  often  does  not  suffer  at  all  in  neuralgia,  but 
in  many  cases,  especially  when  sleeping  and  eating  are  constantly  disturbed  by 
the  attacks  of  pain,  the  disease  gradually  has  a  noticeable  action  on  the  whole 
constitution.  The  patient  becomes  pale  and  emaciated,  and  often  the  persistent 
and  distressing  pain  is  not  without  influence  on  his  mental  condition.  He  becomes 
irritable  and  inclined  to  melancholy.  Patients  have,  in  repeated  instances,  even 
committed  suicide  as  a  result  of  severe  and  incurable  neuralgia. 

The  whole  course  of  neuralgia  shows  the  greatest  diversity.  As  has  been  said 
repeatedly,  the  onset  of  the  disease  in  separate  attacks  is  the  chief  characteristic 
feature.  The  precise  pathogenesis  of  these  attacks  is,  of  course,  entirely  unknown 
to  us.  These  attacks  usually  come  on  every  day  or  several  times  a  day,  or  some- 
times at  greater  regular  or  irregular  intervals.  They  may  last  only  a  few  minutes 
or  several  hours.  During  the  period  between  the  attacks  many  patients  feel  quite 
well,  but  some  have  still  a  certain  sensitiveness  of  the  skin.  The  disease  as  a 
whole  sometimes  lasts  only  a  few  days  or  weeks,  but  sometimes  it  persists  with 
manifold  variations  for  years  and  years,  and,  in  a  word,  is  not  capable  of  im- 
provement; although,  on  the  other  hand,  there  are  recoveries  after  the  disease 
has  lasted  for  years.  In  many  cases,  of  course,  the  disease  depends  upon  the  pres- 
ence of  some  definite  anatomical  cause,  such  as  a  tumor,  a  disease  of  the  bone,  or 
an  aneurism. 

Many  details  as  to  prognosis  and  also  as  to  the  diagnosis  of  neuralgia  will  be 
spoken  of  in  the  following  chapter. 

General  Treatment  of  Neuralgia. — Prophylaxis  of  neuralgia  is  possible  in  this 
way,  that  certain  constitutional  anomalies,  such  as  anaemia  or  a  general  nervous 
predisposition,  favor  its  appearance,  as  we  have  seen ;  and  in  attacking  these  condi- 
tions, we  may  recognize  a  factor  which  can  prevent  to  a  certain  degree  any  subse- 
quent development  of  neuralgia.  It  is  still  more  important,  in  people  who  have 
already  suffered  from  neuralgia,  to  prevent  the  return  of  the  affection  if  we  can. 
For  this  object  we  must  first  consider  the  strengthening  of  the  whole  body,  in 
order  to  make  it  better  resist  the  action  of  any  causes  of  disease.  The  measures 
to  be  chiefly  employed  for  this  purpose  are  proper  food,  good  air,  baths,  sea-bath- 
ing, cold  bathing,  gymnastics,  etc.  Of  course,  we  must  also  particularly  guard 
the  part  of  the  body  that  has  once  been  attacked  from  any  irritation,  such  as  cold, 
mechanical  irritants,  or  over-exertion. 

In  treating  neuralgia  itself  we  must  always  look  first  with  great  care  for  some 
causal  factor,  which  may  be  accessible  to  treatment.  This  fulfillment  of  the 
causal  indication  is  often  possible  in  neuralgias  which  are  due  to  mechanical 
causes.  The  extirpation  of  tumors,  the  excision  of  cicatrices,  the  removal  of  for- 
eign bodies,  the  treatment  of  inflammatory  new  growths,  of  syphilitic  affections, 
of  aneurisms,  etc.,  is  in  many  cases  attended  by  brilliant  success,  but,  of  course,  in 
many  other  cases  the  underlying  disease  is  unfortunately  not  amenable  to  success- 
ful treatment.  We  should  also  carry  out  a  causal  treatment  in  the  neuralgias 
which  are  to  be  referred  to  general  anaemia,  to  a  general  neuropathic  constitution, 
to  hysteria,  etc.  In  such  cases  we  must  always  ascribe  great  value  to  the  general 
treatment,  such  as  diet,  manner  of  life,  baths,  iron,  and  nervines,  as  well  as  to  the 
special  treatment  directed  against  the  neuralgia;  and  the  same  holds  true,  of 
course,  in  the  neuralgias  occurring  in  diabetes,  gout,  and  syphilis.  Lastly,  we  may 
fulfill  the  causal  indication  in  the  malarial  neuralgias.  If  neuralgia  comes  on  at 
approximately  regular  intervals  in  persons  who  come  from  a  malarial  district,  and 


NEURALGIA  IN  GENERAL.  519 

who  perhaps  have  already  suffered  from  other  malarial  affections,  the  exhibition 
of  quinine  in  large  doses,  twenty  to.  forty-live  grains  (grm.  r  5-3*0;  at  once,  will 
usually  speedily  cut  short  the  attack.  In  obstinate  cases  in  which  quinine  does 
no  good,  we  should  try  arsenic,  as  Fowler's  solution.  In  many  toxic  neuralgias, 
too  from  lead,  mercury,  or  alcohol,  our  first  endeavor  in  treatment  should  be  to 
remove  the  cause  of  the  disease. 

In  all  cases  where  the  causal  treatment  can  not  be  carried  out,  or  where  it 
alone  is  not  sufficient,  we  must  consider  those  numerous  remedies  and  methods  of 
treatment  which  correspond  to  the  indicatio  morbi  and  to  the  synmtomatic  indica- 
tions. Starting  with  the  hypothesis  of  an  inflammatory  condition  of  the  nerve,  we 
have  often  tried  to  exert  a  favorable  influence  on  the  disease  by  local  derivatives, 
mustard  plasters,  irritating  embrocations,  such  as  spirits  of  mustard,  veratrine  oint- 
ment (two  and  a  half  per  cent.),  or  tincture  of  iodine,  or  by  blisters,  or  even  by  the 
cautery.  The  remedies  first  mentioned  are  used  only  in  mild  cases.  Vesicatories, 
placed  along  the  course  of  the  affected  nerve,  or  behind  the  ear  in  facial  neu- 
ralgia, sometimes  act  very  well  in  fresh  cases,  especially  those  of  a  "  rheumatic  " 
character.  We  resort  to  the  hot  iron  chiefly  in  old  and  very  severe  cases,  in 
which,  indeed,  especially  in  sciatica,  some  very  favorable  results  have  been  thus 
obtained. 

The  local  electrical  treatment  of  neuralgia  is  more  important  and  more  efficient 
than  the  remedies  mentioned.  Although  we  do  not  know  certainly  how  electricity 
acts,  still  it  is  unquestionably  of  teu  attended  with  great  success  in  the  treatment  of 
neuralgia.  We  many  times  secure  an  improvement  in  the  symptoms,  which  is  of 
course  temporary,  even  in  those  cases  where  the  special  cause  of  the  disease  is  not 
influenced  by  the  electricity,  although  in  idiopathic  neuralgias  in  fresh,  and  some- 
times even  in  old  cases,  we  can  often  obtain  a  complete  cure.  There  are  no  gen- 
eral rules  with  regard  to  the  methods  to  be  employed,  since  different  specialists 
have  their  own  favorite  methods.  The  following  forms  of  application  are  most  in 
use  and  are  most  to  be  recommended :  1.  Stabile  action  of  the  anode  of  a  constant 
current  on  the  affected  nerve-trunk  over  as  great  an  extent  as  possible,  especially 
on  any  painful  points.  We  must  entirely  avoid  any  great  variations  in  the  current 
or  interruptions  of  it.  We  gradually  increase  the  intensity  of  the  current  up  to 
medium  strength.  The  sittings  should  last  three  to  six  minutes,  and  sometimes 
even  longer,  and  must  be  repeated  daily.  2.  In  neuralgia  of  the  larger  nerves  we 
should  use  a  stabile  descending  (sometimes  ascending)  constant  current,  in  which 
the  anode  is  placed  on  the  most  central  point  of  the  nerve-trunk  available,  or  on 
the  vertebral  column,  and  the  cathode  on  different  peripheral  points.  3.  The 
faradic  current  also  frequently  acts  very  well.  We  faradize  the  nerve  either  with 
a  moderately  strong  "  increasing  "  current,  or  we  apply  the  wire  brush  to  the  skin 
over  the  affected  nerves.  The  latter  method  is  very  painful,  but  it  is  often  attended 
with  excellent  results.  4.  Some  electro-therapeutists,  like  Moritz  Meyer,  lay  stress 
upon  the  stabile  application  of  the  anode  of  the  constant  current  to  any  painful 
points  on  the  vertebral  column,  such  as  have  been  described  in  many  neuralgias 
by  Trousseau. 

As  a  general  rule,  it  is  always  well  to  begin  with  a  mild  and  very  cautious  use 
of  electricity,  and  not  to  go  on  to  the  stronger  currents  until  later.  Electricity 
often  acts  brilliantly  at  once,  during  the  attack  of  pain,  but  sometimes  no  improve- 
ment is  seen  until  after  several  sittings.  If,  after  two  or  three  weeks,  we  obtain 
no  result  at  all,  after  employing  different  methods  of  applying  electricity,  it  is  the 
best  plan  to  give  up  electrical  treatment  entirely  as  not  suited  to  the  case. 

In  the  treatment  of  neuralgia  we  must  consider  a  number  of  internal  remedies, 
as  well  as  electricity ;  some  of  these  act  symptomatically,  like  the  narcotics,  while 
others  have  obtained  the  reputation  of  having  a  specific  action.      Among  the. 


520  DISEASES  OF  THE  NERVOUS  SYSTEM. 

latter,  quinine  lias  decidedly  the  greatest  value.  In  severe  cases  quinine  may 
do  excellent  service,  not  only  in  malarial  neuralgias,  although  most  surely  in 
these,  hut  also  in  "idiopathic"  neuralgias.  It  is  in  these  cases  that  the  remedy  is 
given  in  large  doses.  We  begin  with  fifteen  to  thirty  grains  (grni.  1-2)  a  day, 
oest  given  in  one  dose,  and  in  severe  cases  we  may  increase  to  sixty  or  seventy-five 
grains  (grm,  -i-5)  or  more.  We  see  the  best  results  from  quinine  in  trigeminal 
neuralgia,  while  in  other  forms,  like  sciatica,  it  is  much  Jess  efficient.  Some  cures 
have  been  obtained  by  salicylate  of  sodium.  Antipyrine,  in  fifteen  to  thirty  grain 
(grm.  1-2)  doses,  antiiebrine,  in  three  to  seven  grain  (grm.  0 '25-0 -5)  doses,  and  phe- 
nacetine,  in  seven  to  fifteen  grain  (grm.  0  5-1)  doses,  have  lately  been  very  often 
used.  Next  in  rank  come  arsenic  and  bromide  of  potassium.  The  former  is  given 
in  pill  form  or  as  Fowler's  solution,  five  drops  three  times  a  day,  increasing  gradu- 
ally. Bromide  of  potassium  acts  only  in  large  doses,  forty-five  to  seventy-five  to 
a  hundred  and  fifty  grains  a  day  (grm.  3-5-10).  Among  the  many  other  remedies 
which  have  been  recommended,  we  may  mention  here  ergotine,  internally  and 
subcutaneously,  oil  of  turpentine,  oxide  of  zinc,  valerianate  of  zinc,  tincture  of 
gelsemium,  aconitine,  phosphorus,  iodide  of  potassium,  subcutaneous  injections  of 
osmic  acid,  ten  to  fifteen  minims  (grm.  0'5-l)  of  a  one-per-cent.  solution,  etc. 

In  all  severe  neuralgias  the  use  of  narcotics,  especially  of  morphine,  is  unavoid- 
able. Morphine  is  used  almost  exclusively  during  the  attack,  and  is  best  given  as 
a  subcutaneous  injection  of  one-twelfth  to  one-sixth  of  a  grain  (grm.  0-005-001)  in 
the  vicinity  of  the  painful  part.  The  anodyne  effect  almost  invariably  follows» 
but  in  obstinate  and  protracted  cases  the  patient  gradually  becomes  accustomed  to 
the  remedy.  We  must  then  resort  to  still  larger  doses,  and  these,  too,  finally  fail 
in  their  effect.  Among  the  victims  of  the  morphine  habit  we  find  many  patients 
who  have  suffered  or  who  still  suffer  from  severe  neuralgia,  so  that  we  must 
always  be  very  cautious  and  conservative  in  the  protracted  use  of  morphine.. 
We  should  be  especially  cautious  before  deciding  to  put  the  hypodermic  syringe 
into  the  patient's  own  hand.  Many  physicians  ascribe  not  only  a  palliative  but  a 
permanent  benefit  to  injections  of  morphine  in  neuralgia.  We  sometimes  see,  in 
fact,  that  mild  neuralgias  recover  under  the  exclusive  use  of  morphine  injections; 
but  these  are  probably  cases  of  spontaneous  recovery.  The  internal  use  of  mor- 
phine and  opium  preparations  is  decidedly  inferior  to  the  subcutaneous  adminis- 
tration in  certainty  and  rapidity  of  action.  The  external  application  of  narcotic 
ointments,  or  embrocations,  is  much  employed  in  practice,  but  it  appears  to  be  of 
advantage  only  in  milder  cases.  We  prescribe  ointments  with  extract  of  opium 
(one  to  ten),  extract  of  belladonna  (two  to  ten),  extract  of  opium  and  veratrine 
(one  part  of  each  to  twenty  of  simple  ointment),  etc.  We  may  also  use  chloroform 
(equal  parts  of  chloroform  and  oil  of  hyoscyamus)  and  ether.  Chloral  and  also 
paraldehyde  are  often  prescribed  in  chronic  neuralgias  for  their  hypnotic  effect. 
Croton  chloral  has  been  especially  recommended  in  neuralgia.  Finally,  we  must 
add  that  some  physicians  have  praised  the  anodyne  effect  of  subcutaneous  injec- 
tions of  atropine,  gr.  Vi2o  to  Veo  to  Vso*  ferm-  0-0005-0  "001-0 -003!)  at  a  dose, 
sometimes  even  in  cases  where  morphine  does  not  act. 

In  severe  cases  the  surgical  treatment  of  neuralgia  is  often  of  great  importance 
—the  section  of  nerves,  neurotomy,  or  the  excision  of  a  portion  of  the  nerve,  neu- 
rectomy—in  order  to  prevent  the  union  of  the  divided  nerve.  Without  doubt  this 
operation  is  often  attended  with  success ;  but  in  some  cases,  of  course,  it  has  no 
effect  at  all  on  the  disease,  or  else  the  neuralgia  returns  with  its  old  severity  after 
a  temporary  improvement.  We  can  understand  the  success  of  neurotomy  in  cases 
where  we  can  assume  that  the  cause  of  the  abnormal  sensory  irritation  is  peripheral 
to  the  point  of  section ;  but  observations  are  reported  in  literature  where  the  opera- 
tion has  had  a  favorable  influence  even  on  central  neuralgias.     The  operation  is 


THE  INDIVIDUAL  FORMS  OF  NEURALGIA.  521 

to  be  proposed  only  in  severe  cases,  where  all  other  remedies  have  been  tried  in 
vain,  and  the  patient  can  always  be  promised  the  possibility,  or  even  the  proba- 
bility, of  success,  but  never  the  certainty  of  it.  Besides  section  of  the  nerves, 
nerve  stretching-  has  lately  been  frequently  tried  in  neuralgia— sometimes,  but  not 
always,  with  distinctly  good  results. 

The  chief  question  as  to  the  use  of  baths  arises  only  in  the  treatment  of  neural- 
gias in  the  domain  of  the  nerves  of  the  extremities,  especially  in  sciatica,  and 
therefore  these  and  massage  will  be  spoken  of  more  in  detail  in  connection  with 
the  separate  forms  of  neuralgia. 

We  see,  then,  that  a  large  number  of  remedies  are  at  our  command  in  the  treat- 
ment of  neuralgia,  and  that  the  choice  among  them  is  not  always  easy.  In  any 
given  case  we  look  for  the  causal  indication,  and  try  to  fulfill  it  if  possible.  In 
the  many  cases,  however,  where  we  fail  to  find  this,  we  must  first  of  all  try  to 
alleviate  the  pain,  for  which  purpose,  if  external  derivatives  do  not  suffice,  our 
most  effective  remedy  is  morphine.  We  must  then  lay  out  a  special  plan  of  treat- 
ment. We  try  electricity,  or,  if  this  be  not  practicable,  one  of  the  other  remedies 
mentioned  above.  We  put  most  trust  in  quinine,  especially  in  fresh  cases ;  among 
other  remedies,  in  anaemic  persons,  arsenic,  and,  in  more  robust  persons,  bromide 
of  potassium  are  of  service.  If  all  these  and  similar  remedies  give  no  aid,  in 
proper  cases  we  may  still  hope  for  success  from  operative  interference,  or  else  we 
must  confine  ourselves  simply  to  a  purely  symptomatic  treatment  with  narcotics. 


CHAPTER  IV. 
THE   INDIVIDUAL   FORMS    OF   NEURALGIA. 

1.  Neuralgia  of  the  Trigeminus. 

{Prosopalgia.     Tic  douloureux,.     FothergilVs  1 'ace-ache.) 

iEtiology.— Trigeminal  neuralgia  is  one  of  the  commonest  and  most  impor- 
tant neuralgias.  In  its  origin  many  causes  and  predisposing  factors  of  all  sorts 
play  a  part,  as  we  have  learned  in  the  preceding  chapter.  Many  cases,  especially 
the  milder  ones,  come  from  taking  cold.  Sometimes  we  can  not  find  any  definite 
cause.  Malarial  neuralgias  are  very  often  localized  in  the  region  of  the  trigemi- 
nus. The  other  especial  causes  which  may  give  rise  to  trigeminal  neuralgia  are 
diseases  of  the  cranial  bones  and  periosteum,  very  often  diseases  of  the  teeth,  ca- 
ries, exostoses,  and  anomalies. in  development  and  position;  and  also  diseases  of 
the  nasal  and  frontal  cavities  as  well  as  of  the  middle  ear.  Romberg  found  an 
aneurism  of  the  internal  carotid,  pressing  on  the  Gasse rian  ganglion,  as  a  cause 
of  a  severe  and  incurable  case.  We  have  since  seen  a  precisely  analogous  case. 
Lastly,  excessive  use  of  the  eyes  is  not  infrequently  related  to  the  development  of 
trigeminal  neuralgia. 

Symptoms  and  Course.— The  attacks  of  pain  in  neuralgia  of  the  fifth  pair  are 
usually  quite  intense,  and  in  severe  cases  they  may  attain  a  most  distressing  and 
terrible  severity.  They  arise  either  entirely  without  cause,  or  from  some  slight 
influence,  like  washing,  taking  physical  exercise,  or  mental  irritation.  The  pain  is 
usually  limited  to  the  distribution  of  the  different  branches  of  the  trigeminus,  but 
it  sometimes  shoots  into  the  occiput,  the  back  of  the  neck,  the  shoulders,  etc.  We 
can  often  perceive  reflex  twitchings  in  the  face,  especially  blepharospasm,  and 
twitching  of  the  corners  of  the  mouth.  The  vaso-motor  disturbances  are  noticed 
at  first  as  abnormal  pallor,  but  later  usually  as  quite  an  abnormal  redness  of  the 


522  DISEASES  OF  THE  NERVOUS  SYSTEM. 

face  and  conjunctiva.  In  neuralgia  of  the  upper  two  branches  we  often  see,  dur- 
ing the  attack,  an  unusually  great  secretion  of  tears.  An  excessive  flow  of  saliva 
and  an  increased  secretion  from  the  nasal  mucous  membi'ane  are  more  rare. 
Sometimes,  but  still  quite  rarely,  we  see  herpetic  eruptions  in  the  course  of  the 
affected  nerve,  zoster  frontalis,  herpes  of  the  conjunctiva,  etc.  In  some  cases 
too,  more  severe  diseases  of  the  eyes,  belonging  to  the  category  of  neuroparalytic 
ophthalmia,  have  been  observed.  In  neuralgias  that  have  lasted  longer,  we  often 
see  still  further  trophic  disturbances:  changes  in  the  skin  and  subcutaneous  cellu- 
lar tissue,  the  hair  turning  gray  or  falling  out  in  the  frontal  region,  etc. 

Most  trigeminal  neuralgias  are  situated,  not  in  the  whole  distribution  of  the 
nerve,  but  only  in  one  or  more  of  its  branches  (see  Fig.  57,  page  513).  We  accord- 
ingly distinguish  :  1.  Neuralgia  of  the  first  branch  (ophthalmic  neuralgia) 
which  is  especially  frequent  as  supra-orbital  or  frontal  neuralgia.  In  this  we  find 
as  a  rule,  that  pressure  on  the  point  of  exit  of  the  nerve  at  the  supra-orbital  fora- 
men is  more  or  less  painful.  More  rarely  we  find  painful  points  also  on  the  nose, 
at  the  inner  angle  of  the  eye,  or  the  parietal  eminence,  etc.  2.  Neuralgia  of  the 
second  branch  (supra- maxillary  neuralgia)  is  most  frequent  in  the  distribution  of 
the  infra-orbital  nerve,  infra-orbital  neuralgia,  with  the  chief  painful  point  at  the 
infra-orbital  foramen,  and  others  on  the  zygoma,  on  the  upper  lip,  etc.  3. 
Neuralgia  of  the  third  branch  (infra-maxillary  neuralgia  ),  whose  most  frequent 
seat  is  in  the  territory  of  the  inferior  alveolar  nerve  ;  but  neuralgia  also  occurs  in 
the  temporal  region,  in  the  auriculo-temporal  nerve,  and  in  the  tongue,  in  the  lin- 
gual nerve.     The  chief  painful  point  is  at  the  mental  foramen. 

The  general  course  of  neuralgia  of  the  fifth  pair  differs  very  much  in  different 
cases.  We  see  all  forms,  from  the  mildest,  which  rapidly  passes  off,  to  the  sever- 
est and  incurable  types,  which  may  drive  the  patient  to  despair  and  even  to  sui- 
cide. In  general,  neuralgia  of  the  first  branch  usually  belongs  to  the  relatively 
milder  forms  ;  neuralgia  of  the  second,  and  especially  of  the  third  branch  to  the 
severer  forms.  Trousseau  has  termed  a  particularly  sevei'e  form  "  epileptiform 
neuralgia,"  although  we  can  find  no  definite  relation  between  this  disease  and  gen- 
uine epilepsy.  We  can  find  no  cause  for  epileptiform  neui'algia;  the  attacks  of  it 
come  on  with  the  greatest  intensity  either  after  brief  pauses  or  after  intervals  of 
weeks  and  months,  and  they  defy  all  attempts  at  cure  with  the  greatest  obstinacy. 
It  is  worthy  of  note  that  this  form  appears  in  individuals  with  the  neuropathic 
taint. 

Diagnosis. — In  all  pronounced  cases  the  diagnosis  of  trigeminal  neuralgia  is 
easy.  We  must  regard  accurately  the  distribution  of  the  pain,  its  paroxysmal  on- 
set, and  the  points  of  pressure.  Otherwise  in  a  superficial  examination  we  may 
of  course  confuse  it  with  inflammatory  affections  of  the  bones  and  periosteum, 
with  genuine  tooth-ache,  with  migraine,  and  with  other  forms  of  headache  and 
face-ache. 

Prognosis. — The  prognosis  is  never  to  be  made  with  complete  certainty.  It  is 
most  favorable  in  fresh  cases  which  have  a  manifest  cause,  which  may  be  removed, 
as  a  basis  ;  but  if  the  affection  is  due  to  a  coarse  anatomical  cause  which  can  not 
be  removed,  or  if  we  are  dealing  with  old  cases  "  which  have  become  habitual," 
the  prognosis,  unfortunately,  is  often  utterly  unfavorable. 

Treatment. — The  treatment  of  trigeminal  neuralgia  rests  entirely  upon  the 
principles  given  in  the  preceding  chapter.  In  searching  for  the  causal  indications 
we  must  look  chiefly,  in  neuralgia  of  the  second  and  third  branches,  for  diseased 
teeth,  and  also  in  all  cases  for  any  affections  of  the  nose,  of  the  frontal  sinuses,  or 
of  the  middle  ear.  Carious  teeth,  which  are  painful  and  which  seem  to  have  any 
relation  to  the  neuralgia,  should  always  be  removed,  and  any  of  the  other  affec- 
tions mentioned  are  to  be  treated  on  special  principles. 


THE  INDIVIDUAL  FORMS  OF  NEURALGIA.  523 

Of  other  remedies  we  use  first  of  all  electricity,  the  anode  to  the  painful  points, 
with  the  cathode  on  the  back  of  the  neck,  or  the  wire  brush,  etc. ;  we  also  use 
quinine,  Fowler's  solution,  and  in  severe  cases  narcotics.  In  cases  where  the  neu- 
ralgic attacks  come  on  with  approximate  regularity,  quinine  especially  often  does 
excellent  service  ;  we  give  fifteen  to  twenty  grains  (grm.  1-1  "5)  at  first,  two  or 
three  hours  before  the  expected  attack.  If  quinine  does  no  good,  we  try  arsenic 
in  not  too  small  doses,  and  if  these  remedies  are  unsuccessful  we  may  try  one  of 
the  other  drugs  recommended:  butyl  chloral  (croton  chloral)  in  two-  to  five-grain 
capsules  (grm.  0-l-0'3),  or,  according  to  Liebreich's  formula  : 

B  Croton  chloral gr.  Ixxv-  3  ijss.  (grm.  5-10) ; 

Glycerine 3     vj.  (grm.  20)  ; 

Aquae  destill 1     iv.  (grm.  120).     M. 

S.  One  or  more  tablespoonfuls  every  five  or  ten  miautes. 

We  may  also  give  tincture  of  gelsemium  sempervirens,  five  to  twenty  drops  several 
timesaday  ;  aconitine  in  pills  of  V300  to  Viso  °f  agrain  (grm.  0'0003-0-0005),  three 
to  five  times  a  day  ;  nitrite  of  amyl,  ammoniated  copper,  in  powders  of  one  or  two 
thirds  of  a  grain  (grm.  0*02-0"04),  oil  of  turpentine,  [cannabis  indica],  etc.  Special 
indications  for  all  these  remedies  can  not  be  given,  so  that  we  are  recommended 
simply  to  try  different  ones.  In  desperate  cases  Trousseau  has  tried  very  large 
doses  of  opium,  which  he  gradually  increased  until  he  gave  two  to  three 
drachms  (!)  (grm.  8-12)  a  day.  Sometimes  an  attack  may  be  diminished  or  short- 
ened by  compression  of  the  carotid. 

If  a  severe  neuralgia  persists  in  spite  of  rational  treatment  by  electricity  or 
drugs,  we  should  not  delay  too  long  in  proposing  to  the  patient  operative  treat- 
ment if  possible.  In  frontal  and  infra-orbital  neuralgia  especially  the  section  of 
the  nerve  is  a  comparatively  slight  operation,  which — of  course  with  many  failures 
— has  many  excellent  results  to  show.  The  full  description  of  the  technicalities  of 
the  operation,  as  well  as  the  description  of  nerve-stretching,  and  of  the  ligature  of 
one  carotid,  which  has  been  done  in  some  desperate  cases,  must  be  left  to  the  text- 
books on  surgery.  [Unfortunately  the  only  operations  that  promise  permanent 
benefit  are  the  more  serious  ones  of  resection  of  the  nerve  at  the  foramina,  at  the 
base  of  the  skull,  or  excision  of  the  Gasserian  ganglion. — K.] 

2.  Occipital  Neuralgia. 

Of  the  neuralgias  involving  the  sensory  region  of  the  upper  four  cervical 
nerves,  neuralgia  of  the  occipitalis  major  is  the  most  frequent  and  practically  the 
most  important.  Besides  the  factors  to  be  considered  in  all  neuralgias,  we  must 
pay  particular  attention,  in  regard  to  aetiology,  to  diseases  of  the  upper  cervical 
vertebrae — caries  and  new  growths.  The  painful  paroxysms  may  attain  the  great- 
est severity.  They  are  usually  located  in  the  two  occipital  nerves  at  once,  being 
accordingly  bilateral,  although  often  more  severe  on  one  side  than  on  the  other. 
Painful  points  are  most  frequently  found  midway  between  the  mastoid  process 
and  the  upper  cervical  vertebrae.  Vaso-motor  disturbances,  falling  out  of  the  hair, 
etc.,  have  been  often  observed. 

The  prognosis  is  comparatively  favorable  in  cases  which  have  no  severe  anatom- 
ical disease,  such  as  spondylitis,  as  a  basis.  The  most  efficient  remedies  are  strong 
cutaneous  irritants  to  the  back  of  the  neck,  vesicatories  in  fresh  cases,  the  constant 
current,  and  injections  of  morphine. 

Other  neuralgias  in  the  distribution  of  the  cervical  plexus  are  rare.  They 
occur  in  the  distribution  of  the  occipitalis  minor,  which,  according  to  Seeligmül- 
ler, is  quite  frequently  due  to  syphilis,  and  then  is  easily  cured  by  iodide  of  potas- 


524  DISEASES   OF  THE  NERVOUS  SYSTEM. 

sium,  and  in  the  distribution  of  the  great  auricular  and  the  supra-clavicular 
nerves.  A  phrenic  neuralgia  even  has  been  described,  in  which  the  pain  extends 
along  the  course  of  the  phrenic  nerve  to  the  insertion  of  the  diaphragm ;  but  this 
is  at  all  events  very  rare. 

3.  Neuralgia  in  the  Region  op  the  Brachial  Plexus. 

( Cervico-bracldal  Neuralgia.) 

Brachial  neuralgia  is,  on  the  whole,  rare,  and  it  is  hardly  ever  strictly  limited 
to  the  distribution  of  a  single  nerve.  In  general,  the  radial  and  ulnar  nerves  are 
rather  more  frequently  affected  than  the  median.  We  also  see  at  times  neuralgia 
of  the  internal  cutaneous  nerve.  In  regard  to  aetiology,  we  have  to  mention  first 
wounds  and  contusions  of  the  nerves,  and  also  cicatrices  and  foreign  bodies.  The 
amputation  neuralgias  also  belong  to  this  class.  Severe  neuralgia  in  which  the 
pain  may  extend  over  a  greater  part  of  the  whole  arm  is  sometimes  seen  after  in- 
jury of  the  fingers  (crushing,  cuts,  etc.).  In  some  of  these  cases  we  may  have  to  do 
with  an  ascending  neuritis,  starting  from  injury  of  a  small  nerve  branch ;  in  other 
cases  there  are  probably  cicatricial  contractions,  thickenings  of  the  neurilemma, 
or  small  neuromata  developing  after  the  injury,  which  excite  the  pains.  The  "  am- 
putation neuralgias,"  which  are  often  very  severe  in  amputation  stumps,  are  due  to 
neuromata  which  form  on  the  cut  ends  of  nerves.  Severe  neuralgia  often  arises 
from  pressure  on  the  brachial  nerves,  as  in  cases  of  tumors  in  the  axilla  (cancer, 
etc.),  aneurisms  of  the  aorta,  etc.  Rheumatic  neuralgia  may  also  occur.  Double 
brachial  neuralgia  should  always  excite  suspicion  of  disease  in  the  neighborhood  of 
the  upper  posterior  nerve  roots,  especially  of  cervical  pachymeningitis,  spondylitis 
of  the  lower  cervical  vertebrae,  etc. 

We  have  little  to  add  concerning  the  special  symptomatology  of  brachial  neu- 
ralgia. The  pain  is  usually  ascribed  to  the  whole  course  of  the  nerves  without 
being  very  exactly  localized,  as  we  have  stated.  Painful  points  are  sometimes 
found  over  the  brachial  plexus,  over  the  radial  on  the  external  surface  of  the 
upper  arm,  over  the  ulnar  in  the  sulcus  at  the  internal  condyle,  over  the  median 
at  the  inner  border  of  the  biceps,  and  where  the  cutaneous  nerves  emerge  from 
the  fasciae.  Vaso-motor  and  trophic  disturbances  have  sometimes  been  seen,  as 
"glossy  fingers,"  a  peculiar,  shiny,  atrophic  condition  of  the  skin  of  the  fingers. 
In  severe  neuralgia  a  pronounced  atrophy  of  the  whole  arm  has  also  been  observed. 
The  diagnosis  is  usually  easy ;  we  must  bear  in  mind  only  the  risk  of  confusion 
with  articular  affections. 

The  treatment  of  brachial  neuralgia  is  often  no  easy  task,  since  we  frequently 
have  to  do  with  protracted  and  obstinate  diseases.  The  causal  indications  should 
be  met  if  possible ;  besides  these  we  should  make  use  chiefly  of  electricity  (the  de- 
scending galvanic  current  along  the  affected  nerves).  We  may  also  use  narcotics, 
morphine,  cocaine,  sodic  salicylate  to  alleviate  pain,  antipyrine,  phenacetine,  etc. ; 
and  lastly  local  warm  peat  baths.  In  severe  cases  we  must  consider  the  pos- 
sibility of  surgical  interference,  such  as  nerve-stretching,  the  extirpation  of  cica- 
trices, etc. 

4.  Intercostal  Neuralgia. 

( Dorso-intercostal  Neuralgia.) 

The  neuralgias  of  this  class  are  almost  always  pure  intercostal  neuralgias,  since 
the  posterior  dorsal  branches  of  the  thoracic  nerves  are  only  exceptionally  in- 
volved. The  middle  intercostal  nerves,  from  the  fifth  to  the  ninth,  are  usually 
affected,  one  or  more  of  them  being  attacked  at  the  same  time.  The  affection 
is  much  more  frequent  on  the  left  side  than  on  the  right. 


THE  INDIVIDUAL  FORMS  OP  NEURALGIA.  525 

In  regard  to  aetiology,  it  is  important  to  remember  that  obstinate  intercostal 
neuralgias  are  often  a  symptom,  and  for  a  long  time  the  only  symptom,  of  severe 
organic  disease,  especially  affections  of  the  ribs;  diseases  of  the  vertebrae,  such  us 
caries  and  carcinoma;  diseases  of  the  cord,  such  as  tabes  dorsalis,  spinal  men- 
ingitis, and  tumors ;  and  aneurism  of  the  aorta.  Genuine  idiopathic  intercostal 
neuralgia,  however,  is  often  met  with,  as  well  as  these  symptomatic  forms,  espe- 
cially in  anaemic  and  nervous  women  and  girls  in  youth  and  middle  life.  Trau- 
matic lesions  of  the  intercostal  nerves  and  taking  cold  also  play  a  part  in  the 
aetiology. 

The  pain  in  intercostal  neuralgia  may  attain  a  remarkable  severity,  and  is 
usually  increased  by  any  considerable  movement  of  the  thorax.  Hence  the  patient 
avoids  deep  inspirations,  coughing,  loud  talking,  etc.,  as  much  as  possible.  We 
usually  find  three  painful  points — one  near  the  vertebral  column,  one  somewhere 
in  the  middle  of  the  nerve,  and  a  third  near  the  sternum  or  over  the  rectus  abdomi- 
nis. We  may  mention,  among  the  trophic  disturbances,  the  comparatively  fre- 
quent occurrence  of  herpes  zoster.  In  such  cases  we  probably  always  have  an 
actual  neuritis  of  one  or  more  nerves.  The  pain  precedes  the  eruption  of  zoster, 
or  comes  on  at  the  same  time  with  it.  It  often  lasts  for  a  long  time  after  the 
cutaneous  affection  has  healed.  The  formation  of  zoster  has  usually  been  con- 
sidered until  the  present  time  a  "  trophic  disturbance,"  but  recent  careful  anatom- 
ical investigations  (A.  Dubler)  favor  the  hypothesis  that  the  formation  of  vesicles 
arises  simply  from  a  direct  extension  of  the  inflammatory  process  from  the  ter- 
minal branches  of  the  nerves  to  the  skin.  It  is  worthy  of  note  that  the  attacks  of 
zoster  often  exhibit  a  certain  epidemic  and  sometimes  even  an  endemic  distribu- 
tion, so  as  to  suggest  an  infectious  agency.  The  almost  constant  swelling  of  the 
neighboring  lymph-glands,  in  the  axillae,  at  the  lower  border  of  the  pectoral  mus- 
cle, etc.,  perhaps  supports  this  view. 

The  course  of  intercostal  neuralgia  depends  chiefly  upon  the  aetiology  of  the 
affection.  Primary  neuralgias  are  often  quite  obstinate,  but  on  the  whole  they 
usually  give  a  favorable  prognosis.  The  differential  diagnosis  between  genuine 
intercostal  neuralgia  and  rheumatic  affections  of  the  muscles,  incipient  pleurisy, 
etc.,  is  not  always  easy.  In  these  cases  a  careful  physical  examination,  a  con- 
sideration of  the  localization  of  the  pain,  of  the  presence  of  painful  points,  and  of 
the  whole  course  of  the  disease,  are  needed  to  protect  us  from  errors. 

The  treatment  is  governed  by  the  general  rules  given  in  the  previous  chapter. 
Blisters  often  act  very  well  in  fresh  cases.  Electricity  is  given  by  the  faradic 
brush  or  the  constant  current;  with  the  latter,  the  cathode  is  placed  on  the  verte- 
bral column,  and  the  anode  on  the  lateral  and  anterior  painful  points,  using  quite 
a  strong  stabile  current.  In  severe  cases  we  can  not  avoid  injections  of  morphine. 
Herpes  zoster  heals  by  simple  treatment  with  salves  or  by  dusting  on  powders,  like 
one  part  of  zinc  oxide  to  two  of  starch. 

Mastodynia  {Neuralgia  of  the  Mammary  Gland). — Mastodynia  ("irritable 
breast "  of  Astley  Cooper)  is  to  be  considered  as  a  special  neuralgia  in  the  distribu- 
tion of  the  intercostal  nerves.  It  occurs  almost  solely  in  women,  after  the  age  of 
puberty,  and  is  a  very  painful,  distressing,  and  obstinate  affection.  The  pain  is 
either  continuous,  or  it  comes  on  in  separate  paroxysms,  sometimes  accompanied 
by  vomiting.  The  whole  breast  is  extremely  sensitive  to  the  touch.  We  know 
little  that  is  definite  as  to  its  aetiology.  Anaemia,  hysteria,  and  traumatic  action 
seem  to  have  some  influence  on  it.  We  sometimes  feel  little  nodules  in  the  breast, 
which  are  very  painful  (tubercula  dolorosa,  neuromata?),  and  which  may  some- 
times give  rise  to  the  suspicion  of  the  development  of  carcinoma. 

The  disease  may  last  for  years.  Treatment  is  difficult.  Warm  packs  to  the 
breast,  bandaging  the  breast,  and  especially  narcotics,  may  afford  relief.     Elec- 


526  DISEASES  OF  THE  NERVOUS  SYSTEM. 

tricity  may  be  of  distinct  service.  In  the  worst  cases  operative  interference  has 
been  attempted — amputation  of  the  breast,  or  extirpation  of  the  painful  nodules— 
but  its  results  are  uncertain. 

5.   Neuralgia  in  the  Region  op  the  Lumbar  Plexus. 

As  the  neuralgias  of  this  class  are  rare,  and  show  few  peculiarities,  we  will 
content  ourselves  with  a  brief  account  of  the  most  important  forms. 

Lumbo-abdominal  neuralgia  causes  pain  in  the  lumbar  region,  which  shoots 
into  the  buttocks,  the  hypogastrium,  and  the  genitals.  Crural  neuralgia  is  seated, 
in  part,  in  the  region  of  the  external  anterior  cutaneous  nerve  of  the  thigh,  and  in 
part  in  the  region  of  the  cutaneous  branches  of  the  crural  nerve,  the  internal  and 
middle  cutaneous.  Its  distribution  over  the  cutaneous  distribution  of  the  great 
saphenous  nerve,  the  inner  portion  of  the  calves,  and  the  inner  border  of  the  foot, 
is  especially  characteristic.  In  obturator  neuralgia  the  pain  extends  along  the 
inside  of  the  thigh,  down  to  the  vicinity  of  the  knee-joint  (see  Figs.  62  and  63, 
page  515). 

In  their  individual  characteristics,  all  these  neuralgias  agree  with  what  has 
been  said  in  the  previous  chapter.  The  diagnosis  is  not  always  easy,  and  we  must 
pay  special  attention  to  avoid  confusing  them  with  affections  of  the  bones  and 
joints,  with  lumbago,  renal  colic,  etc. 

6.    Sciatica. 

(Ischiatic  Neuralgia.     Malum  Cotunnil.) 

iEtiology. — Next  to  trigeminal  neuralgia,  neuralgia  of  the  sciatic  nerve  is  by 
far  the  most  frequent,  and  practically  the  most  important  form  of  neuralgia.  In 
contrast  to  most  of  the  other  neuralgias,  it  is  more  frequent  in  men  than  in 
women.  Cold,  wet,  and  over-exertion  of  the  leg  are  found  to  be  the  most  frequent 
»etiological  factors.  More  rarely  venous  stasis  in  the  pelvic  veins  (haemorrhoids; 
and  habitual  constipation  give  rise  to  the  development  of  sciatica.  We  see  symp- 
tomatic neuralgia  in  the  region  of  the  sciatic  nerve  in  pelvic  tumors,  caries  of  the 
sacrum,  and  analogous  affections.  Other  traumatic  influences,  and  compression 
of  the  nerve,  as  in  constant,  uncomfortable  sitting,  are  sometimes  evident  causes 
of  the  disease.  Pressure  of  the  gravid  uterus  on  the  sciatic  plexus  may  sometimes 
excite  sciatica,  and  in  women  it  has  been  seen  as  a  result  of  delivery  by  forceps. 

Symptoms  and  Course. — The  pain,  coming  on  usually  with  mild  prodromata 
and  gradually  increasing  to  severe  paroxysms,  generally  begins  at  the  posterior 
surface  of  the  thigh,  in  the  vicinity  of  the  sciatic  notch.  From  this  point  the 
lightning-like  pains  shoot  down,  usually  into  the  peroneal  region,  the  outer  part 
of  the  leg,  and  the  outer  border  and  top  of  the  foot,  or  more  rarely  into  the  tibial 
region,  the  sole  of  the  foot.  They  either  come  on  in  characteristic  neuralgic 
paroxysms,  or  they  are  more  continuous,  and  are  then  described  by  the  patient  as 
"  burning,"  "  boring,"  and  the  like.  They  are  often  worse  at  night.  In  severe 
cases  the  leg  can  scarcely  be  moved,  owing  to  the  pain,  so  that  walking  becomes 
very  difficult  or  almost  impossible,  and  the  affected  leg  is  kept  quiet  in  a  slightly 
flexed  position.  Very  often  the  pain  comes  on  after  long  standing  or  sitting. 
Painful  points  are  often  found  along  the  course  of  the  sciatic,  over  the  gluteus 
maximus,  or  at  its  lower  border,  in  the  popliteal  space  (tibial  nerve),  at  the  head 
of  the  fibula  (peroneal  nerve),  at  the  malleoli,  on  the  top  of  the  foot,  etc. 

Besides  the  pain,  we  often  find  other  disturbances  of  sensibility  in  the  affected 
leg,  such  as  paraesthesia,  hyperaesthesia,  or  slight  anaesthesia.  Reflex  muscular  ten- 
sion, tremors,  and  even  complete  clonic  spasms  have  been  repeatedly  observed  in 
severe  cases.     A  slight  stiffness  and  weakness  of  the  leg  are  very  often  found.     A 


THE  INDIVIDUAL  FORMS  OF  NEURALGIA.  527 

slight  atrophy  of  the  muscles  often  develops,  but  the  higher  degrees  of  atrophy- 
indicate  that  there  are  serious  anatomical  changes  in  the  nerve.  Eruptions  of 
zoster  have  been  repeatedly  observed,  but,  on  the  whole,  it  is  rare. 

The  disease  lasts  several  weeks,  although  sometimes,  in  many  obstinate  cases,  it 
continues  for  months  and  even  years;  but,  except  in  cases  which  have  an  incurable 
anatomical  lesion  as  an  underlying  cause,  the  termination  is  at  last  usually  favor- 
able.    Relapses  are,  of  course,  quite  frequent. 

Diagnosis. — The  diagnosis  of  sciatica  is  easy  in  the  majority  of  typical  cases,  but 
it  may  sometimes  be  quite  difficult.  It  is  chiefly  confused  with  lumbago,  an  acute 
coxitis,  nervous  coxalgia  {vide  infra),  and  psoas  abscess.  We  must  also  bear 
in  mind  the  occurrence  of  sciatic  pain  in  the  beginning  of  tabes  dorsalis.  In 
doubtful  cases  we  can  decide  only  after  the  most  careful  physical  examination, 
embracing  every  part  and  function,  and  by  considering  the  localization  of  the  pain 
and  of  the  painful  points. 

Treatment. — Sometimes  we  can  obtain  favorable  results  by  fulfilling  the  causal 
indication.  In  regard  to  this  we  may  mention  especially  the  improvement  of 
many  cases  of  obstinate  sciatica,  associated  with  habitual  constipation,  by  method- 
ical treatment  with  laxatives,  especially  by  the  springs  at  Marienbad,  or  Kissingen, 
and  also  improvement  after  the  removal  of  tumors,  foreign  bodies,  etc.,  when  they 
exist. 

In  regard  to  the  treatment  of  ordinary  sciatica,  we  must  first  take  care,  in  all 
severe  cases,  to  keep  the  leg  perfectly  quiet  and  in  a  good  position  during  the 
painful  paroxysm.  Usually  the  local  application  of  warmth,  warm  poultices,  or 
bandages,  is  grateful  to  the  patient.  Sometimes  a  vapor  bath  gives  real  relief. 
More  energetic  local  derivatives,  blisters,  or  even  local  blood-letting,  are  of  especial 
use  in  cases  of  "rheumatic  origin."  If  the  pain  be  very  severe,  a  subcutaneous 
injection  of  morphine  is  the  only  certain  remedy,  and  is  sometimes  indispensable. 
Embrocations  of  narcotics  are  also  frequently  prescribed  in  practice. 

Of  the  other  remedies  to  be  considered  we  may  mention,  in  the  first  place,  elec- 
tricity and  massage.  In  electrical  treatment  we  usually  employ  quite  strong 
descending  currents  with  large  electrodes,  which  we  let  act  on  the  nerve  for  five 
or  ten  minutes  a  day,  while  we  include  one  portion  of  the  nerve  after  another  in 
the  current.  Where  there  is  much  stiffness  in  the  leg,  we  open  and  close  the  cur- 
rent a  few  times,  in  order  to  excite  muscular  contraction.  Many  cases  are  suitable 
for  the  use  of  the  faradic  current,  especially  for  the  wire  brush.  Besides  elec- 
tricity, massage  has  often  given  excellent  results  in  sciatica.  Details  of  the  tech- 
nique to  be  employed  may  be  found  in  the  special  treatises  on  this  important 
method  of  treatment.* 

Besides  electricity  and  massage,  baths  deserve  special  consideration  in  tedious 
cases.  Good  results  are  often  obtained  from  the  indifferent  thermal  baths,  such  as 
Teplitz,  Wildbad,  and  Wiesbaden.  We  would  also  recommend  warm  local  douches 
and  hot  sand  baths,  like  Köstritz,  as  particularly  efficient. 

In  general,  we  can  promise  but  slight  results  from  the  very  many  internal 
remedies  recommended  against  sciatica,  but,  if  there  be  a  suspicion  of  syphilis,  we 
must  try  iodide  of  potassium.  Quinine  has  usually  no  effect  in  sciatica.  We  some- 
times see  somewhat  better  results  from  the  exhibition  of  sodic  salicylate,  anti- 
pyrine,  phenacetine,  etc.  We  have  also  very  rarely  seen  any  definite  action  from 
oil  of  turpentine,  which  is  much  used,  especially  in  England.  Some  good  results 
have  lately  been  obtained  by  injections  of  osmic  acid  (see  page  520). 

*  Busch,  "Allgemeine  Orthopädie,  Gymnastik  u.  Massage,"  Leipsic,  Vogel,  1882;  Schreiber, 
"  Praktische  Anleitung  zur  Behandlung  durch  Massage,"  Vienna,  18S3  [translated  by  Mendelson, 
Philadelphia,  1887] ;  Eeibmayr,  "Die  Massage  und  ihre  Verwerthung  in  der  prakt.  Medicin,"  Vienna, 
1883,  etc.  [Graham,  "  A  Treatise  on  Massage,"  New  York,  1890]. 


528  DISEASES  OF  THE  NERVOUS  SYSTEM. 

In  very  severe  and  obstinate  cases,  in  which  all  other  remedies  have  been  tried 
in  vain,  we  are  justified  in  proposing  to  the  patient  to  try  nerve-stretching.  This 
operation  has  been  attended  with  very  good  results  in  some  cases — but  unfortu- 
nately, of  course,  not  in  all.  Some  favorable  action  in  old  cases  has  been  ascribed 
to  the  use  of  the  hot  iron,  and  finally  it  may  be  mentioned  as  a  curiosity  that  dif- 
ferent observers  claim  to  have  obtained  a  recovery  from  sciatica  by  cauterization 
of  the  lobe  of  the  ear ! 

[Mention  should  be  made  here  of  a  method  of  treatment  advocated  by  Weir 
Mitchell,  which  is  occasionally  useful  in  other  forms  of  neuralgia  as  well  as  in 
sciatica.  It  consists  in  absolute  rest  of  the  leg  by  application  of  a  splint.  With 
this  he  combines  the  application  of  cold,  by  an  ice-bag  over  the  length  of  the 
nerve,  which  may  be  continued  for  a  number  of  hours. — E.] 

7.  Neuralgia  of  the  Genitals  and  the  Eectal  Region. 

Neuralgic  affections  of  the  parts  named  are  not  frequent,  but  still  a  number  of 
cases  have  been  described  by  different  observers.  The  pain  has  its  seat  either  in 
the  external  genitals,  or  in  the  urethra,  or  in  the  anal  and  perineal  region.  The 
most  frequent  form  is  spermatic  neuralgia  ("  irritable  testis  "  of  Astiey  Cooper), 
in  which  there  is  the  most  intense  pain  in  the  spermatic  cord  and  the  testicles, 
which  is  almost  always  associated  with  an  extreme  hyperesthesia  of  the  affected 
parts.  The  treatment  of  this  form  of  neuralgia  by  narcotics  and  electricity  is  often 
unsuccessful,  so  that  in  severe  cases  resort  has  sometimes  been  had  even  to  cas- 
tration. In  women,  genuine  uterine  and  ovarian  neuralgia  seem  to  occur  espe- 
cially as  one  symptom  of  hysteria. 

Coccyodynia  is  the  name  of  a  form  of  severe  pain  in  the  coccygeal  region,  seen 
usually  in  women,  which  is  much  increased  by  walking,  defecation,  etc.  The 
affection  is  so  distressing  that  operations  have  been  repeatedly  performed  on 
account  of  it  to  remove  or  to  cut  around  the  coccyx.  We  have  twice  seen  this 
same  symptom  as  a  complication  of  tabes. 


CHAPTER  V. 

NEURALGIA   OF   THE    JOINTS. 

{Articular  Neuroses.) 

Neuralgia  of  the  joints,  first  described  by  the  English  physician  Brodie,  was 
first  generally  known  in  Germany  after  Esmarch  proved,  by  publishing  many 
observations,  that  apparently  severe  and  very  painful  diseases  of  the  joints  are 
often  found,  at  the  basis  of  which  there  is  no  discoverable  anatomical  disease  of 
the  joint,  and  which  we  are  therefore  justified  in  regarding  as  nervous  affections. 
Since  the  localized  pain  in  the  joint  is  the  chief  symptom  in  most  of  the  cases  of 
this  class,  the  term  "neuralgia  of  the  joints"  has  been  quite  fitly  chosen,  al- 
though we  do  not  find  here  such  typical  and  paroxysmal  attacks  of  pain  as  in 
genuine  neuralgia,  and  although,  too,  a  number  of  other  symptoms  are  usually 
present,  which  are  not  seen  in  genuine  neuralgia. 

We  see  neuralgia  of  the  joints  chiefly  in  nervous  hysterical  persons,  and  there- 
fore more  frequently  in  women  and  girls  than  in  men. 

We  can  very  often  make  out  a  psychical  cause  for  the  origin  of  the  disease. 
The  affection  is  often  caused  by  injuries  which  affect  the  joint,  and  which  would 
be  in  themselves  without  significance,  if  they  were  not  associated  with  a  decided 


NEURALGIA  OF  THE  JOINTS.  529 

fright,  and  did  not  direct  the  patient's  thoughts  to  the  affected  limb.  Articular 
neuralgias  do  not,  therefore,  belong  to  the  pure  neuralgias,  but  are  symptoms  of 
hysteria  (traumatic  hysteria).  At  any  rate,  the  name  of  articular  neurosis  is  more 
suitable  than  that  of  articular  neuralgia. 

Either  immediately  after  such  an  occurrence,  or  often  only  some  weeks  later, 
the  patient  begins  to  complain  of  pain.  The  knee-  or  hip-joint  is  almost  always 
affected,  only  rarely  the  joints  of  the  upper  extremity.  The  pain  is  continuous, 
but  it  is  more  severe  at  times,  especially  on  motion,  or  mental  excitement.  At 
other  times,  especially  if  the  patient's  attention  be  diverted  from  the  trouble,  it 
seems  to  diminish  to  a  considerable  extent.  It  is  mainly  localized  in  the  joint,  but 
the  whole  leg  is  often  painful.  Patients  are  usually  very  sensitive  to  pressure,  or 
jarring,  and  sometimes  we  may  even  discover  some  painful  points  on  pressure  over 
the  joints.  The  patients  can  not  walk  at  all,  or  at  least  walking  is  very  painful, 
and  they  limp  badly.  In  severe  cases,  especially  if  the  excessive  sympathy  of  those 
about  them  reduces  the  patients'  power  to  resist  their  suffering,  they  become  com- 
pletely bedridden  for  weeks  or  months.  There  is  usually  a  decided  weakness  in 
the  affected  leg,  which  is  almost  always  associated  with  great  muscular  rigidity 
and  tension.  The  leg  is  extended,  or  flexed  and  rotated  inward,  in  just  the  same 
way  as  in  genuine  coxitis. 

The  diagnosis  of  articular  neurosis  is  often  quite  difficult,  but  it  is  almost 
always  possible,  with  long  observation  of  the  case.  At  first,  of  course,  the  disease 
often  seems  to  be  a  severe  affection  of  the  joint,  on  account  of  the  great  pain,  the 
rigid  position,  and  the  complete  inability  to  use  the  leg.  The  experienced  physi- 
cian, however,  is  usually  struck  by  the  absence  of  any  definite  physical  changes  in 
the  joint,  especially  of  swelling,  and  also  by  the  changes  in  the  intensity  of  the 
complaint,  by  the  influence  of  mental  emotion  on  the  suffering,  and  finally  by  the 
general  impression  he  gets  from  the  patients,  the  way  they  behave,  and  the  con- 
trast between  their  great  complaint  and  their  usual  (though,  of  course,  not  invari- 
able) good  appearance,  appetite,  and  undisturbed  sleep.  In  doubtful  cases  an 
examination  under  chloroform  is  very  advisable.  With  this,  contractures  appar- 
ently the  most  severe  vanish,  and  the  normal  character  and  mobility  of  the  joint 
become  plainly  manifest. 

As  soon  as  the  diagnosis  of  an  articular  neurosis  is  made  the  treatment  has 
quite  definite  indications.  All  embrocations,  poultices,  bandages,  etc.,  are  to  be 
laid  aside.  The  patient  is  to  be  brought  to  the  conviction  that  she  can  walk,  if  she 
will  only  first  learn  to  will  to  walk  again.  We  make  the  patient  practice  walk- 
ing methodically  ;  these  attempts  at  first  prove  very  poor  and  apparently  distress- 
ing to  the  patient,  but  they  often  lead  to  better  results  very  speedily.  These  exer- 
cises are  very  much  aided  by  electrical  treatment  of  the  joint,  passing  a  strong 
current  through  it  or  using  the  faradic  brush,  and  also  by  local  cold  douches  and 
massage.  Under  some  circumstances  the  use  of  internal  remedies  may  be  indi- 
cated, in  many  cases  with  regard  only  to  the  mental  condition.  We  give  iron  to 
anaemic  patients,  and  also  the  nervines.  (See  the  chapters  on  hysteria  and  trau- 
matic neuroses.) 


34 


530  DISEASES  OF  THE  NERVOUS  SYSTEM. 


CHAPTER  VI. 

HABITUAL     HEADACHE. 

( Cejphalma.     Cephalalgia.) 

In  addition  to' the  neuralgias,  we  must  speak  here  of  hahitual  or  "nervous" 
headache,  an  affection  which  is  very  often  met  with  in  practice,  but  in  regard  to 
whose  precise  causes  or  whose  special  nature  our  knowledge  is  still  in  many  re- 
spects very  unsatisfactory. 

We  do  not  term  the  symptomatic  headaches,  so  often  observed,  "nervous  head- 
aches." The  former  come  on  in  acute  febrile  infectious  diseases,  in  pronounced 
general  anaemia,  in  the  different  anatomical  diseases  of  the  brain  and  its  mem- 
branes, of  the  skull,  the  frontal  sinuses,  etc.  Just  as  little  ought  we  to  confuse 
habitual  headache  with  other  painful  and  well-characterized  affections,  especially 
typical  neuralgia  in  the  frontal  branch  of  the  trigeminus,  or  in  the  occipital  nerves, 
or  with  genuine  migraine  or  hemicrania  {vide  infra).  Those  cases,  rather,  belong 
to  this  class  in  which  the  headache  forms  to  a  certain  degree  a  disease  in  itself, 
and  is  the  sole,  or  at  least  the  chief,  symptom  of  which  the  patient  complains,  and 
for  which  he  seeks  aid.  We  know  no  definite  anatomical  basis  for  these  cases. 
We  usually  assume  disturbances  of  circulation  and  of  the  fine  nutrition  as  the  spe- 
cial causes  of  headache  ;  but  it  is  only  in  a  very  few  cases  that  anything  definite 
as  to  the  form  of  these  changes  can  be  stated.  We  can  also  state  little  that  is 
definite  as  to  the  special  place  where  these  pains  arise.  We  do  not  know  whether 
painful  irritations  may  arise  in  the  brain-substance  itself.  The  cerebral  meninges, 
however,  especially  the  dura  mater,  are  decidedly  sensitive,  and  hence  they  may 
usually  be  regarded  as  the  special  seat  of  headache. 

Tbe  manifold  character  of  the  circumstances  under  which  headaches  arise 
renders  it  probable  that  the  causes  of  headache  are  very  different  in  different 
cases.  We  have  to  do  either  with  persons  who  seem  perfectly  healthy  in  other  re- 
spects, or  with  weak  and  anaemic  people,  or  again  with  robust,  very  well  nour- 
ished, "  full-blooded  "  persons  with  red  faces.  Hence  we  look  for  the  cause  of  the 
pain,  according  to  the  general  constitution  of  the  patient,  either  in  an  abnormal 
hyperaemia  or  anaemia  of  the  brain  and  its  membranes— a  hyperaemic  or  anaemic 
cephalalgia.  We  very  often  find  headache,  too,  as  the  chief  symptom  in 
nervous,  neurasthenic  people — neurasthenic  cephalalgia.  To  this  class  belong 
especially  people  who  are  overworked  physically  and  mentally — scholars,  offi- 
cials, students  before  an  examination,  etc.  If  we  believe  that  we  can  make  out 
"rheumatic"  influences,  such  as  taking  cold,  or  toxic  influences,  such  as  alcohol, 
nicotine,  or  chronic  lead  poisoning,  we  speak  of  a  rheumatic  or  a  toxic  cephalal- 
gia. Patients  with  habitual  headache  often  suffer  at  the  same  time  from  chronic 
gastric  disturbances  or  habitual  constipation,  so  that  the  latter  disorders,  in  many 
cases,  stand  perhaps  in  a  causal  relation  to  the  headaches.  Finally,  it  is  a  very 
important  point  that  headache  is  sometimes,  associated  with  chronic  diseases  of 
neighboring  organs,  especially  of  the  nose,  the  naso-pharynx,  and  the  ear.  In  very 
many  cases,  however,  we  can  find  no  definite  cause  at  all  for  the  affection,  so  that 
we  have  to  do  with  a  genuine  idiopathic  disease.  It  is  worthy  of  mention,  merely, 
that  in  not  very  rare  cases  a  pronounced  hereditary  predisposition  to  habitual 
headache  seems  to  exist.  [One  of  the  frequent  causes  of  persistent  headache  is  eye- 
strain due  to  the  persistent  unconscious  effort  of  the  muscles  of  accommodation 
to  overcome  some  error  of  refraction,  such  as  astigmatism  or  hypermetropia.  In 
some  cases  this  eye-strain  may  be  associated  with  insufficiency  of  some  of  the  ex- 
ternal muscles  of  the  eye.     This  condition  may  be  associated  with  normal  visual 


HABITUAL  HEADACHE.  531 

power,  so  that  the  patient  often  maintains  that  there  can  be  no  trouble  with  the 
eyes  ;  this  is  especially  true  where  the  refractive  error  is  slight,  less  than  one 
dioptric.  It  is  therefore  essential  in  every  case  of  persistent  headache,  to 
have  a  thorough  examination  of  the  eyes,  in  order  to  determine  whether  there 
is  astigmatism  or  hypermetropia.  The  adjustment  of  proper  glasses,  or,  in  rare 
cases,  tenotomy  of  some  of  the  external  muscles,  will  often  give  marked  relief, 
although  even  in  these  cases  attention  must  also  be  paid  to  the  general  condi- 
tion.— K.] 

Habitual  headache  is  a  chronic  disease.  It  may  last  for  months  or  years,  or 
even  through  the  whole  life,  either  being  present  continually,  or,  what  is  more 
frequent,  coming  on  in  separate  attacks  and  lasting  several  hours  or  days.  These 
attacks  sometimes  come  without  any  evident  cause,  but  they  may  often  be  referred 
to  definite  influences,  to  mental  excitement,  physical  exertion,  errors  of  diet,  etc. 
The  pain  is  felt  either  in  the  forehead  or  in  the  occiput,  or  sometimes  over  the 
whole  head.  It  is  sometimes  limited  to  a  definite  and  quite  sharply  defined  part 
of  the  head.  The  precise  form  of  the  pain  is  described  in  different  ways,  either 
as  boring,  or  tearing,  or  as  if  the  head  were  pressed  together  from  without,  or  as 
if  it  would  split  open.  In  many  cases  the  intensity  of  the  pain  is  not  great;  there 
is  merely  a  dizziness  and  a  feeling  of  ''pressure"  in  the  head,  but  in  other  cases 
the  pain  is  very  severe.  In  such  cases  there  is  also  at  times  a  pronounced  hyper- 
Eesthesia  of  the  skin  of  the  head,  so  that  it  may  cause  pain  even  to  touch  the  hair. 

The  general  health  is  almost  always  disturbed  in  headache.  The  patient  can 
not  work,  he  is  often  ill-tempered  and  irritable,  and  he  loses  his  appetite.  We 
sometimes  see  more  marked  gastric  symptoms,  especially  nausea  and  vomiting, 
and  sometimes  copious  perspiration.  Severe  cases  of  the  disease  are  of  great  im- 
portance, since  by  an  attack  the  patient  is  rendered  almost  wholly  unable  to 
attend  to  his  business. 

The  treatment  of  headache  is  always  a  difficult  task.  In  the  first  place,  of 
course,  we  should  try  to  adapt  our  treatment  to  the  aetiology  of  the  disease  if  it  is 
evident.  We  should  therefore  never  neglect  to  make  a  thorough  examination  of 
all  the  organs  which  are  to  be  considered  (nose,  ear,  stomach,  heart,  kidneys  [eyes], 
etc.).  In  such  a  case  the  existing  primary  disease  requires  special  treatment.  If 
there  is  any  suspicion  of  syphilis,  which  must  especially  be  considered  if  the  pain 
is  worse  at  night,  we  must  first  of  all  try  iodide  of  potassium.  For  anaemic  pa- 
tients we  prescribe  iron,  arsenic,  a  country  residence,  strengthening  diet,  etc. 
We  order  full-blooded  persons,  especially  if  they  also  suffer  from  indigestion,  to 
drink  bitter  waters,  or  we  send  them  to  health  resorts  like  Marienbad  or  Carlsbad. 
Nervous  headaches  in  hysterical  and  neurasthenic  patients  require  a  rational  gen- 
eral treatment :  electricity,  general  faradization,  galvanism  to  the  head,  or  to  the 
sympathetic,  cold-water  cures,  etc.  For  persons  who  have  overworked,  we  most 
urgently  advise  complete  physical  and  mental  rest.  We  send  them  to  the  country 
or  to  try  sea-bathing. 

The  number  of  symptomatic  remedies  recommended  to  relieve  headache  is 
very  considerable.  In  most  of  the  tedious  cases  the  patient  himself  has  learned 
to  know  his  disease  perfectly  well.  Many  know  that  there  is  no  remedy  for 
"  their  old  headaches,"  and  they  merely  desire  to  rest,  waiting  until  the  pain  ceases 
of  itself.  Others  have  become  accustomed  to  employ  certain  domestic  remedies : 
they  put  poultices  on  the  head,  take  a  cold  or  a  hot  foot-bath,  put  a  mustard  plas- 
ter to  the  back  of  the  neck,  bathe  the  forehead  with  cologne- water,  bind  a  towel 
tightly  about  the  head,  drink  strong  tea,  smell  ammonia  or  "  smelling-salts,"  etc. 
We  sometimes  see  good  results,  although  frequently  we  do  not,  from  the  internal 
remedies.  These  may  be  used,  either  during  the  attack  or  for  a  longer  period,  to 
prevent  the  return  of  the  pain.     There  are  no  special  indications  for  the  different 


532  DISEASES  OF  THE  NERVOUS  SYSTEM. 

remedies,  so  that  we  must  try  to  see  which  one  is  the  most  efficacious.  Antipyriue 
is  most  used  of  late  in  doses  of  seven  to  twenty  grains  (grm.  0-5-l-5).  Its  efficacy 
in  migraine  is  undoubted,  but  it  sometimes  gives  distinct  relief  in  other  forms  of 
headache.  We  may  also  use  autifebrine,  in  doses  of  three  to  seven  grains  (grm. 
0 '25-0 -5),  phenacetine,  seven  to  fifteen  grains  (grm.  0"5-l),  and  quinine,  six  to  ten 
grains  (grm.  0  3-0  75).  In  headaches  which  come  on  after  exposure  to  cold, 
draughts,  etc.,  we  may  try  sodic  salicylate,  half  a  drachm  to  a  drachm  (grm.  2-4). 
Of  otlier  remedies  we  may  mention  paullinia  serbilis  (guarana,  which  contains  caf- 
feine), in  seven  to  thirty  grain  powders  (grm.  0*5-2),  three  to  six  one-grain 
ergo  tine  pills  (grm.  0*05)  a  day  in  hyperaemic  headache,  potassic  bromide  half  a 
drachm  to  a  drachm  (grm.  2-4),  arsenic,  [cannabis  indica],  etc. 

Electrical  treatment  {vide  supra)  has  given  decidedly  good  results  in  many 
cases,  but  we  must  always  begin  it  with  great  caution,  and  try  first  what  method 
is  best  borne.  Cold-water  cures,  too,  are  sometimes  beneficial,  or  residence  in  the 
country,  at  the  seashore,  or  in  the  mountains. 

We  can  sometimes  do  the  patient  good  service  with  the  remedies  mentioned, 
but  in  other  cases  the  evil  obstinately  defies  all  attempts  at  cure.  Then,  however, 
the  patient  has  still  the  encouragement  left  that  the  disease  often  ceases  at  last 
spontaneously  in  advanced  age,  after  lasting  years  and  years. 


CHAPTER  VII. 
ANOMALIES   OF   THE    SENSE   OF   SMELL. 

Anomalies  of  smell,  which  depend  iipon  a  disease  of  the  olfactory  nerve  itself, 
or  of  its  terminal  apparatus,  or  of  its  central  termination,  are  not  infrequently 
observed,  but  they  have  no  great  practical  interest.  It  is  well  known  that  only 
the  upper  two  tui'binated  bones  and  the  upper  part  of  the  septum  of  the  nares,  the 
olfactory  region,  are  supplied  by  fibers  of  the  olfactory  nerve.  The  branches  of  the 
olfactory  nerve  pass  into  the  cranial  cavity  through  the  openings  of  the  lamina 
cribrosa  and  form  the  trunk  of  the  nerve.  Nothing  certain  is  known  as  to  their 
further  central  course.  The  hemianosmia,  in  affections  of  the  posterior  portion 
of  the  internal  capsule,  is  worthy  of  notice,  and  also  the  anosmia  of  the  left  nasal 
cavity  which  has  sometimes  been  claimed  to  be  observed  in  cases  where  there  was 
also  right  hemiplegia  and  aphasia. 

In  testing  the  sense  of  smell,  we  use  substances  which  do  not  at  the  same  time 
irritate  the  sensory  fibers  of  the  trigeminus  in  the  nasal  cavity.  The  best  sub- 
stances to  use  are  cologne-water,  ethereal  oils,  such  as  oil  of  cloves  or  oil  of  berga- 
mot,  oil  of  turpentine,  camphor,  musk,  valerian,  asafcetida,  etc. 

Hyperesthesia  of  the  sense  of  smell  (hyperosmia)  makes  itself  manifest  either 
by  a  remarkably  fine  perception  of  odors,  or  by  an  abnormal  sensitiveness  to  them. 
The  latter  symptom  is  often  noticed,  especially  in  the  hysterical.  Patients  have 
headaches,  or  attacks  of  fainting,  from  slight  odors,  which  healthy  persons  notice 
but  little.  Subjective  sensations  of  smell  (hallucinations  of  smell)  are  quite  fre- 
quent among  the  insane,  and  sometimes  during  the  aura  of  an  epileptic  attack. 

A  diminution  of  the  power  of  smell  (olfactory  anaesthesia,  anosmia)  is  also  not 
infrequent.  We  see  it  in  the  different  diseases  of  the  nose — coryza.  etc. ;  also  in 
affections  of  the  base  of  the  skull,  such  as  tumors,  and  acute  and  chronic  menin- 
gitis, which  involve  the  trunk  of  the  olfactoiw  sympathetically,  and  also  in  cere- 
bral disease,  tumors,  etc.,  and  most  frequently  in  severe  hysteria.  In  far-advanced 
tabes  dorsalis  we  have  sometimes  found  pronounced  anosmia,  dependent,  perhaps, 


ANOMALIES  OF  THE  SENSE  OF  TASTE. 

upon  an  atrophy  of  the  olfactory  nerve.  It  is  important  to  state  that  in  every 
marked  enfeeblement  of  the  smell  the  "taste"  for  many  forms  of  food  suffers, 
since  it  is  well  known  that  their  "aroma,"  as  in  roast  meats,  wines,  and  tin:  differ- 
ent sorts  of  cheese,  is  due  chiefly  to  the  co-existing  sensations  of  smell. 

The  treatment  of  anomalies  of  smell  almost  always  coincides  with  the  treatment 
of  the  primary  disease.  In  case  the  disturbance  of  smell  makes  special  interfer- 
ence desirable,  we  can  try  electrization  of  the  nasal  mucous  membrane,  or  painting 
it  with  a  one-per-cent.  solution  of  nitrate  of  strychnine  in  olive-oil. 


CHAPTER  VIII. 
ANOMALIES   OF   THE    SENSE    OF   TASTE. 

Sensations  of  taste  are  obtained  from  two  nerves — the  glossopharyngeal,  and 
the  lingual  nerve  from  the  third  branch  of  the  trigeminus.  The  glossopharyn- 
geal is  the  nerve  of  taste  for  the  posterior  third  of  the  tongue  and  the  palate,  the 
lingual  for  the  anterior  two  thirds  of  the  tongue.  The  gustatory  fibers  of  the  lin- 
gual, all,  or  at  least  a  great  part  of  them,  pass  over  to  the  chorda  tympani,  and 
reach  with  this  the  trunk  of  the  facial ;  they  do  not  remain  in  the  facial,  how- 
ever, as  many  pathological  experiences  have  most  plainly  shown,  but  they  finally 
come  back  to  the  trigeminus,  and,  probably  chiefly  by  the  great  superficial  petrosal 
nerve  and  the  Vidian  nerve  to  the  spheno-palatine  ranglia,  in  this  way  they  pass 
to  the  second  branch  of  the  trigeminus.  There  may  be  some  other  channels,  how- 
ever, by  which  the  gustatory  fibers  finally  unite  again  with  the  trigeminus,  and 
enter  the  brain  with  its  trunk.  We  know  nothing  definite  as  to  their  further 
course  and  their  central  termination. 

Hyperesthesia  of  taste  is  rare,  and  it  has  been  seen  almost  exclusively  in  the 
hysterical.  Paresthesia  of  taste  is  sometimes  found  in  patients  with  facial  paraly- 
sis, who  complain  of  an  abnormal  taste  in  their  mouths.  In  the  insane,  too,  sub- 
jective sensations  of  taste  (hallucinations  of  taste)-may  occur.  Anaesthesia  of  the 
gustatory  nerves  (gustatory  anaesthesia,  ageusia)  is,  however,  quite  frequent.  As 
follows  from  what  has  gone  before,  this  may  be  seen :  (1)  In  affections  of  the 
peripheral  terminal  organs  of  the  gustatory  nerves,  as  in  disease  of  the  mucous 
membrane  of  the  tongue ;  (2)  in  affections  of  the  glossopharyngeal,  such  as  com- 
pression ;  (3)  in  affections  of  the  lingual  nerve,  and  of  the  trigeminus  within  the 
cranial  cavity ;  (4)  in  affections  of  the  chorda  tympani,  from  diseases  of  the  mid- 
dle ear ;  (5)  in  affections  of  the  facial  nerve  between  the  entrance  of  the  chorda 
tympani  and  the  geniculate  ganglion;  but  we  know  from  experience  that  any 
obstacle  to  conduction  in  this  nerve,  above  or  below  the  points  named,  causes 
no  disturbance  of  the  sense  of  taste.  Central  disturbances  of  taste  have  been 
observed  in  affections  of  the  posterior  portion  of  the  internal  capsule.  Disturb- 
ances of  taste  are  very  common  in  hysteria  and  allied  conditions  (traumatic  neu- 
roses, etc.). 

The  test  of  the  sense  of  taste  must  be  performed  separately  for  all  the  different 
varieties  of  the  sensation  of  taste,  since  partial  paralyses  of  taste  are  not  infre- 
quent. The  test  is  performed  by  putting  small  amounts  of  the  substance  to  be 
tasted  in  solution  on  the  tongue  with  a  glass  rod  or  a  brush.  The  anterior  and  pos- 
terior parts  are  to  be  tested  separately.  A  solution  of  quinine  or  tincture  of  nux 
vomica  serves  as  a  test  for  bitter,  a  solution  of  sugar  for  sweet,  vinegar  or  dilute 
muriatic  acid  for  sour,  and  a  solution  of  common  salt  for  salt.  We  may  also  use 
as  a  test  for  taste  the  well-known  galvanic  taste,  which  is  strongest  at  the  anode, 


534 


DISEASES  OF  THE  NERVOUS  SYSTEM. 


but  is  also  detected  at  the  cathode  in  even  very  weak  currents,  and  hence  is  so 
often  noticed  from  by -currents  in  galvanizing  the  head,  neck,  etc. 

An  accurate  diagnosis  as  to  the  seat  and  cause  of  disturbances  of  taste  can  be 
made  only  by  considering  the  other  symptoms  which  are  also  present.  Direct 
treatment  may  best  be  employed  by  the  aid  of  electricity 


SECTION  II. 
Diseases  of  the  Motor  Nerves. 

CHAPTER  I. 
GENERAL  REMARKS  UPON   THE   DISTURBANCES   OF   MOTILITY. 

1.  Paralysis. 

General  Classification  of  Paralyses.— By  "paralysis  "  we  mean  the  loss  of  vol- 
untary motion  in  the  muscles  of  the  body  controlled  by  the  will.  We  usually  dis- 
tinguish between  the  complete  loss  of  the  power 
of  active  motion  (paralysis)  and  the  mere  weak- 
ening of  it  (paresis).  In  complete  paralysis  of 
any  part  of  the  body,  or  of  a  single  muscle,  the 
slightest  voluntary  motion  can  not  be  produced 
in  it;  while  in  paresis  in  a  diseased  part  certain 
movements  are  still  possible,  but  they  are  more 
or  less  below  the  normal  in  strength,  extent,  atid 
duration. 

In  every  portion  of  the  tract  that  leads  from  the 
motor  portions  of  the  cortical  gray  matter  of  the 
brain  to  the  muscles — that  is,  in  every  part  of  the 
so-called  great  "cortico-muscular  conduction-path" 
or  ''  pyramidal  tract " — disease  may  lead  to  paraly- 
sis if  it  takes  away  from  the  part  affected  its  power 
to  conduct  voluntary  motor  irritations.  Every  de- 
struction or  inhibition  of  function  of  the  motor  cen- 
ters in  the  cerebral  cortex,  with  whose  integrity  the 
initiation  of  voluntary  innervation  is  associated, 
must  also  lead  to  a  paralysis  in  the  corresponding 
muscular  region.  Finally,  it  is  conceivable,  at  least 
a  priori,  that  diseases  of  the  muscles  may  also  lead 
to  a  paralysis,  since  the  muscles  may  either  have 
their  contractile  substance  injured,  or  lose  their 
power  to  respond  by  a  contraction  to  any  nervous 
irritation  that  reaches  them ;  but  an  absolute  con- 
firmation of  such  "  myopathic  paralyses  "  is  associ- 
ated with  great  difficulties,  because  diseases  of  the 
special  muscular  substance  can  scarcely  be  sepa- 
rated from  diseases  of  the  terminal  branches  and 
terminal  apparatus  of  the  motor  nerves. 
If  we  represent  to  ourselves  briefly  the  precise  course  of  the  chief  tract  for 
exciting  voluntary  movements,  as  far  as  it  is  now  known,  we  must  put  the  begin- 


Fig.  64. — Horizontal  section  through 
the  right  cerebral  hemisphere, 
NC.  Caudate  nucleus.  Th.  Optic 
thalamus.  LK.  Lenticular  nu- 
cleus (first,  second,  and  third  di- 
visions). vS.  Anterior  limb  of  the 
internal  capsule.  hS.  Posterior 
limb  of  the  internal  capsule.  Fa. 
Fibers  belonging  to  the  facial 
nerve.  Pi).  Pyramidal  tract  (mo- 
tor). S.  Sensory  tract  (probably 
cutaneous  nerves  and  those  of 
special  sense).   0.  Occipital  lobes. 


REMARKS  UPON  THE   DISTURBANCES  OP  MOTILITY. 


>35 


ning  of  this  tract,  according  to  all  recent  experiments,  in  the  region  of  the  central 
convolutions  of  the  cerebrum  and  of  the  paracentral  lobule.  Here  we  find  the  so- 
called  psycho-motor  centers  (see  the  details  in  the  chapter  on  cerebral  localization), 
from  which  the  motor  libers  in  the  corona  radiata  converge  and  pass  downward. 
The  latter,  after  they  have  united  into  quite  a  compact  bundle,  enter  the  internal 
capsule,  which  they  traverse  obliquely.  As  we  see  in  a  horizontal  section  through 
the  cerebral  hemispheres  (see  Pig.  64),  the  internal  capsule  consists  of  two  limbs 
— an  anterior,  between  the  lenticular  and  the  caudate  nuclei,  and  a  posterior, 
between  the  lenticular  nucleus  and  the  optic 
thalamus.  The  two  limbs  form  an  obtuse 
angle,  opening  outward,  whose  top — that  is, 
the  junction  of  the  anterior  and  posterior 
limbs  of  the  internal  capsule — is  termed  the 
"  knee  of  the  capsule."  The  motor  tract  (Py) 
lies  in  the  posterior  limb  of  the  internal  cap- 
sule about  the  posterior  end  of  its  middle 
third.  In  this  it  runs  downward  rather 
obliquely,  so  that  in  the  upper  part  of  the 
internal  capsule  it  lies  somewhat  farther  for- 
ward than  in  the  lower.  From  the  internal 
capsule  the  pyramidal  tract  enters  the  crusta. 
It  lies  first  in  the  third  quarter,  counting  from 
the  inside,  then  farther  down  in  the  middle 
third  of  the  crusta  (see  Pig.  65),  and  from  this 
point  it  passes  into  the  anterior  half  of  the 
pons.  In  the  pons  the  fibers  of  the  pyram- 
idal tract  are  somewhat  separated,  but  they 
come  together  below  it  into  the  compact  bundle  of  the  pyramids  on  the  anterior 
surface  of  the  medulla.  At  the  lower  end  of  the  pyramids  the  decussation  of 
the  (lower)  motor  pyramids  takes  place — that  is,  the  motor  fibers  of  each  pyramid 
pass  over,  for  the  most  part,  into  the  lateral  column  of  the  opposite  half  of  the 
spinal  cord,  and  here  form  the  distinct  bundle  of  the  lateral  pyramidal  tract  (PyS, 
see  Figs.  66  and  67).  A  small  part  of  the  pyramids,  which  sometimes  seems  to  be 
entirely  wanting,  remains  uncrossed,  and  passes  downward  in  the  anterior  column 


Fig.  65.— Transverse  section  through  the 
crura  cerebri  in  secondary  degeneration 
of  the  right  pyramidal  tract.  (From 
Charcot.)  sn.  Substantia  nigra,  p.  The 
degenerated  and  therefore  translucent 
pyramidal  tract.  III.  Oculo  -  motor 
nerves.    AS.  Aqueduct  of  Sylvius. 


fyS 


Fig.  66. 


Fig.  67. 


Fig.  66.— Transverse  section  through  the  cervical  enlargement  of  the  spinal  cord.  PyS.  Lateral  pvramidal 
tract.    PyV.  Anterior  pyramidal  tract  (in  this  case  present  only  on  one  side). 

Fig.  67.— Transverse  section  through  the  lumbar  enlargement.  Pi/S.  Lateral  pyramidal  tract.  (The 
anterior  tract  is  no  longer  present  in  the  lumbar  portion  of  the  cord.) 

of  the  cord  on  the  same  side  as  the  so-called  anterior  pyramidal  tract  (PyV,  Fig. 
66).  From  the  lateral  column,  or  the  anterior  column  of  the  cord,  the  motor  fibers 
pass  into  the  anterior  gray  columns  of  the  cord,  and  are  here  directly  connected 
with  the  large  motor  ganglion-cells  of  the  anterior  cornua.     The  anterior  root- 


536  DISEASES  OF  THE  NERVOUS  SYSTEM. 

fibers  pass  out  from  these  gang-lion-cells,  as  is  well  known,  and  become  the  ante- 
rior spinal  roots  of  the  peripheral  nerves.  Through  the  latter  the  motor  impulses, 
coming  from  the  cerebrum,  finally  reacb  the  special  motor  apparatus,  the  volun- 
tary muscles. 

Tbe  long  motor  tract,  just  described,  the  cortico-muscular  path  or  the  pyram- 
idal tract,  has  been  quite  accurately  determined  in  its  details  by  the  results  of 
pathological  observations  (Tiirck,  Charcot),  and  investigations  into  the  history  of 
its  development  (Flechsig).  It  forms,  at  all  events,  the  chief  path  for  the  conduc- 
tion of  voluntary  innervation.  It  is  possible  that  there  are  other  motor  paths  of 
conduction  besides  this  tract,  but  we  know  nothing  definite  concerning  them. 

If  we  pay  attention  to  the  course  of  the  motor  tracts  described,  we  shall  easily 
understand  certain  peculiarities  in  the  distribution  of  motor  paralyses,  which  are 
of  great  importance  in  diagnosis.  Since  the  motor  centers  for  separate  parts  of  the 
body,  such  as  the  face,  the  arm,  or  the  leg,  are  separated  from  one  another  in  the 
cerebral  cortex,  and  are  distributed  over  a  comparatively  large  surface,  as  we  shall 
see  more  fully  later  on,  it  is  easily  explained  why  affections  of  the  cortex,  if  they 
are  not  very  extensive,  may  lead  to  paralysis  of  only  a  single  part  of  the  body. 
We  call  such  an  isolated  paralysis  of  one  part  of  the  body  monoplegia,  and  thus 
we  speak  of  a  cortical  facial  or  brachial  monoplegia.  Farther  downward  in  the 
brain,  in  the  internal  capsule  and  the  crus  cerebri,  however,  as  we  have  seen,  all 
the  motor  fibers  are  collected  into  one  bundle,  whose  diameter  takes  up  compara- 
tively little  space.  Hence  we  comprehend  that  any  disease  of  the  brain,  which  is 
situated  in  this  part  of  the  motor  tract,  may  easily  make  this  tract  incapable  of 
conduction  throughout  its  whole  extent,  or  at  least  throughout  the  greatest  part 
of  it.  The  result  must  be,  then,  a  more  or  less  complete  paralysis  of  the  facial 
muscles,  the  arm,  and  the  leg  at  the  same  time — that  is,  of  the  entire  half  of  the 
body — a  form  of  paralysis  which  is  termed  hemiplegia  or  unilateral  paralysis.  We 
may  note  here  that,  as  a  result  of  the  passage  of  the  motor  fibers  to  the  other  half 
of  the  cord  in  the  decussation  of  the  pyramids,  the  paralysis  must  develop  on  the 
side  of  the  body  opposite  to  the  focus  of  disease  in  the  hrain.  Farther  down  in 
the  medulla  and  the  cord  the  fibers  coming  from  both  hemispheres,  and  belonging 
to  the  two  sides  of  the  body,  lie  quite  near  each  other.  Since  many  diseases  of  the 
cord  have  a  tendency  to  affect  the  two  halves  of  the  cord  at  once,  or  gradually  to 
extend  over  the  whole  transverse  section  of  the  cord,  a  simultaneous  paralysis  of 
the  corresponding  portion  of  the  two  sides  of  the  body  will  readily  arise  as  a  result 
of  this.  This  form  of  paralysis  we  call  paraplegia.  Diseases  in  the  cervical  cord 
may  have  as  a  result  a  paralysis  of  all  four  extremities  or  of  the  two  arms — cervi- 
cal, brachial,  or  superior  paraplegia;  diseases  in  the  dorsal  and  lumbar  cord  a 
paraplegia  of  the  two  legs — inferior  paraplegia,  often  called  simply  "  paraplegia," 
without  further  prefix.  In  affections  of  the  peripheral  nerves  we  have,  of  course, 
again  a  limitation  of  the  paralysis  to  the  region  of  the  affected  nerve.  The  paraly- 
sis may  be  quite  extensive  in  diseases  of  a  nervous  plexus — paralysis  of  a  periph- 
eral plexus ;  or  it  may  confine  itself  wholly  to  the  region  of  a  single  nerve,  or  even 
of  a  single  branch  of  the  nerve — paralysis  of  a  peripheral  nerve. 

We  will  have  to  add  many  more  details  to  what  has  just  been  said,  but  as  a 
fundamental  principle  we  may  now  note  that  hemiplegia  is  the  chief  form  of 
cerebral  paralysis,  while  paraplegia  is  the  chief  form  of  spinal  paralysis.  Mono- 
plegias are  tisually  either  cortical  cerebral  paralyses,  or  peripheral  paralyses. 

General  iEtiology  of  Paralysis.— The  kind  of  lesion  which  leads  to  paralysis 
may,  in  the  different  cases,  be  very  diverse.  From  easily  understood  reasons  we 
can  very  rarely  decide  as  to  the  kind  of  lesion  from  the  intensity  and  extent  of 
the  paralysis,  but  only  from  the  manifest  serological  factors,  from  the  develop- 
ment and  course  of  the  paralysis,  from   other  morbid  symptoms  that  are  also 


BEMARKS  UPON  THE  DISTURBANCES  OF  MOTILITY.  537 

present,  etc.  In  general,  we  may  divide  the  paralyses  into  two  groups,  according 
to  the  nature  of  their  cause:  into  paralyses  from  causes  that  can  be  discovered 
anatomically,  and  into  the  so-called  functional  paralyses,  in  which  no  anatomical 
cause  for  the  paralysis  can  be  found;  but  since  our  anatomical,  and  especially  our 
histological,  methods  of  investigation  have  become  better  developed  and  are  more 
employed,  the  domain  of  functional  paralyses  has  become  gradually  more  and 
more  restricted,  and  a  definite  anatomical  cause  has  now  been  found  for  many 
paralyses  which  were  once  regarded  as  functional. 

All  the  diseases  of  the  nervous  system  may  be  anatomical  causes  of  paralysis, 
if  they  lie  in  a  spot  where  they  damage  or  destroy  the  paths  of  motor  conduction. 
Inflammation,  degeneration,  new  growths,  haemorrhages,  and  severe  disturbances 
of  circulation,  with  their  results,  especially  embolic  and  thrombotic  softening,  are 
found  in  the  brain,  the  cord,  and  the  peripheral  nerves,  and  under  some  circum- 
stances give  rise  to  the  appearance  of  paralysis.  Mechanical  lesions  of  the  nervous 
system  also  play  a  great  part  in  the  pathogenesis  of  paralysis,  especially  traumatic 
injuries,  and  compression  of.  the  brain,  the  cord,  and  the  peripheral  nerves  by 
swellings,  new  growths,  and  other  diseases  in  their  vicinity. 

We  also  know  certain  toxic  substances  which  produce  paralysis  from  their  per- 
sistent action  on  the  organism.  Of  these  toxic  paralyses,  lead  paralysis  is  the  most 
important  in  its  clinical  relations ;  but  other  poisonous  substances,  such  as  copper, 
arsenic,  and  certain  vegetable  alkaloids,  may  cause  paralysis.  In  regard  to  lead 
paralysis  {vide  infra),  which  was  once  considered  a  purely  functional  paralysis, 
we  now  know  that  anatomical  changes  form  its  basis.  These  can  be  plainly  made 
out,  especially  in  the  peripheral  nerves. 

We  may  group  a  large  number  of  paralyses  together  under  the  term  of  "  paraly- 
sis after  acute  diseases."  Since  in  these  cases  we  always  have  to  do  with  acute 
infectious  diseases,  we  may  assume,  as  their  most  probable  cause,  certain  changes 
in  the  nervous  system,  sometimes  in  the  brain,  but  more  frequently  in  the  cord  or 
the  peripheral  nerves,  which  stand  in  direct  relation  to  the  specific  infectious 
material.  There  seem  to  be  chemical  poisons  ("  ptomaines  ")  which  form  in  the 
body  in  infectious  diseases,  and  cause  degeneration  of  certain  nerve  fibers,  in  the 
same  way,  for  example,  as  lead.  We  most  frequently  see  paralysis  appear  after 
diphtheria,  diphtheritic  paralysis  (vide  infra),  or  more  rarely  after  typhoid,  small- 
pox, dysentery,  the  acute  exanthemata,  etc.  The  paralyses  which  may  arise  in 
certain  chronic  infectious  diseases,  especially  in  syphilis  and  tuberculosis,  usually 
have  another  origin.  Here  we  usually  have  to  do  with  the  specific  morbid  product 
itself  (gumma,  tubercle),  which  may  invade  various  parts  of  the  nervous  system. 

Those  paralyses  which  come  on  most  manifestly  because  of  exposure  to  cold 
are  termed  paralyses  from  exposure  to  cold,  or  "refrigeratory,"  or  frequently 
"  rheumatic  "  paralyses.  Although  many  spinal  diseases,  like  myelitis,  may  pei'- 
haps  be  referred  to  exposure  to  wet  or  cold,  we  usually  reckon  among  rheumatic 
paralyses  only  certain  peripheral  paralyses,  like  that  in  the  region  of  the  facial 
nerve.  Tbe  functional  disturbance  of  the  nerves  in  these  cases  probably  depends 
upon  mild  inflammatory  changes  in  them  produced  by  cold,  and  is  accordingly  of 
an  anatomical  and  not  merely  of  a  functional  nature. 

There  are,  however,  quite  a  comprehensive  group  of  paralyses  which  we  must 
to-day  still  term  functional  paralyses.  To  this  class  belong  the  hysterical  paralyses, 
the  paralyses  from  psychical  causes,  like  paralysis  from  fright,  the  "  paralyses  from 
imagination,"  etc.  We  shall  learn  to  recognize  these  more  fully  in  the  chapter  on 
hysteria. 

In  conclusion,  we  must  bear  in  mind  the  "reflex  paralyses,"  whose  a?tiology  is 
not  yet  fully  explained — that  is,  paralyses  which  come  on  in  the  course  of  diseases 
of  certain  internal  organs,  especially  of  the  intestine,  and  of  the  urinary  and 


53S  DISEASES  OF  THE  NERVOUS  SYSTEM. 

sexual  organs.  An  attempt  has  been  made  to  explain  their  origin,  from  analogy 
with  well-known  physiological  experiments,  by  the  idea  that  a  "  reflex  inhibition  " 
is  excited  in  certain  motor  regions  by  a  sensory  irritation  arising  in  the  diseased 
organs,  a  theory  which  has  not  yet  been  fully  confirmed.  Leyden's  hypothesis  is 
somewhat  more  probable,  but  it  is  by  no  means  proved  beyond  a  doubt.  Accord- 
ing to  it  the  paralyses  of  this  class  are  explained  by  an  ascending  neuritis,  arising 
from  the  organs  originally  affected  (see  the  chapter  on  neuritis).  Generally 
speakiug,  the  whole  conception  of  "  reflex  paralyses  "  is  still  far  from  clear,  and 
we  will  do  well  to  be  extremely  guarded  in  their  diagnosis.  Lepine  has  also 
regarded  the  paralysis  of  the  arm  of  the  affected  side,  seen  in  some  cases  of  empy- 
ema, especially  after  operative  interference,  as  a  "  reflex  paralysis,"  an  explanation 
which  may  be  proper  in  some  cases,  but  in  regard  to  which  we  should  be  the  more 
cautious,  as  metastatic  abscesses  of  the  bi'ain  are  not  very  infrequently  found  in 
empyema  (see  the  chapters  on  purulent  meningitis  and  cerebral  abscess). 

General  Symptomatology  of  Paralyses. — We  can  recognize  the  existence  of  a 
paralysis,  except  from  the  patient's  statements  as  to  the  impossibility  of  perform- 
ing certain  motions  and  functions,  only  by  a  careful  and  thorough  physical  exam- 
ination of  the  power  of  voluntary  motion.  This  examination  in  patients  with 
nervous  disease  must  extend  to  all  parts  of  the  body,  and  demands  an  accurate 
knowledge  of  all  the  movements  that  can  normally  be  executed  by  the  different 
joints,  and  of  the  muscles  and  nerves  requisite  to  produce  them.  In  the  descrip- 
tion of  the  different  single  forms  of  paralysis  we  will  go  more  into  detail  in  regard 
to  the  anomalies  of  motion  to  be  observed. 

In  each  individual  case  of  paralysis  some  other  symptoms  must  be  considered 
besides  immobility — first  the  condition  of  the  paralyzed  muscles,  and  then  certain 
accompanying  symptoms  that  are  often  present  with  the  paralysis. 

In  regard  to  the  first  point,  the  trophic  condition  of  the  pai'alyzed  muscle  is  of 
the  greatest  diagnostic  and  practical  importance.  In  comparing  a  large  number 
of  paralyses,  a  very  evident  difference  in  this  respect  strikes  us  at  once.  We  see 
on  the  one  hand  paralyses  where  the  paralyzed  muscles  retain  their  normal  vol- 
ume and  their  normal  state  of  nutrition  entirely,  or  almost  entirely,  for  years,  and 
on  the  other  hand  we  see  cases  in  which  there  is  a  considerable  atrophy  in  the 
paralyzed  muscles  in  a  few  weeks  or  months.  This  difference  is  so  effectual  that 
all  the  last-named  paralyses  have  been  classed  together  under  the  name  of  "  atro- 
phic paralyses."  Since  muscular  atrophy  does  not  occur  in  every  case  of  paralysis, 
it  can  not  be  simply  the  result  of  the  rest  and  inactivity  of  the  muscles,  but  it  must 
have  its  special  cause. 

If  we  once  more  represent  to  ourselves  the  whole  course  of  the  motor  tracts, 
from  the  cerebral  cortex  to  the  voluntary  muscles,  we  shall  remember  that  the 
nerve-fibers  through  this  long  route  undergo  a  single  interruption— namely,  by 
the  interposition  of  the  large  ganglion-cells  of  the  anterior  cornua  of  the  gray 
matter  of  the  spinal  cord.  Clinical  and  anatomical  experience  teaches  us  that,  in 
all  those  paralyses  where  the  cause,  that  is,  the  break  in  conduction  of  the  motor 
fibers,  lies  in  the  first  portion,  that  is,  between  the  cortex  and  the  cells  in  the  ante- 
rior cornua,  there  is,  as  a  rule,  no  atrophy,  or  only  a  slight  amount  of  atrophy,  in 
the  paralyzed  muscles,  while  in  those  paralyses  where  the  cause  is  situated  in  these 
ganglion-cells  themselves,  or  in  the  portion  of  the  motor  ti-act  peripheral  to  them, 
a  pronounced  muscular  atrophy  rapidly  develops.  The  only  possible  interpretation 
of  this  fact  is,  that  the  large  motor  ganglion-cells  of  the  anterior  cornua  have,  as 
we  express  it,  a  trophic  influence  on  the  muscles.  If  these  cells  are  intact,  and  the 
conduction  from  them  to  the  muscles  is  not  interrupted,  the  muscles  keep  approxi- 
mately their  normal  condition  of  nutrition,  even  if  they  are  paralyzed,  while  an 
affection  of  the  ganglion-cells  themselves,  or  an  interruption  of  conduction  in  the 


REMARKS  UPON  THE  DISTURBANCES  OF  MOTILITY.         539 

peripheral  nerves,  rendering  the  transmission  of  the  trophic  influences  from  the 
cells  to  the  muscle  impossible,  necessarily  results  in  an  atrophy  of  the  muscles. 
This  atrophy  is  not  confined  merely  to  the  muscles  separated  from  their  "  trophic 
center,"  that  is,  from  the  ganglion-cells  in  the  anterior  cornua  of  the  cord,  as  we 
must  note  here,  but  the  nerves  proceeding  downward  from  the  point  of  the  lesion 
also  take  part  in  the  atrophy.  Since  this  atrophy,  both  of  nerve  and  muscle,  is 
associated  with  a  destruction  of  tissue  to  be  more  fully  described  later — a  genuine 
"  degeneration  "  of  the  fibers — we  speak  of  a  "  degenerative  atrophy  "  of  the  nerves 
and  muscles,  in  contrast  to  the  simple  muscular  atrophy  which  occurs  iu  almost 
all  severe  diseases,  in  starvation,  etc.  The  degeneration  of  the  nerves  is,  of  course, 
not  evident  to  our  sight  and  touch  during  life,  but  it  is  proved,  as  we  shall  soon 
see,  by  certain  changes  in  their  electrical  excitability. 

From  the  above  statements  the  following  extremely  important  points  in  the 
anatomical  diagnosis  of  paralysis  are  at  once  evident  :  that  in  cerebral  paralyses 
there  is  never  a  degenerative  atrophy  in  the  paralyzed  muscles  ;  that  atrophy  is 
present  in  spinal  paralyses  only  when  the  large  ganglion-cells  in  the  anterior 
cornua  of  the  cord,  belonging  to  the  muscles,  are  destroyed  or  injured  in  their 
functions  by  the  cause  of  the  paralysis  ;  but  that  in  all  long-continued  peripheral 
paralyses  a  degenerative  atrophy  of  the  paralyzed  muscles  and  nerves  must  inev- 
itably develop.  These  fundamental  principles  may  suffice  for  the  present  ;  fur- 
ther deductions  from  them  must  he  postponed  until  the  special  chapters  on  the 
various  forms  of  pai^alysis. 

We  observe  a  further  distinction  in  the  condition  of  the  paralyzed  muscles  if 
we  perform  passive  motion  in  the  paralyzed  parts.  There  are  paralyses  where  we 
can  perform  passive  motion  in  the  paralyzed  parts  at  any  joint  with  perfect  ease 
and  freedom,  and  without  perceiving  the  slightest  resistance.  We  term  such 
paralyses  "flaccid  paralyses,"  but  there  are  also  paralyses  where  passive  motion 
meets  with  considerable  muscular  resistance,  so  that  it  can  be  performed  only  with 
a  certain  greater  or  less  amount  of  exertion,  or  only  within  certain  limits,  or  not 
at  all.  This  difficulty  in  performing  passive  motion  may  have  different  causes. 
It  is  most  frequently  caused  by  the  development  of  persistent  shortening  in  the 
paralyzed  muscles  themselves,  or  in  their  antagonists  (the  so-called  contractures), 
which  prevent  the  free  performance  of  passive  motion.  In  other  cases  there  is  no 
special  contracture,  but  the  paralyzed  muscles  exhibit  a  peculiar  rigidity.  There 
are  all  sorts  of  muscular  contractions,  which  either  are  to  be  regarded  as  symptoms 
of  direct  motor  irritation  {vide  infra),  or  have  a  reflex  origin.  Paralyses  in  which 
the  performance  of  passive  motion  is  hindered  by  such  muscular  contractions  are 
termed  "spastic  paralyses."  The  details  of  all  these  symptoms  will  be  spoken  of 
in  the  special  chapters. 

Finally,  in  every  case  of  paralysis,  we  must  consider  the  other  nervous  symp- 
toms which  accompany  it,  since  these  may  also  be  of  great  importance  in  judging 
of  the  cause  of  the  paralysis.  We  must  first  of  all  investigate  the  condition  of 
the  reflexes  (vide  infra)  in  the  paralyzed  parts,  from  which  many  conclusions  can 
be  drawn  as  to  the  seat  of  the  lesion  which  causes  the  paralysis.  We  must  also 
test  the  state  of  the  sensibility,  both  in  the  skin  and  in  the  muscles  themselves. 
Certain  attendant  trophic  and  vaso-motor  symptoms  are  also  to  be  regarded.  The 
skin  over  the  paralyzed  parts  sometimes  appears  cyanotic,  or  marble-like ;  it  feels 
cool,  is  oedematous,  and  sometimes  is  peculiarly  dry,  hard,  and  scaly. 

2.  Symptoms  of  Motor  Irritation. 
As  we  have  termed  the  symptoms  of  motor  deficiency  "  paralysis,"  we  group 
the  symptoms  of  motor  irritation  in  general  together  under  the  name  of  "spasm." 
We  mean  by  this  all  the  morbid  movements  occurring  in  the  muscles  involunta- 


540  DISEASES  OF  THE  NERVOUS  SYSTEM. 

rily  and  even  against  the  will.  Although  we  may  find  spasm  in  the  smooth  mus- 
cles, which  generally  are  not  controlled  by  the  will,  as  in  spasm  of  the  bronchial 
muscles,  spasm  of  the  vessels,  etc.,  we  will  concern  ourselves  here  only  with  the 
spasmodic  movements  in  the  voluntary  muscles.  We  must  look  for  the  cause  of 
these  in  abnormal  irritation  exerted  in  some  way  on  the  motor  tracts,  but  we 
know  very  little  of  the  precise  nature  and  character  of  this  irritation  in  most 
cases.  The  abnormal  irritation  often  acts  directly  on  the  motor  nervous  region, 
as  in  the  frequent  spasms  in  affections  in  the  neighborhood  of  the  cortical  motor 
centers;  but  the  motor  irritations  often  seem  to  be  excited  secondarily  tln'ough 
some  reflex  channel — reflex  spasms. 

For  a  long  time  two  kinds  of  spasm  have  been  distinguished  symptomatically. 
We  term  those  spasms  clonic  where  the  abnormal  muscular  contraction  lasts 
only  a  short  time,  and  then  is  interrupted  by  a  short  period  of  relaxation,  to  come 
on  again  afresh.  The  affected  parts  of  the  body  are  thus  put  in  a  constant  con- 
vulsive motion.  In  distinction  from  this  we  term  those  abnormal  muscular  con- 
tractions tonic  spasms  where  the  muscle  remains  spasmodically  contracted  for  a 
longer  time — minutes,  hours,  or  days.  The  affected  part  of  the  body  is  thus  kept 
motionless  in  some  abnormal  position.  Both  forms  of  spasm,  however,  show 
many  transitions  and  combinations,  so  that  we  must  often  speak  of  "tonic-clonic  " 
spasms. 

A  more  careful  examination  of  the  symptoms  of  motor  irritation,  however, 
gives  a  still  greater  number  of  different  forms.  We  will  here  group  together  the 
most  important  varieties  of  morbid  involuntary  movements  without  giving  a  com- 
pletely exhaustive  review  of  the  manifold  forms  of  spasm. 

1.  Epileptiform  convulsions  are  severe,  and  usually  clonic  spasms,  at  times 
tonic-clonic,  spread  over  the  whole  body  or  limited  to  one  half  or  one  portion  of 
the  body.  By  them  the  whole  body  or  the  part  affected  is  put  into  violent 
motion,  usually  thrashing  and  shaking  movements.  The  pure  epileptic  spasm  in 
epilepsy  is  the  type  of  this  form  of  spasm,  but  precisely  analogous  spasms,  "  epi- 
leptiform" spasms,  are  seen  in  organic  diseases  of  the  brain,  in  hysteria,  etc. 

2.  Rhythmical  contractions  in  single  groups  of  muscles  are  sometimes  seen  in 
certain  cerebral  diseases,  such  as  apoplexy  and  sclerosis,  and  also,  as  we  have  lately 
observed,  after  acute  myelitis.  In  these  the  part  of  the  body  affected  is  put  in 
motion  by  continuous,  separate,  weaker  or  stronger  thrusts,  which  follow  one 
another  in  a  regular  rhythm.  Rhythmical  contractions  are  also  seen  as  precur- 
sors or  at  the  end  of  epileptiform  spasms. 

3.  Trembling  motions,  or  tremor,  as  we  say  in  ordinary  parlance,  are  moderate 
motions,  rapidly  following  one  another,  with  a  not  very  marked  excursion.  If  the 
tremor  is  more  pronounced,  we  term  it  "  shaking."  Tremor  is  an  important  symp- 
tom, almost  pathognomonic  in  many  nervous  diseases,  such  as  paralysis  agitans, 
but  we  know  almost  nothing  in  regard  to  the  more  intimate  manner  of  its  origin. 
We  often  see  pronounced  tremor,  especially  in  the  hands  in  exophthalmic  goitre. 
We  know  that  tremor  is  often  present  in  old  people — senile  tremor ;  and  in  alco- 
holic subjects — alcoholic  tremor.  Tremor  sometimes  appears  in  muscles  at  rest, 
that  is,  not  innervated  by  the  will,  and  sometimes  only  in  those  which  are  moved 
voluntarily.  This  latter  form  of  tremor,  which  is  seen  most  frequently  in  multiple 
sclerosis  (vide  infra),  is  termed  "intention  tremor."  Very  marked  intention 
tremor,  which  is  increased  by  any  mental  excitement,  is  seen  as  a  symptom  in 
chronic  mercurial  poisoning  (mercurial  tremor),  particularly  in  mirror-makers, 
etc. 

We  may  mention  here  the  so-called  essential  tremor,  that  is,  a  condition  where 
the  ti'emor,  which  is  most  marked  in  the  hands,  is  the  only  morbid  symptom  and 
can  be  referred  to  no  known  cause.     This  form  of  tremor  is  sometimes  seen  in 


REMARKS  UPON  THE  DISTURBANCES  OF  MOTILITY.  541 

comparatively  young  people,  and  even  in  children.  A  distinct  hereditary  pre- 
disposition is  often  present,  so  that  several  "tremblers"  are  found  in  the  same 
family. 

We  very  often  find  trembling  in  "nervous  "  persons,  which  is  at  once  increased 
by  any  emotion.     There  is  also  a  pure  hysterical  tremor. 

4.  Single  contractions,  either  sudden  twitchings,  or  in  the  form  of  a  slow  con- 
traction of  the  muscle,  are  seen  with  especial  frequency  in  diseases  of  the  cord. 
They  are  either  single,  or  frequent  and  persistent.  Their  mode  of  origin  is  not 
always  plain.  They  may  depend  on  direct  motor  irritation  or  they  may  have  a 
reflex  origin. 

5.  Fibrillary  muscular  contractions  are  little  contractions  in  the  separate 
muscular  bundles,  which  may  be  seen  on  a  close  examination  of  the  muscles,  but 
which  do  not  have  any  special  influence  on  motion.  If  the  fibrillary  contractions 
in  a  muscle  are  very  pronounced,  there  may  develop  an  actual  "wave"  in  the 
muscular  substance.  We  see  this  symptom  especially  in  atrophied  muscles,  par- 
ticularly in  spinal  progressive  muscular  atrophy  (vide  infra). 

6.  Choreic  movements  are  either  slight  contractions  or  quite  complicated  and 
extensive  movements,  which  usually  appear  in  the  face,  in  one  limb,  or  some- 
times over  the  whole  body,  without  regard  to  rule.  In  severe  cases  they  are 
almost  continuous,  but  in  milder  cases  they  are  interrupted  by  shorter  or  longer 
pauses.  They  form  the  chief  symptom  of  chorea  proper,  but  they  are  also  pres- 
ent in  other  cerebral  affections,  such  as  symptomatic  chorea,  post-hemiplegic 
chorea,  etc. 

7.  Movements  of  athetosis  is  the  name  we  give  to  peculiar  involuntary  and 
usually  quite  slow  movements,  which  are  seen  especially  in  the  arm  and  hands, 
but  also  in  the  head,  the  trunk,  etc.  The  fingers  make  slow  but  often  very  exten- 
sive movements,  are  extended,  spread  apart,  flexed,  and  moved  over  and  around 
one  another  in  the  most  remarkable  way.  This  form  of  motor  irritation  occurs  as 
a  special  disease,  "  athetosis"  or  as  a  symptom  in  certain  central  nervous  diseases, 
especially  the  cerebral  paralysis  of  children  {vide  infra). 

8.  Constant  or  co-ordinated  spasms  are  symptoms  of  motor  irritation  in  which 
the  patient  performs  complicated  movements  by  comptilsion — forced  movements. 
Among  these  are  classed  the  compulsory  going  forward  or  moving  in  a  circle,  the 
turning  about  the  axis  of  the  body  (forced  attitudes),  and  also  certain  peculiar  com- 
plicated forms  of  spasm,  such  as  spasms  of  jumping,  laughing,  screaming,  with  all 
sorts  of  spasms  of  the  respiratory,  pharyngeal,  and  laryngeal  muscles,  associated 
with  hiccoughing  and  belching  sounds,  etc.  They  are  seen  most  frequently 
in  severe  cases  of  hysteria,  but  epilepsy  may  also  occur  exceptionally  in  the  form 
of  co-ordinated  spasms.  The  forced  movements  and  attitudes  mentioned  above 
are  seen  chiefly  in  affections  of  the  cerebellum  and  the  cerebellar  peduncles. 

9.  Tonic  spasm,,  as  has  been  said,  is  the  name  for  all  morbid  nrascular  contrac- 
tions that  continue  for  a  long  time.  Tonic  spasm  in  the  muscles  of  mastication, 
the  masseters,  is  termed  trismus.  Tonic  spasm  in  the  muscles  of  the  back  and 
neck,  by  which  the  whole  body  is  drawn  backward,  and  the  vertebral  column  is 
bent  into  an  arch  with  the  convexity  in  front,  is  called  opisthotonos.  Tonic 
rigidity  of  the  whole  body  is  termed  tetanus.  Tonic  spasms  are  seen  in  tetanus, 
tetany,  hysteria,  etc. 

10.  Cataleptic  rigidity  is  the  name  of  that  tonic  condition  of  the  muscles  in 
which  the  limbs  are  deprived  of  the  influence  of  the  will,  but  are  held  in  position 
by  the  muscles  in  any  position  given  to  them  passively.  It  is  seen  chiefly  in  cer- 
tain cases  of  hysteria,  but  cataleptic  states  are  also  present  in  other  cerebral  dis- 
eases, such  as  meningitis  (see  the  chapter  on  catalepsy). 

11.  Associated  movements  are  abnormal  movements  which  appear,  while  mak- 


542  DISEASES  OF  THE  NERVOUS  SYSTEM. 

iuo-  voluntary  movements,  in  muscles  which  have  no  connection  with  the  move- 
ment willed.  Thus  in  hemiplegia  associated  movements  sometimes  take  place 
in  the  arm  when  the  patient  wills  to  move  the  leg  alone.  In  spinal  cases,  as  we 
have  seen,  the  movement  of  one  leg  is  accompanied  also  by  an  unintentional 
movement  of  the  other  leg.  Associated  movements  are  commonest  in  the  muscles 
of  the  same  limb.  Thus  we  often  see  in  hemiplegia  or  in  spastic  spinal  paralysis 
that  patients  can  not  draw  the  leg  up  on  the  body  without  at  the  same  time 
producing  a  marked  dorsal  extension  of  the  foot  as  an  associated  movement.  In 
old  peripheral  facial  paralysis  (q.  v.)  we  very  often  see  associated  movements  in 
the  facial  muscles. 

Besides  the  conditions  of  motor  irritation,  other  attendant  nervous  symptoms 
often  occur  at  the  same  time.  Symptoms  of  motor  paralysis  and  irritation  are 
very  often  combined  with  each  other,  since  the  different  forms  of  spasm  may 
appear  not  only  in  groups  of  muscles  whose  motion  is  otherwise  normal,  but  also 
in  paretic  or  paralyzed  muscles.  In  general  convulsions  the  state  of  the  con- 
sciousness deserves  special  attention.  Genuine  epileptic  attacks  are  usually 
associated  with  complete  loss  of  consciousness,  but  in  most  of  the  other  forms  of 
spasm  the  consciousness  is  unaffected.  Finally,  it  is  worthy  of  mention  that  tonic 
spasms  especially  are  attended  by  a  feeling  of  decided  pain,  which  is  probably  due 
to  an  irritation  of  the  intra-muscular  sensory  nerves.  Such  painful  tonic  muscu- 
lar conti'actions  are  termed  cramps.  Among  them  are  the  well-known  painful 
spasms  in  the  calves  after  physical  exertion. 

3.  Ataxia. 

In  executing  all  normal  complicated  movements  we  need  the  simultaneous 
action  of  several  muscles.  Consider  the  numerous  muscles  which  must  be  put  in 
activity  in  walking,  in  grasping,  and  in  all  the  manifold  employments  of  the 
hands.  Hence,  in  order  to  perform  such  movements  correctly,  it  is  not  only 
necessary  that  all  the  muscles  concerned  should  be  innervated  by  the  will— that 
is,  that  they  be  not  paralyzed— but  that  we  should  also  be  able  so  to  modify  the  in- 
nervation of  each  individual  muscle  that  its  contraction  corresponds  precisely  to 
the  special  part  of  the  work  belonging  to  it.  A  prescribed  voluntary  motion  can 
take  place  only  when,  first,  all  the  muscles  requisite  for  it  come  into  no  less  but 
also  no  greater  action ;  second,  when  each  individual  muscle  contracts  only  so  far 
and  so  much  as  its  special  task  requires;  and,  third,  when  the  conditions  in  the 
time  of  innervation  take  their  normal  course— that  is,  when  all  the  muscles  in- 
volved contract  at  the  same  time  or  in  the  proper  order  after  one  another.  A 
movement  which  is  executed  in  such  a  prescribed  manner  we  call  a  co-ordinated 
movement,  and  the  process  of  modifying  properly  the  innervation  of  the  different 
muscles  necessary  for  a  complicated  movement  we  call  the  co-ordination  of  motion. 
We  must  especially  bear  in  mind  that  the  simultaneous  action  of  several  muscles 
is  so  far  necessary,  even  for  what  seem  to  be  the  simplest  movements,  that  muscles 
antagonistic  to  those  moved  must  also  come  into  activity.  Only  by  the  aid  of  the 
ever-ready  antagonistic  muscles  can  we  grade  our  movements  as  finely,  or  check 
or  hasten" them  as  rapidly,  as  is  demanded  for  the  execution  of  almost  all  compli- 
cated movements. 

Nervous  pathology  is  rich  in  facts  which  can  make  the  idea  and  the  necessity 
of  the  co-ordination  of  motion  clear  to  us.  We  often  see  disturbances  of  motility 
which  make  the  patient  incapable  of  any  fine  motor  acts,  and  yet  which  do  not 
depend  at  all  upon  any  motor  weakness  or  paralysis,  but  only  upon  a  disturbance 
in  the  co-ordination  of  motion.  Such  a  disturbance  we  call  ataxia,  and  we  speak 
of  an  ataxia  of  the  arms,  of  the  legs,  etc.,  when  the  parts  named  can  perform  all 


REMARKS  UPON  THE  DISTURBANCES  OF  MOTILITY.  543 

the  motions  and  retain  their  full  strength,  but  these  movements  show,  usually  at 
once,  a  striking,  disordered,  uncertain  "  ataxic  "  character. 

Many  theories  have  been  advanced  as  to  the  precise  cause  of  ataxia,  upon 
which  we  must  enter  in  the  special  chapters.  We  can  remark  here  only  that 
ataxia  is  seen  both  in  cerebral  diseases,  especially  in  affections  of  the  cerebellum 
(cerebellar  ataxia),  and  in  diseases  of  the  spinal  cord  (spinal  ataxia).  Among  the 
latter,  degeneration  of  the  posterior  columns  especially  (locomotor  ataxia,  tabes  dor- 
salis)  has  ataxia  as  one  of  its  chief  symptoms.  Therefore  we  will  discuss  the  charac- 
ter of  the  symptoms  and  the  cause  of  ataxia  more  fully  in  describing  this  disease. 

4.  General  Remarks  upon  testing  the  Reflexes  and  upon  the  Condition 

OP  THEM. 

In  testing  the  reflexes,  which  should  never  be  omitted  in  any  case  of  nervous 
disease  on  account  of  its  frequent  great  diagnostic  importance,  we  must  distin- 
guish the  two  chief  groups  of  reflexes  from  each  other:  the  cutaneous  reflexes,  and 
the  "tendon  reflexes." 

Cutaneous  Reflexes.— We  term  the  muscular  contractions,  excited  reflexly  by 
irritation  of  the  sensory  centripetal  cutaneous  nerves,  cutaneous  reflexes.  These 
are  usually  present  only  to  a  slight  degree  in  the  upper  extremities ;  but  we  can 
sometimes  excite  reflexes  even  here  by  pricking  or  pinching  the  skin,  especially 
that  of  the  fingers.  The  very  marked  reflex  in  many  people  caused  by  tickling  the 
axilla  is  well  known.  The  test  of  the  cutaneous  reflexes  in  the  lower  extremities  is 
much  more  important.  The  soles  of  the  feet  are  the  most  sensitive  parts  for  excit- 
ing a  reflex.  Simply  tickling  the  soles  with  the  finger  is  a  sufficient  irritation  (the 
tickling  reflex),  and  so  is  the  prick  of  a  pin  (the  prick  reflex),  or  striking  the  skin 
hard  with  a  blunt  object,  usually  the  handle  of  a  percussion- hammer  (the  blow 
reflex).  Thermal  irritants  are  also  very  suitable  for  exciting  a  reflex,  especially 
bits  of  ice  held  to  the  skin  (cold  reflex).  It  is  often  advisable  to  try  all  these 
methods,  since  with  diminished  reflex  irritability  a  reflex  contraction  in  the  leg 
can  often  be  excited  only  by  some  one  of  them.  We  should  also  examine  the 
reflex  irritability  of  the  rest  of  the  skin,  as  well  as  the  soles  of  the  feet,  by  a  pin- 
prick, by  pinching  a  fold  of  the  skin,  etc.  We  should  especially  remember  that 
in  nervous  diseases  there  is  often  a  delay  in  the  reflex,  so  that  the  reflex  contrac- 
tion appears  only  when  the  irritation  has  lasted  for  a  certain  time.  Thus  in  many 
diseases  of  the  cord,  as  we  have  repeatedly  seen,  the  reflex  follows  only  after  we 
have  pinched  a  fold  of  skin  continuously  for  several  (ten  or  fifteen)  seconds,  a 
delay  which  has  a  connection  with  the  fact  of  the  "  summation  of  reflex  irrita- 
tion" known  from  physiology.  The  fact  also  deserves  mention  that  in  many 
patients  the  reflexes  are  easily  excited  in  certain  parts  of  the  skin,  but  in  other 
parts  with  difficulty  or  not  at  all — the  "  place  of  easiest  reflex  irritability." 

In  general,  the  reflex  contractions  are  confined  to  the  limb  irritated.  On 
pricking  the  sole  of  the  foot,  a  dorsal  extension  of  the  toes  or  of  the  foot  follows, 
or  a  greater  or  less  flexion  of  the  leg.  The  reflex  rarely  involves  the  rest  of  the 
body,  but  under  pathological  conditions  there  is  such  an  increased  reflex  irrita- 
bility that,  on  irritating  the  soles  of  the  feet,  both  legs,  or  even  the  whole  body, 
fall  into  contraction.  Such  a  condition  is  sometimes  seen  in  hysteria,  in  tetanus, 
in  hydrophobia,  in  strychnine  poisoning,  etc. 

We  must  also  mention  two  special  forms  of  cutaneous  reflex  which  are  often 
examined:  the  abdominal  reflex,  consisting  of  a  contraction  of  the  abdominal 
muscles  on  the  same  side,  when  we  stroke  the  skin  of  the  abdomen  with  the  finger 
or  the  handle  of  the  percussion-hammer  ;  and  the  cremaster  reflex — that  is,  the 
reflex  retraction  of  the  testicle,  when  we  stroke  the  internal  surface  of  the  thigh. 


5±4  DISEASES  OF  THE  NEEVOUS  SYSTEM. 

or  exert  a  marked  pressure  a  hand's  breadth  above  the  internal  condyle.  The 
creinaster  reflex  appears  first  on  the  side  irritated,  but  not  very  infrequently  on 
both  sides  at  once.  Other  cutaneous  reflexes,  such  as  the  gluteal  reflex,  the  niam- 
millary  reflex,  etc.,  have  less  significance  and  are  often  absent. 

Judgment  in  regard  to  any  pathological  condition  of  the  cutaneous  reflexes  is 
rendered  difficult  by  the  fact  that  their  inteusity  varies  considei'ably  even  under 
normal  conditions.  Many  healthy  people  have  much  livelier  reflexes  than  others. 
Hence  we  may  judge  most  accui'ately  of  a  patient  if,  in  unilateral  affections,  we  can 
compare  the  reflex  symptoms  in  the  two  halves  of  the  body  with  each  other.  The 
precise  condition  of  the  reflexes  in  the  different  forms  of  disease  will  be  spoken  of 
in  the  special  chapters.  We  can  state  here  only  that  a  diminution  or  a  complete 
absence  of  the  cutaneous  reflexes  must,  of  course,  be  seen  where  the  reflex  conduc- 
tion—through the  centripetal  nerve,  the  gray  matter,  the  special  anterior  cornu, 
and  the  motor  nerve— is  interrupted  at  any  point,  as  may  be  the  case  both  in  dis- 
eases of  the  peripheral  nerves  and  of  the  spinal  cord.  On  the  other  hand,  how- 
ever, the  cutaneous  reflexes  may  lose  their  intensity,  or  even  disappear  entirely,  if 
the  reflex  centers  lose  then*  irritability  from  an  irritation  of  the  reflex-inhibitory 
centers  or  fibers.  We  see  an  abnormal  increase  of  the  cutaneous  reflexes  when 
either  the  irritability  of  the  parts  that  aid  in  producing  the  reflex  is  increased,  as 
in  many  cases  of  cutaneous  hyperesthesia,  in  strychnine  poisoning, 'and  in  many 
general  neuroses ;  or  when  the  inhibitory  processes  which  normally  act  upon  the 
reflex  centers  are  abolished,  as  in  certain  diseases  of  the  brain  and  spinal  cord. 
The  increase  of  the  cutaneous  reflexes  is  shown  partly  by  the  fact  that  the  reflex 
movements  are  particularly  lively,  and  appear  with  a  comparatively  slight  irrita- 
tion of  the  skin,  and  partly  by  their  extension  to  more  distant  groups  of  muscles 
than  usual. 

Tendon  Reflexes. — Of  almost  greater  practical  importance  than  the  investiga- 
tion of  the  cutaneous  reflexes  is  the  test  of  the  phenomena  classed  under  the  name 
of  the  "  tendon  reflexes,"  and  first  carefully  investigated  and  described  by  Erb  and 
Westphal  in  the  year  1875.  We  understand  by  these  those  muscular  contractions 
which  >  arise  from  the  mechanical  irritation  of  the  tendons  and  analogous  parts, 
such  as  the  periosteum  and  fascia?.  By  this  the  sensory  nerves  of  the  tendon  are 
irritated,  and  excite  a  reflex  muscular  contraction  by  means  of  the  spinal  cord.  If 
we  give  a  quick  blow  to  the  ligamentum  patellae  (the  tendon  of  the  quadriceps 
extensor)  with  the  ulnar  side  of  the  hand,  or,  better,  with  a  percussion-hammer, 
while  the  leg  hangs  down  laxly,  or,  if  the  person  examined  be  in  bed,  while  the 
leg  is  in  a  passive  position  of  slight  flexion,  it  is  followed  almost  invariably  in 
healthy  persons  by  a  more  or  less  vigorous  contraction  of  the  quadriceps,  by  which 
the  leg  is  extended.  This  is  termed  "  patellar  reflex,"  "  knee  phenomenon  "  (West- 
phal) [or  "knee-jerk"].  In  order  to  produce  it,  it  is  especially  necessary  for  the 
person  examined  to  avoid  all  active  muscular  tension  in  the  leg,  especially  in  the 
extensor.  If  we  examine  patients  who  are  not  in  bed,  we  can  test  the  patellar  re- 
flex by  making  the  patient  cross  the  leg  to  be  tested  over  the  other,  and  by  strik- 
ing the  patellar  tendon  as  the  leg  hangs  loose  ;  but  it  seems  to  us  more  con- 
venient to  direct  the  patient  to  extend  the  leg  until  it  forms  an  obtuse  angle  with 
the  thigh  with  the  opening  of  the  angle  below.  If  the  sole  be  set  fully  on  the 
floor  the  extensor  cruris  is  made  tense  in  this  position,  and  we  can  very  easily  and 
plainly  excite  the  contraction  of  the  quadriceps  by  striking  the  patellar  tendon. 
If  the  patellar  reflex  be  weak  and  hard  to  detect,  we  should  try  the  proceeding  ad- 
vised by  Jendrassik,  which  consists  in  testing  the  reflex  while  the  patient  grips 
the  two  hands  together,  and  tries  with  all  his  strength  to  pull  them  apart.  By  this 
ingenious  tension  of  the  muscles  of  the  upper  extremities  the  muscles  of  the  legs 
are  probably  greatly  relaxed,  wThile  any  voluntary  innervation  is  avoided,  and 


ff 

REMARKS  UPON  THE  DISTURBANCES  OF  MOTILITY.         545 

thus  is  explained  the  increase  of  the  reflex,  which  is  often  pronounced.  If  by 
the  help  of  this  "  Jendrassik's  test "  no  reflex  is  to  be  elicited,  we  may  regard  it 
as  absent. 

The  second  important  tendon  reflex  to  be  provoked  in  the  lower  extremity  is 
the  Achilles'  tendon  reflex.  If  we  give  to  the  foot  of  the  person  examined  a  pas- 
sive position  of  slight  dorsal  extension,  so  that  the  tendo  Achillis  is  a  little  tense, 
and  then  strike  the  tendon  a  quick  blow,  a  marked  contraction  of  the  gastrocne- 
mius follows.  Under  normal  conditions  this  reflex  is  often  absent.  Where  the 
tendon  reflexes  are  abnormally  increased,  however,  it  is  very  vigorous,  and  then 
we  can  very  often  produce  it  in  the  following  especially  characteristic  manner. 
If  we  make  a  sudden,  short,  vigorous,  passive,  dorsal  extension  of  the  foot,  the  tendo 
Achillis  is  suddenly  made  tense,  and  thus  is  irritated  mechanically.  As  a  result 
of  this,  there  is  a  reflex  plantar  flexion  of  the  foot.  If  now,  by  persistent  passive 
dorsal  extension  of  the  foot,  the  tendo  Achillis  is  again  made  tense,  there  follow 
by  turns  new  plantar  and  dorsal  movements  of  the  foot,  so  that  the  foot  is  thus 
put  into  a  vigorous  tremor.  This  symptom,  which  can  only  exceptionally  be  pro- 
voked in  healthy  persons,  is  termed  ankle  clonus  (foot  clonus),  or  "  foot  phenom- 
enon" (Westphal).  Where  there  is  a  very  great  increase  of  the  tendon  reflexes 
the  tremor  is  sometimes  not  confined  to  the  foot,  but  the  whole  leg  falls  into  a 
vigorous  clonus,  a  symptom  which  was  once  given  the  unsuitable  name  of  spinal 
epilepsy.  We  can  also  obtain  the  patellar  reflex  in  the  form  of  a  clonus  if  we 
pull  the  patella  firmly  down  with  the  finger  and  force  it  downward  by  a  sudden 
blow  on  the  finger. 

The  two  symptoms  described — the  patellar  reflex,  and  the  Achilles'  tendon  reflex 
or  foot  phenomenon — are  practically  the  most  important,  and  are  the  most  often 
tested,  but  they  are  by  no  means  the  only  reflexes  in  the  lower  extremity.  Besides 
the  reflexes  from  the  special  tendons,  we  also  frequently  obtain  muscular  contrac- 
tions by  striking  the  periosteum  and  the  fasciae,  which  have  been  termed  the  peri- 
osteal and  fascia  reflexes.  Thus  a  contraction  in  the  quadriceps  often  follows  a 
blow  on  the  anterior  surface  of  the  tibia.  We  also  see  contractions  frequently  in 
the  adductors  of  the  thigh  on  striking  the  internal  condyle  of  the  femur,  contrac- 
tions in  the  muscles  of  the  posterior  aspect  of  the  thigh  in  striking  the  calves,  etc. 

Under  normal  conditions  the  tendon  reflexes  in  the  upper  extremities  are  often 
insignificant  or  entirely  absent,  but  where  the  irritability  is  abnormally  increased 
we  see  even  here  the  most  various  and  vigorous  reflexes.  The  most  important 
and  most  constant  are  the  periosteal  reflexes  in  the  supinator  longus,  biceps,  and 
deltoid,  from  a  blow  on  the  lower  end  of  the  radius  and  ulnar,  and  also  the  tendon 
reflex  in  the  biceps  from  a  blow  on  the  biceps  tendon  at  the  elbow-joint,  or  in  the 
triceps  from  a  blow  on  the  triceps  tendon  above  the  olecranon.  A  persistent  clonus 
in  the  hand  upon  passive  volar  flexion  sometimes  occurs,  but  it  is  rare. 

In  many  places  in  the  special  chapters  we  shall  go  more  fully  into  the  exact 
conditions  and  diagnostic  significance  of  the  tendon  reflexes.  We  shall  see  that 
the  absence  of  tendon  reflex  is  characteristic  of  certain  spinal  diseases,  such  as 
poliomyelitis  and  tabes  dorsalis,  and  also  of  most  peripheral  paralyses  (traumatic 
paralyses  and  neuritis).  We  see  an  abnormal  increase  of  tendon  reflex  in  many 
diseases  of  the  cord,  especially  in  that  form  of  spinal  paralysis  which  is  termed 
spastic  spinal  paralysis,  and  very  often,  too,  in  cerebral  paralyses.  The  increase 
of  the  reflex  in  these  cases  is  probably  always  due  to  a  disappearance  of  certain 
influences  which  normally  inhibit  the  reflex. 

Although  we  have  so  far  tacitly  assumed  the  reflex  nature  of  the  symptom 
termed  "tendon  reflex "  as  certain — a  theory  first  propounded  by  Erb,  and  now 
shared  by  most  nervous  pathologists  on  the  ground  of  many  clinical  and  experi- 
mental facts — we  can  not  conceal  the  fact  that  the  reflex  nature  of  the  phenomena 
35 


546  DISEASES  OF  THE  NERVOUS  SYSTEM. 

in  question  is  not  recognized  by  another  party,  headed  by  "Westphal.  West- 
phal  holds  the  "  tendon  phenomena  "  to  be  the  result  of  a  direct  mechanical  irrita- 
tion of  the  muscle  provoked  by  the  jarring  or  stretching  of  the  muscle.  Since, 
however,  careful  experimental  investigations,  repeatedly  performed,  have  of  late 
almost  without  exception  decided  in  favor  of  the  reflex  nature  of  the  phenomena 
in  question,  and  since  many  clinical  facts,  such  as  the  occurrence  of  contractions 
in  distant  muscles,  crossed  contractions,  etc.,  can  be  explained  only  in  this  way,  we 
will  hold  in  the  sequel  to  the  term  "  tendon  reflex. " 

Mechanical  Muscular  Irritability  and  Paradoxical  Contraction.— In  addition  to 
the  description  of  tendon  reflexes  we  must  make  brief  mention  here  of  two  symp- 
toms which  must  also  be  considered  in  the  examination  of  nervous  patients. 
"  Direct  mechanical  irritability  of  the  muscles  "  is  shown  by  the  occurrence  of 
contractions  from  a  direct  blow  on  the  belly  of  the  muscle,  in  which,  of  course,  we 
can  not  definitely  separate  the  direct  muscular  irritation  from  some  mechanical 
irritation  of  the  muscular  nerves.  Sometimes  the  muscular  contraction  is  perhaps 
also  a  reflex,  arising  from  the  mechanical  irritation  of  the  fascia  drawn  over  the 
muscle ;  but  it  is  worthy  of  mention  that  in  cases  where  the  tendon  reflex  has 
wholly  disappeared,  as  in  tabes  dorsalis,  the  direct  mechanical  muscular  irrita- 
bility is  usually  retained.  The  so-called  idio-muscular  contractions  must  be  espe- 
cially distinguished.  We  see  these  most  plainly  if  we  give  a  vigorous  blow  with 
the  ulnar  side  of  the  hand  to  the  belly  of  a  muscle,  like  the  biceps.  A  circum- 
scribed muscular  swelling  forms  at  the  point  struck,  and  gradually  disappears 
again.  The  test  for  mechanical  muscular  irritability  has  not  yet  attained  any 
special  practical  importance. 

"  Paradoxical  contraction  "  is  the  name  which  Westphal  has  given  to  a  symp- 
tom seen  especially  in  the  tibialis  anticus,  and  rarely  also  in  the  flexors  of  the  leg 
and  forearm.  It  is  when  the  foot,  after  being  put  in  passive  dorsal  extension,  re- 
mains in  this  position  even  after  the  expiration  of  a  considerable  time  (several 
minutes),  and  a  marked  prominence  of  the  tendon  of  the  tibialis  anticus  is  usually 
visible.  We  can  not  at  the  present  time  give  an  explanation  of  this  phenomenon, 
which  so  far  has  been  observed  in  different  spinal  and  cerebral  diseases,  multiple 
sclerosis,  paralysis  agitans,  etc. 

5.  General  Remarks  upon  the  Changes  of  Electrical  Excitability  in  the 
Motor  Nerves  and  Muscles.* 

Electricity,  since  the  investigations  of  Duchenne,  Remak,  Benedikt,  Moritz 
Meyer,  von  Ziemssen,  Brenner,  Erb,  and  others,  has  become  not  only  one  of  the 
most  prominent  therapeutic  aids  in  the  treatment  of  nervous  diseases,  but  it  also 
plays  an  extremely  important  part  in  the  examination  of  nervous  patients,  since 
the'  test  of  the  electrical  excitability  of  diseased  nerves  and  muscles  gives  us  a 
large  amount  of  valuable  information  in  regard  to  diagnosis  and  prognosis. 

Every  complete  electrical  examination  must  be  made  with  both  currents— the 
faradic  or  induction  current  (usually  the  secondary  current),  and  the  galvanic  or 
constant  current.  One  "  indifferent "  pole  is  usually  put  on  the  sternum  or  the 
back  of  the  neck,  and  the  other  "testing"  pole  on  the  nerve  or  muscle  to  be 
tested.  The  excitement  of  the  muscle  from  the  nerve  is  called  indirect;  the  excite- 
ment from  placing  the  electrode  on  the  muscle  itself  (where,  of  course,  the  excite- 
ment of  the  intra-muscular  nerves  can  not  be  excluded)  is  called  direct.  Those 
points  on  the  human  body  where  the  different  nerves  and  muscles  are  most  easily 


*  In  regard  to  all  the  details  of  electrical  diagnosis  and  electro-therapeutics  we  would  refer  to  Erb's 
"  Handbuch  der  Elektrotherapie."  Leipsic,  Vogel,  1882.  [Translated  by  De  Watteville.  New  York  : 
Wm.  Wood  &  Co.,  1887.] 


REMARKS  UPON  THE  DISTURBANCES  OF  MOTILITY. 


547 


accessible  to  the  electrical  excitement  are  to  be  found  in  Figs.  08  to  7:3,  taken  from 
Erb's  hand-book. 

In  faradic  examination  the  rule  is  that  we  can  provoke  marked  muscular  con- 
tractions both  from  the  nerves  and  from  direct  excitement  of  the  muscles  at  the 
points  generally  accessible  to  excitement.  We  designate  the  strength  of  the  cur- 
rent required  by  the  distance  between  the  two  coils  of  the  induction  apparatus 
(coil  distance,  Rollenabstand)  at  which  the  first  minimal  contraction  of  the  muscle 
occurs.  On  increasing  the  current,  the  minimal  contraction  gradually  passes  into 
a  vigorous  tetanic  contraction  of  the  muscles. 

Galvanic  examination  is  performed  by  the  aid  of  a  "current  reverser,"  by 
which  the  testing  pole  can  be  made  either  the  negative  pole  (the  cathode  or 
zinc  pole)  or  the  positive  pole  (the  anode  or  copper  or  carbon  pole).      By  this 


Frontalis 

Facial 
{upper  branch) 

Corrugator  supercilii 

Orbicul .  palpebrarum. 
Nasal  muscles.  < 

Zygomatici. 
Orbicularis  oris. 
Facial  {middle  br'ch) 
Masseter. 

Levator  menti. 

Quadratus  menti. 

Triangularis  menti. 

Hypoglossals. 

Facial  {lower  branch). 

Platysma  myoides. 

Hyoid  muscles.  \ 


Omo-hyoid 


Anterior  thoracic 
(Pectoralis  major;. 


Region  of  the  central 
convolutions. 


Region  of   the    third 
frontal  convolution 
and  the  insula 
(speech  center;. 

Temporalis. 

Facial  {upper)   in 
front  of  ear. 

Facial  {trunk) . 
Posterior  auricular. 
Facial  {middle  br'ch). 
Facial  {lower  branch). 
Splenius. 

Sterno-cleido-mastoid . 

Spinal  accessory. 
Levator  anguli 

scapulas. 
Trapezius. 

Dorsalis  scapidce. 
Axillary  {circumflex). 

Long  thoracic  (serra- 
tus  magnus;. 


Phrenic.        Supraclavicular  point.         Brachial  plexus. 
(Erb\s  point.    Deltoid, 
biceps,  brachialis  anticus, 
and  supinator  longus.) 

Fig.  68. 

"polar  method  of  investigation"  (Brenner)  the  following  law  of  contraction  is 
obtained,  which  holds  equally  for  the  normal  motor  nerves  and  for  the  muscles. 

With  a  weak  current  no  noticeable  excitement  takes  place.  If  we  gradually 
increase  the  strength  of  the  current,  the  first  weak  contraction  of  the  muscle 
occurs  at  the  closure  of  the  cathode— that  is,  when  the  current  is  closed  so  that 
the  cathode  is  made  the  testing  pole.  On  opening  the  cathode,  or  on  closing  or 
opening  the  anode,  nothing  follows.  If  we  increase  the  strength  of  the  current 
still  more,  the  cathodic  closure  contractions  become  stronger,  and  the  anodic 
closure  and  anodic  opening  contractions  appear,  now  the  one  being  earlier  and 
stronger,  and  now  the  other.  Opening  of  the  cathode  has  still  no  effect.  Only 
with  a  very  strong  current,  in  which   the  cathodic  closure  contractions  have 


548 


DISEASES  OF  THE  NERVOUS  SYSTEM. 


already  become  tetanic-that  is,  they  still  persist  after  the  closure  of  the  current- 
provoke  weak  cathodic  opening  contractions.     Expressed  in  the  abbrevia- 


can  we 


Triceps  (long  head). 

Triceps  (internal  head). 
Ulnar. 


Flexor  carpi  ulnaris 
Flexor  profundus  digitorum 


Flexor  sublimis  digitorum 
(II  and  IU). 


Flexor  sublimis  digitorum 
■  land  IV). 

Ulnar. 


Palmaris  brevis. 

Abductor  minimi  digiti. 

Flexor  brevis  minimi  digiti. 

Opponens  minimi  digiti. 

Lumbricales. 


Supinator  longus. 
Pronator  radii  teres. 
—  Flexor  carpi  radialis. 


Deltoid  (anterior 
half). 


Musculo-cutaneous 
Biceps. 
Brachialis  anticus. 


Flexor  sublimis  digitorum. 

Flexor  longus  pollicis. 
Median. 

Abductor  pollicis. 
Opponens  pollicis. 
Flexor  brevis  pollicis. 
Adductor  pollicis. 


Fig 


tions  now  in  general  use  in  electrical  diagnosis,  the  law  of  contraction  for  normal 
muscles  and  nerves  in  man  is  as  follows:* 

1    Lowest  degree  with  weak  currents :  Kabz,  KaO— ,  Anb— ,  Anu     . 

2.  Middle  degree  with  stronger  currents:  KaSZ,  KaO-,  AnSz  AnUZ 

3.  Highest  degree  with  very  strong  currents:  KaSTe,  KaOz,  AnSZ,  AnOZ. 


*Ka  signifies  cathode,  An  =  anode,  S  =  closure,  0  =  opening,  .  ^^f^tn^^l 
Z  =  stronger  contraction,  Te  =  tetanus.     Sometimes  the  increasing  strength  of  the   contiactions 


REMARKS  UPON  THE  DISTURBANCES  OF  MOTILITY. 


549 


The  variations  from  the  normal  state  seen  under  pathological  conditions  con- 
sist of  quantitative  and  also  of  qualitative  changes  in  the  Jaw  of  contraction.  We 
term  the  simple  increase  or  diminution  of  the  electrical  excitability  in  nerves  or 
muscles,  without  simultaneous  changes  in  the  quality  and  order  of  the  occurrence 
of  muscular  contractions,  quantitative  changes.  The  discovery  of  increased  or 
diminished  irritability  of  nerve  and  muscle  can  be  made  most  easily  in  unilateral 
diseases,  where  we  can  compare  the  strengths  of  current  required  to  obtain  the 
minimal  contraction  on  the  diseased  and  healthy  sides  with  each  other.    If  we  are 


Deltoid  (posterior  half). 


Radial  (musculo-spiral). 
Brachialis  anticus. 

Supinator  longus. 
Extensor  carpi  radialis  longior. 
Extensor  carpi  radialis  brevior. 

Extensor  communis  digitorum.  < 
Extensor  indicis. 

Extensor  ossis  metacarpi  pollicis. 
Extensor  primi  internodii  pollicis. 


Dorsal  interossei,  I  and  II 


Triceps  (long  head). 


Triceps  (external  head). 


Extensor  carpi  ulnaris. 
Supinator  brevis. 

Extensor  minimi  digiti. 
Extensor  indicis. 


Extensor  secundi  internodii 
pollicis. 


-Abductor  minimi  digiti. 

)  Dorsal  interossei, 
-  f      HI  and  IV. 


dealing  with  bilateral  or  general  diseases  this  is  much  harder  to  make  out.  We 
must  then  draw  our  comparisons  from  the  conditions  of  excitability  in  normal 
individuals,  where  the  different  obstacles  to  conduction  can  be  carefully  estimated 
by  the  aid  of  a  galvanometer,  or  by  comparing  the  excitability  of  the  nerve-trunks 
in  the  different  parts  of  the  body  with  one  another.     For  this  purpose  we  are 


abbreviated  by  the  signs  Z,  Z'  and  Z".  [Many  English  and  American  writers  on  electricity  use  letters 
derived  from  the  English  names.  Thus  C  stands  for  cathode,  closure,  and  contraction.  A  and  O  have 
the  same  meaning.  It  seems  to  us  clearer  and  conducive  to  greater  harmony  to  retain  the  German 
abbreviations,  which  are  simple  and  definite. — Trans.] 


550 


DISEASES  OF  THE  NERVOUS  SYSTEM. 


usually  content  (following  Erb's  example)  with  comparing  the  superficial  nerves, 
such  as  the  frontal,  accessory,  ulnar,  and  peroneal,  which  are  easily  excited.  An 
increase  of  electrical  excitability  is  found  in  many  fresh  peripheral  paralyses,  and 
also  in  tetany.  A  diminution  of  electrical  excitability  is  found  quite  frequently  in 
bulbar  and  spinal  paralyses,  in  progressive  muscular  atrophy,  etc. 


Crural.  -- 


Adductor  magnus.  — L 
Adductor  longus.  — I- 


Crureus. 


Vastus  internus. 


>  Tensor  vaginas  femoris. 


Sartorius. 

Quadriceps  femoris  (common  point). 

Rectus  femoris. 

* 

Vastus  externus. 


Fig.  71. 


A  significant  advance  in  the  investigation  of  the  quantitative  conditions  of  ex- 
citability has  been  rendered  possible  by  the  introduction  of  the  "  absolute  galvanom- 
eter" (Hirschmann,  Edelmann,  etc.),  by  which  the  strength  of  the  current  can  be 
read  off  directly  in  milliamperes.  By  extensive  investigations  on  healthy  persons 
Stintzing  has  found  certain  limits  within  which  the  normal  excitability  of  the 
different  nerves  varies.  Deviations  from  these  figures  above  or  below  accordingly 
permit  us  to  recognize  an  increase  or  a  diminution  of  the  galvanic  excitability. 
These  limits  are,  for  instance,  for  the  frontal  nerve,  l-2'5  milliamperes  ;  for  the 
accessory  nerve,  0 '1-0 '44  ma. ;  for  the  ulnar  nerve  (at  a  point  one  or  two  inches 
above  the  olecranon),  0*2-0-9  ma. ;  for  the  peroneal  nerve,  0'2-2'0  ma.  In  these 
cases  it  is  necessary,  in  order  to  obtain  results  that  may  be  compared,  always  to  use 
electrodes  of  the  same  area  ("  unit  electrode  "  of  3  sq.  cm).*  An  accurate  measure 
of  the  absolute  strength  of  the  faradic  current  has  not  yet  been  found.  We  there- 
fore content  ourselves  with  the  statement  of  the  position  of  the  outer  coil  [of  the 
DuBois-Eeymond  apparatus]  over  the  inner  (coil  distance,  Rollenabstand),  at 
which  the  first  perceptible  contraction  occurs.  Stintzing  found  as  an  average 
position  for  the  frontal  nerve,  128  "5  mm. ;  for  the  accessory  nerve,  137  mm. ;  for 


[*  This  is  Stintzing's  unit.    Erb  has  proposed  a  larger  one,  a  "  normal  electrode  "  of  10  sq.  cm.— K.] 


REMARKS  UPON  THE  DISTURBANCES  OF  MOTILITY. 


551 


the  ulnar  nerve,  130  mm. ;  and  for  the  peroneal  nerve,  115  mm.     Wc  must  refer 
to  the  special  works  for  further  details. 

Much  more  important,  however,  than  the  simple  quantitative  changes  of  <  Lee 
trical  excitability  are  those  not  merely  quantitative  but  also  qualitative  deviations 
from  the  normal  law  of  contraction,  which  were  first  discovered  in  certain  forms 
of  paralysis  by  Baierlacher  in  1859,  and  were  soon  generally  confirmed.  Erb  has 
given  these  the  name  of  the  "  reaction  of  degeneration,"  because  they  are  closely 
connected  with  the  progress  of  certain  anatomical  changes  in  the  paralyzed  mus- 
cles and  nerves. 

In  order  to  make  the  relations  of  the  reaction  of  degeneration  clear,  let  us 
select  as  an  example  any  fresh  peripheral  paralysis  and  follow  the  changes  in 
excitability  to  the  two  currents  in  the  nerves  and  muscles.  In  a  short  time  (two 
or  three  days)  after  the  onset  of  the  paralysis  a  gradually  increasing  decline  in  the 
faradic  and  galvanic  excitability  in  the  nerve  begins.     After  one  or  two  weeks 


Sciatic 

Biceps  femoris  (long  head) 

Biceps  femoris  (short  head). 


Peroneal. 


Gastrocnemius  (external  head). 


Soleus, 


Flexor  longus  hallucis. 


Gluteus  maximus. 


Adductor  magnus. 

® J —  Semitendinosus. 

Semimembranosus. 


Posterior  tibial. 

Gastrocnemius  (internal  head). 
Soleus. 

—  Flexor  longus  digitorum. 
Tibial. 


Fig.  72. 

the  excitability  is  completely  lost,  so  that  from  the  nerve  we  can  no  longer 
provoke  any  trace  of  muscular  contraction  with  the  strongest  faradic  or  con- 
stant current.  During  this  time  the  excitability  of  the  paralyzed  muscles  to- 
the  faradic  current  has  also  rapidly  diminished,  and  finally  has  wholly  disap- 
peared.    The  case  is  quite  different  with  direct  galvanic  excitement  of  the  mus- 


552 


DISEASES  OF  THE  NERVOUS  SYSTEM. 


cles.  Here  we  find  at  first  a  slight  diminution,  which  in  the  second  week  passes 
to  a  decided  increase  of  the  galvanic  muscular  excitability.  We  now  obtain 
marked  muscular  contractions  with  relatively  very  weak  currents.  Besides  that, 
two  other  very  important  peculiarities  are  to  be  noted:  1.  The  muscular  contrac- 
tions are  not  short  and  lightning-like,  as  under  normal  conditions,  but  they  seem 
quite  sluggish,  protracted,  "  worm-like,"  and  often  persist  during  the  whole  dura- 
tion of  the  closure  of  the  current.  2.  The  muscular  contractions  occur  not  only 
chiefly  at  cathodic  closure  (KaS),  as  under  normal  conditions,  but  the  anodic 


Tibialis  anticus. 
Extensor  longus  digitorum.  — 


Peroneus  brevis. 


Extensor  proprius  pollicis. 


Peroneal. 

Gastrocnemius  (external). 
ri«  *~\ * —  Peroneus  longus. 


Soleus. 


Flexor  longus  hallucis. 


Dorsal  interossei.  X   -  f''*^^       •/- 


Extensor  brevis  digitorum. 
Abductor  minimi  digiti. 


Fig.  73. 

closure  contractions  are  as  strong  as  the  cathodic  closure  contractions  (KaSZ),  or. 
even  plainly  exceed  them.  The  cathodic  opening  contraction  (KaOZ)  is  also  fre- 
quently stronger.  3.  It  may  also  be  mentioned  here  that  the  mechanical  irrita- 
bility of  the  muscles  in  such  cases  is  usually  increased. 

This  second  degree  of  the  reaction  of  degeneration  lasts  from  four  to  eight 
weeks.  If  the  paralysis  be  severe  and  long  continued,  or  incurable,  at  the  end  of 
this  period  comes  a  decline  of  the  galvanic  muscular  excitability.  The  contractions 
become  weaker,  the  strength  of  current  necessary  to  produce  them  greater,  and, 
finally,  in  incurable  cases,  even  with  the  strongest  currents,  we  can  obtain  only 
a  little  slow  anodic  closure  contraction,  or  none  at  all.  It  is  different,  however,  in 
the  milder,  curable  cases.  In  these  the  passage  to  the  normal  condition  gradually 
follows  either  the  increase  of  the  galvanic  muscular  excitability,  or,  in  more  pro- 
tracted cases,  its  secondary  decline.  The  contractions  become  more  vigorous  and 
shorter,  the  cathodic  closure  contraction  (KaSZ)  again  predominates,  the  faradic 
muscular  excitability  and  the  faradic  and  galvanic  excitability  of  the  nerves 


REMARKS  UPON   THE  DISTURBANCES  OP  MOTILITY.  553 

finally  return,  and  with  them  the  old  normal  conditions  are  restored.  A  fact  to  he 
observed  in  these  cases  is  of  great  interest,  namely,  that  the  voluntary  motion  in 
such  cases  often  returns  decidedly  earlier  than  the  electrical  excitability  of  the 
peripheral  nerves.  We  see,  then,  that  a  diseased  nerve  may  be  capable  of  con- 
ducting irritations  coming  from  the  brain,  while  the  taking  up  of  irritation,  its 
direct  excitability,  is  still  completely  lost.*  In  such  cases  we  can  obtain  a  mus- 
cular contraction  by  electrical  irritation  of  the  nerve  above  the  point  of  lesion. 

Besides  tbe  complete  reaction  of  degeneration  just  described,  there  is  also  a  so- 
called  partial  reaction  of  degeneration,  which  is  not  infrequent  in  milder  cases. 
This  may  show  itself  in  several  forms,  but  it  is  chiefly  when  the  diminution 
of  the  faradic  and  galvanic  excitability  in  the  nerves  and  the  diminution  of 
faradic  excitability  in  the  muscles  is  only  of  a  slight  degree,  while  the  character- 
istic changes  in  the  direct  galvanic  excitement  of  the  muscles— increased  excita- 
bility, slow  contractions,  and  predominance  of  anodic  closure  contractions— are 
fully  developed.  In  some  cases  the  occurrence  of  slow  contractions  on  faradic 
excitement  of  nerves  and  muscles  has  lately  been  observed—"  faradic  reaction  of 
degeneration."  In  the  course  of  atrophic  paralyses  we  often  see  that  the  different 
varieties  of  reaction  of  degeneration  pass  into  one  another  as  the  process  advances 
or  improves  (Stintzing). 

Anatomical  Changes  of  the  Nerves  and  Muscles  in  the  Reaction  of  Degenera- 
tion ;  its  Significance  in  Diagnosis  and  Prognosis.— As  we  have  seen  on  page  538, 
all  paralyses  may  be  divided  into  two  great  groups— into  atrophic  paralyses,  and 
paralyses  without  marked  atrophy  of  the  affected  muscles.  We  have  learned  to 
recognize  the  necessary  hypothesis  of  the  "  trophic  "  influence  of  the  ganglion- 
cells  in  the  anterior  cornua  of  the  spinal  cord  as  the  foundation  of  this  distinction. 
In  all  cases  where  the  disease  affects  these  ganglion-cells,  or  is  situated  in  the 
peripheral  nerves,  so  that  the  trophic  influence  of  the  ganglion-cells  on  the  mus- 
cles can  no  longer  be  of  influence,  we  have  a  degenerative  atrophy  of  the  periph- 
eral portion  of  the  nerve,  and  of  the  muscle  belonging  to  it.  This  degenerative 
atrophy  is  the  anatomical  cause  of  the  symptoms  of  the  electrical  reaction  of  de- 
generation. 

If  we  have  to  do  with  a  peripheral  paralysis,  such  as  a  traumatic  lesion  of  a 
nerve-trunk,  the  portion  of  the  nerve  peripheral  to  the  point  of  lesion  is  separated 
from  its  ''trophic  center"  in  the  cord,  and  begins  to  undergo  secondary  degenera- 
tion. The  first  anatomical  sign  of  the  degeneration  is  a  breaking  down  of  the 
medullary  sheath  into  large  and  small  flakes  and  drops.  The  axis  cylinder  is  also 
soon  destroyed,  so  that  the  sheath  of  Schwann  finally  incloses  only  homogeneous 
fluid  contents,  which  are  in  great  part  rapidly  absorbed.  At  the  same  time  there 
is  an  increase  of  the  nuclei  in  the  sheath  of  Schwann,  and  this  increase,  when  the 
process  is  long  continued,  leads  to  a  decided  increase  of  the  interstitial  connective 
tissue  in  the  nerve.  The  diminution  and  final  loss  of  electrical  irritability  in  the 
nerve  are  perfectly  parallel  to  these  anatomical  changes,  as  we  can  easily  under- 
stand. 

The  degeneration  of  the  nerve  involves  its  finest  terminal  branches  in  the 
muscles;  but  the  muscle  itself  does  not  remain  unchanged.  The  muscular  fibers 
undergo  a  marked  atrophy.  They  become  much  smaller,  their  transverse  striatum 
is  less  distinct,  and  they  show  in  part  a  fatty  and  "  granular  "  degeneration  of  their 
contents.     The  motor  end-plates  of  the  nerves  in  the  muscles  are  spared  for  a  com- 

*  This  is  also  connected  with  the  repeated  observations  by  Erb,  Bernhardt,  and  others,  that  in 
lesions  of  peripheral  nerves,  and  perhaps  also  in  spinal  diseases,  reaction  of  degeneration  can  some- 
times be  made  out  even  in  those  muscles  which  show  no  essential  limitation  of  their  voluntary  mobil- 
ity. In  these  cases  the  electrical  examination  points  to  finer  anatomical  disturbances  which  have  not 
led  to  the  loss  of  voluntary  excitability. 


554  DISEASES  OF  THE  NERVOUS  SYSTEM. 

paratively  long  time,  and  they  disappear  only  when  the  degeneration  of  the  mus- 
cles has  reached  the  highest  degree.  In  regeneration,  however,  the  end-plates  are 
already  completely  restored  at  a  time  when  the  nerve-fibers  themselves  are  still 
found  destroyed  (Gessler).  Some  fibers  show  that  peculiar  yellow  homogeneous 
character  which  we  call  "  waxy  degeneration."  In  addition  to  this,  there  is  a  con- 
siderable increase  of  the  muscular  nuclei,  and  in  the  later  stages  a  great  new 
growth  of  interstitial  connective  tissue,  often  associated  with  a  marked  deposit  of 
fat.  These  muscles,  thus  altered,  now  react  only  to  the  galvanic  current,  and  in 
the  manner  above  described.  The  particular  cause  of  this  remarkable  fact  is,  of 
course,  still  completely  unknown  to  us. 

In  the  incurable  cases  the  processes  of  degenei-ation  just  described  gradually 
advance,  but,  in  the  cases  that  recover,  a  number  of  processes  of  regeneration  begin 
sooner  or  later.  We  can  not  here  go  into  the  finer  details,  which  are  still,  in  many 
respects,  the  subject  of  controversy;  but  it  is  certain  that  new  nervous  and  muscu- 
lar fibers  are  formed,  and  that,  hand  in  hand  with  the  anatomical  processes  of 
regeneration,  first  the  voluntary  motion,  and  later  the  electrical  excitability  of  the 
paralyzed  parts,  gradually  return  again. 

The  same  anatomical  changes,  which  we  have  just  described  as  a  secondary 
degeneration  in  lesions  of  the  peripheral  motor  nerves,  also  develop,  if  the  primary 
disease  has  its  seat  in  the  anterior  cornua  of  the  gray  matter  of  the  spinal  cord — 
that  is,  in  the  trophic  centers  themselves.  In  these  cases,  of  course,  the  form  of  the 
disease  has  nothing  to  do  with  it.  Both  in  the  different  forms  of  inflammation 
and  of  primary  atrophy,  and  also  in  new  growths,  which  affect  the  antei'ior  gray 
matter  of  the  cord,  a  secondary  degeneration,  with  pronounced  reaction  of  degen- 
eration, develops  from  the  anterior  roots  of  that  portion  of  the  cord  affected  to 
the  ends  of  the  peripheral  nerves,  and  even  to  the  corresponding  muscles.  We 
shall  also  learn  to  recognize  a  number  of  primary  degenerations  of  the  peripheral 
nerves,  such  as  primary  neuritis,  diphtheritic  and  toxic  paralyses,  etc.,  which  like- 
wise show  the  same  anatomical  changes,  and  likewise  give,  as  a  result  of  these,  elec- 
trical reaction  of  degeneration.  In  all  cerebral  paralyses,  however,  and  in  those 
spinal  paralyses  where  the  cause  of  the  paralysis  is  situated  above  the  part  of  the 
anterior  gray  cornua  concerned,  the  degenerative  atrophy,  and  also  the  reaction 
of  degeneration,  are  entirely  wanting. 

We  thus  see  that  the  reaction  of  degeneration,  in  regard  to  diagnosis,  at  once 
permits  us  to  decide  that  the  disease  is  situated  in  the  gray  matter  of  the  cord, 
or  in  the  peripheral  nerves.  It  does  not  permit  any  further  distinction.  In  regard 
to  prognosis,  it  teaches  us  that  anatomical  changes  have  taken  place  in  the  nerves 
and  muscles,  from  which  a  restoration  is  still  very  possible,  but  at  all  events  it  can 
take  place  only  after  the  lapse  of  a  longer  time,  at  least  two  or  three  months.  We 
will  soon  learn  to  recognize  a  number  of  mild  peripheral  paralyses  in  which  there 
is  generally  no  reaction  of  degeneration.  From  the  absence  of  reaction  of  degen- 
eration we  can  then  draw  the  conclusion,  with  certainty,  that  no  coarse  anatom- 
ical changes  are  present  in  the  nerve,  and  that  we  may  expect  after  the  trouble  a 
much  more  rapid  recovery,  perhaps  in  three  or  four  weeks.  The  partial  reaction 
of  degeneration,  above  mentioned,  is  also  an  important  symptom  in  regard  to 
prognosis.  It  shows  that  severe  anatomical  changes  have  taken  place  in  the  mus- 
cles but  not  in  the  nerves,  and  hence  it  always  permits  a  more  favorable  prognosis 
as  to  time  than  in  the  cases  with  complete  reaction  of  degeneration. 


THE  DIFFERENT  FORMS  OF  PERIPHERAL  PARALYSIS.       555 

CHAPTER  II. 
THE   DIFFERENT   FORMS   OF   PERIPHERAL   PARALYSIS. 

1.  Paralysis  op  the  Ocular  Muscles. 

.ffitiology, — The  largest  part  of  all  the  ocular  paralyses  arise  from  affections 
which  involve  either  the  peripheral  nerves  or  their  nuclei  in  the  brain-stem.  We 
accordingly  make  a  distinction  between  peripheral  and  nuclear  paralyses  of  the 
ocular  muscles.  As  we  shall  take  up  the  latter  more  fully  in  the  description  of 
chronic  bulbar  paralysis,  we  have  here  to  mention  only  the  most  important  and 
most  frequent  causes  of  the  peripheral  ocular  paralyses.     These  are  as  follows: 

1.  Traumatic  injuries,  which  directly  affect  the  nerve-trunks  or  their  branches : 
blows  on  the  eye,  knife-stabs,  fractures  of  the  skull  involving  the  orbit  or  the  base 
of  the  skull,  and  the  like. 

2.  Compression  of  the  nerves  from  morbid  processes  in  their  neighborhood. 
Tumors  of  the  base  of  the  skull,  especially,  very  often  lead  to  ocular  paralyses. 
Periostitis  at  the  base  of  the  skull  or  in  the  orbit  may  also  cause  similar  symptoms, 
and  so  do  syphilitic  diseases  of  the  nerves  and  their  surroundings,  the  meninges  or 
periosteum,  aneurisms  of  the  basilar  artery,  acute  or  chronic  meningitis  in  its  dif- 
ferent forms,  etc.  In  all  these  cases  we  usually  have  to  do  with  a  pure  mechanical 
compression  of  the  affected  nerves  by  the  morbid  new  growths  in  their  immediate 
vicinity.  More  rarely  the  pathological  process  directly  invades  the  nerves  them- 
selves. 

3.  The  so-called  rheumatic  ocular  paralyses  are  quite  common.  These  arise 
after  some  decided  exposure  to  cold,  such  as  a  draught  from  an  open  window,  and 
are  in  all  probability  very  largely  of  a  peripheral  nature.  They  depend,  as  is 
supposed,  upon  an  acute  neuritis  of  the  affected  nerve,  and  hence  are  to  be  re- 
garded as  completely  analogous  to  the  other  rheumatic  paralyses,  like  rheumatic 
facial  paralysis.  Among  the  "  rheumatic  paralyses  "  we  usually  class  the  paraly- 
ses which  apparently  come  on  spontaneously  and  completely  recover,  for  which 
no  other  special  cause  can  be  made  out. 

4.  The  ocular  paralyses  that  sometimes  arise  after  certain  acute  diseases  are 
also  of  a  peripheral  nature,  and  are  due  to  a  degenerative  neuritis  of  the  affected 
nerves.  They  are  most  frequent  as  a  result  of  diphtheria,  and  are  much  more 
rare  in  typhoid,  acute  rheumatism,  etc.  Of  chronic  diseases,  diabetes  mellitus  may 
sometimes  give  rise  to  ocular  paralyses,  especially  to  paralysis  of  accommodation. 

A  fuller  account  of  the  very  important  ocular  paralyses  in  tabes  dorsalis  will 
be  found  in  the  description  of  that  disease. 

Symptoms.— Since  we  must  refer  to  the  text-books  of  ophthalmology  in  regard 
to  the  more  precise  symptomatology,  and  the  more  special  methods  of  ophthalmic 
investigation,  we  will  here  give  only  a  brief  review  of  the  chief  symptoms  of  ocu- 
lar paralyses  which  are  important  in  nervous  pathology. 

The  disturbance  in  the  mobility  of  one  eye  is  noticed  by  the  patient  himself 
from  the  appearance  of  double  images— double  vision,  or  diplopia.  These  arise 
because,  on  looking  to  one  side,  the  eye  on  the  paralyzed  side  can  not  be  brought 
into  the  corresponding  position,  and  consequently  the  retinal  images  no  longer 
fall  upon  the  same  spots.  In  pathological  convergence  of  the  visual  axes  homolo- 
gous double  images  arise,  in  pathological  divergence  crossed  images— that  is,  in 
the  first  case,  on  closing  one  eye,  the  image  disappears  on  the  same  side,  in  the 
second  case  it  disappears  on  the  opposite  side.  By  alternately  fixing  the  gaze  on 
one  or  the  other  of  two  fingers  held  in  line  with  each  other,  and  by  regarding  the 
disappearance,  on  closing  one  eye,  of  the  double  image  of  the  finger  not  fixed,  we 
can  easily  demonstrate  this  on  ourselves.     If,  then,  crossed  double  images  arise, 


556  DISEASES  OF  THE  NERVOUS  SYSTEM. 

for  example,  on  looking  to  the  right,  we  must  have  a  divergent  strabismus — that 
is,  an  imperfect  function  of  the  left  internus;  but  if  there  are  homonymous 
double  images,  there  must  be  a  convergent  strabismus,  and  consequently  a  weak- 
ness in  the  right  abducens.  It  makes  it  much  easier  to  test  the  double  images  if 
we  put  a  colored  glass  before  one  of  the  patient's  eyes.  False  projections  of  the 
visual  field  arise,  as  a  result  of  the  double  images  and  of  the  abnormal  strength  of 
innervation  which  the  patient  exerts,  so  that  the  patient's  judgment  of  the  position 
of  external  objects  is  uncertain.  In  the  more  extensive  ocular  paralyses  this  often 
leads  to  a  pronounced  feeling  of  dizziness.  In  order  to  avoid  this  unpleasantness 
many  patients  confine  themselves  to  monocular  vision,  close  the  affected  eye,  or 
put  their  heads  in  a  position  to  avoid  the  double  images. 

Physical  examination  gives  the  following  results,  according  to  the  extent  of 
the  paralysis: 

In  complete  paralysis  of  one  ocnlo-motor  nerve  (the  levator  palpebras  superioris, 
the  superior,  inferior,  and  internal  recti,  the  inferior  oblique,  the  sphincter  of  the 
iris,  and  the  ciliary  muscle)  the  first  thing  that  is  noticed,  besides  the  disturbance 
in  the  movements  of  the  eye,  is  the  more  or  less  complete  drooping  of  the  upper 
lid — ptosis.  If  we  ask  the  patient  to  follow  with  his  eyes  the  motion  of  any 
object,  like  the  finger,  held  before  him,  keeping  his  head  still,  we  notice  at  once 
that  the  affected  eye  does  not  move  upward,  downward,  or  inward.  The  pupil  is 
dilated  (mydriasis)  and  no  longer  contracts  to  light.  Accommodation  is  lost,  and 
distinct  vision  for  near  objects  is  impossible.  As  a  rule,  the  whole  eye  seems 
rather  prominent  (paralytic  exophthalmus),  because  the  backward  traction  of  the 
recti  is  very  largely  absent.  In  old  oculo-motor  paralysis  there  is  often  a  second- 
ary contracture  in  the  unparalyzed  external  rectus  (and  superior  oblique),  by 
which  the  eye  is  persistently  drawn  outward.  Partial  oculo-motor  paralyses  are 
not  infrequent,  especially  isolated  ptosis,  isolated  paralysis  of  the  internal,  inferior, 
or  superior  rectus,  or  isolated  paralysis  of  accommodation,  and  they  may  usually 
be  easily  recognized  from  what  has  been  said. 

Paralysis  of  the  abducens  is  characterized  by  the  inability  to  move  the  external 
rectus.  The  eye  can  no  longer  be  moved,  or  it  can  be  moved  only  imperfectly, 
outward  beyond  the  median  line.  In  old  paralysis  the  eye  is  drawn  inward  from 
a  secondary  contracture  of  the  internal  rectus,  and  convergent  strabismus  arises. 
Paralysis  of  the  abducens  may  be  isolated,  bilateral,  or  combined  with  other  ocu- 
lar paralyses. 

Paralysis  of  the  trochlear  nerve,  the  superior  oblique  muscle,  is  not  perfectly 
easy  to  recognize;  but  it  is  rarely  of  special  practical  importance.  The  action 
of  the  superior  oblique  coincides  with  that  of  the  inferior  rectus.  The  paralysis 
of  the  former,  therefore,  is  soonest  recognized  by  the  retardation  of  the  eye  in 
movements  downward  and  also  inward,  and  sometimes  by  the  failure  of  the  eye 
to  revolve,  which  rotation  normally  takes  place  on  looking  downward,  and  is 
due  to  the  superior  oblique  muscle.  This  latter  movement  takes  place  in  each  eye 
inward,  toward  the  nose,  about  a  sagittal  axis,  in  such  a  way  that  the  left  eye  is 
turned  from  the  left  and  up  to  the  left  and  downward,  and  the  right  eye  from 
the  right  and  up  to  the  right  and  downward.  In  regard  to  diagnosis  it  is  also 
characteristic  that  the  double  images  in  trochlear  paralysis  appear  only  in  the 
lower  half  of  the  field  of  vision,  and  especially  on  looking  downward.  Hence  it 
happens  that  the  disturbance  of  vision  is  especially  manifest  in  going  up  or  down 
stairs. 

Finally,  we  must  mention  a  symptom  to  be  observed  in  almost  every  ocular 
paralysis — the  so-called  secondary  deviation  of  the  healthy  eye.  If,  after  the 
sound  eye  has  been  covered,  we  have  the  paretic  eye  fix  itself  upon  a  point  which 
it  can  not  reach  at  all,  or  which  it  can  reach  only  after  the  utmost  exertion,  we 


THE  DIFFERENT  FORMS  OF  PERIPHERAL  PARALYSIS.       557 

see,  when  the  covering  hand  is  taken  away  from  the  sound  eye,  that  the  latter 
has  been  moved  much  too  far  in  the  corresponding  direction.  The  abnormal 
exertions  of  innervation  with  the  affected  eye,  somewhat  after  the  analogy  of 
certain  associated  movements,  pass  over  to  the  associated  muscle  of  the  healthy 
side  and  cause  in  it  too  extensive  a  contraction. 

The  following  must  be  added  in  regard  to  the  separate  forms  of  ocular  paraly- 
sis: Rheumatic  ocular  paralysis  affects  the  abducens  most  frequently,  and  not 
infrequently  the  oculo-motor  or  one  of  its  branches,  as  in  isolated  ptosis.  A  case 
observed  by  us  a  short  time  ago  is,  at  any  rate,  rare,  in  which  exposure  to  severe 
cold  had  been  followed  by  a  complete  paralysis  of  all  the  muscles  of  the  right 
eye,  with  complete  ptosis,  and  almost  absolute  immobility  of  the  eye  in  any  direc- 
tion. The  rheumatic  ocular  paralyses  are  almost  always  acute  in  their  onset,  and 
they  are  often  during  the  first  period  associated  with  sensations  of  pain  about  the 
eye  and  in  the  head.  Vomiting  (of  reflex  origin  ?)  is  also  not  rare  at  the  beginning 
of  the  affection.  The  course  of  most  cases  is  favorable,  since  they  usually  com- 
pletely recover  in  a  few  weeks,  though  sometimes  not  for  months.  In  some  cases 
the  paralysis  may  remain  stationary.  The  diphtheritic  ocular  paralyses  usually 
appear,  like  the  other  diphtheritic  paralyses,  a  week  or  two  after  the  termination 
of  the  disease.  They  most  frequently  affect  the  muscles  of  accommodation,  so  that 
the  patient  complains  chiefly  of  indistinct  vision  for  near  objects ;  but  we  some- 
times see  paralyses  of  the  external  ocular  muscles  also,  the  abducens  or  the  inter- 
nal rectus.  The  prognosis  of  diphtheritic  paralyses  is  almost  invariably  favor- 
able. Finally,  we  must  mention  here  the  "  periodical  oculo-motor  paralysis,"  to 
which  Mobius  and  others  have  lately  called  attention,  and  whose  nature  is  still 
almost  wholly  inexplicable.  In  the  cases  of  this  sort  repeated  paralyses  of  one 
oculo-motor  nerve,  often  associated  with  headache  and  vomiting,  just  as  in  mi- 
graine, come  on  at  longer  or  shorter  intervals  (in  women  sometimes  at  the  men- 
strual period)  in  the  same  individual,  who  has  often  had  them  since  childhood. 
The  individual  attack  sometimes  lasts  only  a  few  days,  but  often  some  weeks. 
The  attacks  usually  become  gradually  more  severe  later  on. 

Nothing  generally  applicable  can  be  said  as  to  the  course  and  prognosis  of  the 
other  forms  of  ocular  paralyses,  since  in  them  everything  depends  upon  the  form 
of  the  underlying  disease. 

Treatment. — In  regard  to  the  fulfillment  of  any  possible  causal  indication  we 
must  remember  especially  that  a  syphilitic  origin  of  ocular  paralysis  is  not  very 
rare.  Iodide  of  potassium  and  energetic  mercurial  inunction  may  sometimes  give 
very  good  results  in  such  cases.  Hence  these  remedies  must  also  be  tried  in 
doubtful  cases. 

Of  other  remedies  galvanic  treatment  gives  the  speediest  relief.  We  pass  weak 
currents  transversely  through  the  temples,  or,  what  is  usually  better,  put  the  anode 
to  the  back  of  the  neck  and  apply  the  labile  cathode  to  the  closed  eye,  especially 
to  the  region  corresponding  to  the  paralyzed  muscles.  GTreat  caution,  weak  cur- 
rents, and  the  avoidance  of  any  great  variations  in  the  currents  are  of  course 
necessary.  We  may  also  try  preparations  of  strychnine  internally,  or,  better, 
subcutaneously  in  the  vicinity  of  the  eye.  We  must  refer  to  special  treatises  with 
regard  to  a  correction  of  the  double  images  by  prismatic  spectacles,  or  in  regard  to 
operations,  such  as  tenotomy,  that  are  sometimes  performed. 

2.  Paralysis  of  the  Motor  Branch  of  the  Trigeminus. 

(Paralysis  of  the  Muscles  of  Mastication.) 

Pai'alysis  of  the  muscles  of  mastication,  the  masseters  and  temporals,  supplied 
by  the  third  branch  of  the  trigeminus,  is  a  rare  affection.  It  is  most  frequently 
seen  in  diseases  of  the  base  of  the  skull  which  compress  the  motor  branch  of  the 


558 


DISEASES  OF  THE  NERVOUS  SYSTEM. 


fifth.  We  shall  also  learn  later  on  to  recognize  paralysis  of  the  muscles  of  mas- 
tication as  a  rare  symptom  of  chronic  bulbar  affections. 

The  chief  symptom  of  motor  paralysis  of  the  trigeminus  is  the  difficulty  or 
impossibility  of  chewing.  In  unilateral  paralysis  the  patient  can  chew  only  on 
the  healthy  side ;  in  bilateral  paralysis  he  can  no  longer  chew  at  all.  The  lower 
jaw  hangs  loosely  down  and  can  also  no  longer  be  moved  sideways,  from  the 
co-existing  paralysis  of  the  pterygoids.  There  are  often  sensory  disturbances  in 
the  distribution  of  the  trigeminus  at  the  same  time. 

The  prognosis  and  treatment  depend  upon  the  primary  disease.  Local  faradi- 
zation or  galvanization  of  the  paralyzed  muscles  is  to  be  tried. 

3.  Facial  Paralysis. 

(Mimetic  Facial  Paralysis.     PelPs  Palsy.) 

iEtiology. — Facial  paralysis  is  one  of  the  commonest  peripheral  paralyses,  as 
•we  can  understand  from  the  exposed  position  of  the  nerve  and  its  course  through 
the  narrow  Fallopian  canal.  The  most  important  causes  of  it  are  :  1.  Exposure 
to  cold,  draughts,  sleeping  by  an  open  window,  riding  in  the  cars  with  the  win- 
dow open,  etc.  The  paralyses  arising  in  this  way  are  termed  "  rheumatic,"  and  we 
also  include  in  this  class  those  peripheral  paralyses  which  are  apparently  spon- 
taneous— that  is,  those  without  any  marked  exposure  to  cold  that  can  be  dis- 
covered. In  all  these  cases  we  probably  have  to  do  with  a  neuritis  of  the  nerve- 
trunk,  which  comes  on  in  a  way  as  yet  unknown.  [In  a  recent  autopsy  of  a  case 
of  so-called  "  rheumatic  "  facial  paralysis,  Minkowski  found  a  simple  degenerative 
parenchymatous  neuritis,  without  any  swelling  of  the  nerve  sheath  or  increase 
of  connective  tissue. — K.]  2.  Diseases  of  the  middle  ear  and  caries  of  the 
petrous  bone.     As  the  facial  passes  through  the  Fallopian  canal,  which  is  in  the 

immediate  vicinity  of  the  tympanic 
cavity,  we  can  easily  understand  how, 
in  caries  of  the  petrous  bone  and  in 
purulent  affections  of  the  middle  ear, 
inflammation  may  often  invade  the 
trunk  of  the  facial,  or  how  the  facial 
may  be  compressed  by  inflammatory 
exudations,  etc.  3.  In  rare  cases  a 
pressure  paralysis  of  the  facial  nerve 
arises  in  swelling  of  the  parotid  gland 
or  tumors  in  its  vicinity.  4.  Dis- 
eases of  the  base  of  the  skull  or  brain, 
tumors,  syphilitic  new  growths,  and 
acute  or  chronic  inflammations,  often 
give  rise  to  the  development  of  a  fa- 
cial paralysis  by  invasion  of  the  trunk 
of  the  facial  or  compression  of  it.  5. 
We  shall  have  to  speak  repeatedly  of 
the  frequent  implication  of  the  facial 
nerve  in  diseases  of  the  brain  and  me- 
dulla in  the  following  sections. J 

Symptoms  and  Course.— The  mani- 
fold character  and  different  functions 
of  the  nerves,  which  unite  in  the  trunk 
of  the  facial,  are  the  cause  of  the  quite 
The  paralysis  of  the  facial  muscles  of 
The  paralyzed  half 


Fig.  74.— Right  facial  paralysis  (after  Seeligmüller). 
The  folds  are  smoother!  out  and  in  part  entirely  ab- 
sent on  the  paralyzed  side,  while  they  are  strongly 
marked  on  the  left.  The  mouth  and  nose  are  drawn 
to  the  left. 

large  array  of  symptoms  in  facial  paralysis 

expression  is  the  most  striking  and  characteristic  (see  Fig.  74) 


THE  DIFFERENT  FORMS  OF  PERIPHERAL  PARALYSIS.       559 

of  the  face  is  lax  and  expressionless,  the  wrinkles  in  the  forehead  are  obliterated, 
the  eye  is  abnormally  wide  open  and  waters  (epiphora),  the  naso-labial  fold  is  oblit- 
erated, the  corner  of  the  mouth  droops,  and  saliva  frequently  Hows  from  it.  The 
paralysis  becomes  still  more  marked  on  any  movement  of  the  face,  on  wrinkling 
the  forehead,  turning  up  the  nose,  laughing,  talking,  whistling,  or  inflating  the 
cheeks.  The  eye  can  be  only  partly  closed.  On  attempting  it,  the  upper  lid  sinks 
down  from  its  weight  (a  weakening  of  the  levator  palpebral  superioris),  the  eye  is 
turned  upward,  so  that  the  pupil  is  covered,  but  quite  a  wide  space  is  left  between 
the  eyelids  (lagophthalmus).  This  defective  closure  of  the  lids  facilitates  the 
entrance  of  dust,  etc.,  into  the  eye,  and  sometimes  gives  rise  to  conjunctivitis,  or 
even  to  severer  inflammation  of  the  eye.  Speech  is  rendered  difficult  and  indis- 
tinct from  defective  movements  of  the  lips,  and  mastication  becomes  impaired 
from  the  imperfect  movement  of  the  cheeks.  In  many  cases  we  also  find  a  paresis 
of  the  soft  palate  on  the  affected  side ;  the  fibers  from  the  facial  pass  through  the 
superficial  petrosal  nerve  to  the  spheno-palatine  ganglion,  and  thence  to  the  soft 
palate.  It  droops  more,  and  on  phonation  the  soft  palate  is  raised  obliquely  to 
the  healthy  side.  No  general  rule  can  be  given  as  to  the  position  of  the  uvula,  as 
this  varies  very  much  even  under  normal  conditions. 

Disturbances  of  taste  in  the  anterior  two  thirds  of  the  tongue  have  been  repeat- 
edly found  on  the  paralyzed  side,  but  they  usually  attain  only  a  slight  degree. 
They  are  explained  by  an  affection  of  the  fibers  of  the  chorda  tympani,  which  run 
for  some  distance  in  the  facial,  as  has  been  described  on  page  533.  At  the  begin- 
ning of  the  paralysis  many  patients  complain  of  subjective  sensations  of  taste. 
Later  on  the  dullness  of  taste  may  often  be  discovered  by  careful  testing.  Tactile 
sensibility  in  the  tongue  is  only  exceptionally  diminished  (sensory  fibers  in  the 
chorda?).  There  is  sometimes  a  diminished  secretion  of  saliva  (fibers  in  the 
chorda),  which  produces  an  abnormal  feeling  of  dryness  in  the  patient's  mouth  on 
the  paralyzed  side.  Disturbances  of  hearing  are  frequent,  but  they  are  usually 
due  to  some  complicating  aural  trouble  (vide  supra),  or  to  a  co-existing  affection 
of  the  acoustic  nerve.  Paralysis  of  the  stapedius  muscle,  however,  sometimes 
seems  to  cause  symptoms,  including  a  marked  sensitiveness  to  all  loud  sounds,  and 
even  an  abnormal  acuteness  of  hearing,  especially  for  low  notes  (hyperacusis  oxyo- 
koia).  This  symptom  is  due  to  the  fact  that  in  paralysis  of  the  stapedius  its 
antagonist,  the  tensor  tympani,  causes  a  greater  tension  of  the  membrana  tym- 
pani. Reflex  movements,  winking,  etc.,  are,  of  course,  lost  in  complete  peripheral 
facial  paralysis.  For  the  special  reflexes,  which  are  often  seen  in  the  later  stages 
of  facial  paralysis,  vide  infra. 

By  testing  all  the  symptoms  described,  in  most  cases  we  can  decide  with  accu- 
racy upon  the  place  where  the  break  in  conduction  in  the  facial  must  occur.  If  we 
examine  the  accompanying  plan  of  the  facial  (Fig.  75),  devised  by  Erb,  we  can 
easily  understand  the  following  chief  symptomatic  forms  of  facial  paralysis : 

1.  Paralysis  of  the  facial  muscles;  but  taste,  secretion  of  saliva,  hearing,  and 
soft  palate  normal ;  seat  of  the  affection  in  the  portion  between  1  and  2,  usually 
the  trunk  of  the  facial  below  the  Fallopian  canal. 

2.  Paralysis  of  the  facial  muscles,  disturbance  of  taste,  and  eventually  dimin- 
ished secretion  of  saliva ;  but  hearing  and  soft  palate  normal ;  seat  of  the  affection 
within  the  Fallopian  canal  between  2  and  3. 

3.  Paralysis  of  the  facial  muscles,  disturbance  of  taste,  diminished  secretion 
of  saliva,  abnormal  acuteness  of  hearing ;  but  soft  palate  normal ;  seat  between  3 
and  4. 

4.  Paralysis  of  the  facial  muscles,  disturbance  of  taste,  diminished  secretion  of 
saliva,  abnormal  acuteness  of  hearing,  and  paresis  of  the  soft  palate ;  seat  in  the 
geniculate  ganglion  between  4  and  5. 


560 


DISEASES  OF  THE  NERVOUS  SYSTEM. 


5.  Paralysis  of  the  facial  muscles,  diminished  secretion  of  saliva,  abnormal 
acuteness  of  hearing,  paresis  of  the  soft  palate,  but  no  disturbance  of  taste ;  seat 
above  the  geniculate  ganglion  between  5  and  6.     [Gowers  doubts  whether  there  be 

paralysis  of  the  soft  palate  in  le- 
sions of  the  facial  nerve.  If  it  ex- 
ist at  all  it  is  very  rare.  Conse- 
quently the  conclusions  just  given 
can  hardly  be  accepted  in  f  ull.— K.] 
The  changes  in  electrical  ex- 
citability, and  some  other  changes, 
may  be  best  described  in  connec- 
tion with  the  course  of  facial  pa- 
ralysis. The  paralysis  usually 
begins  quite  suddenly;  less  fre- 
quently it  is  more  gradual.  Some- 
times there  are,  for  a  short  time, 
subjective  prodromata,  such  as  ab- 
normal sensations  of  taste,  slight 
ringing  in  the  ears,  and  above  all 
painful  sensations  in  the  ear  and 
face,  which  symptoms  may  be  re- 
ferred to  the  beginning  of  acute 
inflammatory  processes  in  the 
nerve.  In  a  few  cases  the  occur- 
rence of  herpes  vesicles  has  been 
observed  in  the  distribution  of  the 
affected  facial,  a  condition  which 
may  be  soonest  explained,  in  ac- 
cordance with  what  was  said  on 
page  525,  by  reference  to  the  nu- 
merous anastomoses  between  the 
branches  of  the  facial  and  those 
of  the  trigeminus. 

In  regard  to  the  further  course 
we  distinguish  the  three  follow- 
ing forms: 

1.  The  mild  form  of  facial  paralysis,  to  which  especially  many  rheumatic 
paralyses  belong.  The  affection  is  usually  referred  only  to  the  facial  muscles, 
disturbances  of  taste,  etc.,  being  wholly  absent.  Electrical  excitability  in  the 
facial  and  the  paralyzed  muscles  remains  entirely  normal.  Recovery  is  rapid, 
usually  in  two  or  three  weeks.  In  these  cases  we  may  certainly  suppose  that 
there  are  no  severe  and  deep-seated  anatomical  changes  in  the  nervous  or  mus- 
cular fibers. 

2.  The  middle  form  of  facial  paralysis  (Erb).  In  this  there  is  no  complete 
reaction  of  degeneration,  but  only  a  partial  one.  The  excitability  of  the  nerve  is 
somewhat  diminished,  but  it  is  not  lost.  In  the  muscles,  however,  in  about  two 
or  three  weeks,  there  appears  a  decided  increase  of  galvanic  excitability  to  direct 
excitement.  The  anodic  closure  contraction  (AnSZ)  is  also  greater  than  the 
cathodic  closure  contraction  (KaSZ),  and  the  contractions  are  slow.  In  regard 
to  prognosis  we  may  decide  from  this  that  the  recovery  will  still  be  quite  rapid. 
It  usually  follows  in  from  four  to  six  weeks. 

3.  The  severe  form  of  facial  paralysis  is  that  in  which  there  is  a  complete 
reaction  of  degeneration  in  the  nerve  and  muscles,  the  details  of  which  we  have 


Fig.  75. — Schematic  representation  of  the  trunk  of  the  facial 
from  the  base  of  the  skull  to  the  pes  ansermus.  Differ- 
ent localizations  of  the  lesion  in  paralysis.  N.f.  Facial 
nerve.  N.p.s.  Great  superficial  petrosal.  N.c.c.p.t. 
Nerve  communicating  with  the  tympanic  plexus.  N.st. 
Stapedius.  Ch.t.  Chorda  tympani.  Gf.  Fibers  of  taste. 
Si>s.  Nerve  governing  the  secretion  of  saliva.  N.a. 
Acoustic  nerve.  G.g.  Geniculate  ganglion.  F.st.  Stylo- 
mastoid foramen.    N.a.p.  Posterior  auricular  nerve. 


THE  DIFFERENT  FORMS  OF  PERIPHERAL  PARALYSIS.       501 

learned  in  the  previous  chapter,  loss  of  faradic  and  galvanic  excitability  of  the 
nerve,  loss  of  faradic  excitability  of  the  muscles,  and  quantitative  and  qualitative 
changes  in  the  galvanic  excitability  of  the  muscles.  In  this  form  there  are  always 
coarse  processes  of  degeneration  in  the  nerve  and  muscles,  so  that  recovery  fol- 
lows, if  at  all,  only  after  two  to  six  months,  or  even  later,  because  the  processes  of 
regeneration  require  at  least  as  much  time  for  their  accomplishment.  We  often 
see  in  the  later  stages  of  these  cases  special  symptoms  of  motor  irritation  (Hitzig). 
These  consist,  first,  of  a  more  or  less  marked  tonic  contracture  of  the  paralyzed 
muscles,  which  is  sometimes  very  striking;  second,  of  single  spasmodic  contrac- 
tions of  the  muscles;  third,  of  special  associated  movements — if  the  patient  closes 
his  eyes,  winks,  etc.,  there  always  follows  a  marked  distortion  of  the  corner  of 
the  mouth,  which  can  not  be  suppressed ;  fourth,  of  an  increased  reflex  irrita- 
bility— on  pricking  the  skin,  or  blowing  on  it,  vigorous  muscular  contractions 
follow.  We  have  often  ourselves  seen  contractions  in  the  affected  facial  muscles 
following  a  blow  on  the  bridge  of  the  nose,  on  the  nasal  bone,  or  on  the  forehead 
on  the  healthy  side.  These  reflexes  come  from  the  skin,  or  perhaps  in  part  from 
the  periosteum  and  the  fasciae  also.  All  these  symptoms  may  last  for  a  very  long 
time — for  years  in  incurable  or  in  imperfectly  cured  cases.  The  above-described 
associated  movement  in  the  angle  of  the  mouth  on  shutting  the  eyes  we  have 
repeatedly  seen  in  students  who  have  had  an  injury  of  a  peripheral  branch  of  the 
facial  in  a  duel. 

Prognosis. — The  prognosis  of  facial  paralysis  depends,  of  course,  in  the  first 
place,  upon  the  primary  disease,  if  any  exists.  Paralysis  in  tumors  of  the  base  of 
the  brain,  caries  of  the  petrous  bone,  etc.,  is  almost  always  incurable.  The  course 
of  the  paralysis  in  affections  of  the  middle  ear  depends  upon  the  curability  of  the 
latter  disease.  Very  important  data  for  the  accurate  prognosis  of  rheumatic 
paralysis  are  given  by  the  electrical  examination,  as  has  been  carefully  described 
above.  Of  course,  we  can  never  form  a  definite  judgment  from  this  at  the  begin- 
ning of  the  paralysis,  but  only  at  the  end  of  the  first  week.  If,  at  the  end  of  the 
first  week  or  fortnight,  the  electrical  excitability  of  the  nerve  still  remains  normal, 
we  can  almost  certainly  prophesy  a  rapid  and  favorable  course.  If  reaction  of 
degeneration  appears,  we  can  not  count  upon  recovery  in  the  most  favorable  cases 
before  two  or  three  months.  As  a  rule,  relapses  do  not  occur,  but  we  saw  a  man 
of  about  thirty  who  had  a  peripheral  facial  paralysis  four  times  within  a  few  years, 
which  disappeared  each  time  after  a  few  weeks— a  condition  which  possibly  is  to 
be  regarded  as  analogous  to  the  "  periodical  oculo-motor  paralysis  "  (see  page  557;. 

Diagnosis. — The  symptoms  of  facial  paralysis  are  so  pronounced  that  the  paraly- 
sis itself  can  always  be  easily  recognized.  In  regard  to  the  precise  form  of  the 
paralysis  and  its  cause,  we  can  often  decide  only  by  considering  .the  aetiological 
factors,  such  as  injuries,  exposure  to  cold,  or  aural  affections.  In  distinguishing 
between  peripheral  and  central  (bulbar  or  cerebral)  paralyses,  the  other  co-exist- 
ing bulbar  or  cerebral  symptoms  must  also  be  considered.  We  shall  learn  to 
recognize  more  accurately  later  the  different  modes  in  which,  in  these  cases, 
facial  paralysis  may  be  combined  with  paralysis  of  the  other  cerebral  nerves,  or 
the  nerves  of  the  extremities.  In  doubtful  cases  electrical  examination  is  often  of 
decisive  value.  Reaction  of  degeneration  can  be  present  only  in  peripheral  paraly- 
sis, or  in  such  bulbar  paralyses  as  affect  the  fibers  of  the  facial  below  the  facial 
nucleus  or  affect  the  nucleus  itself.  In  all  the  genuine  cerebral  paralyses  the 
electrical  excitability  is  perfectly  retained.  It  may  also  be  mentioned  here  briefly 
that  in  all  cerebral  facial  paralyses  the  frontal  portion  of  the  facial  is  usually  un- 
affected, while  in  peripheral  paralysis  it  also  is  paralyzed.  The  power  to  close  the 
eye  is  usually  not  affected  in  cerebral  facial  paralysis. 

Treatment. — The  treatment  of  the  underlying  disease  is  of  the  greatest  impor- 
36 


562  DISEASES  OF  THE  NERVOUS  SYSTEM. 

tance  in  all  cases  where  any  aural  affection,  any  removable  compressing  swelling, 
as  of  the  parotid,  or  syphilis,  lies  at  the  bottom  of  the  trouble.  The  methods  of 
treatment  indicated  in  such  cases  are  self-evident.  In  other  cases  electricity  is 
the  only  remedy  which  can  give  sure  results,  although  we  must  not  overestimate 
its  efficiency.  In  fresh  facial  paralysis  we  may  recommend  the  stabile  conduction 
of  a  weak  constant  current  through  the  auriculo-mastoid  fossae,  four  to  six  times  a 
week  for  two  or  three  minutes,  at  first  the  anode,  then  the  cathode,  to  the  affected 
side.  Later  on  tbe  chief  treatment  is  peripheral  galvanization,  or  eventually 
faradization  of  tbe  muscles.  We  place  the  anode  in  the  auricular  fossa  and  slowly 
stroke  the  different  nerve-branches  and  the  muscles  with  the  cathode.  We  can 
often  confirm  the  fact,  immediately  after  each  sitting,  that  the  eye  closes  better 
after  galvanization  of  the  orbicularis.  Faradization  pei*haps  excites  a  reflex 
irritation  of  the  nerves  from  irritation  of  the  skin,  and  hence  is  of  service. 

Of  other  remedies  we  may  mention  subcutaneous  injections  of  strychnine, 
seven  to  fifteen  minims  of  a  one-per-cent.  solution  of  the  sulphate  three  or  four 
times  a  week,  although  it  is  only  rarely  of  use.  In  secondary  contractures 
we  may  obtain  favorable  results  by  methodical  stretching  of  the  muscles  by 
wooden  wedges  inserted  under  the  cheeks  and  by  massage. 

4.  Paralyses  in  the  Region  of  the  Muscles  of  the  Shoulder. 

Isolated  paralyses  of  these  muscles  are  rare,  with  the  exception  of  the  practi- 
cally important  paralysis  of  the  serratus.  Disturbances  in  their  functions  are 
more  frequent,  as  one  symptom  in  complicated  paralytic  states,  especially  in  pro- 
gressive muscular  atrophy.  The  diagnosis  of  these  paralyses  in  detail  is  often  very 
difficult. 

Paralysis  of  the  Sterno-cleido-mastoid  (spinal  accessory  nerve). — The  chin 
is  somewhat  raised  and  turned  toward  the  affected  side  in  consequence  of  the 
antagonistic  contracture  of  the  other  sterno-mastoid.  Motion  in  the  opposite 
direction  is  difficult.  In  bilateral  paralysis  of  this  muscle  it  is  very  difficult  to  tum 
the  head  with  the  chin  raised,  and  it  can  be  done  only  imperfectly. 

Paralysis  of  the  Trapezius  (spinal  accessory  nerve). — The  sbmilder  sinks 
downward  and  forward  so  that  the  supra-clavicular  fossa  becomes  deeper.  The 
median  border  of  the  scapula  is  not  parallel  to  the  vertebral  column,  as  under 
normal  conditions,  but  it  runs  obliquely  from  below  and  inward,  upward  and  out- 
ward. Voluntary  raising  of  the  shoulder,  "  shrugging  the  shoulder,"  is  impaired, 
and  it  can  be  done  only  by  the  levator  scapulae.  The  drawing  back  of  the  shoul- 
der, approximating  it  to  the  vertebral  column,  is  difficult,  and  can  be  done  only 
by  the  rhomboidei.  Raising  the  arm  above  the  horizontal  is  also  affected,  from 
the  impaired  fixation  of  the  scapula. 

Paralysis  of  the  Pectoralis  Major  and  Minor  (anterior  thoracic  nerves). 
— Abduction  of  the  upper  arm  is  difficult  or  impossible.  The  hand  can  no  longer 
be  placed  on  the  shoulder  of  the  healthy  side. 

Paralysis  of  the  Rhomboidei  and  the  Levator  Anguli  Scapula  (dorsalis 
scapulas  nerve)  can  be  certainly  recognized  only  when  tbe  trapezius  is  also  para- 
lyzed. Then  the  approximation  of  the  scapula  to  the  vertebral  column  (rhom- 
boidei) and  the  raising  of  the  scapula  (levator  anguli  scapulae)  are  completely 
abolished. 

Paralyses  of  the  Latissimus  Dorsi  (subscapular  nerves). — There  is  no 
deformity  when  at  rest,  but  the  arm  can  not  be  strongly  adducted,  and  the  hand 
can  not  be  placed  on  the  sacrum. 

Paralysis  of  the  Rotators  of  the  Humerus  Inward  and  Outward. — In 
paralysis  of  the  inward  rotators,  the  teres  major  and  subscapular,  innervated  by 
the  subscapular  nerves,  the  arm,  when  rotated  outward,  can  not  be  brought  back 


THE  DIFFERENT  FORMS  OF  PERIPHERAL  PARALYSIS.       563 

again  to  its  normal  position.  All  manipulations,  too,  which  the  paralyzed  arm 
tries  to  make  on  the  opposite  side  of  the  body,  are  considerably  impaired.  In 
paralysis  of  the  outward  rotators — the  infra-spinatus,  innervated  by  the  supra- 
scapular nerve,  and  the  teres  minor,  innervated  by  the  axillary — rotation  of  the 
arm  outward  is  abolished.  In  writing-  and  sewing-  (using  the  needle;,  the  paraly- 
sis causes  very  marked  disturbance. 

Paralysis  of  the  Serratus  Anticus  Major  (paralysis  of  the  long  thoracic 
nerve). — This  paralysis  is  quite  common,  and  therefore  is  of  practical  importance. 
Its  most  frequent  cause  is  traumatic  action  on  the  nerve;  therefore  it  is  espe- 
cially common  in  porters,  soldiers,  etc.  Besides  this,  serratus  paralysis  sometimes 
arises  from  exposure  to  cold,  "rheumatic  serratus  paralysis,"  and  also  as  a  result 
of  infectious  diseases,  such  as  typhoid,  and  as  one  symptom  of  progressive  mus- 
cular atrophy,  especially  in  the  juvenile  form. 

As  the  arm  hangs  down  quietly,  the  scapula  on  the  paralyzed  side  stands  out  a 
little  from  the  chest- wall,  from  the  action  of  the  antagonists  (the  rhomboidei,  the 
levator  anguli  scapulae,  and  the  trapezius),  its  lower  angle  is  a  little  appi'oximated 
to  the  vertebral  column,  and  therefore  its  median  edge  runs  obliquely  upward  and 
outward.  If  the  patient  tries  to  raise  his  arm,  he  can  raise  it  only  to  the  hori- 
zontal position,  and  we  fail  to  see  the  projection  of  the  tense  indentations  of  the 


Fig.  76.— Paralysis  of  the  right  serratus.    (From  a  photograph  by  Duchenne.) 

serratus  on  the  lateral  wall  of  the  chest;  but  as  soon  as  we  seize  the  scapula 
firmly  and  push  it  forward — that  is,  supply  the  missing  action  of  the  serratus— the 
patient  can  at  once  raise  the  arm.     If  the  arm  is  raised  upward  to  the  horizontal 


564  DISEASES  OF  THE  NERVOUS  SYSTEM. 

Hue,  the  scapula  approaches  the  vertebral  column ;  if  it  is  raised  forward,  there 
appears  a  very  characteristic  wing-like  projection  of  the  inner  border  of  the  scap- 
ula, so  that  we  can  touch  with  the  hand  the  inner  surface  of  the  scapula  (see  Fig. 
76).  Adduction  of  the  arm  and  laying  the  hand  on  the  other  shoulder  are  also 
disturbed.     The  cutaneous  sensibility  of  the  chest  is,  as  a  rule,  normal. 

The  course  of  serratus  paralysis  is  usually  tedious.  Recovery  does  not  take  place 
for  several  months,  as  a  rule.  Many  cases  are  incurable.  Treatment  consists 
chiefly  in  the  application  of  electricity  to  the  paralyzed  nerve  and  muscles. 

5.  Paralyses  of  the  Muscles  of  the  Back. 

Of  the  paralyses  of  the  muscles  of  the  back,  which  are  rarely  seen  except  as  a 
complication  of  more  extensive  paralyses,  paralysis  of  the  extensors  of  the  spine 
in  the  lumbar  region  (the  erector  spina?  and  its  divisions,  the  sacro-lumbalis  and 
longissimus  dorsi)  is  the  only  one  that  has  a  practical  interest.  This  is  seen  com- 
paratively often  in  the  muscular  atrophy  or  pseudo-hypertrophy  of  children  (vide 
infra),  and  causes  a  remarkably  characteristic  and  easily  recognizable  picture.  If 
we  make  the  little  patient  stand  up,  the  peculiar  carriage  of  the  body  strikes  us  at 
once.  The  lumbar  vertebrae  are  arched  forward  in  lordosis,  the  belly  is  very 
prominent,  and  the  upper  part  of  the  body  is  bent  backward.  The  trunk  is  bal- 
anced on  the  hips  and  the  gait  is  waddling.  The  paralysis  of  the  erectors  appears 
most  plainly  if  the  child  has  stooped  to  get  any  object  and  tries  to  straighten  up 
again.  He  can  bring  the  upper  part  of  his  body  into  the  erect  posture  only  by 
supporting  himself  with  his  hands  on  his  knees,  and  slowly  climbing  up  his 
thighs. 

6.  Paralyses  in  the  Region  of  the  Upper  Extremity. 

Paralysis  of  the  Deltoid  Muscle  {axillary  [circumflex*]  nerve). — Deltoid 
paralysis  occurs  either  as  one  symptom  of  complicated  paralyses  arising  from  the 
brachial  plexus,  or  as  an  isolated  traumatic  and  rheumatic  paralysis ;  that  is,  neu- 
ritic,  beginning  with  pains  in  the  region  of  the  shoulder.  It  may  be  recognized  by 
the  impossibility  of  raising  the  upper  arm  at  all.  We  can  easily  distinguish  it 
from  an  anchylosis  of  the  shoulder-joint  by  passive  motion.  If  tbe  paralysis 
lasts  a  long  time  there  is  a  very  marked  atrophy  of  the  muscle,  and  there  is  the 
electrical  reaction  of  degeneration  in  it.  Paralysis  of  the  teres  minor,  which  is 
also  innervated  by  the  axillary,  can  not  be  diagnosticated  with  certainty. 

Paralysis  of  the  Biceps  and  Brachialis  Anticus  (musculo-cutaneous  nerve) 
is  only  exceptionally  isolated,  but  is  quite  often  seen  combined  with  other  paraly- 
ses. The  forearm,  when  in  supination,  can  not  be  flexed,  but  in  pronation  the 
supinator  longus  it  can  still  display  its  action  of  flexion.  The  action  of  supina- 
tion by  the  biceps,  which  it  exerts  when  the  forearm  is  flexed,  is  also  absent.  We 
sometimes  see  at  the  same  time  a  disturbance  of  sensibility  on  the  radial  side  of 
the  forearm  from  an  affection  of  a  cutaneous  branch  of  the  musculo-cutaneous 
nerve. 

Radial  [Musculo- spiral]  Paralysis. — The  anatomical  course  of  the  radial  nerve 
causes  pressure  paralysis  of  this  nerve  to  be  among  the  commonest  peripheral 
paralyses.  It  is  seen  especially  when  the  nerve  is  pressed  against  the  humerus 
during  sleep  by  the  body  or  head  lying  on  it,  in  drunkenness,  sleeping  with  the 
arm  hanging  over  the  arm  of  a  chair,  etc.  The  paralysis  is  usually  noticed  imme- 
diately on  waking.  Other  traumatic  influences,  direct  injuries  of  the  nerve,  com- 
pression in  dislocation  of  the  shoulder,  in  fractures  of  the  humerus,  in  pressure 
from  crutches,  in  bandaging  the   arm,  etc.,  are   also  frequent  causes  of   radial 

*  We  have  followed  Henle's  nomenclature  for  the  peripheral  nerves. — Trans. 


THE  DIFFERENT  FORMS  OF   PERIPHERAL  PARALYSIS.       565 


paralysis.  Exposure  to  cold,  rheumatic  radial  paralysis,  plays  a  very  subordinate 
part.  For  lead  paralysis,  which  is  localized  chiefly  in  the  distribution  of  the  radial, 
vide  infra. 

The  radial  innervates  the  triceps  and  the  muscles  on  the  extensor  side  of  the 
forearm.  Paralysis  of  the  triceps  is  present  only  in  the  cases  where  the  point  of 
lesion  is  situated  quite  high  up,  as  in  crutch  paralyses,  dislocation  paralyses,  plexus 
paralyses,  etc.,  but  it  is  absent,  or  at  least  it  is  only  faintly  manifest,  in  most  of 
the  ordinary  pressure  paralyses,  in  which  the  place  where  the  radial  turns  about 
the  humerus  is  the  point  of  compression.  Triceps  paralysis  is  readily  recognized 
by  the  impossibility  of  extending-  the  forearm,  but  we  must  always  make  the  ex- 
periment with  the  upper  arm  raised,  so  as  to  exclude  the  action  of  gravity  in  ex- 
tending the  forearm. 

Paralysis  of  the  muscles  on  the  extensor  side  of  the  forearm  may  at  once  be 
recognized,  since  the  hand  hangs  down  relaxed  in  a  flexed  position  (see  Fig.  77). 
Any  dorsal  extension  by  the  extensor  carpi  ulnaris  and  the  extensor  carpi  radialis 
longus  and  brevis  is  impossible,  and  the  lateral  movements  of  the  hand  in  abduction 
and  adduction  are  rendered  difficult.  The  fingers  are  flexed,  the  first  phalanx  can 
not  be  extended  by  the  extensor  communis  digitorum,  extensor  indicis,  and  extensor 
minimi  digiti;  but  if  the  first  phalanges  be  extended  passively  and  supported,  the 
extension  of  the  terminal  phalanges  is  perfectly  normal,  from  the  action  of  the 
inter ossei  which  are  sup- 
plied by  the  ulnar  nerve. 
The  thumb  is  flexed  and 
adducted,  and  can  neither 
be  abducted  nor  extended 
actively  (extensores  ossis 
metacarpi  et  primi  et  se- 
cundi  internodii  pollicis). 
If  the  forearm  be  extend- 
ed and  pronated  it  can  not 
be  supinated  (supinator 
brevis),  but  the  flexed  fore- 
arm can  be  supinated  by 
the  biceps.     Flexion  of  the 

forearm  in  supination,  which  is  done  by  the  biceps  and  brachialis  anticus,  is 
retained,  but  flexion  when  half  pronated  ("  middle  position  ")  is  weakened,  from 
the  paralysis  of  the  supinator  longus.  If  we  have  the  patient  make  short  and 
rapid  movements  of  flexion  of  the  forearm  in  this  position  we  do  not  see  the 
characteristic  normal  prominence  of  the  tense  supinator  longus.  The  very 
characteristic  prominence  of  this  muscle  is  also  wanting  if  the  patient  tries  to 
hold  his  pronated  and  semi-flexed  forearm  firm  against  forcible  attempts  at 
extension. 

The  functional  disturbance  of  the  hand  in  radial  paralysis  is  very  considerable. 
The  action  of  the  flexors  is  also  weakened,  since  their  points  of  insertion  are 
approximated,  on  account  of  the  constant  drooping  of  the  hand.  We  often  see, 
too,  sensory  disturbances  as  well  as  motor  in  the  distribution  of  the  radial,  but 
these  are  usually  slight.  The  chief  seat  is  on  the  radial  half  of  the  back  of  the 
hand  and  the  dorsal  surface  of  the  thumb,  and  index  and  middle  fingers  (compare 
Fig.  61).  The  electrical  excitability  of  the  paralyzed  parts  corresponds  to  the  laws 
that  generally  obtain.  At  the  onset,  and  in  mild  cases,  it  is  normal ;  at  a  later 
period,  in  severe  cases,  there  are  pronounced  atrophy  and  reaction  of  degeneration. 
It  is  worthy  of  note  that  in  all  forms  of  radial  paralysis,  especially  in  lead  paraly- 
sis, we  very  often  find  a  peculiar  chronic  thickening  and  swelling  of  the  tendons 


Fig. 


"7. — Position  of  the  hand  in  paralysis  of  the  radial  nerve. 
(From  Seeligmüller.) 


566 


DISEASES  OF  THE  NERVOUS  SYSTEM. 


on  the  back  of  the  hand,  the  chief  cause  of  which  is  probably  the  mechanical 
tension  of  the  tendons. 

Ulnar  Paralysis. — Except  from  the  frequent  implication  of  the  muscles  sup- 
plied by  the  ulnar  nerve  in  extensive  paralyses  and  atrophies,  especially  in  pro- 
gressive muscular  atrophy,  ulnar  paralysis  arises  chiefly  from  traumatic  influ- 
ences, pressure,  wounds,  fractures  of  the  humerus,  dislocations  of  the  shoulder- 
joint,  etc.     Neuritic  paralyses  are  more  rare. 

Flexion  of  the  hand,  and  especially  its  lateral  movement  to  the  ulnar  side,  is 
disturbed  (flexor  carpi  ulnaris).  Flexion  of  the  last  three  fingers  is  imperfect 
from  partial  paresis  of  the  flexor  profundus  digitorum,  and  the  little  finger  can 
not  be  moved  at  all  (hypothenar  muscles).  Paralysis  of  the  interossei  is  most 
striking,  by  which  flexion  of  the  primary  phalanges  and  extension  of  the  terminal 
phalanges  of  the  fingers  becomes  impossible.  Spreading  the  fingers,  and  still 
more  bringing  them  together  again,  is  also  much  impaired  (interossei,  lumbri- 
cales).  The  thumb  can  not  be  firmly  adducted  against  the  metacarpal  bone  of  the 
index-finger  (adductor  pollicis). 

In  almost  all  old  cases  of  ulnar  paralysis  a  very  characteristic  position  of  the 
hand  is  developed,  besides  the  muscular  atrophy  which  is  especially  noticeable  in 
the  interosseal  furrows  of  the  back  of  the  hand.  By  the  contraction  of  the  mus- 
cles antagonistic  to  the  paralyzed  interossei  (extensor  and  flexor  communis  digi- 
torum), the  first  phalanges  are  put  in  marked  dorsal  extension,  but  the  tercninal 
phalanges  are  completely  flexed,  so  that  the  hand  assumes  an  actual  clawing  posi- 
tion— "claw-like  hand,"  main  en  griffe  (see  Fig.  78). 

The  disturbance  of  sensibility,  if  it  be  present  at  all,  affects  the  volar  surface  of 
the  last  two  fingers,  the  dorsal  surface  of  the  last  three  fingers,  and  a  portion  of 
the  back  of  the  hand  (see  Figs.  59  and  60). 

Median  Paralysis. — Median  paralysis  is  seen  chiefly  as  a  traumatic  paralysis. 
It  is  often,  too,  one  symptom  of  more  extensive  paralyses,  in  progressive  muscular 
atrophy,  etc. 

The  disturbances  of  motion  are  very  striking.  Pronation  of  the  forearm  is 
almost  wholly  abolished  (pronator  radii  teres  and  quadra tus).     The  hand  can  he 

flexed  only  toward  the  ulnar 
side  by  the  flexor  carpi  ulnaris 
(paralysis  of  the  flexor  carpi 
radialis).  The  terminal  pha- 
langes of  the  fingers  can  no 
longer  be  flexed  (flexor  sub- 
limis  digitorum  and  a  part  of 
the  profundus),  but  flexion  of 
the  primary  phalanges  is  nor- 
mal by  means  of  the  interossei. 
Si«,.         ^      s  The  patient  can  grasp  an  ob- 

Fig.  78.— Claw-shaped  hand,  main  en  griffe.    (From  Duchenne.)     ject     Only    by    the     last     three 

fingers,  which  can  still  be 
partly  flexed  by  the  flexor  profundus  digitorum  (ulnar  nerve).  The  thumb  can 
no  longer  be  flexed  or  opposed  (flexor  longus  pollicis  et  brevis,  opponens),  and 
usually  lies  on  the  hand. 

If  thei'e  is  any  disturbance  of  sensibility,  it  is  found  on  the  volar  surface  of  the 
thumb  and  the  two  adjacent  fingers,  and  also  on  the  dorsal  surface  of  the  terminal 
and  middle  phalanges  of  the  index  and  middle  fingers,  and  the  radial  side  of  the 
ring-finger  (see  Figs.  60  and  61).  We  quite  frequently  see  in  severe  cases  trophic 
disturbances,  vesicles  on  the  fingers,  a  shining  atrophic  skin,  and  changes  in  the 
nails.  , 


THE  DIFFERENT   FORMS  OF  PERIPHERAL  PARALYSIS.       567 

Combined  Paralyses  of  the  Arm.— Combined  paralyses,  in  which  the  affected 
muscles  belong  to  the  distribution  of  several  nerves,  occur  in  various  forms,  espe- 
cially as  a  result  of  injuries  which  affect  tbe  brachial  plexus  in  the  neck — plexus 
paralyses.  To  this  class  belong  also  a  great  part  of  the  paralyses  following  dislo- 
cation of  the  humerus — dislocation  paralyses. 

A  combined  plexus  paralysis,  first  described  by  Erb,  and  since  then  repeatedly 
observed,  deserves  special  mention.  In  this  the  deltoid,  biceps,  hrachialis  anticus, 
and  supinator  longus  (muscles  whose  nerves  all  rise  from  the  roots  of  tbe  fifth 
and  sixth  cervical  nerves)  are  paralyzed  at  the  same  time.  The  arm  hangs  down 
relaxed,  and  can  not  be  raised  at  all,  the  forearm  can  not  be  flexed  at  all,  but  the 
hand  and  fingers  have  their  normal  mobility.  The  cause  of  the  paralysis  must 
have  its  seat  at  the  point  where  the  nerve-fibers  for  the  muscles  mentioned  lie 
near  one  another  (see  Fig.  68).  Sometimes  the  infra-spinatus  is  also  paralyzed,  so 
that  when  the  arm  is  rotated  inward  it  can  not  be  rotated  outward. 

This  same  combination  of  paralyzed  muscles  is  found  in  a  part  of  the  delivery 
paralyses  first  described  by  Duchenne.  These  are  sometimes  seen  in  infants  after 
hard  labor,  and  are  the  result  of  traumatic  injuries  of  the  brachial  plexus  in  turn- 
ing, in  the  Prague  method,  in  extracting  the  child  by  the  shoulders,  etc. 

In  some  cases  of  complicated  paralyses  of  the  brachial  plexus,  which  are  usu- 
ally traumatic  (Seeligmüller  and  others),  co-existing  symptoms  on  the  part  of  the 
sympathetic  have  been  observed,  consisting  of  contraction  of  the  pupil,  narrowing 
of  the  opening  of  the  lids,  and  a  retraction  of  the  eyeball  on  the  paralyzed  side. 
These  symptoms,  pointing  to  a  paralysis  of  sympathetic  nerves  (vide  infra,  page 
591),  probably  depend,  as  follows  from  clinical  and  experimental  investigations 
(Klumpke),  always  upon  a  lesion  of  the  ramus  communicans  of  the  first  dorsal 
nerve.  Vaso-motor  symptoms  in  the  face  are  usually  absent,  but  we  sometimes 
find  a  peculiar  flattening  of  the  cheeks,  which  has  not  yet  been  correctly  ex- 
plained. 

General  Prognosis  and  Treatment  of  the  Peripheral  Paralyses  of  the  Upper 
Extremity. — In  the  prognosis  of  the  peripheral  paralyses  of  the  arm  the  same 
points  hold  good  that  have  been  spoken  of  in  the  prognosis  of  facial  paralysis. 
In  this,  too,  there  are  mild  and  severe  cases,  the  latter  having  complete  reaction  of 
degeneration,  and  a  course  that  lasts  at  least  several  months  before  recovery.  A 
number  of  traumatic  paralyses  can  be  cured  only  up  to  a  certain  point,  or  they 
may  be  even  entirely  incurable. 

The  treatment  can  fulfill  a  causal  indication  only  in  comparatively  rare  cases, 
when  we  can  succeed  in  removing  by  operation  any  compressing  tumors,  cica- 
trices, splinters  of  bone,  formations  of  callus,  etc. 

In  other  cases  the  electrical  treatment  of  paralyses  promises  the  best  success. 
We  use  the  galvanic  current  chiefly,  although  we  generally  employ  the  faradic  cur- 
rent at  the  same  time.  In  regard  to  the  method  of  application,  we  may  employ  the 
stabile  action  of  the  constant  current  on  the  very  point  of  the  lesion,  especially  in 
fresh  cases,  but  the  chief  method  is  the  electrical  irritation  of  the  paralyzed  nerves 
and  muscles.  We  treat  the  nerve  above  the  point  of  the  lesion  in  order  to  act  in 
some  degree  against  the  hindrance  to  conduction  from  above  and  to  overcome  it. 
The  muscles  are  irritated  by  galvanism  by  stroking  the  cathode  over  the  separate 
paralyzed  muscles.  If  there  is  reaction  of  degeneration,  with  anodic  contractions 
predominating  or  exclusively  present,  we  use  the  anode  for  the  testing  pole.  The 
other  pole  is  placed  on  the  back  of  the  neck  or  on  the  seat  of  the  lesion.  Fara- 
dization of  the  muscles  may  also  be  of  service,  especially  if  the  muscles  react  to 
faradism ;  but,  even  if  this  is  not  the  case,  the  sensory  faradic  irritation  has  per- 
haps a  favorable  influence,  since  it  produces  a  reflex  irritation  of  the  motor 
nerves.     The  single  sittings  should  last  five  or  ten  minutes,  and  should  take  place 


568  DISEASES  OP  THE  NERVOUS  SYSTEM. 

daily  or  three  or  four  times  a  week.  The  fresher  the  paralysis,  the  more  favor- 
ahle,  comparatively,  is  the  prognosis,  but  even  in  old  and  severe  cases  we  may 
sometimes  obtain  noticeable  results  by  patience  and  perseverance.  The  treatment 
must  in  such  cases  be  kept  up  for  months,  and  even  longer,  with  occasional  inter- 
ruptions. 

Embrocations  with  spirits  and  with  similar  substances  must  often  be  prescribed 
in  practice,  but  they  act  favorably  only  when  associated  with  methodical  massage 
of  the  paralyzed  muscles.  We  sometimes  see  a  certain  advantage,  too,  from  local 
warm  bathing,  or  from  the  use  of  the  baths  in  Teplitz,  Wiesbaden,  Wildbad,  etc. 

7.  Paralyses  of  the  Diaphragm. 

Isolated  paralysis  of  the  diaphragm  occurs  but  rarely,  in  wounds  of  the  phrenic 
nerve  in  the  neck,  as  a  "  rheumatic  "  paralysis,  and  finally  in  hysteria.  Muscular 
paresis  of  the  diaphragm  seems  to  develop  sometimes  as  a  result  of  inflammation 
of  the  serous  layer  of  the  diaphragm.  The  paralysis  of  the  diaphragm  which 
comes  on  as  one  symptom  in  more  extensive  paralyses,  is  more  frequent  and  prac- 
tically more  important.  In  diseases  of  the  npper  cervical  cord,  in  ascending 
myelitis,  in  progressive  muscular  atrophy,  in  multiple  neuritis,  etc.,  the  develop- 
ment of  paralysis  of  the  diaphragm  is  the  cause  of  the  rapidly  fatal  termination 
which  follows  the  appearance  of  disturbance  of  respiration. 

The  symptoms  of  paralysis  of  the  diaphragm  are  readily  recognized,  especially 
in  the  ordinary  bilateral  affection.  We  detect  the  modification  of  the  respiratory 
movements  at  the  first  glance.  While  we  are  struck  by  the  marked  upper  thoracic 
respiration,  which  becomes  very  labored  on  the  slightest  cause,  the  visible  and 
palpable  protrusion  of  the  epigastrium  on  inspiration  is  entirely  absent.  Instead 
of  this  there  is  usually  an  inspiratory  retraction  in  the  epigastric  region.  The 
respiration  is  but  little  accelerated  in  simple  paralysis  of  the  diaphragm  as  long  as 
the  patient  is  perfectly  quiet;  but  in  other  cases  the  development  of  a  severe 
bronchitis,  from  the  defective  respiration  in  the  lower  lobes  of  the  lungs,  causes 
constant  dyspnoea.  The  cause  of  the  bronchitis  may  be  found  in  the  fact  that  the 
action  of  abdominal  pressure  is  very  much  diminished  in  the  constant  high  posi- 
tion of  the  diaphragm,  which  may  be  made  out  by  percussion,  and  consequently 
the  cough  and  the  expectoration  of  secretion  are  very  imperfect. 

The  prognosis  is  favorable  only  in  hysterical  and  rheumatic  paralyses;  other- 
wise it  is  usually  very  unfavorable.  In  regard  to  treatment,  the  only  thing  that 
can  be  tried  is  to  excite  the  diaphragm  from  the  phrenic  in  the  neck  by  faradism 
or  galvanism,  while  the  other  pole  is  placed  on  the  region  of  the  insertion  of  the 
diaphragm  in  the  thorax.  A  transverse  conduction  of  the  constant  current 
through  the  diaphragm,  associated  with  changes  of  the  current,  may  also  have  a 
favorable  influence. 

8.  Paralyses  in  the  Region  of  the  Lower  Extremity. 

Paralysis  of  the  Crural  Nerve.— Crural  paralysis  is  but  rarely  isolated. 
It  is  seen  after  injuries,  after  compression  of  the  nerve  by  tumors  of  the  pelvis  or 
thigh,  in  disease  of  the  vertebrae,  psoas  abscess,  etc. 

The  symptoms  are  readily  recognized.  The  thigh  can  not  be  flexed  on  the 
trunk,  and  the  trunk  can  not  be  raised  from  the  recumbent  position  (ilio-psoas 
muscle).  The  leg  when  flexed  can  not  be  extended  (quadriceps  extensor).  Walk- 
ing and  standing  are  very  difficult  or  almost  impossible.  Paralysis  of  the  sar- 
torius  and  pectineus  causes  no  special  symptoms.  If  there  is  any  disturbance  of 
sensibility  it  is  found  in  the  lower  half  of  the  anterior  surface  of  the  thigh  and 
on  the  inner  side  of  the  leg  down  to  the  great  toe  (saphenous  nerve,  see  Figs.  62 
and  63). 


THE  DIFFERENT  FORMS  OF  PERIPHERAL  PARALYSIS.       569 

Paralysis  of  the  Obturator  Nerve  is  very  rarely  seen  as  an  isolated  phe- 
nomenon. The  chief  symptom  is  the  defective  adduction  of  the  thigh  (the  ad- 
ductor magnus,  longus,  and  brevis,  and  the  gracilis),  and  the  impossibility  of  cross- 
ing one  leg  over  the  other.  Rotation  of  the  thigh  outward  is  also  disturbed  (ob- 
turator externus).  Some  disturbance  of  sensuality  may  be  found  on  the  inner  side 
of  the  thigh. 

Paralyses  in  the  Distribution  of  the  Gluteal  Nerves  are  not  uncommon.  We 
have  seen  them  in  progressive  muscular  atrophy  and  in  multiple  neuritis. 
Paralysis  of  the  glutaeus  maximus  is  rendered  noticeable  by  the  fact  that  this 
muscle  extends  the  thigh  on  the  pelvis.  It  is  therefore  especially  called  into  play 
in  going  up-stairs,  climbing  mountains,  and  rising  from  a  sitting  position.  All 
these  movements  are  rendered  nearly  impossible  when  the  muscles  are  paralyzed. 
The  glutaeus  medius  and  glutaeus  minimus  are  abductors  of  the  thigh,  and  also  fix 
the  thigh  on  the  pelvis.  If  they  are  paralyzed  the  patient  has  a  very  characteristic 
waddling  gait.  On  account  of  the  predominance  of  the  adductors  the  feet  are 
then  advanced  near  each  other  or  even  one  over  the  other.  Rotation  of  the  thigh 
inward  is  also  due  in  part  to  fibers  of  the  glutaeus  medius,  but  chiefly  to  the  ob- 
turator internus. 

Paralyses  in  the  Region  of  the  Sciatic  are  quite  frequently  seen.  They  come 
from  traumatic  lesions,  from  compression  of  the  separate  nerve-branches  in.  dis- 
eases of  the  vertebra?,  in  pelvic  tumors,  in  hard  labors,  rarely  from  rheumatic  in- 
fluences, sciatic  neuritis  etc. 

Paralysis  of  the  Peroneal  Nerve,  which  is  also  frequently  isolated,  may  at 
once  be  recognized  by  the  flaccid  drooping  of  the  foot.  On  walking,  this  becomes 
very  marked,  and  the  tip  of  the  foot  often  sticks  to  the  floor.  The  patient,  there- 
fore, has  to  raise  the  thigh  higher,  and  to  put  the  foot  down  awkwardly,  toe  first. 
Dorsal  extension  of  the  foot  (tibialis  anticus)  and  of  the  toes  (extensor  communis 
digitorum  longus  and  extensor  hallucis  longus),  and  also  abduction  of  the  foot 
and  raising  its  outer  border  (the  peronei),  are  almost  impossible.  In  old  cases  a 
permanent  toe-drop  (talipes  equinus  or  varo-equinus)  develops,  usually  as  a  result 
of  secondary  contracture  of  the  muscles  of  the  calf. 

Paralysis  of  the  Tibial  Nerve  makes  plantar  flexion  of  the  foot  impos- 
sible (gastrocnemius  and  soleus).  The  patient  can  no  longer  rise  on  his  toes. 
Adduction  of  the  foot  (tibialis  posticus)  and  plantar  flexion  of  the  toes  (flexor 
communis  digitorum  and  flexor  hallucis  longus)  are  also  abolished.  As  a  result 
of  secondary  contractures,  talipes  calcaneus  sometimes  develops,  and  also  a  claw- 
like  position  of  the  toes,  with  dorsal  extension  of  the  first  and  plantar  flexion  of  the 
last  phalanges  from  paralysis  of  the  interossei. 

In  Paralyses  of  the  Trunk  of  the  Sciatic  there  is  added  to  the  symptoms 
mentioned  the  inability  to  flex  the  leg  backward  on  the  thigh  (to  be  tested  when 
the  patient  is  lying  on  his  side  or  standing),  which  is  due  to  a  paralysis  of  the  bi- 
ceps, semi-membranosus,  and  semi-tendinosus.  In  unilateral  paralysis  of  the 
sciatic,  walking  is  still  possible,  since  the  leg  is  fixed  at  the  knee  by  the  quadriceps 
extensor  and  is  rigid  like  a  wooden  leg. 

The  distribution  of  the  disturbance  of  sensibility  on  the  posterior  surface  of  the 
whole  leg  is  given  in  Fig  63.  Vaso-motor  and  trophic  disturbances,  cyanosis  and 
coldness  of  the  skin,  and  atrophy  of  the  muscles,  are  often  present. 

Treatment  follows  the  same  rules  as  are  given  for  the  management  of  periph- 
eral paralyses  in  the  upper  extremity. 

9.  Toxic  Paralyses. 
Lead  Paralysis. — Of  all  the  toxic  paralyses,  that  from  lead  poisoning  is  prac- 
tically the  most  important.     It  is  a  common  symptom  of  chronic  lead  poisoning. 


570  DISEASES  OF  THE  NERVOUS  SYSTEM. 

and  is  seen  chiefly  in  those  people  whose  occupation  gives  rise  to  a  long-con- 
tinued taking  of  small  amounts  of  lead  into  the  system,  especially,  therefore,  in 
type-setters,  type-cutters,  and  type-founders;  in  artists  and  house-painters,  from 
lead  colors;  in  potters,  from  lead  glaze,  etc. 

As  to  the  special  anatomical  causes  of  lead  paralysis,  we  have  not  yet  reached 
a  complete  harmony  in  our  theories.  While  some  seek  the  starting-point  of  the 
paralysis  in  the  muscles  themselves,  most  authors  at  present  assume,  as  a  cause  of 
the  paralysis,  an  affection  of  the  nervous  system  excited  by  the  toxic  action  of  the 
lead.  Since  lead  paralysis  belongs  to  the  genuine  atrophic  paralyses  (vide  supra), 
as  we  shall  soon  see,  we  have  to  do  only  with  a  disease  of  the  anterior  gray  cornua 
in  the  cord,  or  with  a  degeneration  of  the  peripheral  motor  nerves.  The  positive 
lesions  found  at  present  do  not  fully  agree,  but  there  can  be  scarcely  a  doubt, 
after  the  discoveries  of  Leyden,  Zunker,  and  others,  that,  at  least  in  most  cases, 
the  degenerative  atrophy  of  the  peripheral  motor  nerve-fibers  is  primary,  and  that 
the  degenerative  atrophy  of  muscles  supplied  by  tbe  nerves  follows  secondarily  in 
the  ordinary  way.  In  many  cases,  however,  there  is  perhaps,  besides  the  periph- 
eral degeneration,  an  affection  of  the  cord,  especially  in  the  anterior  gray  cornua, 
caused  by  the  toxic  action  of  the  lead. 

Lead  paralysis  shows  an  extremely  typical  localization  in  the  great  majority  of 
cases,  and  it  affects  by  far  the  most  frequently  a  part  of  the  radial  distribution.  A 
paralysis  of  the  extensor  communis  digitorum  comes  on  rapidly  or  slowly.  Ex- 
tension of  the  primary  phalanx  of  the  middle  and  ring,  and  later  of  the  index  and 
little  fingers,  becomes  impossible,  but  the  extension  of  the  terminal  phalanges  by 
the  interossei  remains  normal.  There  often  follows  later  a  paralysis  of  the  exten- 
sor longus  pollicis  and  the  extensor  brevis,  and  of  the  abductor  pollicis  and  the 
extensors  of  the  wrist,  while  the  supinator  longus  and  the  triceps  almost  always 
remain  free  in  a  remarkable  way.  In  much  rarer  cases  lead  paralysis  affects  the 
deltoid,  biceps,  brachialis  anticus,  and  supinators.  Paralysis  of  the  lower  extremi- 
ties is  also  very  rare. 

Lead  paralysis  is  usually  bilateral.  In  all  severe  cases  a  pronounced  atrophy 
and  electrical  reaction  of  degeneration  develop  in  the  paralyzed  muscles.  It  is  an 
interesting  point  that  the  latter  may  sometimes  be  made  out  in  muscles  which  can 
be  perfectly  well  moved  by  the  will  (see  page  553).  The  sensibility  is  almost  inva- 
riably perfectly  normal,  so  that  the  sensoiy  nerves  are  manifestly  unaffected  by 
the  lead. 

Lead  paralysis  permits  a  favorable  prognosis  in  the  cases  where  the  patient 
can  be  removed  from  the  injurious  influence  of  the  poison.  Recovery  takes  place 
after  several  weeks,  or  in  severe  cases  after  some  months.  Relapses  and  compli- 
cations with  other  morbid  results  of  chronic  lead  poisoning,  however,  are,  of 
course,  frequent. 

The  treatment  is  the  same"  as  in  all  other  peripheral  paralyses.  Electricity  is 
first  to  be  considered.  Local  sulphur  baths  and  the  internal  use  of  iodide  of  potas- 
sium are  also  recommended. 

[It  is  well  to  mention  here  that  chronic  lead  poisoning  may  give  rise  to  symp- 
toms closely  resembling  those  of  almost  every  chronic  disease  of  the  nervous  sys- 
tem. It  is  often  so  difficult  to  detect  the  source  of  the  lead  that  it  is  well  in  all 
obscure  nervous  diseases  to  test  the  urine  for  the  metal  after  iodide  of  potassium 
has  been  administered  in  five-  to  ten -grain  doses  thrice  daily  for  a  week.  For  the 
precautions  to  be  observed  in  carrying  out  this  test  the  reader  is  referred  to  works 
on  medical  chemistry.  If  large  doses  of  the  iodide  are  administered  there  is  dan- 
ger lest  the  lead  be  liberated  too  rapidly  and  cerebral  symptoms  supervene.  J.  J. 
Putnam  has  shown,  however,  that  lead  is  often  found  in  the  urine  of  persons  in 
apparent  good  health.    Lead  may  also  cause  simple  anaemia,  and  it  is  occasionally 


THE  DIFFERENT  FORMS  OF  LOCALIZED  SPASM.  571 

found  in  the  urine  of  patients  with  degenerative  diseases  of  the  spinal  cord,  espe- 
cially combined  sclerosis,  ataxic  paraplegia,  and  chronic  myelitis.] 

Arsenical  Paralysis. — Arsenical  paralysis  is  much  rarer  than  that  from  lead. 
In  distinction  from  that  it  comes  on  especially  after  acute  poisoning  with  arsenic, 
and  usually,  though  not  always,  it  follows  immediately  the  other  symptoms  of 
poisoning.  The  localization  of  the  paralysis  is  not  as  typical  as  in  lead  paralysis. 
The  paralysis  is  sometimes  very  extensive  over  the  arms  and  legs,  but  it  usually 
chiefly  affects  only  the  lower  extremities.  The  paralyzed  muscles  rapidly  atrophy. 
It  has  not  yet  been  certainly  decided  whether  reaction  of  degeneration  occurs. 
The  accompanying  disturbances  of  sensibility  are  very  characteristic,  either  anaes- 
thesia, or  especially  paresthesia  and  severe  pains  in  the  sacrum  and  legs.  Trophic 
disturbances  in  the  nails,  hair,  etc.,  have  been  repeatedly  observed.  Nothing  cer- 
tain is  known  as  to  the  anatomical  cause  of  arsenical  paralysis,  but  the  theory  of 
its  peripheral  origin  is  most  probable  on  account  of  the  initial  pains. 

The  course  is  usually  favorable,  sometimes  rapid  and  sometimes  lasting  for 
months.     The  treatment  is  the  same  as  in  lead  paralysis. 


Copper  paralysis,  zinc  paralysis,  etc.,  are  very  rare,  and  therefore  they  will 
not  be  described  fully  here.  The  essentials  in  regard  to  alcoholic  paralysis  may  be 
found  in  the  chapter  on  neuritis  (vide  infra).  We  may  mention  here  briefly 
that,  after  subcutaneous  injections  of  ether  on  the  extensor  side  of  the  forearm, 
paralysis  of  the  extensor  communis  digitorum  has  been  observed  in  a  few  cases. 


CHAPTER  III. 
THE   DIFFERENT  FORMS   OF   LOCALIZED   SPASM. 

1.  Spasm  in  the  Motor  Distribution  of  the  Trigeminus. 

Tonic  spasm  of  the  muscles  of  mastication  is  called  trismus.  As  an  independ- 
ent disease  it  is  very  rare,  but  it  often  occurs  as  one  symptom  in  complicated 
forms  of  spasm  and  other  nervous  affections,  as  in  tetanus,  in  the  epileptic  attack, 
in  hysteria,  meningitis,  etc.  Both  jaws  are  pressed  firmly  together,  and  we  can 
feel  through  the  cheeks  the  hard  and  tense  masseters.  In  unilateral  spasm  of  the 
pterygoids  the  lower  jaw  is  pushed  laterally  in  the  opposite  direction. 

Clonic  spasm  of  the  muscles  of  mastication — masticatory  facial  spasm— consists 
of  a  paroxysmal  and  constant  movement  of  the  lower  jaw,  almost  always  in  a 
vertical,  but  rarely  in  a  horizontal  direction.  The  single  movements  follow 
one  another  usually  in  a  regular,  rapid  rhythm,  and  produce  an  audible  chatter- 
ing of  the  teeth.  The  mucous  membrane  of  the  mouth  and  the  tongue  is  often 
injured. 

The  cause  of  these  spasms  can  not  always  be  established.  Sometimes  they 
seem  to  be  of  reflex  origin,  as  in  affections  of  the  lower  jaw,  the  teeth,  or  even  of 
distant  parts.  We  once  saw  a  case  which  lasted  for  a  year  which  was  said  to 
have  arisen  from  a  severe  fright,  and  also  a  case  of  chronic  spasm  in  the  masseters 
and  mylo-hyoids  of  hysterical  origin  in  a  ten-year-old  boy. 

The  treatment,  apart  from  the  treatment  of  the  primary  affection,  must  aim  at 
removing  the  cause  of  the  disease,  if  there  be  one,  such  as  decayed  teeth.  In  other 
respects  electricity  is  of  value  in  many  cases,  applied  either  by  passing  the  constant 
current  through  the  muscles,  or  by  faradizing  them,  or  by  using  the  wire  brush. 


572  DISEASES  OF  THE  NERVOUS  SYSTEM. 

Of  internal  remedies  we  may  try  narcotics,  such  as  morphine,  cannabis  indica, 
bromide  of  potassium,  atropine,  arsenic,  iodide  of  potassium,  valerianate  of 
zinc,  etc. 

Artificial  feeding  is  of  great  importance,  if  the  patient  can  not  take  food  volun- 
tarily from  a  persistent  trismus.  It  is  best  to  introduce  a  small  oesophageal  tube 
through  the  nose  into  the  oesophagus.  Eectal  feeding  is  insufficient  for  a  perma- 
nent method,  but  still  it  is  sometimes  of  service.  In  some  cases  a  successful 
attempt  has  been  made  to  overcome  the  closure  of  the  jaws  gradually  by  push- 
ing wooden  wedges  between  the  teeth. 

2.   Clonic  Facial  Spasm. 

{Mimetic  Facial  Spasm.     Convulsive  Tic.) 

We  know  little  that  is  definite  as  to  the  aetiology  of  facial  spasm,  the  most  fre- 
quent and  practically  the  most  important  form  of  spasm.  We  can  rarely  make 
out  any  cause  for  its  origin.  In  some  cases,  perhaps,  the  disease  is  to  be  referred 
to  a  lesion  of  the  trunk  of  the  facial,  from  exposure  to  cold,  aural  affections,  or  dis- 
turbances at  the  base  of  the  skull,  or  else  to  a  reflex  irritation  of  the  nerve  in  tri- 
geminal neuralgia,  and  also  in  diseases  of  the  sexual  organs,  etc.  It  may  be  that 
many  cases  are  not  of  peripheral  but  of  central  origin,  from  the  facial  center  in 
the  cerebral  cortex.  The  disease  may  also  appear  after  violent  mental  excitement. 
Finally,  imitation  and  the  habit  of  grimacing  play  a  part  in  many  cases,  espe- 
cially in  children,  that  is  not  to  be  underestimated.  Repeated  observations  have 
established  the  fact  that  the  disposition  to  the  disease  is  heightened  by  a  general 
hereditary  neuropathic  taint. 

The  symptoms  of  convulsive  tic  consist  of  alternating,  short,  lightning-like 
contractions  in  almost  all  the  muscles  supplied  by  the  facial.  The  disease  is  usu- 
ally unilateral,  often  extending  over  the  whole  distribution  of  the  facial,  but  some- 
times confined  only  to  individual  parts,  the  partial  facial  spasm.  Sometimes 
the  contractions  are  almost  constant,  though  varying  in  intensity,  so  that  the 
patient  involuntarily  makes  the  strangest  faces  ;  but  they  often  appear  in  sepa- 
rate attacks,  which  last  but  a  short  time,  and  are  interrupted  by  completely  free 
intervals.  The  attacks  arise  without  any  special  cause,  or  they  may  be  excited  by 
talking,  voluntary  movements,  sensory  and  mental  impressions,  etc.  In  some 
very  severe  cases  the  contractions  also  invade  the  neighboring  territory — the  mus- 
cles of  mastication,  the  tongue,  and  the  muscles  of  the  neck.  Voluntary  motion 
in  the  muscles  is  perfectly  normal,  except  for  the  disturbing  influence  of  the  spas- 
modic movements.  All  sensory  disturbances  are  also  wanting;  thei'e  is  neither 
anaesthesia  nor  pain. 

A  common  partial  form  of  facial  spasm,  which  is  entirely  or  almost  entirely 
isolated,  deserves  special  mention — blepharospasm,  or  spasm  of  the  eyelids — that 
is,  a  tonic  or  clonic  spasm  in  the  orbicularis  palpebrarum.  The  tonic  form 
may  be  of  reflex  origin  in  affections  of  the  eye,  but  sometimes  it  is  excited  from 
other  regions  of  the  trigeminus.  It  is,  as  a  rule,  bilateral,  and  may  last  for  days 
or  weeks,  sometimes  with  occasional  interruptions.  The  pressure  points,  which 
are  found  in  this  form,  and  which  were  first  carefully  described  by  Graefe,  are 
very  remai'kable.  They  are  usually  found  at  the  points  of  exit  of  the  branches 
of  the  trigeminus,  but  sometimes  on  the  vertebral  column  or  on  other  parts  of  the 
body.  By  pressure  on  these  points  the  spasm  at  once  ceases,  so  that  the  lids  "  fly 
up  as  if  by  a  spring."  Clonic  spasm  of  the  lids,  nictitating  spasm,  consists  of  a 
spasmodic  winking  and  contraction  of  the  eyes,  which  is  sometimes  almost  con- 
stant. Here,  too,  we  can  often  make  out  a  reflex  origin  for  the  spasm,  but  fre- 
quently we  can  not  find  any  cause. 


THE  DIFFERENT  FORMS   OF  LOCALIZED   SPASM.  573 

Facial  sj)asm,  in  its  severe  forms,  is  always  a  troublesome  disease  for  tbe  patient, 
and  causes  very  much  disturbance,  especially  in  blepharospasm.  Tbe  course  is 
often  very  tedious.  Sometimes  there  are  long  intervals,  as  we  have  seen  during 
pregnancy,  and  then  the  spasm  begins  anew.  In  not  very  rare  cases  the  affection 
becomes  habitual  and  lasts  for  life. 

Treatment  is,  therefore,  usually  a  difficult  and  thankless  task.  The  best  results 
may  be  obtained  where  we  can  succeed  in  removing  any  reflex  cause  of  the  spasm, 
as  in  extracting  decayed  teeth,  treating  affections  of  the  eye,  or,  in  some  cases, 
resection  of  the  supra-orbital  nerve.  In  applying  electricity,  our  chief  attention 
must  be  directed  to  any  pressure  points,  to  which  we  make  a  stabile  application  of 
the  anode  of  the  constant  current.  If  there  are  no  pressure  points,  we  put  the 
anode  on  the  trunk  of  tbe  facial  and  the  different  branches  of  the  pes  anserinus. 
In  cases  of  reflex  origin  Berger  obtained  good  results  by  applying  the  anode  to  the 
occiput,  just  under  the  protuberance,  while  the  cathode  was  held  in  the  hand — 
galvanization  of  the  medulla.  The  single  sitting  should  last  five  or  ten  minutes. 
The  faradic  current — a  slowly  "  swelling  current "  * — has  also  been  recommended. 
Of  internal  remedies  we  should  first  try  bromide  of  potassium,  and  then  arsenic, 
atropine,  curare,  or  oxide  of  zinc.  Their  action  is  always  very  uncertain.  A 
favorable  result,  however,  has  been  obtained  by  nerve-stretching,  in  a  part  of  the 
cases  operated  on,  at  least  so  far  that  the  ensuing  paralysis  troubles  the  patient 
less  than  the  constant  twitching.  When  the  paralysis  ceases  the  twitchings  usu- 
ally begin  again,  but  in  some  cases  the  benefit  has  been  permanent.  Finally,  we 
must  mention  that  the  use  of  the  red-hot  iron  has  sometimes  been  followed  by  a 
decided  improvement  of  the  spasm  in  old  cases.  We  employ  cauterization  along 
the  cervical  vertebrae,  on  the  trunk  of  the  nerve,  or  on  any  existing  pressure 
points,  by  means  of  Paquelin's  thermo-cautery. 

[Convulsive  tic  (Maladies  des  tics  convulsifs). — Under  this  term  Gilles  de  la 
Tourette  has  described  an  affection  allied  to  hysteria,  which  usually  begins  in 
young  children,  especially  those  with  a  neurotic  heredity.  It  is  characterized  by 
spasmodic  twitchings  of  the  facial  muscles,  and  sometimes  of  the  other  muscles  of 
the  body,  and  by  explosive  utterances.  These  utterances  may  be  a  repetition  of 
some  word  which  the  child  hears  (echolalia),  or  the  repetition  of  some  profane  or 
filthy  word  (coprolalia).  Actions  may  also  be  imitated.  Coprolalia  is  one  of  the 
most  distinctive  symptoms.  Other  mental  symptoms,  particularly  certain  forms 
of  imperative  conceptions,  are  occasionally  observed.  The  prognosis  is  bad.  The 
treatment  is  largely  the  same  as  that  of  hysteria  (q.  v.). — K.] 

3.  Spasm  in  the  Region  of  the  Hypoglossal  Nerve.    Lingual  Spasm. 

Although  the  tongue  is  often  implicated  in  complicated  forms  of  spasm,  such  as 
hysterical  or  epileptic  spasms,  isolated  spasms  in  it  are  very  rarely  seen.  They 
occur,  however,  either  in  a  clonic  or  a  tonic  form,  and  then  they  cause  a  marked 
disturbance  of  speech,  or  even  of  respiration,  if  the  spasm  draw  the  tongue  back- 
ward. In  the  latter  case  it  may  be  necessary  to  use  inhalations  of  chloroform, 
and  to  draw  the  tongue  forward  by  force. 

4.  Spasms  in  the  Muscles  op  the  Neck. 

Tonic  and  clonic  spasms  in  the  region  of  the  muscles  of  the  neck  are  not  very 
frequent,  but  they  appear  in  very  various  forms,  and  are  at  times  a  very  severe 
and  persistent  affection.  We  can  usually  discover  nothing  definite  as  to  the  aeti- 
ology of  this  condition.     Only  in  a  few  cases  can  we  make  out  coarse  anatomical 

[*  A  current  that  begins  weak,  and  is  gradually  made  stronger  and  then  weaker. — Traks.] 


574 


DISEASES   OF  THE  NERVOUS  SYSTEM. 


disease  of  the  nervous  system  or  of  the  cervical  vertebra?,  rheumatic  or  other  evil 
factors,  reflex  influences,  etc.  Although  the  spasms  in  the  different  muscular 
regions  are  often  combined  with  one  another,  we  can  still  distinguish  the  chief 
separate  forms. 

Spasms  in  the  Distribution  of  the  Accessory  (Circubiflex)  Nerve. — In 
clonic  spasm  of  the  accessory  there  are  paroxysmal  twitchings  of  the  head,  which 
may  attain  great  severity.  Where  there  is  a  predominating  unilateral  spasm  of 
the  sterno-mastoid,  the  head  is  turned  to  the  opposite  side  at  every  contraction  of 
this  muscle,  and  the  chin  is  also  somewhat  raised.  In  unilateral  spasm  of  the 
trapezius  the  head  is  drawn  backward  toward  the  affected  side  against  the  shoul- 
der. In  bilateral  and  combined  spasm  of  these  muscles  we  see  severe  shaking  and 
nodding  movements  of  the  head — the  so-called  nodding  spasms,  "  salaam  convul- 
sions " — which  have  been  observed  chiefly  in  children.  They  may  also  be  excited 
in  like  manner  by  contractions  of  other  muscles  of  the  neck.     In  tonic  spasm  of 

the  accessory  the  head  is  constantly  fixed 
in  the  abnormal  position  described  above, 
and  it  can  not  be  brought  back  passively 
to  its  normal  position  at  all,  or  only  in- 
completely. The  oblique  position  of  the 
head  in  unilateral  tonic  spasm  of  the  ster- 
no  mastoid  is  called  spastic  torticollis  (ca- 
put obstipum  spasticum),  or  rheumatic 
torticollis,  if  exposure  to  cold  be  regarded 
as  the  cause. 

Tonic  and  clonic  spasm  of  the  splenius 
(Fig.  79)  is  also  isolated,  or  combined  with 
spasm  of  the  accessory.  In  this  the  head 
is  drawn  backward  and  toward  the  affected 
side,  and  thus  we  can  feel  the  muscular 
swelling  protruding  to  the  outside  of  the 
cervical  portion  of  the  trapezius. 

Spasm  of  the  obliquus  capitis  is  proba- 
bly the  cause  of  the  so-called  rotatory  tic, 
in  which  there  are  genuine  spasmodic  ro- 
tatory movements  of  the  head.  The  recti 
capitis  antici  and  postici  are  perhaps  im- 
plicated in  many  cases  of  nodding  spasm. 
The  prognosis  of  the  forms  of  spasm  described  is  usually  doubtful.  There  are 
many  mild  "  rheumatic  "  cases  which  recover  in  a  short  time,  but,  on  the  other 
hand,  many  of  these  forms  of  spasm  develop  into  a  chronic  affection.  In  these 
cases  any  steady  occupation,  such  as  reading  or  writing,  is  rendered  almost  impos- 
sible by  the  constantly  recurring  spasmodic  lateral  and  rotatory  movements  of 
the  head.  Any  excitement,  a  feeling  that  he  is  noticed,  etc.,  increase  the  patient's 
spasms,  while  they  become  milder  when  he  is  completely  at  ease.  Many  cases  of 
combined  tonic-clonic  spasm  of  the  muscles  of  the  neck  form  a  very  severe  affec- 
tion, which  may  last  for  years  or  for  life,  which  is  extremely  distressing  and  pain- 
ful to  the  patient,  and  which  may  also  reduce  the  strength  and  the  nutrition  to  the 
utmost  degree. 

Treatment. — In  some  cases  electricity  has  brought  about  recovery,  or  at  least 
improvement.  The  method  of  treatment  consists  in  the  application  of  the  anode 
to  the  affected  nerves  and  muscles,  or  in  the  use  of  a  swelling  faradic  current,  or 
of  thefai'adic  brush  to  the  skin  over  the  affected  muscles.  Very  often  we  have  to 
change  the  method,  and  we  must  try  to  find  out,  by  testing,  the  most  efficient  way 


Fig.  79.— Spasm  of  the  right  splenius  capitis. 
(From  Duchenne.) 


THE  DIFFERENT  FORMS  OF  LOCALIZED   SPASM.  575 

to  employ  electricity.  Of  other  remedies,  nai*cotics,  such  as  suhcutaneous  injec- 
tions of  morphine,  are  indispensable  in  severe  cases.  We  may  also  try  bromide  of 
potassium,  antipyrine,  valerianate  of  zinc,  arsenic,  and  other  nervines.  In  severe 
cases  we  resort  to  the  use  of  the  red-hot  iron  to  the  back  of  the  neck.  Other 
observers,  and  we  ourselves,  have  seen  good  results  from  it,  hut  of  course  benefit 
does  not  always  follow.  We  may  also  advise  nerve-stretching-,  but  it  is  of  doubt- 
ful advantage.  Finally,  it  must  be  mentioned,  that  we  may  give  great  relief  to 
many  patients  by  suitably  applied  mechanical  supports,  the  more  so  because  in 
some  cases  the  spasms  occur  only  when  the  head  is  kept  free,  but  if  they  lean  their 
heads  on  anything,  as  in  lying  or  sitting,  the  spasms  cease  at  once. 

5.  Spasms  in  the  Muscles  of  the  Shoulder  and  Arm. 

Clonic  spasms  in  the  upper  extremity  are  probably  usually  of  central  origin. 
They  are  rarely  isolated,  as  in  the  pectoralis  major,  but  are  more  frequently  com- 
bined with  other  forms  of  spasm  and  other  nervous  symptoms.  They  sometimes 
seem  to  be  of  reflex  origin,  as  in  the  clonic  spasrns  associated  with  brachial  neu- 
ralgia, and  also  the  spasms  sometimes  seen  in  amputation-stumps. 

Isolated  tonic  spasms,  in  single  muscles,  or  groups  of  muscles,  in  the  upper 
extremity,  have  been  repeatedly  observed.  Tonic  spasm  of  the  rhomboidei  causes 
an  oblique  position  of  the  scapula,  so  that  its  inner  border  runs  obliquely  upward 
and  outward  from  below  and  inward.  This  makes  it  hard  to  raise  the  arm  above 
the  horizontal  line,  as  in  serratus  paralysis,  but  the  separation  of  the  scapula  from 
the  chest-wall,  which  is  so  very  characteristic  of  the  latter,  is  wanting.  Tonic 
spasm  in  the  levator  anguli  scapulae  is  rare,  except  in  connection  with  spasm  of  the 
rhomboidei  or  trapezius.  In  it  the  shoulder  is  raised  and  the  head  is  bent  a  little 
to  the  affected  side.  Isolated  tonic  spasms  in  the  pectoralis  major,  latissimus  dorsi, 
deltoid,  etc. ,  are,  on  the  whole,  easy  to  recognize,  but  they  are  only  of  very  rare 
occurrence.  Tonic  flexor  spasms  of  the  hand  and  fingers  are  more  common.  We 
have  ourselves  seen  several  such  cases,  which  lasted  for  months.  In  one  case  the 
spasm  could  at  once  be  relieved  by  placing  the  anode  of  a  moderately  strong  gal- 
vanic current  on  the  median  nerve.  In  another  'case  the  flexor  spasm  of  the 
fingers  had  followed  a  mild  acute  inflammation  of  the  wrist-joint. 

The  special  causes  of  all  these  spasms  are  still  wholly  unknown  to  us.  Prog- 
nosis and  treatment  follow  the  same  general  rules  which  are  given  for  other  forms 
of  spasm.  Most  is  to  be  expected  from  electricity :  the  stabile  action  of  the  anode, 
the  faradic  brush,  or  faradization  of  the  antagonistic  muscles. 

6.  Spasms  in  the  Muscles  op  the  Lower  Extremity. 

Clonic  spasms  in  the  muscles  of  the  lower  extremity  are  always,  with  rare 
exceptions,  a  symptom  of  spinal  or  cerebral  disease.  Of  the  tonic  spasms  the 
most  frequent  and  the  best  known  are  the  painful  spasms  in  the  calves,  or  cramps, 
which  are  apt  to  come  on  after  great  muscular  exertion,  mountain-climbing,  or 
dancing.  Many  persons  have  an  especially  marked  predisposition  to  such  cramps, 
which  readily  come  on,  especially  after  making  certain  movements  or  holding  the 
foot  in  a  certain  position.  Similar  painful  cramps  sometimes  come  in  other  mus- 
cles besides  the  calves,  as  in  the  abductor  hallucis,  etc.  Other  tonic  spasms  in  the 
muscles  of  the  lower  extremity  are  rare,  but  individual  cases  of  isolated  tonic 
spasm  in  the  abductors,  in  the  ilio-psoas,  in  the  muscles  of  the  calves,  etc.,  have 
been  observed.  More  extensive  tonic  contractures  of  the  muscles  of  the  leg  are 
not  very  rare  in  hysteria,  especially  in  the  hysteria  of  children. 

Saltatory  Reflex  Spasm. — In  this  place  we  may  mention  a  peculiar  form  of 
spasm,  to  which  Bamberger  has  given  the  name  of  "saltatory  reflex  spasm.'1 


576  DISEASES  OF  THE  NERVOUS  SYSTEM. 

This  shows  itself  in  the  muscles  of  the  lower  extremities,  never  when  the  patient 
is  quiet  in  bed,  but  only  when  he  tries  to  stand  or  to  walk.  As  soon  as  the  soles 
of  the  feet  touch  the  floor,  such  vigorous  contractions  are  set  up  in  the  muscles  of 
the  legs  as  to  force  the  patient  to  keep  up  a  constant  hopping,  jumping,  or  tripping. 
The  heels  are  also  usually  raised  spasmodically,  and  in  many  cases  the  patient 
would  certainly  fall  if  he  were  not  supported.  In  the  pure  forms  of  saltatory 
spasm,  on  physical  examination  we  can  usually  make  out  nothing  but  an  extraor- 
dinary increase  of  the  reflexes,  especially  of  the  tendon  reflexes,  but  in  some  cases 
there  may  also  be' other  nervous  symptoms.  In  general,  it  seems  that  saltatory 
reflex  spasm  is  not  to  be  regarded  as  a  special  disease,  but  as  a  peculiar  symptom, 
which  may  arise  in  different  neuroses  in  consequence  of  a  very  decided  exaggera- 
tion of  the  reflexes.     Many  cases  especially  seem  to  us  to  be  hysterical. 

[Certain  similar  affections  exist  as  endemic  neuroses.  In  the  ''  jumpers "  of 
Maine  the  spasms  may  be  produced  by  any  excitement.  In  other  forms  the  vic- 
tims are  compelled  to  imitate  everything  they  see  or  hear.  The  curious  affections 
observed  in  Siberia,  Java,  and  elsewhere,  known  as  latah  or  emeryaki  (myriachit), 
are  allied  to  this  trouble.  Alcoholism,  cold,  and  privation  seem  to  be  important 
serological  factors,  and  they  probably  have  some  relation  to  hysteria. — K.] 

Arthrogryposis. — As  an  appendix  we  would  here  consider  briefly  a  remarkable 
disease,  the  so-called  arthrogryposis,  which  occurs  chiefly  in  children  in  the  first 
years  of  life,  and  consists  of  persistent  tonic  spasms  and  contractures  of  one  or 
often  of  all  four  extremities.  The  disease  usually  develops  quite  acutely,  and  may 
run  its  course  with  fever  and  rather  severe  general  symptoms.  The  legs  are  found 
either  in  a  position  of  rigid  extension,  or  they  are  drawn  up  spasmodically  to  the 
body,  and  can  not  be  extended  passively  even  with  violence.  The  arms  are  flexed, 
and  the  hands  and  fingers  are  also  fixed  in  some  position  of  contracture.  The 
milder  cases  may  recover  after  a  few  weeks,  but  we  have  also  seen  two  cases 
which  ended  fatally,  in  which  the  autopsy  gave  a  perfectly  negative  result.  The 
nature  of  this  quite  rare  affection  is  still  wholly  unknown  to  us.  In  regard  to 
treatment,  prolonged  warm  baths  are  especially  to  be  recommended. 

[Paramyoclonus  multiplex. — Under  this  term  Friedreich  has  described  a  peculiar 
affection  consisting  of  clonic  bilateral  spasms  of  several  muscles  of  a  physiological 
group.  Hence  the  movements  seem  to  have  a  purposive  character.  The  spasms 
are  rapidly  repeated  from  fifty  to  one  hundred  and  eighty  times  a  minute,  and 
occur  in  paroxysms.  The  muscles  chiefly  affected  are  those  attached  at  one  or 
both  ends  to  the  trunk.  Fascicular  tremors  of  the  affected  muscles  are  observed 
in  the  intervals.  The  reflexes  are  exaggerated,  and  the  attacks  may  be  brought  on 
by  irritation  of  the  skin  or  tendons.  The  nature  of  the  affection  is  unknown. 
The  prognosis  is  favorable.  The  most  effective  treatment  has  been  the  application 
of  strong  galvanic  currents  to  the  spine  and  neck. 

Electrical  Chorea.— This  term  was  first  applied  to  an  affection  met  with  chiefly 
in  northern  Italy.  It  consists  of  sudden  muscular  contractions,  resembling  those 
caused  by  electrical  stimulation.  With  these  are  associated  progressive  paralysis 
and  muscular  wasting.  Many  of  the  cases  terminate  fatally.  Similar  sudden 
contractions  are  seen  in  ordinary  chorea,  hysterical  spasmodic  conditions,  etc., 
and  hence  the  term  has  been  frequently  applied  to  these.  Compare  the  chapter 
on  hysteria. — K.] 

The  form  of  tonic  spasm  known  as  tetany  will  be  described  in  a  special  chapter. 

7.  Spasms  in  the  Respiratory  Muscles. 

Tonic  spasm  of  the  diaphragm  has  been  seen  in  a  few  rare  cases.  The  lower 
part  of  the  thorax  is  much  expanded,  the  epigastrium  is  protruded,  and  the  respira- 


WRITER'S  CRAMP  AND  ALLIED  PROFESSIONAL  NEUROSES.  577 

tion,  which  shows  intense  dyspnoea,  can  be  performed  only  by  the  upper  part  of 
the  thorax.  The  depression  and  immobility  of  the  diaphragm  can  be  made  out  on 
percussion.  Many  patients  have  a  severe  pain  in  the  region  of  the  diaphragm. 
The  condition  is  not  without  danger  and  demands  instant  interference:  inhalations 
of  chloroform,  subcutaneous  injections  of  morphine,  a  warm  bath  with  a  cool 
shower-bath  after  it,  faradization  of  the  skin  in  the  region  of  the  diaphragm,  gal- 
vanization of  the  phrenics,  etc. 

Clonic  Spasm  of  the  Diaphragm. — Singultus.— The  well-known  "hiccough" 
or  "  sob,"  due  to  a  sudden  spasmodic  contraction  of  the  diaphragm,  is  in  its  mild 
forms  a  very  frequent  condition,  which  soon  passes  off;  but  it  sometimes  in- 
creases to  a  persistent,  obstinate,  and  very  troublesome  affection,  which  may  last 
for  weeks  or  months.  It  sometimes  comes  on  after  mental  excitement,  and  is  a 
not  very  rare  symptom  of  hysteria.  Persistent  hiccough  may  also  be  excited  re- 
flexly  in  affections  of  the  stomach,  intestines,  peritoneum,  etc.  In  some  cases  the 
hiccough  depends  upon  a  direct  lesion  of  the  phrenic  nerve,  as  we  have  seen  in 
one  case  of  tubercular  mediastino-pericarditis.  We  have  also  seen  hiccough  last- 
ing for  hours  in  cerebral  apoplexy,  and  also  in  chronic  myelitis  extending  to  the 
cervical  cord. 

In  the  milder  cases  hiccough  soon  passes  off  without  special  treatment.  Hold- 
ing the  breath,  pressure  on  the  closed  glottis,  blows  on  the  back,  etc.,  are  proce- 
dures generally  known  by  the  laity,  and  often  used  to  suppress  hiccough.  In  more 
severe  cases  we  must  try  narcotics,  opium,  cannabis  indica,  or  inhalations  of  chlo- 
roform. The  faradic  brush  to  the  region  of  the  diaphragm,  or  the  direct  action  of 
electricity  on  the  phrenic  nerve,  is  sometimes  of  advantage.  In  hysterical  hic- 
cough we  may  obtain  very  rapid  results  in  this  way,  or  sometimes  by  one  of  the 
different  nervines,  valerian,  zinc,  atropine,  or  Fowler's  solution. 

Complicated  respiratory  spasms,  either  in  the  form  of  spasmodically  accelerated 
and  forced  breathing,  or  spasms  combined  with  all  sorts  of  other  symptoms,  with 
many  gurgling  noises,  eructations,  etc. ,  are  almost  exclusively  confined  to  hysteria. 
We  have  ourselves  counted  in  one  such  case  over  two  hundred  respirations  a  min- 
ute !  The  best  remedy  against  most  of  these  forms  of  spasm,  and  one  which  often 
acts  instantly,  is  a  cool  bath  with  energetic  cold  shower-baths.  The  yawning 
spasm  (chasmus,  oscedo),  sneezing  spasm  (sternutatio  convulsiva,  ptarmus), 
laughing  and  weeping  spasms,  coughing  spasm,  etc.,  also  belong  to  the  respiratory 
spasms.  We  once  saw  a  very  remarkable  example  of  the  latter  in  a  boy  ten  years 
old.  A  peculiar,  reflex,  hollow,  barking  cough  came  on,  either  spontaneously  or 
on  pinching  any  part  of  the  skin.  The  affection  lasted  for  some  weeks,  and  then 
disappeared  quite  suddenly. 


CHAPTER  IV. 
WRITER'S   CRAMP   AND   ALLIED   PROFESSIONAL   NEUROSES. 

Writer's  cramp  (graphospasm,  mogigraphia)  is  the  commonest  form  of  a 
whole  class  of  peculiar  disturbances  of  motion,  to  which  Benedikt  gave  the  appro- 
priate name  of  "professional  neuroses  of  co-ordination."  Their  characteristic 
feature  is  that  the  disturbance  in  a  certain  group  of  muscles  appears  only  when 
these  muscles  come  into  harmonious  action,  in  quite  a  definite  and  usually  a 
delicate  and  complicated  occupation.  Although  the  persons  who  suffer  from 
writer's  cramp  can  move  and  use  the  muscles  of  their  right  arm  and  hand  for 
ordinary  purposes  in  a  perfectly  normal  manner,  these  same  muscles  at  once 
37 


578  DISEASES  OF  THE  NERVOUS  SYSTEM. 

refuse  their  service  when  the  patient  begins  to  write.  In  this  case  the  disturbance 
can  not  he  in  the  innervation  of  the  individual  muscles  themselves,  but  it  must  be 
referred  to  the  form  of  their  associated  action — that  is,  it  must  be  a  disturbance  of 
co-ordination ;  but  the  details  of  this  disturbance  are  still  entirely  unknown  to  us, 
nor  do  we  know  in  what  part  of  the  nervous  system  we  are  to  look  for  the  seat  of 
the  disease.  Over-exertion  in  writing  plays  the  most  important  part  as  an  sero- 
logical factor.  Writer's  cramp  is  therefore  seen  chiefly,  but  of  course  not  ex- 
clusively, in  those  persons  whose  occupation  is  connected  with  continuous  writ- 
ing, especially  in  secretaries,  merchants,  bureau  officials,  etc.  A  general  nervous 
predisposition  seems  also  to  increase  the  tendency  to  writer's  cramp.  Attention 
has  also  been  called  to  the  fact  that  bad  pens,  such  as  hard  steel  pens,  bad  methods 
of  holding  the  pen  in  writing,  etc.,  may  favor  the  development  of  writer's  cramp. 

Symptoms. — The  essential  symptom  of  writer's  cramp  is  the  appearance  of 
certain  disturbances  at  every  attempt  to  write,  which  render  writing  very  difficult 
or  entirely  impossible.  The  affection  visually  begins  gradually,  but  increases  quite 
rapidly.  For  the  precise  characterization  of  the  disturbance  Benedikt  has  dis- 
tinguished three  forms  of  writer's  cramp,  but  they  run  into  one  another  in  various 
ways.  The  spastic  form  is  the  most  frequent.  The  patient  scarcely  begins  to  write 
when  contractions  or  tonic  spasms  come  on  in  the  different  fingers,  so  that  the  pen 
can  no  longer  be  held  firmly,  or  it  makes  abnormal  irregular  movements,  or  it  is 
firmly  pressed  into  the  paper,  etc.  We  very  often  see  a  tonic  spasm  of  the  pixma- 
tors  of  Ü\e  forearm  set  in  on  each  attempt  to  wi'ite.  Writing  is  wholly  impossi- 
ble, or  it  is  done  only  with  the  greatest  exertion,  and  the  characters  are  also  utterly 
distorted,  unequal,  and  mingled  with  false  strokes  and  blots.  In  the  paralytic 
form  *  the  disturbance  in  writing  is  chiefly  a  rapidly  arising  tired  feeling,  like 
paralysis,  in  the  right  arm,  which  is  often  associated  with  painful  sensations. 
Finally,  in  the  tremulous  form  of  writer's  cramp  there  is  such  a  marked  tremor  in 
the  right  hand  at  every  attempt  to  write  that  the  letters  are  completely  illegible. 
We  have  seen  several  such  cases  in  children,  which  we  have  regarded  as  distinctly 
hysterical. 

As  has  already  been  said,  motility  in  every  other  respect  is  perfectly  normal, 
but  sometimes  analogous  symptoms  also  appear  in  the  same  patient  in  many  other 
fine  employments,  such  as  sewing,  piano-playing,  etc.  The  sensibility  is  usually 
perfectly  normal,  except  for  the  muscular  pains  already  mentioned,  and  a  frequent 
feeling  of  numbness  in  the  forearm  and  fingers.  A  few  painful  pressure-points 
have  sometimes  been  found  on  the  cervical  and  dorsal  vertebrae.  We  should  also 
examine  the  peripheral  nerves,  since  painful  thickenings  are  sometimes  to  be 
detected  in  them,  which  possibly  stand  in  a  causal  relation  to  the  disease.  If  we 
are  dealing  with  people  who  are  generally  neurotic,  they  often  complain  at  the 
same  time  of  headaches,  mental  uneasiness,  and  general  weakness. 

The  diagnosis  of  writer's  cramp  is  almost  always  easy.  We  must  guard  against 
confusing  it  with  other  nervous  diseases,  such  as  chorea,  paralysis  agitans,  multiple 
sclerosis,  beginning  muscular  atrophy,  or  agraphia,  which,  of  course,  under  some 
circumstances  may  lead  to  disturbances  in  writing. 

The  prognosis  is  always  to  be  given  with  reserve.  Complete  recoveries  with- 
out doubt  do  occur,  but  many  cases  are  extremely  obstinate  and  others  are  incur- 
able. Relapses  are  also  very  common  even  after  improvement  has  set  in.  Many 
patients  are  obliged  to  choose  another  calling  in  consequence  of  their  trouble. 

The  treatment  begins  first  with  the  command  to  give  up  writing  entirely  for 
several  weeks  or  months.     If  this  command  can  be  obeyed,  the  mere  rest  may  be 

*It  is  particularly  illogical  to  class  this  disturbance  with  writer's  cramp,  since  we  can  not  speak 
of  the  "  paralytic  "  form  of  a  "  cramp." 


SIMPLE  AND  MULTIPLE  DEGENERATIVE  NEURITIS.  579 

of  service  in  mild  incipient  cases.  Certain  contrivances  for  writing,  which  the 
patient  can  best  test  himself,  are  often  of  advantage,  such  as  sticking  the  pen- 
holder through  a  cork,  using  a  large  pen-holder,  a  change  in  the  way  of  holding 
the  pen  and  in  the  position  of  the  arm,  etc.  Nussbaum  has  lately  invented  a  kind 
of  bracelet  to  which  the  pen-holder  is  fastened,  and  which  is  held  firmly  by  the 
outspread  fingers.  Learning  to  write  with  the  left  hand,  which  is  often  tried  by 
patients,  usually  leads  to  no  good  result,  since  the  cramp  very  soon  appears  in  the 
left  hand  also  with  remarkable  rapidity. 

Of  the  special  methods  of  treating  writer's  cramp  the  application  of  galvanism 
deserves  the  first  mention.  Avoiding  all  strong  currents  and  variations  of  the 
current,  we  apply  the  stabile  anode  to  the  brachial  plexus,  and  also  to  the  different 
nerves  (especially  if  they  be  sensitive  to  pressure)  and  the  affected  muscles,  for  five 
or  ten  minutes.  The  cathode  is  placed  in  the  vicinity  of  the  cervical  vertebrae. 
If  painful  points  are  found,  they  receive  special  treatment.  We  may  also  use  gal- 
vanism, as  an  experiment,  through  the  head.  Of  late,  massage  and  methodical 
gymnastics  have  shown  still  more  favorable  results  than  electrical  treatment,  but 
the  use  of  them  demands  special  technical  skill,  and  therefore  they  have  so  far 
obtained  excellent  results  chiefly  in  the  hands  of  certain  specialists.  We  can  very 
rarely  promise  success  from  internal  remedies  such  as  subcutaneous  injections  of 
strychnine,  atropine,  etc.,  but  those  methods  of  treatment  often  act  favorably 
which  aid  the  general  strength  of  the  nervous  system,  such  as  cold-water  cures,  sea- 
bathing, and  residence  at  a  mountain  resort. 

As  an  appendix  we  will  mention  here  some  other  professional  neuroses  that 
are  occasionally  seen.  They  are  the  piano-player's  cramp,  which  is  seen  espe- 
cially in  young  conservatory  pupils,  violin-  and  'cello-player's  cramp,  telegrapher's 
cramp,  tailor's  cramp,  milker's  cramp,  the  peculiar  disturbances  of  innervation  in 
the  hands  which  often  occur  in  cigar-rollers,  etc.  In  the  lower  extremities  there 
seems  to  be  an  analogous  affection  in  ballet-dancers,  and  also  in  sewing-machine 
girls,  turners,  etc.  We  have  seen  a  professional  cramp  in  the  tongue  in  a  clario- 
net-player. The  special  points  in  the  symptomatology  and  treatment  of  all  these 
forms  of  cramp  are  in  large  part  analogous  to  the  conditions  described  in  writer's 
cramp.  In  piano-players  the  neurosis  appears  chiefly  in  the  paretic  form — mild 
fatigue — and  is  usually  associated  with  quite  severe  pains,  that  come  on  during 
playing,  in  certain  parts  of  the  arm.  In  regard  to  treatment,  the  best  results  are 
obtained  by  energetic  massage.  Finally,  it  may  here  be  noted  that  in  certain 
laborious  occupations  that  are  persistently  practiced,  a  severe  group  of  nervous 
symptoms  may  also  arise.  For  example,  B.  Hirt  has  lately  described  an  affection 
which  occurs  in  sewing-machine  girls,  and  is  characterized  by  disturbances  of  sen- 
sibility, pain,  paresthesia,  and  in  some  cases  anaesthesia,  ataxia,  absence  of  the 
tendon  reflexes,  and  swaying  with  the  eyes  shut.  The  disease  thus  recalls  very 
closely  the  picture  of  locomotor  ataxia,  but  it  is  curable  with  proper  treatment. 
Therefore  Hirt  suspected  an  affection  of  the  peripheral  nerves.  Like  symptoms 
are  also  seen  in  other  classes  of  laborers,  as  in  farm-hands  after  laborious  toil  in 
the  fields. 


CHAPTER  V. 

SIMPLE   AND   MULTIPLE   DEGENERATIVE   NEURITIS. 

.ffitiology  and  Pathology. — We  term  those  changes  in  the  nerves  acute  neuritis 
(inflammation  of  the  nerves)  where  their  vessels  become  very  hyperaemic,  and 
where  the  transudation  of  fluid  and  cellular  elements  takes  place  from  the  walls 


580  DISEASES  OF  THE  NERVOUS  SYSTEM. 

of  the  vessels  into  the  surrounding  tissue.  The  inflamed  nerve  is  therefore  swollen 
and  thickened,  its  color  is  manifestly  reddened  from  the  marked  vascular  hyper- 
aeinia,  and  we  can  aften  recognize  with  the  naked  eye  a  few  or  many  small  haem- 
orrhages. Microscopic  examination  shows  an  abundant  infiltration  of  round  cells 
into  the  nerve  sheaths  and  the  interstitial  tissue,  and  these  may  he  so  numerous 
that  the  inflammation  in  some  cases  may  be  recognized,  even  on  macroscopic 
examination,  as  a  purulent  neuritis.  The  nerve-fibers  themselves  sometimes  show 
no  visible  changes,  but  in  more  severe  neuritis  we  usually  find  an  evident  disin- 
tegration of  the  medullary  sheaths  and  the  axis-cylinders,  and  finally  a  complete 
destruction  of  the  nerve-fibers.  The  "  fatty  granular  cells  "  which  are  seen  in 
these  cases  are  probably  white  blood-corpuscles  (perhaps,  also,  endothelial  cells  ?), 
which  have  taken  up  the  fat  from  the  disintegrated  medullary  substance.  The 
destruction  of  the  nerve-fibers,  "  parenchymatous  inflammation,"  is  partly  a  me- 
chanical result  of  their  compression  by  the  surrounding  exudation,  but  very 
largely  probably  the  result  of  the  direct  injury  which  the  nerve-fibers  undergo 
from  the  causes  that  provoke  the  inflammation. 

In  its  further  course  the  neuritis  advances  to  the  stage  of  the  new  formation  of 
connective  tissue  and  the  regenerative  processes.  The  nerve  appears  firmer  and 
denser  than  normal;  a  lai-ge  amount  of  interstitial  connective  tissue  is  formed 
between  the  single  nerve-fibers  that  are  still  preserved,  which,  if  produced  in 
excess,  like  a  sort  of  callus  formation,  may  lead  to  quite  considerable  partial  thick- 
enings of  the  nerve,  the  so-called  neuritis  nodosa.  The  capacity  for  regeneration 
of  the  peripheral  nerves  is  relatively  very  considerable,  so  that  in  moderate  and 
even  in  severe  degrees  of  neuritis  we  may  have  a  complete  restitutio  ad  integrum. 
There  may  be  a  partial  regeneration  of  the  nerve-fibers  even  in  the  worst  cases. 
Chronic  neuritis  either  proceeds  from  acute  neuritis,  or  it  develops  de  novo  in  an 
insidious  fashion.  In  the  latter  case  the  first  acute  stage  of  hyperasmia  and  cellu- 
lar infiltration  is  entirely  absent,  and  the  destruction  of  the  nerve-fibers  and  the 
new  growth  of  connective  tissue  proceed  in  a  chronic  manner  from  the  beginning. 
In  such  cases  the  interstitial  inflammatory  changes  in  the  connective  tissues  and 
the  vessels  are  often  so  subordinate  to  the  degenerative  processes  in  the  nerve- 
fibers  themselves  that  we  have  almost  a  genuine  parenchymatous  degeneration. 
Such  conditions,  perhaps,  can  not  be  properly  termed  "  neuritis  "  at  all,  but  rather 
"primary  chronic  degenerative  atrophy  of  the  nerves."  They  arise  especially  as 
a  result  of  certain  infectious  and  toxic  influences  (vide  infra),  which  have  a 
directly  deleterious  action  upon  the  nerve-fibers.  They  often  appear  in  many 
nerves  at  the  same  time,  and  consist  of  a  slowly  progressive  disintegration  of  the 
medullary  sheath,  and  later  of  the  axis-cylinders  also.  It  is  possible  that  these 
last-named  changes  begin  in  the  terminal  branches  of  the  peripheral  nerves,  and 
gradually  advance  from  them  toward  the  centers,  but  this  has  not  yet  been  cer- 
tainly confirmed ;  at  any  rate,  the  affection  often  remains  confined  to  the  periph- 
eral nerves.  The  anterior  spinal  roots  and  the  cord  itself  in  such  cases  are  found 
perfectly  intact,  or  altered  only  in  a  subordinate  way.  [According  to  recent 
observations  distinct  changes  may  be  found  in  the  cord,  chiefly  in  the  white  sub- 
stance, especially  in  the  more  chronic  forms  of  neuritis,  and  the  forms  of  toxic  ori- 
gin.—K] 

In  inquiring  into  the  causes  of  neuritis  we  encounter  first  the  same  injurious 
influences  which  play  the  chief  part  in  the  inflammations  of  other  organs.  We 
very  often  speak  of  a  traumatic  neuritis,  which  is  supposed  to  mean  a  neuritis 
produced  by  various  mechanical  injuries  of  the  nerve.  As  far  as  this  implies 
open  wounds — like  stabs,  cuts,  gun-shot  wounds,  etc. — that  involve  the  nerve,  the 
development  of  a  genuine  traumatic  neuritis  can  not  be  doubted ;  but  in  such  cases 
we  not  only  have  to  do  with  mechanical  lesions,  but  with  an  accidental  complica- 


SIMPLE  AND  MULTIPLE  DEGENERATIVE  NEURITIS.  581 

tion  of  the  wound,  with  the  entrance  of  organized  agents  of  inflammation  through 
the  wound  into  the  nerves.  Only  in  this  case  can  there  be  an  inflammation 
(ascending  neuritis,  neuritis  migrans)  advancing  continuously  or  by  leaps  in 
the  nerve-trunk  from  tbe  point  of  lesion  in  the  nerve,  whereas,  if  the  wound 
remains  aseptic,  as  the  experiments  of  Rosenbach  and  Kast  have  shown,  such  a 
propagation  of  the  inflammation  above  the  point  of  lesion  never  occurs.  In 
the  subcutaneous  injuries  of  the  nerve-trunk  from  a  blow,  from  pressure,  from 
dislocations  of  the  bones,  etc.,  we  are,  of  course,  not  justified  in  speaking  of  a 
traumatic  neuritis ;  but  in  such  cases  we  have  a  purely  mechanical  destruction 
of  the  nervous  elements,  which  is  followed  by  the  regular  processes  of  secon- 
dary degeneration  (vide  supra),  increase  of  connective  tissue,  and  final  restora- 
tion. 

Another  cause  for  the  origin  of  a  genuine  neuritis  lies  in  the  extension  of  an 
inflammation  from  the  neighboring  organs  to  the  nerves.  In  inflammations  of 
the  bones,  as  in  caries  of  the  bones  of  the  skull  and  of  the  vertebrae,  of  the  joints 
and  of  the  different  internal  organs,  the  inflammatory  process  may  directly  involve 
a  nerve-trunk  by  contiguity.  In  this  way,  perhaps,  are  developed  the  atrophy 
and  paralysis  of  the  neighboring  muscles  which  are  often  seen  after  affections  of 
the  joints.  Leyden  has  also  tried  to  explain  a  number  of  the  so-called  ''  reflex 
paralyses  " — that  is,  paralyses  which  sometimes  develop  as  a  result  of  inflamma- 
tory affections  of  certain  internal  organs,  especially  the  intestines  and  the  urinary 
and  sexual  organs — by  a  neuritis  arising  from  the  organ  originally  affected,  and 
even  extending  to  the  spinal  cord. 

Primary  neuritis,  however,  is  of  special  interest.  This  may  either  be  caused 
by  some  evident  agency,  or  it  may  develop,  apparently  spontaneously,  without 
any  cause  as  far  as  known.  We  have  already  learned  to  recognize  one  group  of 
these  primary  neuritides  in  the  preceding  chapters :  those  which,  in  all  probabil- 
ity, underlie  most  of  the  "  rheumatic "  paralyses  on  the  one  hand,  and  certain 
forms  of  neuralgia,  such  as  sciatica,  intercostal  neuralgia  with  zoster,  etc.,  on  the 
other.  As  we  have  said,  little  that  is  definite  is  known  as  to  the  precise  cause  of 
these  neuritides.  Some  of  them  seem  to  arise  from  external  agencies,  such  as 
exposure  to  cold;  others,  perhaps,  from  infectious  influences.  Certain  toxic 
paralyses  belong  to  a  second  group  of  primary  neuritides,  among  them,  for 
instance,  the  lead  and  arsenic  paralyses  already  described,  and  the  disease  of  the 
nerves  produced  by  chronic  alcoholism,  which  will  be  more  fully  described  below. 
Finally,  the  so-called  multiple  neuritis  forms  the  third  recognized  group,  a  special 
form  of  disease  in  which  several  nerves  are  usually  affected  at  the  same  time  or 
soon  after  one  another.  As  will  be  stated  in  the  description  of  the  course  of  the 
disease,  we  probably  have  in  these  cases  a  definite  form  of  infectious  disease, 
which  is  localized  exclusively,  or  at  least  mainly,  in  the  peripheral  nerves.  In 
the  acute  cases  the  anatomical  changes  in  the  nerves  seem  to  be  really  of  an 
inflammatory  nature,  but  in  the  chronic  cases  a  simple  degenerative  atrophy  of 
the  nerves  underlies  the  morbid  symptoms.  The  aatiological  position  of  these 
chronic  cases  of  multiple  neuritis,  however,  is,  in  our  opinion,  to  be  judged  with 
caution,  since  at  least  a  part  of  the  cases  so  far  published  are  certainly  to  be  classed 
with  alcoholic  neuritis  (vide  infra). 

Clinical  History  of  the  Different  Forms  of  Neuritis. 

1.  Secondary  Neuritis. — The  chief  symptom  of  secondary  neuritis,  following 
wounds,  inflammations  of  neighboring  organs,  etc. ,  is  pain,  which  comes  on  with 
great  intensity,  not  only  in  the  region  of  distribution  of  the  affected  nerve,  but 
also  along  the  whole  trunk  of  the  nerve.     In  these  cases  there  is  also  a  marked 


582  DISEASES   OF  THE  NERVOUS   SYSTEM. 

sensitiveness  of  the  nerve  to  pressure.  In  many  cases  we  can  succeed  in  feeling 
the  thickened  nerve  plainly  through  the  skin. 

Besides  these  direct  symptoms,  the  inflammation  soon  renders  the  necessary 
results  of  disturbed  nervous  conduction  apparent.  There  is  a  dullness  of  sensibility 
in  the  distribution  of  the  affected  nerve,  at  first  in  the  form  of  a  subjective  feeling 
of  numbness,  but  later  as  a  manifest  objective  anaesthesia,  which,  however,  rarely 
reaches  a  very  high  degree.  The  motor  symptoms  at  first  show  themselves  as 
motor  weakness,  which  in  severe  cases  becomes  a  pi^onounced  paralysis.  It  goes 
without  saying  (see  page  538)  that  the  paralysis,  in  all  severe  cases,  is  followed  by 
a  degenerative  atrophy  of  the  paralyzed  muscles,  and  the  appearance  of  electrical 
reaction  of  degeneration.  Iu  the  skin,  trophic  and  vaso-motor  disturbances  have 
been  repeatedly  observed,  especially  slight  oedema  of  the  subcutaneous  cellular 
tissue,  eruptions  of  herpes,  etc. 

The  course  of  simple  secondary  neuritis  may  vary.  Its  onset  is  usually  quite 
acute,  or  more  rarely  it  begins  gradually.  Many  cases  seem  to  recover  before  the 
severer  consequences  are  reached,  while  others  take  a  chronic,  tedious  course,  and 
lead  to  permanent  disturbances  of  function. 

2.  Primary  Simple  Neuritis. — We  must  seek  for  the  cause  of  many  primary 
paralyses  (that  is,  paralyses  coming  on  without  special  cause  or  after  cold,  etc.) 
in  the  distribution  of  individual  peripheral  nerves  in  a  pure  neuritis.  For  exam- 
ple, "  rheumatic  "  facial  paralysis  is  certainly  due  to  a  mild  or  a  severe  neuritis  of 
the  facial  nerve.  Precisely  similar  primary  neuritic  paralyses  occur,  although 
more  rarely,  in  the  distribution  of  other  nerves,  especially  in  the  upper  and  more 
rarely  in  the  lower  extremities ;  thus  we  see  neuritic  axillary  or  deltoid  paralysis, 
ulnar  paralysis,  peroneal  paralysis,  etc.  All  these  cases  are  characterized  by  the 
fact  that  they  begin  with  more  or  less  severe  pain  or  paresthesia  in  the  territory 
of  the  affected  nerve.  Motor  paralysis  sooner  or  later  develops,  which  in  the 
severer  cases  leads  to  degenerative  atrophy  of  the  affected  muscles  with  reaction 
of  degeneration.  Sensory  disturbances  in  tbe  skin  can  usually  be  plainly  detected, 
at  least  to  a  slight  degree,  on  careful  examination.  The  prognosis  of  these  paraly- 
ses is,  as  a  rule,  favorable  ;  but  sometimes  permanent  disturbances  of  function 
remain,  and  they  may  also  recur. 

3.  Primary  Multiple  Degenerative  Neuritis. — Primary  multiple  neuritis  is 
probably  not  a  very  rare  disease,  but  yet  it  has  been  carefully  investigated  only  in 
the  last  few  years.  The  first  definite  observations  lipon  it  were  made  in  the  years 
1864  and  1866  in  France  by  Dumenil.  Since  then  a  whole  series  of  well-established 
cases  have  been  published  by  Eichhorst,  Eisenlohr,  Joffroy,  Leyden,  Vierordt,  the 
writer,  and  others,  so  that  the  type  of  the  disease  is  at  present  quite  accurately 
known.  Probably  in  former  days  multiple  neuritis  was  often  confused  with 
poliomyelitis  and  certain  cases  of  "acute  ascending  paralysis"  (vide  infra).  An 
interesting  discovery  was  first  made  by  Scheube,  that  the  peculiar  disease,  of 
endemic  occurrence,  long  known  in  Japan  and  the  East  Indies  as  '*  Jcak-Jce  "  or 
"  beri-beri,"  is  in  its  clinical  and  anatomical  relations  a  well-characterized  multiple 
peripheral  neuritis.  With  us,  also,  multiple  neuritis  occasionally  shows  an  epi- 
demic increase  in  frequency  (Eisenlohr).  [Cases  have  been  observed  among 
sailors,  fishermen,  etc.,  in  the  seaport  towns  of  New  England,  where  the  symp- 
toms resembled  those  of  neuritis  and  were  akin  to  beri-beri.  J.  J.  Putnam  thinks 
that  in  1881  and  1889  there  were  epidemics  of  this  disease  in  the  fishing  towns  of 
Massachusetts,  characterized  by  pain,  loss  of  power,  numbness,  and  oedema,  the 
trouble  being  chiefly  in  the  legs. — K.] 

Multiple  neuritis  usually  begins  acutely,  sometimes  almost  in  an  apoplecti- 
form manner,  and  without  any  definite  occasion,  precisely  like  an  acute  infectious 
disease.    Febrile  symptoms,  with  temperatures  from  102°  to  104°  (39°-40°  C),  come 


SIMPLE  AND  MULTIPLE  DEGENERATIVE  NEURITIS.  583 

on  in  persons  previously  in  good  health,  usually  in  adults  in  youth  or  middle  life, 
with  severe  general  disturbance,  loss  of  appetite,  dullness,  headache,  and  some- 
times even  mild  delirium.  In  these  acute  cases  albuminuria  and  a  slight  enlarge- 
ment of  the  spleen  have  sometimes  been  observed,  which  symptoms  also  point 
toward  the  infectious  nature  of  the  disease.  In  other  cases  the  initial  symptoms 
are  less  severe,  but  they  are  almost  never  entirely  absent.  The  pains,  which  are 
hardly  ever  absent,  are  very  characteristic.  They  are  described  as  pulling  and 
tearing,  are  felt  chiefly  in  the  loins  and  the  extremities,  and  sometimes  follow 
approximately  the  course  of  the  large  nerve-trunks.  Since  in  some  cases  a  num- 
ber of  the  joints  are  swollen,  the  disease  at  first  may  be  mistaken  for  acute  articu- 
lar rheumatism.  The  first  symptoms  of  paralysis,  usually  in  the  lower  extremi- 
ties, appear  very  soon  after  these  initial  symptoms,  or  at  the  same  time  with  them. 
The  patient  notices  that  he  can  not  readily  move  one  leg,  and  soon  after  he  notices 
the  same  of  the  other.  The  paralysis  often  extends  rapidly  to  one  or  both  arms. 
If  we  examine  the  paralyzed  parts  more  carefully  we  find  a  perfectly  atonic  and 
more  or  less  extensive  paralysis.  The  legs  are  often  not  paralyzed,  but  distinctly 
ataxic,  a  condition  which  is  often  seen  in  alcoholic  neuritis  {vide  infra).  The  re- 
flexes are  almost  always  diminished,  the  tendon  reflexes  are  usually  entirely  ab- 
sent, and  the  cutaneous  reflexes  are  weak,  or  they  also  have  almost  wholly  disap- 
peared. In  only  a  few  cases  are  the  reflexes  increased — a  symptom  which  is  to  be 
regarded  as  analogous  to  cutaneous  hyperesthesia.  We  can  usually  make  out, 
after  a  few  days,  a  decided  diminution  of  electrical  excitability  in  the  affected 
nerves  and  muscles,  which  finally  becomes  a  pronounced  reaction  of  degeneration. 
If  the  paralysis  is  of  longer  duration,  there  is  a  decided  atrophy  of  the  muscles. 
In  these  cases  the  severe  initial  symptoms  of  sensory  irritation,  as  a  rule,  rapidly 
disappear,  although  slight  pains,  paresthesia,  and  especially  a  considerable  sensi- 
tiveness of  the  paralyzed  parts  to  pressure  and  to  passive  motion,  often  last  for  a 
long  time.  In  many  acute  cases  the  hyperesthesia  of  the  skin  and  of  the  deeper 
parts  reaches  a  very  high  degree,  but  it  is  remarkable  that  the  objective  disturbances 
of  sensibility  are  very  slight  in  the  great  majority  of  cases.  Marked  anesthesia  is  a 
rare  exception,  so  that  we  may  rightly  suppose  that  primary  multiple  neuritis  affects 
chiefly  the  motor  nerve-fibers.  We  usually  find  no  disturbances  in  the  distribution 
of  the  cerebral  and  bulbar  nerves.  An  affection  of  the  optic  nerve  has  been  men- 
tioned in  only  a  few  cases.  The  marked  increase  in  the  frequency  of  the  pulse, 
which  is  usually  present,  is  important,  and  probably  depends  upon  a'disturbance  of 
the  vagus.  Trophic  disturbances  in  the  skin,  hair,  and  nails  are  not  very  rare.  (Ede- 
matous swelling  of  the  affected  extremities  has  also  been  repeatedly  observed.  The 
functions  of  the  bladder  and  rectum,  however,  almost  always  remain  undisturbed. 
In  regard  to  the  course  of  the  disease,  in  the  severest  cases  it  may  soon  termi- 
nate fatally,  almost  always  because  the  paralysis  extends  to  the  muscles  of  respira- 
tion. The  inspirations  are  labored,  and  are  performed  with  the  upper  part  of  the 
thorax  only,  while  the  epigastrium  is  motionless,  or  sinks  in  on  inspiration  from 
the  paralysis  of  the  diaphragm.  There  is  also  paralysis  of  the  other  muscles  of 
respiration,  the  abdominal  muscles,  etc.,  so  that,  after  the  disease  has  lasted  a  week 
or  ten  days,  death  ensues  with  all  the  signs  of  respiratory  insufficiency.  A  second 
class  of  cases  also  begins  quite  acutely,  but  then  takes  a  chronic  course.  The  ini- 
tial acute  febrile  symptoms  cease  after  a  few  days,  and  the  paralysis  develops 
to  some  extent.  Then  the  affection  seems  to  come  to  a  stand-still,  and  the  first 
signs  of  improvement  gradually  begin  to  appear.  Since  there  is  a  more  or  less 
pronounced  atrophy  of  the  muscles  in  these  cases,  it  always  takes  quite  a  long 
time— usually  several  months— for  recovery.  A  third  class  of  cases  follow  a 
chronic  course  from  the  outset,  although  even  in  these  cases  there  may  be  more 
acute  exacerbations  of  the  disease.     In  these  cases  quite  extensive  atrophic  paraly- 


584.  DISEASES  OF  THE  NERVOUS  SYSTEM. 

sis  gradually  develops  in  the  lower  extremities,  and  usually  in  the  upper  extremi- 
ties also.  The  reflexes  disappear;  the  sensibility  is  as  a  rule  somewhat,  but  very 
rarely  much  diminished.  Pains  are  always  present  at  first,  but  later  on  in  the 
disease  they  often  become  subordinate.  The  bladder  and  rectum  usually  remain 
intact  in  their  functions.  If  the  disease  advance  gradually  it  may  terminate 
fatally  even  at  a  late  period,  after  a  course  of  months,  usually  from  a  final  paraly- 
sis of  respiration ;  but,  on  the  other  hand,  even  after  a  protracted  course,  the  disease 
may  come  to  a  stand-still,  and  even  to  a  complete  or  at  least  to  a  partial  recovery. 
It  is  worthy  of  note  that  a  combination  of  multiple  neuritis  and  pulmonary  tuber- 
culosis has  quite  frequently  been  observed ;  but  nothing  definite  is  yet  known  as 
to  the  form  of  connection  between  the  two  diseases. 

The  diagnosis  of  multiple  neuritis  is,  as  a  rule,  easy,  for  one  who  is  acquainted 
with  the  disease  and  notes  the  different  symptoms  carefully.  In  regard  to  diag- 
nosis, the  chief  importance  should  be  placed  on  the  generally  acute  beginning, 
with  pronounced  symptoms  of  sensory  irritation,  with  frequently  a  very  consid- 
erable sensitiveness  of  the  nerves  to  pressure  and  general  cutaneous  hyperes- 
thesia ;  and  also  on  the  appearance  of  a  rapidly  extending  paralysis,  whose  periph- 
eral nature  may  be  attested  by  the  presence  of  reaction  of  degeneration,  muscu- 
lar atrophy,  and  the  absence  of  the  cutaneous  and  tendon  reflexes.  Such  a  paraly- 
sis can  be  produced  by  nothing  but  an  affection  of  the  peripheral  nerves  or  polio- 
myelitis {vide  infra).  As  we  have  shown  above,  this  latter  disease  may,  in  fact, 
often  be  confused  with  multiple  neuritis,  but  a  careful  attention  to  the  initial 
symptoms,  especially  to  the  disturbances  of  sensation,  will  usually  make  the  dif- 
ferential diagnosis  possible. 

The  prognosis  of  multiple  neuritis  is  doubtful,  as  is  shown  by  the  description 
of  the  course  of  the  disease,  but  it  is  by  no  means  very  imfavorable.  If  the  first 
acute  stage  of  the  disease  has  been  gone  through  with  without  accident,  we  may 
hope  for  recovery,  or  at  least  actual  improvement,  even  with  extensive  paralysis. 
Such  striking  results  in  the  way  of  recovery,  after  paralysis  that  has  lasted  for 
months,  are  also  important  in  regard  to  diagnosis,  since  such  extensive  processes 
of  regeneration  are  possible  in  affections  of  the  peripheral  nerves,  but  scarcely  in 
spinal  diseases ;  and  hence  they  are  sometimes  an  additional  confirmation  of  the 
diagnosis  of  a  neuritis. 

Treatment .—  In  the  first  stage  of  the  disease,  especially  if  severe  pains,  swelling 
of  the  joints,  or  high  fever  be  present,  it  is  advisable  to  try  the  exhibition  of  sali- 
cylic acid,  from  which  several  observers  have  seen  a  favorable  effect.  We  give 
ten  grains  (grm.  0'5)  of  the  acid  every  hour,  or  a  few  larger  doses,  a  drachm  to  a 
drachm  and  a  half  (grm.  4-6)  of  salicylate  of  sodium.  Instead  of  salicylic  acid  we 
have  lately  used  antipyrine  and  phenacetine  with  good  results.  When  the  pain  is 
very  severe  we  must  use  narcotics,  such  as  injections  of  morphine.  Embrocations 
of  chloroform,  and  sometimes  protracted  warm  baths,  have  also  a  palliative  effect. 
In  the  further  course  of  the  disease  proper  care,  a  suitable  position  for  the  limbs, 
and  diet— nourishing  food— are  the  main  things  for  the  patient.  The  regenerative 
processes  of  recovery  begin  spontaneously,  if  at  all,  but  we  may  hasten  recovery 
and  make  it  complete  by  a  subsequent  electrical  treatment,  especially  galvanism. 
For  the  completion  of  the  recovery,  bathing  (simple  warm  baths,  salt  baths,  etc.) 
is  serviceable,  and  also  the  baths  at  Teplitz,  Wiesbaden,  and  Eehme. 

4.  The  Chronic  Neuritis  of  Alcoholic  Subjects. 

{Pseudotabes  of  Alcoholic  Subjects,  Ataxia  of  Drinkers.) 

It  has  long  been  known  that  peculiar  nervous  affections  often  occur  in  alco- 
holic subjects  (M.  Huss,  Lendet,  and  others) ;  but  up  to  the  present  time  a  disease 


SIMPLE  AND   MULTIPLE  DEGENERATIVE  NEURITIS.  585 

of  the  spinal  cord  has  heen  assumed  to  he  the  cause  of  the  symptoms,  and  only  of 
late  have  we  obtained  the  knowledge  that  at  least  a  great  part  of  the  cases  of  this 
class  are  to  be  regarded  as  a  special  form  of  chronic  multiple  neuritis  (Lancereaux, 
Moeli,  and  others).  The  jiractical  importance  of  this  alcoholic  neuritis  is  not 
slight ;  first,  because  it  may  easily  be  confused  with  other  nervous  diseases,  espe- 
cially with  tabes  dorsalis,  and,  second,  because  its  p roper  and  timely  diagnosis  is 
of  great  significance  in  regard  to  treatment. 

Alcoholic  neuritis  occurs  chiefly  in  two  forms:  in  one  form  actual  atrophic 
paralysis  develops  chiefly  in  the  lower  extremities,  but  in  the  other  form  the 
paresis  is  subordinate  to  the  other  disturbances  of  innervation.  The  first  symptom 
of  the  disease  is  usually  tearing  and  drawing  pains  in  different  parts  of  the  lower, 
or,  more  rarely,  of  the  upper,  extremities.  The  pains  are  usually  quite  severe, 
but  sometimes  only  of  moderate  strength.  Sooner  or  later,  but  sometimes  not  for 
years,  a  pronounced  disturbance  of  the  gait  is  added  to  the  pains.  More  careful 
examination  shows  that  in  such  cases  there  is  partly  an  actual  paresis  of  the 
muscles  of  the  legs,  and  partly  a  form  of  ataxia — a  defective  innervation  which  is 
manifest  by  an  uncertainty,  a  staggering  and  reeling  in  the  gait.  If  there  be 
marked  paresis,  the  affected  muscles  are  quite  atrophic,  and  electrical  examination 
usually  gives  a  decided  diminution  of  excitability,  or  even  pronounced  reaction  of 
degeneration.  The  patellar  reflex  is  usually  lost  quite  early.  The  sensibility,  too, 
is  very  rarely  perfectly  normal ;  we  find  sometimes  quite  marked  anaesthesia,  es- 
pecially in  the  lower  legs,  and  also  in  other  parts  of  the  skin.  The  cutaneous 
reflexes  are  also  often  feeble  and  slow.  There  is  sometimes  considerable  tender- 
ness on  pressure  on  the  deeper  parts  and  over  the  nerves.  The  course  of  the 
disease  is  usually  chronic.  If  the  cause  of  the  evil— the  abuse  of  alcohol— be  re- 
moved in  time,  perfect  recovery  is  possible;  but  in  far-advanced  cases  the  disease 
may  go  on  to  complete  paralysis  even  of  the  upper  extremities,  and  to  a  fatal 
termination.  [In  women,  especially,  mental  symptoms  are  often  pronounced.  It 
is  a  characteristic  feature  of  the  delusions  of  alcoholic  neuritis,  that  the  patient 
will  tell  of  walks  taken,  and  of  people  seen,  although  at  the  time  he  is  helpless  in 
bed.— K.] 

As  may  be  seen,  the  disease  is  decidedly  like  tabes  dorsalis,  and  in  the  early 
stages,  with  pain,  ataxia,  and  absence  of  patellar  reflex,  the  differential  diagnosis 
has  no  slight  difficulty.  In  regard  to  this  it  must  be  borne  in  mind  that  the 
reflex  immobility  of  the  pupils,  the  girdle  sensation  and  disturbances  of  the  bladder, 
seem  to  be  absent  in  alcoholic  neuritis,  at  least  as  a  rule,  while,  on  the  other  hand, 
the  development  of  atrophic  paralyses  may  almost  certainly  exclude  tabes. 

The  treatment  demands,  in  the  first  place,  the  entire  abandonment  of  the 
further  use  of  alcohol,  if  possible.  In  mild  cases  we  can  obtain  a  decided  improve- 
ment by  this  alone.  In  more  advanced  cases  electrical  treatment  and  tepid  baths 
do  the  best  service.  We  would  also  recommend  the  internal  or  subcutaneous  use 
of  preparations  of  strychnine. 


CHAPTER  VI. 

NEW  GROWTHS  IN  THE  PERIPHERAL  NERVES. 

The  new  growths  in  the  peripheral  nerves  are  usually  divided  into  false  and 
true  neuromata.  The  former  are  not  newly  formed  nervous  tissue  proper,  but  are 
fibromata,  myxomata,  sarcomata,  etc.,  which  develop  on  the  nerves.  Infectious 
tumors,  also,  especially  syphilitic  gummata,  and  still  more  frequently  the  new 
growths  arising  in  leprosy,  may  have  their  seat  on  the  peripheral  nerves.     The 


58G  DISEASES  OF  THE  NERVOUS  SYSTEM. 

true  neuromata  consist  of  newly  formed,  usually  medullated,  nerve-fibers  (neu- 
roma myelinicum  of  Virchow),  which  are  imbedded  in  a  frequently  very  abun- 
dant connective-tissue  stroma.  These  neuromata  develop  most  frequently  in  the 
cut  ends  of  nerves  in  amputation-stumps  (amputation  neuromata),  but  they  may 
form  after  other  injuries  of  the  nerves,  and  probably  many  neuralgias  and  per- 
sistent paius  after  injuries  are  due  to  the  formation  of  such  little  neuromata.  The 
multiple  occurrence  of  neuromata,  which  has  also  been  repeatedly  observed,  is 
very  remarkable.  These  develop  by  hundreds  in  the  same  individual,  chiefly  on 
the  spinal  nerves,  only  occasionally  and  exceptionally  on  the  sympathetic  or 
cranial  nerves.  In  such  cases  the  different  tumors  are  by  no  means  metastases 
from  one  original  tumor,  but  are  the  expression  of  a  general  and  often  hereditary 
predisposition  of  the  peripheral  nervous  system  to  the  formation  of  tumors. 
Sometimes  multiple  neuromata  are  combined  with  other  anomalies  of  the  nervous 
system,  such  as  cretinism.  Besides  the  medullated  neuromata,  there  are  also  new 
growths  of  non-medullated  nerve-fibers  (neuroma  amyelinicum),  but  their  histo- 
logical diagnosis  is  always  very  difficult. 

The  symptoms  of  neuromata  vary  very  much  in  different  cases.  Many  of 
them  cause  no  symptoms  at  all,  but  in  other  cases  they  are  the  cause  of  extremely 
severe  and  persistent  neuralgias  and  neuralgiform  pains,  which  come  on  with 
varying  intensity,  are  usually  remittent  or  intermittent,  and  are  often  iencrased 
by  external  causes,  the  influence  of  the  weather,  etc.  Marked  symptoms  of 
pressure,  especially  anaesthesia  and  motor  paralysis,  are  only  exceptionally  devel- 
oped, but  they  sometimes  do  occur,  especially  in  neuromata  of  the  cauda  equina. 
Direct  or  reflex  symptoms  of  motor  irritation,  such  as  tremor  or  tonic  spasms,  are 
somewhat  more  frequent. 

The  so-called  tubercula  dolorosa  deserve  special  mention.  By  this  term  we 
mean  little  nodules  which  may  be  felt  beneath  the  skin,  and  are  usually  readily 
movable  and  very  sensitive  to  pressure.  They  are  not  very  rare,  and  are  usually 
associated  with  drawing  pains,  which  are  rarely  decidedly  neuralgic  and  are  not 
very  strictly  localized.  They  are  situated  in  the  extremities,  especially  in  the 
arms,  and  in  the  back,  the  neck,  etc.  It  is  worthy  of  note  that  the  symptoms  are 
only  at  times  very  prominent,  and  then  they  disappear  again,  and  that  with  this 
disappearance  is  certainly  sometimes  associated  a  spontaneous  disappearance  of 
the  nodule.  The  anatomical  nature  of  the  tubercula  dolorosa  is  not  always  to  be 
established  with  certainty.  Many  of  them  are  true  neuromata,  but  others  belong 
to  other  kinds  of  new  growths. 

The  course  of  neuromata  is  of  course  very  chronic.  In  some  cases  the  per- 
sistent severe  pain  may  give  rise  to  considerable  general  disturbance,  but  a  final 
spontaneous  cessatiou  of  the  symptoms,  and  even  a  disappearance  of  the  new 
growths,  have  also  been  observed. 

The  diagnosis  of  neuromata  is  possible  only  when  the  tumors  can  be  felt  through 
the  skin,  and  when  their  seat,  as  well  as  their  clinical  symptoms,  correspond  to 
the  course  and  distribution  of  a  nerve.  In  multiple  neuromata  the  diagnosis  has 
been  repeatedly  confirmed  by  the  excision  and  examination  of  one  of  the  tumors. 

The  only  successful  treatment  of  neuromata  is  extirpation,  which  is  to' be 
undertaken  only  when  the  symptoms  are  very  severe.  If  extirpation  be  not 
practicable,  or  if  we  have  to  do  with  multiple  neuromata,  the  patient's  trouble 
can  be  alleviated  only  by  symptomatic  means,  narcotics,  and  electricity.  If  we 
can  compress  the  nerve  above  the  neuroma,  we  can  often  cause  by  this  means  a 
temporary  cessation  of  the  pain. 


I 

VASO-MOTOE,  TKOPHIC,  AND  SECRETORY  DISTURBANCES.  587 


II. — Vaso-motor  and  Trophic  Neuroses. 


CHAPTER  I. 

PRELIMINARY  REMARKS  UPON  VASO-MOTOR,  TROPHIC,  AND 
SECRETORY  DISTURBANCES. 

Besides  the  disturbances  of  sensibility  and  motility  described  in  the  preceding 
sections,  we  also  see  in  nervous  patients  frequent  anomalies  of  the  vaso-motor  and 
trophic  functions,  but  up  to  the  present  time  we  know  comparatively  little  that  is 
certain  as  to  the  precise  nature  of  their  occurrence. 

Physiology,  as  is  well  known,  distinguishes  two  varieties  of  vaso-motor  nerves 
— the  vaso-constrictors  and  the  vaso-dilators ;  but  since  experiments  have  detected 
the  latter  variety  in  only  a  few  places — for  example,  in  the  chorda  tympani,  the 
nervi  erigentes,  and  the  sciatic — they  have  not  acquired  a  very  great  significance  in 
human  pathology.  We  are  at  present  much  more  disposed  to  refer  every  abnor- 
mal constriction  of  the  vessels  to  an  irritation,  and  every  abnormal  dilatation  of 
the  vessels  to  a  paralysis  of  the  vaso-constrictor  nerves,  although  perhaps  patho- 
logical conditions  of  irritation  of  the  vaso-dilators  may  not  be  at  all  rare.  In 
regard  to  the  precise  anatomical  course  of  the  vaso-motor  nerves,  we  must  first 
state  that  vaso-motor  irritations  may  certainly  proceed  from  the  cerebrum,  as  is 
shown  by  the  well-known  symptoms  of  blushing  and  pallor  from  mental  emo- 
tions. In  experiments  on  clogs,  Eulenburg  and  Landois  have  succeeded  in  pro- 
ducing a  fall  of  temperature  on  the  opposite  side  by  irritating  certain  portions  of 
the  cortex  in  the  immediate  vicinity  of  the  motor  centers,  and  by  extirpation  of 
the  same  parts  they  have  produced  a  rise  in  temperature.  Furthermore,  we  know 
with  certainty  that  there  is  an  important  vaso-motor  center  in  the  medulla  oblon- 
gata (in  the  region  of  the  upper  olivary  body  in  rabbits),  the  irritation  of  which, 
directly  or  reflex] y,  is  followed  by  an  almost  universal  vascular  constriction,  and 
its  destruction  by  an  almost  universal  vascular  dilatation.  We  must  probably 
seek  the  further  course  of  the  vaso-motor  nerves  very  largely  (or  exclusively  ?)  in 
the  lateral  columns,  from  which  they  pass  out  chiefly  by  the  anterior  roots ;  but 
there  are  also  experimental  data  (Strieker)  suggesting  the  presence  of  vaso-motor 
nerves  in  the  posterior  roots.  It  is  not  known  with  certainty  whether  there  is 
any  decussation  of  the  vaso-motor  fibers,  or,  if  there  is,  where  it  occurs.  The 
larger  part  of  the  vaso-motor  nerves  collect,  at  any  rate;  in  the  principal  trunks 
of  the  sympathetic,  from  which,  as  is  well  known,  the  separate  plexuses  that  sur- 
round the  vessels  arise.  It  is  not  improbable,  however,  that  there  is  also  in  part  a 
direct  passage  of  vaso-motor  fibers  from  the  cord  into  the  peripheral  nerves.  In 
conclusion,  we  must  mention  that,  according  to  Goltz's  experiments,  there  are 
reflex  vaso-motor  centers  in  the  cord  for  the  different  parts  of  the  body. 

The  clinical  vaso-motor  symptoms  are  chiefly  to  be  observed  in  the  external 
skin.     We  distinguish  them  as  follows : 

1.  Symptoms  of  Vaso-motor  Paralysis. — We  conclude  that  there  is  a  paral- 
ysis of  the  vaso-motors  if  there  is  an  abnormal  redness  of  the  skin.  Such  a  red- 
ness is  almost  always  associated  with  an  objective  and  often  a  subjective  feeling 
of  an  increase  of  temperature.  Such  conditions  are  observed  either  in  connection 
with  other  nervous  symptoms — as  in  fresh  spinal  or  cerebral  paralyses,  and  also 


588  DISEASES  OF  THE  NERVOUS  SYSTEM. 

very  often  in  certain  functional  neuroses,  such  as  hysteria  and  neurasthenia — or  in 
the  form  of  independent  affections — the  pure  vaso  motor  neuroses,  injuries  of  the 
cervical  sympathetic,  etc.  There  are  cases  in  which  the  only  symptoms  are  a 
persistent  or  paroxysmal  redness  of  the  skin,  especially  of  the  head,  associated 
with  a  great  feeling  of  heat,  with  palpitation  of  the  heart,  strong  pulsation  of  the 
arteries,  anxiety,  ringing  in  the  ears,  and  sweating.  If  the  affection  he  confined 
to  a  single  extremity,  in  which  there  are  paroxysmal  redness,  diffuse  swelling,  and 
pain,  we  have  the  condition  described  by  Weir  Mitchell  as  erythromelalgia.  As 
was  stated  above,  it  is  at  present  impossible  to  decide  whether  many  of  the  symp- 
toms just  mentioned  do  not  perhaps  depend  upon  an  irritation  of  the  vaso-dilator 
nerves. 

2.  Symjrtoms  of  Vaso-motor  Spasm. — Spasm  of  the  small  vessels  becomes 
apparent  by  a  striking  pallor  and  coolness  of  the  skin.  There  is  often,  with  this, 
a  decided  feeling  of  formication  and  stiffness  in  the  affected  parts,  which  may 
even  increase  to  an  actual  feeling  of  pain.  Such  vaso-motor  spasms  affect  the 
hands  especially,  and  form  a  chronic  trouble  that  is  not  very  rare.  They  are 
usually  seen  in  people  who  are  generally  nervous  and  irritable,  and  sometimes 
also  in  washerwomen.  A  vascular  spasm  is  sometimes  seen  in  the  extremities  as 
one  symptom  of  complicated  paroxysms,  such  as  nervous  angina  pectoris  (q.  v.), 
especially  at  the  beginning  of  the  paroxysm.  A  persistent  spasm  of  the  small 
arteries  may  give  rise  to  considerable  subsequent  trophic  disturbance.  At  least, 
the  rare  cases  of  so-called  "  spontaneous  symmetrical  gangrene  "  [Raynaud's  dis- 
ease of  the  extremities],  and  also  certain  forms  of  scleroderma  and  some  similar 
affections,  are  referred  by  many  observers  to  a  primary  spasm  of  the  vessels. 
[Other  observers  are  disposed  to  attribute  many  if  not  all  the  cases  of  symmetrical 
gangrene  to  arterio-sclerosis  or  syphilitic  endarteritis  affecting  the  smaller  vessels. 
— K.]  There  is  a  condition,  seen  especially  in  the  hands,  in  which,  without  known 
cause,  the  skin  becomes  dark  blue  and  icy  cold,  and  the  epidermis  is  raised  in  dif- 
ferent parts  into  bullae.  This  condition  may  even  attain  to  a  circumscribed  gan- 
grene— spastic  gangrene. 

We  have  much  less  information  concerning  the  trophic  nerves  than  we  have 
concerning  the  vaso-motor.  As  is  well  known,  the  controversy  is  still  going  on 
as  to  whether  we  have  any  right  to  assume  the  existence  of  special  trophic  nerves. 
Clinical  facts  speak  decidedly  in  favor  of  this  assumption,  although  we  have 
already  stated  that  many  trophic  disturbances  are  probably  due  to  vaso-motor 
changes,  and  also  that  the  anaesthesia  of  many  parts  is  a  very  favorable  circum- 
stance for  the  occurrence  of  disturbances  of  nutrition  (compare  what  was  said  in 
regard  to  anaesthesia  of  the  trigeminus  on  page  514). 

Those  changes  in  the  skin  which  depend  essentially  upon  an  abnormally  great 
exudation  from  the  vessels  form  a  transition  between  vaso-motor  and  trophic  dis- 
turbances. Among  them  are,  first,  peculiar  cases  of  disease  which  have  been 
termed  "  acute  angioneurotic  oedema"  (Quincke,  Strübing,  and  others).  In  these 
cases  cedematous  swellings  appear  suddenly  in  various  parts  of  the  body,  and 
sometimes  disappear  after  a  few  hours,  hut  they  may  be  very  often  repeated.  Dan- 
gerous symptoms  may  arise  if  the  oedema  affect  the  pharynx  or  the  entrance  to 
the  larynx.  The  patient's  health  otherwise  is  sometimes  perfectly  good,  but  in 
other  cases  it  is  more  or  less  affected.  Gastric  disturbances  especially  (attacks  of 
vomiting  and  gastralgia)  have  been  observed  at  the  same  time  in  such  patients. 
Acute  angioneurotic  oedema  is  manifestly  closely  allied  to  urticaria  and  ery- 
thema exudativum.  In  regard  to  the  occurrence  of  herpes  zoster  in  nervous  dis- 
eases, compare  what  was  said  on  page  525.  Vesicle  formations  analogous  to  herpes 
zoster  intercostalis  may  also  occur  along  the  track  of  other  nerve-trunks  in  periph- 
eral, or  even  in  purely  spinal  (?)  nervous  affections. 


VASOMOTOR,  TROPHIC,  AND  SECRETORY  DISTURBANCES.  589 

Among  those  symptoms  which,  chiefly  support  the  theory  of  the  existence  of 
specific  trophic  nervous  influences,  we  have  already  learned  to  recognize  Die 
degenerative  atrophy  of  the  muscles  and  nerves  (see  page  588).  Various  other 
sorts  of  trophic  disturbances  in  the  skin  and  the  deeper  parts  are  seen  in  nervous 
diseases.  Especially  after  wounds  of  the  peripheral  nerves  we  often  notice  a 
peculiar  shining,  smooth,  atrophic  condition  of  the  skin— the  "glossy  skin"  or 
"glossy  fingers"  of  the  English  authors.  In  other  cases  anomalies  in  the  pig- 
mentation of  the  skin  seem  to  be  connected  with  the  nervous  disturbances ;  thus 
spots  deprived  of  pigment  {vitiligo)  often  develop  as  a  result  of  severe  neural- 
gias. We  must  also  bring  to  mind  here  the  appearance  of  changes  in  pigmenta- 
tion from  nervous  causes,  especially  the  aetiology  of  Addison's  disease  (vide  infra) 
and  the  occurrence  of  the  so-called  nervous  nsevi.  Among  the  severe  neuro- 
trophic disturbances  of  the  skin  many  observers,  especially  Charcot,  class  the 
appearance  of  acute  bedsores  in  many  spinal  and  cerebral  paralyses,  but  we  have 
never  been  able  to  convince  ourselves  of  the  occurrence  of  a  "  neurotrophic  decubi- 
tus," and  we  believe  that  every  bedsore  is  due  in  the  first  instance  to  external  in- 
fluences, uncleanliness,  and  pressure  on  the  skin. 

We  may  here  mention  myxoedema  (cachexie  pachydermique  of  Charcot),  which 
was  first  described  in  England  by  William  Gull  and  Ord.  The  disease  has  taken 
its  name  from  a  peculiar  thickening  and  swelling  of  the  skin,  which  is  most 
marked  in  the  face,  but  which  is  sometimes  seen  in  the  extremities,  the  trunk,  the 
tongue,  and  even  in  the  internal  organs.  This  swelling  is  not  oedema,  but  it  is 
due  to  the  development  of  a  sort  of  myxomatous  new  growth,  rich  in  mucine, 
in  the  connective  tissue.  Other  trophic  disturbances  usually  co-exist:  atrophy  of 
the  teeth  and  nails  [spade-like  hands,  coarseness  and]  loss  of  hair,  failure  in  the 
sweat  secretion  and  consequent  dryness  of  the  skin,  etc.  Besides  these  there  gradu- 
ally develops  a  general  physical  and  mental  weakness,  which  may  increase  to  great 
hebetude  or  even  to  complete  dementia.  Disturbances  of  the  sensory  functions 
may  also  occur.  It  is  a  fact  of  especial  interest  that  we  find  quite  commonly  a 
diminution  and  even  a  complete  atrophy  of  the  thyroid  gland.  It  is  not  improb- 
able that  all  the  symptoms  of  the  disease  may  arise  from  the  failure  of  function 
of  the  thyroid  gland.  This  hypothesis  is  confirmed  by  the  repeated  experiments 
of  Kocher  and  others,  that  after  complete  extirpation  of  the  thyroid  in  man  almost 
the  same  symptoms  ensue  as  in  myxoedema  (cachexia  strumipriva).  From  this 
we  must  suppose  that  certain  injurious  substances  accumulate  in  the  body  which 
can  no  longer  be  made  innocuous  by  the  thyroid  gland. 

Besides  the  trophic  disturbances  in  the  skin,  we  often  see  analogous  changes  in 
the  nails  and  hair  in  nervous  patients.  The  nails  become  brittle  and  cracked,  as- 
sume a  darker  color,  and  often  show  a  considerable  thickening  (onychogryphosis). 
We  also  see  at  times  a  loss  of  the  nails.  A  loss  of  hair  is  seen  in  frontal  neural- 
gia, in  certain  forms  of  headache,  and  not  infrequently  as  an  apparently  independ- 
ent nervous  disease  (alopecia).  A  very  rapid  whitening  of  the  hair  after  mental 
excitement  is  well  known  to  have  occurred  in  some  cases. 

Among  the  trophic  disturbances  of  the  deeper  parts  the  symptoms  sometimes 
seen  in  the  bones  and  joints  deserve  a  brief  mention.  The  implication  of  the 
bones  in  atrophic  processes  is  seen  chiefly  in  progressive  unilateral  facial  atrophy 
(vide  infra).  A  retarded  growth  of  bone  in  the  affected  extremities  is  also  a 
symptom  frequently  seen  in  the  spinal  and  even  in  the  cerebral  paralyses  that 
develop  in  childhood,  which  proves  most  plainly  that  the  processes  of  growth  de- 
pend upon  the  nervous  system. 

A  "  trophic  disturbance  "  chiefly  of  the  bones,  but  also  involving  the  soft  parts, 
forms  the  basis  of  that  peculiar  and  rare  disease  recently  termed  acromegaly 
(P.  Marie,  Erb,  etc.).     The  affection  develops  slowly  in  women  and  men,  usually 


590  DISEASES  OF  THE  NERVOUS  SYSTEM. 

in  youth  or  middle  age.  Besides  the  general  symptoms  of  dullness,  fatigue,  and 
quite  severe  neuralgic  or  rheumatic  pains  in  the  head  and  the  extremities,  there 
gradually  develops  a  striking  increase  in  the  size  of  the  hands  and  feet,  and  thick- 
ness and  plumpness  of  the  face,  due  chiefly  to  enlargement  of  the  nose,  chin,  and 
lips,  which  become  puffed  out  to  a  considerable  size.  The  hands  and  feet  become 
actual  paws.  Later  in  the  disease  the  legs  and  forearms  also  increase  in  circum- 
ference. The  hypertrophy  seems  to  affect  the  bones  chiefly,  but  in  some  cases 
the  skin  also  seems  thicker,  without  showing  those  marked  changes  characteristic 
of  myxcedema.  In  a  case  we  have  lately  seen  the  tongue  also  showed  distinct  en- 
largement; sugar  was  also  occasionally  present  in  the  urine,  and  with  this  there 
was  a  profuse  and  almost  uninterrupted  secretion  of  sweat.  The  voice  was  weak, 
deep,  and  hoarse,  as  a  result  of  an  evident  paresis  of  the  vocal  cords.  The  few 
autopsies  in  acromegaly  have  thus  far  not  been  able  to  contribute  much  in  the 
way  of  explanation  of  this  remarkable  affection.  In  all  cases  hyperplasia  of  the 
hypophysis  cerebri  was  a  striking  lesion,  and  in  the  case  of  Klebs  the  persistence 
and  hyperplasia  of  the  thymus  gland.  Erb  found  in  his  cases  a  dullness  in  the 
upper  sternal  region,  which  he  is  disposed  to  attribute  to  a  persistent  thymus.  In 
our  case  this  dullness  could  not  be  detected.  The  significance  of  all  these  discov- 
eries is  still  an  utter  enigma. 

Trophic  affections  of  the  joints  have  been  repeatedly  confirmed  in  cerebral  and 
spinal  diseases,  especially  in  tabes  dorsalis  (vide  infra).  As  a  special  vaso-mo- 
tor-trophic  articular  neurosis  we  may  mention  here  the  so-called  hydrops  articu- 
lorum  intermittens.  We  mean  by  this  a  very  rare  but  perfectly  typical  disease, 
in  which  large  swellings,  usually  of  the  knee-joint,  but  sometimes  of  the  other 
large  joints,  develop  at  perfectly  regular  intervals  of  one  to  four  weeks.  They 
continue  without  fever,  and  usually  without  any  great  pain,  and  disappear  again 
in  a  few  days.  Such  attacks  may  be  repeated  at  intervals  of  different  lengths, 
during  years  and  years.  Their  nervous  character  is  attested  especially  by  the 
rapid  onset  and  disappearance  of  the  affection,  and  also  by  the  combination  of  it 
with  other  nervous  disturbances,  such  as  angina  pectoris,  exophthalmic  goitre, 
vaso-motor  symptoms,  etc.,  which  combination  has  often  been  observed.  In  re- 
gard to  treatment  we  may  try  salicylic  acid,  quinine,  Fowler's  solution,  and  subcu- 
taneous injections  of  ergotine. 

In  addition  to  the  trophic  disturbances  we  must  consider  the  disturbances  of 
secretion.  These  are  not  infrequent.  We  have  already  learned  to  recognize 
anomalies  in  the  secretion  of  saliva  in  facial  paralysis,  and  of  the  lachrymal  secre- 
tion in  trigeminal  neuralgia,  Analogous  symptoms  are  occasionally  noticed  in 
other  nervous  diseases.  Disturbances  of  the  sweat  secretion  are  the  easiest  to 
confirm.  Our  understanding  of  them  comes  substantially  from  the  discovery  of 
the  "swreat  nerves,"  arising  mainly  from  the  sympathetic,  which  was  first  made 
by  Luchsinger.  In  nervous  patients  we  have  seen  quite  frequently,  on  the  one 
hand,  an  abnormal  increase  of  the  sweat  secretion  (hyperidrosis,  ephidrosis),  and, 
on  the  other,  a  diminution  or  a  complete  disappearance  of  it.  The  former  is  seen 
on  the  paralyzed  side  in  many  hemiplegias  and  in  spinal  paralyses,  the  latter  in 
tabes  dorsalis.  Anomalies  of  the  sweat  secretion  are  quite  frequent,  and  are  usu- 
ally combined  with  vaso-motor  disturbances,  in  certain  general  neuroses,  such  as 
hysteria  and  neurasthenia.  In  a  few  rare  cases  a  genuine  haematidrosis  (bloody 
sweat)  has  been  confirmed.  The  condition  known  as  unilateral  hyperidrosis  (uni- 
lateral sweating)  is  also  especially  interesting.  In  this  there  is  an  abnormal  secre- 
tion of  sweat,  chiefly  in  one  half  of  the  face,  more  rarely  in  one  arm  or  over  the 
whole  of  one  side.  The  affection  has  usually  been  observed  in  connection  with 
hemicrania,  exophthalmic  goitre,  hysteria,  etc.,  and,  in  at  least  a  number  of  cases, 
it  seems  to  be  due  to  direct  lesions  of  the  sympathetic.     On  the  other  hand,  we 


HEMICRANIA.  501 

have  repeatedly  seen  persons,  who  were  otherwise  perfectly  healthy,  in  whom  the 
secretion  of  sweat,  coming  on  under  normal  conditions  from  heat  or  physical  exer- 
tion, remained  limited  to  one  half  of  the  body,  especially  the  face. 

In  conclusion,  we  would  briefly  mention  here  the  symptoms  which  have  been 
observed  in  direct  injuries  of  the  cervical  sympathetic,  wounds,  pressure  of  neigh- 
boring tumors,  etc.  If  we  have  to  do  with  a  paralysis  of  the  sympathetic,  we  see 
almost  constantly  on  the  affected  side  a  contraction  of  the  pupil  from  paralysis  of 
the  dilator  pupillae  supplied  from  the  sympathetic,  in  many  cases  associated  with 
a  slow  reaction  to  light.  We  also  frequently  see  a  narrowing  of  the  opening  of  the 
lids  from  paralysis  of  Mtiller's  muscle,  and  in  old  cases  a  retraction  of  the  bulbus 
oculi,  and  occasionally  increased  redness  and  warmth  in  the  ear  and  cheeks  from 
vaso-motor  disturbance.  In  a  few  cases  we  see  an  increased  sweat  secretion.  We 
may  add  that,  according  to  Möbius,  the  normal  reflex  dilatation  of  the  pupil,  from 
a  painful  irritation  of  the  skin  of  the  face,  is  absent  in  paralysis  of  the  sympa- 
thetic. The  opposite  symptoms  are  found  in  conditions  of  irritation  of  the  sym- 
pathetic. In  both  cases  there  are  sometimes  slight  trophic  disturbances  in  the 
cheeks.  It  is  also  worthy  of  note  that  in  tumors  of  the  neck,  and  after  injuries  of 
the  brachial  plexus,  there  are  sometimes  disturbances  in  the  sympathetic,  especially 
changes  in  the  pupils,  which  are  due,  as  is  supposed,  to  a  lesion  of  the  communi- 
cating branches  between  the  principal  trunk  of  the  sympathetic  and  the  brachial 
plexus.  The  occurrence  of  sympathetic  symptoms  in  certain  injuries  of  the  bra- 
chial plexus  has  already  been  mentioned  above  (page  567). 


CHAPTER  II. 

HEMIORANIA. 

( Migraine.) 

iEtiology. — By  hemicrania  we  mean  a  peculiar  form  of  unilateral  headache, 
due  probably  to  vaso-motor  disturbances,  or  at  least  almost  always  associated  with 
vaso-motor  symptoms.  The  affection  occurs  especially  in  women,  more  rarely  in 
men,  and  almost  always  begins  in  youth,  generally  at  the  period  of  puberty,  but 
typical  cases  of  migraine  have  been  repeatedly  observed  in  school-children.  Quite 
freqiiently,  but  not  always  by  any  means,  the  disease  affects  women  who  must  be 
regarded  as  "  generally  neryous,';  who  are  anaemic,  or  who  suffer  from  disturbances 
of  menstruation.  Heredity  often  plays  a  part,  since  hemicrania  is  both  hereditary 
as  such,  and  often  appears  in  families  which  have  suffered  from  other  nervous 
diseases,  such  as  epilepsy,  hysteria,  or  the  psychoses.  We  may  mention  as  exciting 
causes,  which  may  be  made  answerable  both  for  the  onset  of  the  disease  and  quite 
often  for  the  individual  attacks,  physical  and  mental  overexertion,  great  mental 
excitement,  and  disturbances  of  digestion.  [Eye-strain  (vide  supra)  may  be  a 
cause  of  migraine  as  well  as  of  other  forms  of  headache,  and  a  careful  search  for 
any  errors  of  refraction  should  be  made  in  every  case. — K.] 

We  do  not  know  the  special  cause  of  hemicrania.  Considering  the  accompa- 
nying vaso-motor  symptoms,  which  are  present  in  migraine  as  a  rule  ( vide  infra), 
it  is  almost  universally  assumed  that  we  must  regard  the  disease,  from  its  chief 
cause,  as  an  affection  of  the  sympathetic ;  but  we  must  agree  with  Möbius  that  this 
assumption  is  by  no  means  confirmed,  and  that  it  is  possible  that  the  accompany- 
ing sympathetic  symptoms  may  be  only  secondary  and  of  reflex  origin,  in  conse- 
quence of  the  pain.  We  also  have  no  definite  information  as  to  the  special  seat 
of  the  pain  in  migraine,  but  it  is  most  probably  to  be  placed  in  the  meninges — the 
pia  and  dura  mater. 


592  DISEASES  OF  THE  NERVOUS  SYSTEM. 

Symptomatology. — Migraine  always  comes  on  in  separate  attacks,  which  are 
repeated  at  intervals  of  varying  lengths,  although  some  cases  often  show  a 
remarkably  great  regularity.  The  onset  of  the  attack  in  women  often  has  some 
relation  to  the  menses.  The  left  half  of  the  head  is  much  more  frequently  affected 
than  the  right.  In  some  cases  it  happens  that  the  pain  affects  the  right  and  the 
left  sides  alternately ;  in  others  it  is  not  generally  very  strictly  limited  to  one 
side. 

The  attack  of  migraine  usually  begins  with  certain  prodromal  symptoms,  which 
the  patient  soon  recognizes  as  sure  signs  of  his  approaching  suffering.  These 
prodromal  symptoms  consist  of  general  uneasiness,  discomfort,  pressure  in  the 
head,  vertigo,  at  times  tinnitus,  spots  before  the  eyes,  chills,  malaise,  abnormal 
yawning,  etc.  In  a  short  time  the  pain  begins.  It  is  felt  most  either  in  the  ante- 
rior frontal  region  or  in  the  temporal  or  parietal  region ;  it  generally  shows  a  con- 
tinuous character,  not  intermittent  as  in  neuralgia,  and  may  increase  to  a  very 
great  intensity.  Special  painful  points  are  usually  absent,  but  the  whole  skin 
over  the  head  on  the  affected  side  is  usually  hyperassthetic.  The  general  malaise 
continues  with  it;  the  patient  has  absolutely  no  appetite;  there  is  often  great 
nausea,  and  almost  always  a  great  sensitiveness  to  external  impressions,  to  any 
bright  light,  or  to  any  noise.  In  many  cases  of  ophthalmic  hemicrania  ocular 
disturbances  are  especially  prominent;  bright  scintillations  before  the  eyes,  scin- 
tillating scotoma,  and  quite  often  a  pronounced  hemianopsia,  may  be  made  out 
during  the  attack. 

The  vaso-motor  symptoms  are  of  special  interest  because  they  are  of  value  in 
the  theory  of  the  disease.  From  them  migraine  is  usually  divided  into  two  sub- 
divisions— hemicrania  sympathico-tonica  or  spastica,  and  hemicrania  sympathi- 
co-paralyiica  or  angio-paralytica. 

In  hemicrania  spastica,  first  described  by  Du  Bois-Reymond  from  observations 
on  himself,  the  forehead  and  ear  on  the  affected  side  are  pale,  the  skin  is  cool,  the 
temporal  arteries  contracted,  the  pupil  is  often  decidedly  dilated,  the  secretion  of 
saliva  increased— in  short,  there  are  a  whole  row  of  symptoms  present  which  all 
agree  in  pointing  to  a  condition  of  irritation  in  the  sympathetic  {vide  supra). 

In  hemicrania  paralytica,  however,  which  wTas  first  described  by  Möllendorff, 
also  from  observations  on  himself,  the  face  is  reddened  on  the  affected  side,  it  feels 
hot,  the  temporal  arteries  are  dilated  and  pulsate  strongly,  there  is  sometimes 
unilateral  sweating  of  the  face,  the  pupil  is  contracted— all  symptoms  which  can 
depend  only  on  a  paralysis  of  the  sympathetic. 

As  has  already  been  hinted,  the  significance  of  all  these  symptoms  is  not  abso- 
lutely certain,  and  we  must  also  add  that  the  cases  which  occur  in  practice  can 
not  by  any  means  always  be  inserted  into  one  or  the  other  typical  scheme  without 
further  ceremony.  The  vascular  symptoms  are  sometimes  but  slight,  conditions 
of  paralysis  and  of  irritation  of  the  sympathetic  sometimes  seem  to  alternate  with 
each  other  in  the  same  attack,  and  we  may  even  frequently  meet  with  apparently 
contradictory  symptoms  at  the  same  time,  such  as  pallor  joined  with  contraction  of 
the  pupil.  The  peculiar  method  of  the  origin  of  the  pain  is  at  present  also  almost 
wholly  unexplained.  If  we  assume  primary  vascular  changes  in  hemicrania,  we 
must  look  for  the  cause  of  the  pain  in  the  disturbance  of  the  circulation,  or  per- 
haps, in  spastic  hemicrania,  in  the  spasmodic  contraction  of  the  vessels  itself. 

The  duration  of  the  attacks  of  migraine  differs  very  much  in  different  cases. 
It  usually  lasts  several  hours,  or  a  whole  day;  then  the  pain  gradually  disappears, 
and  there  is  often  considerable  vomiting  and  sometimes  a  profuse  discharge  of 
urine  toward  the  end  of  the  attack.  In  the  intervals  between  the  different  attacks 
most  patients  are  perfectly  well  and  free  from  pain. 

The  whole  course  of  migraine  is  very  chronic,  and  may  last  for  years  and 


HEMICRANIA.  593 

years.  It  is  usually  a  trouble  to  which  the  patient  finally  becomes  accustomed. 
We  must  generally  be  quite  guarded  in  our  prognosis,  for  many  cases  resist  very 
obstinately  all  attempts  at  cure.  We  can  give  the  patient  only  the  consolation 
that  the  trouble  generally  disappears  of  itself  in  advanced  life.  It  is  not  usually 
attended  with  any  special  danger.  In  only  a  few  cases  has  it  been  noticed  that 
attacks  of  hemicrania  of  years' duration  bave  preceded  a  severe  cerebral  disease 
that  developed  later,  or  tabes  dorsal  is. 

Treatment. — Very  many  patients  who  suffer  from  migraine  finally  renounce 
any  special  treatment,  after  they  have  exhausted  all  possible  remedies.  They 
withdraw  to  their  rooms  when  the  attack  comes  on,  darken  the  windows,  take 
nothing  but  some  tea,  Seltzer-water,  or  cracked  ice,  put  a  cold  compress  about 
the  head,  perhaps  try  a  foot-bath,  and  for  the  rest  wait  quietly  until  the  attack  is 
over.  In  fact,  our  remedies  for  cutting  the  attack  short  are  quite  uncertain.  They 
sometimes  aid,  but  they  often  leave  us  in  the  lurch,  especially  if  used  repeatedly. 
We  must  note  especially  that  narcotics,  such  as  morphine,  are  almost  always  ill 
borne  in  migraine,  and  do  no  good;  but  antipyrine,  sodic  salicylate  (20-.'j0  grains 
[grm.  1'5-2'u],  in  strong  black  coffee),  antifebrine,  and  phenacetine  in  many  cases 
undoubtedly  have  a  favorable  action.  Which  remedy  acts  the  best  must  usually 
be  tested  in  the  individual  case.  We  have  ourselves  seen  excellent  results  former- 
ly from  sodic  salicylate,  and  lately  from  antipyrine ;  the  attacks  of  migraine,  when 
the  remedy  was  taken  immediately  upon  the  onset  of  the  first  symptoms,  have  be- 
come distinctly  milder  and  have  run  their  course  more  rapidly.  Of  course  the  ac- 
tion often  ceases  with  time,  and  we  must  then  try  another  of  the  remedies  men- 
tioned. Of  the  other  remedies  used  we  may  mention  guarana  {Paullinia  sorbilis). 
half  a  drachm  to  a  drachm  (grm  2-4)  of  the  powder,  and  caffeine,  or  sodio-salicylate 
of  caffeine,  in  three-  to  five-grain  doses  (grm.  0'2-0-3),  which  is  sometimes  very  serv- 
iceable. On  theoretical  grounds,  inhalations  of  nitrite  of  amy],  three  to  five  drops 
on  a  napkin,  have  been  used  in  spastic  hemicrania,  and  subcutaneous  injections 
of  ergotine  in  the  paralytic  form  (aqueous  extract  of  ergot,  2"5;  dilute  alcohol  and 
glycerine,  each  5 ;  or  one  part  of  dialyzed  ergotine  in  four  parts  of  distilled  water ; 
injections  of  either,  three  to  fifteen  minims).  Many  other  nervines,  such  as  bro- 
mide of  potassium  and  Fowler's  solution,  have  been  recommended  for  continued 
use,  and  also  extract  of  cannabis  indica ;  and,  lately,  nitrite  of  sodium,  two  parts 
in  120  of  water,  a  teaspoonful  one  to  three  times  a  day.  Its  action  is  analogous  to 
that  of  nitrite  of  amyl.  Nitro-glycerine,  in  troches  containing  ^  to  -^  grain  (grm. 
0-0005-0  '001),  also  has  the  same  dilating  action  on  the  vessels.  In  ophthalmic 
migraine  the  treatment  by  large  doses  of  bromide  of  potassium  is  praised,  espe- 
cially in  France,  as  being  very  successful. 

In  many  cases  the  general  treatment  is  very  important.  Preparations  of  iron, 
sea-bathing,  a  mountain  residence,  and  cold-water  cures  are  often  of  distinct  serv- 
ice. In  patients  with  co-existing  gastric  symptoms  a  course  at  Carlsbad  is  some- 
times of  permanent  benefit.  The  persistent  application  of  electricity  bas  also 
shown  some  good  results,  but  we  must  not  build  very  great  hopes  upon  it.  In  the 
spastic  form  the  action  of  the  anode  on  the  sympathetic  is  to  be  especially  tried, 
and  in  the  paralytic  form  the  action  of  the  cathode,  while  the  other  electrode  is  to 
be  placed  on  the  cervical  cord,  or  as  high  as  possible  on  the  occiput  in  the  region 
of  the  medulla.  Cautious  galvanization  of  the  head,  and  weak  primary  faradic 
currents,  may  also  be  used.  Specialists  in  massage  praise  their  mode  of  treatment 
in  migraine ;  they  massage  either  certain  painful  spots  in  the  head,  or  the  gastric 
region.  Finally,  we  must  mention  that  migraine  often  seems  to  be  connected 
with  diseases  of  the  nose,  especially  with  hyperplasia  of  the  erectile  tissue  in  the 
nose,  and  that  in  such  cases  treatment  of  the  primary  disease  with  the  galvano- 
cautery  may  result  in  the  cessation  of  the  migraine. 
33 


594 


DISEASES  OF  THE  NERVOUS  SYSTEM. 


CHAPTER  III. 

PROGRESSIVE    FACIAL    HEMIATROPHY. 

(  Unilateral  Progressive  Facial  Atrophy.) 

Unilateral  facial  atrophy  is  an  extremely  rare  disease,  of  which  only  about 
ninety  cases  have  been  recorded  in  literature  up  to  the  present  time.  The  disease 
consists  in  a  very  slow  and  gradual  but  usually  constantly  progressive  atrophy  of 
one  half  of  the  face,  and  affects  the  skin,  and  also  the  fatty  tissue,  the  muscles, 
and  the  bones,  either  in  a  uniform  or  a  very  diverse  manner.  The  affection 
usually  begins  in  youth.  The  female  sex  seems  to  be  more  disposed  to  the  disease 
than  the  male. 

The  atrophy,  which  has  its  seat  much  more  frequently  on  the  left  side  than  on 
the  right,  begins  usually  in  a  circumscribed  spot  either  on  the  cheeks  or  on  the 

chin.  The  skin,  as  a  rule,  gradually 
assumes  a  whitish  or  brownish  color. 
The  affected  part,  and  finally  the 
whole  half  of  the  face,  gradually  sink 
in  more  and  more,  so  that  the  disease 
can  be  recognized  at  the  first  glance. 
The  atrophy  shows  a  sharp  limitation 
at  the  median  line.  In  many  cases 
the  muscles  apparently  remain  al- 
most wholly  intact,  but  in  some  cases 
they  show  a  marked  atrophy,  espe- 
cially the  muscles  of  mastication. 
<y|l||§§§l|\     "^     W dntiniH  The  corresponding  half  of  the  tongue 

and  the  soft  palate  has  sometimes 
been  found  implicated.  Exceptional- 
ly, the  atrophy  involves  the  neighbor- 
ing region  of  the  shoulder  and  the 
upper  extremity.  The  bones  also  at- 
rophy, especially  in  the  cases  which 
arise  in  early  youth.  The  hair  on 
the  affected  half  of  the  head  often 
falls  out  in  great  amount,  and  it  be- 
comes thin  and  atrophic.  The  sen- 
sibility remains  perfectly  intact. 
Marked  vaso-motor  and  secretory  disturbances  have  only  rarely  been  observed. 
The  accompanying  illustration  (Fig.  80)  shows  a  patient  who  was  described  by 
Romberg  about  thirty  years  ago,  and  who  at  present  still  frequents  the  German 
cliniques  in  order  to  show  himself. 

Nothing  definite  is  kuown  in  regard  to  the  nature  of  the  affection.  Most 
observers  at  present  agree  that  it  is  a  trophic  neurosis,  an  affection  of  trophic 
nerves  or  nerve-centers,  but  where  we  are  to  look  for  the  special  seat  of  the  dis- 
ease, whether  in  the  trigeminus  or  in  the  sympathetic,  we  do  not  know.  Mendel 
lately  found  in  a  case  which  came  to  autopsy  a  distinct  neuritis  in  the  trigeminus. 
The  disease  is  not  dangerous  in  itself,  and  usually  causes  no  special  subjective 
disturbance,  but  it  seems  to  be  incurable.  In  cases  at  their  beginning  we  can  at 
most  make  an  attempt  to  bring  the  disease  to  a  standstill  by  a  long-continued 
application  of  electricity. 

As  an  appendix  it  may  be  briefly  mentioned  here  that  there  is  a  unilateral  hy- 
pertrophy, which  is  also  possibly  connected  with  neurotrophic  disturbances. 


Fig.  80.— Left  facial  hemiatrophy. 


We 


EXOPHTHALMIC  GOITRE.  595 

have  at  present  under  observation  a  ten-year-old  boy,  otherwise  perfectly  healthy, 
in  whom  a  striking  hypertrophy  of  the  left  side  of  his  face  and  of  the  left  arm  has 
gradually  developed. 


CHAPTER  IV. 

EXOPHTHALMIC   GOITRE. 

(Graves's  Disease.     Morbus  Gravesii.    Basedow's  Disease.    Morbus  Basedowii.     Glotzau/jenkrankheit.) 

iEtiology. — The  special  group  of  symptoms  to  which  the  name  of  exoph- 
thalmic goitre  has  been  given,  and  whose  three  cardinal  symptoms  are  accelera- 
tion of  the  pulse,  goitre,  and  exophthalmus,  was  first  carefully  described  in  Ger- 
many, in  the  year  1840,  by  the  Merseburg  physician  Basedow,  although  similar  but 
less  precise  observations  had  been  published  in  England  by  Graves  five  years  ear- 
lier. The  anatomical  cause  of  this  disease  is  still  entirely  unknown  to  us,  but  the 
whole  type,  and  almost  all  the  single  symptoms  of  the  affection,  point  definitely 
to  an  affection  of  the  nervous  system,  which,  with  regard  to  the  most  prominent 
symptoms,  is  usually  considered  a  "  vaso-motor  neurosis  "  or  an  "  affection  of  the 
sympathetic  " ;  although,  as  may  be  seen  from  what  follows,  this  hypothesis  still 
lacks  any  basis  in  fact. 

With  reference  to  the  special  aetiology  of  the  disease  all  those  factors  are 
prominent  which  generally  play  the  first  part  in  the  aetiology  of  neuroses.  In 
many  cases  a  hereditary  predisposition  can  certainly  be  discovered.  The  disease 
has  been  repeatedly  seen  in  several  members  of  the  same  family.  Further- 
more, exophthalmic  goitre  is  also  quite  frequent  in  those  families  in  which  there 
is  a  hereditary  predisposition  to  neuroses  in  genei'al — epilepsy,  the  psychoses,  or 
hysteria.  Among  the  exciting  causes  we  must  first  mention  great  mental  excite- 
ment— grief,  terror,  anger.  Sometimes  real  injuries,  as  well  as  these  "  psychical 
injuries,"  seem  to  have  an  influence  on  the  development  of  the  disease — that  is, 
great  general  bodily  concussion,  such  as  a  fall.  Many  authors  have  laid  consider- 
able weight  on  diseases  of  the  female  sexual  organs,  but  the  importance  of  this  fac- 
tor seems  to  us  to  be  exaggerated.  It  is  certain,  however,  that  the  first  symptoms 
of  exophthalmic  goitre  often  develop  at  the  period  of  pregnancy. 

The  influence  of  sex  upon  the  origin  of  the  disease  is  plain,  since  women,  espe- 
cially somewhat  anaemic,  "  nervous  "  women,  are  much  more  frequently  affected 
than  men.  Exophthalmic  goitre  usually  appears  in  middle  life,  while  it  is  seen 
only  exceptionally  in  children  and  old  people. 

Symptomatology. — Of  the  three  cardinal  symptoms  of  exophthalmic  goitre 
named  above,  of  which,  of  course,  one  or  another  is  often  absent  or  only  slightly 
developed,  the  acceleration  of  the  pulse  is  the  most  constant  and  usually  the  ear- 
liest. The  frequency  of  the  pulse  averages  100  to  120,  sometimes  only  80  or  90, 
but  in  other  cases  even  140  or  160.  It  is  not  alike  at  all  times,  but  has  many  vari- 
ations— the  symptoms  lasting  for  long  periods  and  coming  on  in  single  parox- 
ysms. A  very  vigorous  action  of  the  heart,  and  as  a  rule  the  subjective  feeling 
of  palpitation,  are  usually  associated  with  th£  acceleration  of  the  pulse.  There  is 
a  vigorous  pulsation  of  the  carotids,  and  sometimes  of  the  smaller  arteries.  We 
do  not  discover  any  qualitative  changes  of  the  pulse.  The  pulse  is  usually  quite 
regular,  but  arhythmia  has  been  repeatedly  observed.  In  some  cases  the  patients 
suffer  from  pronounced  angina  pectoris. 

Physical  examination  of  the  heart  in  many  cases  shows  nothing  particiliar, 
except  an  accelerated  and  violent  action  of  the  heart,  but  we  sometimes  find,  as 
we  can  affirm  from  several  cases  in  our  own  experience,  a  manifest  hypertrophy 


596  DISEASES  OF  THE  NERVOUS  SYSTEM. 

of  the  left  ventricle,  and  also  dilatation  of  the  heart,  and  even  actual  valvular 
disease.  In  the  diagnosis  of  the  latter  some  caution  is  necessary,  because  func- 
tional heart  murmurs  are  often  present  in  exophthalmic  goitre. 

The  goitre  usually  develops  somewhat  later  than  the  first  symptoms  in  the 
heart.  In  many  cases  it  is  entirely  absent,  or  present  only  in  a  slight  degree. 
The  swelling  of  the  thyroid  gland  is  generally  only  exceptionally  very  marked. 
There  are  sometimes  marked  variations  in  it  in  the  course  of  the  same  case.  The 
comparative  softness  of  the  tumor,  the  frequent  and  strong  pulsations  in  it,  and  the 
loud  vascular  murmurs,  which  are  often  but  not  always  heard,  and  which  arise  in 
the  dilated  vessels  of  the  thyroid  gland,  are  characteristic  of  the  goitre  in  Graves's 
disease.     By  laying  the  hand  on  it  we  can  often  feel  the  thrill  and  pulsation. 

The  exophthalmus,  the  protrusion  of  the  eyeballs  from  their  orbits,  is  always 
bilateral,  although  it  is  sometimes  more  marked  on  one  side  than  on  the  other. 
In  many  cases  it  is  entirely  absent ;  in  others  it  may  attain  so  high  a  degree  that 
an  actual  "  dislocation  of  the  eyeball "  has  been  described.  In  the  marked  degrees 
of  exophthalmus  there  is  often  a  peculiar  staring  expression  to  the  countenance. 
A  peculiar  symptom,  first  described  by  Graefe,  is  also  worthy  of  mention.  On 
raising  and  lowering  the  eyes,  the  corresponding  associated  movements  of  the 
upper  eyelid,  which  are  always  present  under  normal  conditions,  are  absent.  This 
"  Graefe  symptom  "  may  sometimes  be  one  of  the  earliest  signs  of  the  disease,  and 
may  therefore  be  of  diagnostic  value ;  but  we  must  lay  stress  upon  the  fact  that,  in 
our  own  experience,  this  symptom  is  at  any  rate  only  rarely  pronounced.  Some- 
times severe  inflammatory  processes  have  been  seen  in  the  eye,  which  are  probably 
to  be  referred  to  the  impaired  protection  of  the  eye  by  the  upper  lid  as  a  result  of 
the  exophthalmus.  Disturbances  of  the  pupils  and  of  accommodation  are  unknown 
in  exophthalmic  goitre,  but  we  have  ourselves  repeatedly  observed  anomalies  in 
the  movements  of  the  eyeball,  especially  temporary  strabismus.  We  might  men- 
tion one  symptom,  which  Möbius  has  first  noticed,  and  which  we  also  have  repeat- 
edly but  not  constantly  seen,  especially  in  patients  with  more  marked  exophthalmus. 
It  consists  in  the  fact  that  one  eye  very  soon  deviates  outward  if  we  have  the 
patient  converge  the  eyes  strongly,  as  in  fixation  of  a  near  object — "  insufficiency 
of  convergence." 

Besides  the  chief  symptoms  of  exophthalmic  goitre  thus  far  described,  we  must 
also  mention  a  list  of  other  symptoms  which  come  to  our  observation,  both  in 
the  typical  cases  and  still  more  often  in  anomalous  cases — the  so-called  " formes 
frustes"  of  the  French.  Among  them  are  some  other  nervous  symptoms,  espe- 
cially a  peculiar  tremor  to  which  Marie  in  particular  has  lately  called  attention. 
This  tremor  affects  the  whole  body,  or  the  extremities  alone ;  it  shows  at  times 
temporary  remissions  and  exacerbations,  and  it  may  be  so  severe  as  to  form  the 
patient's  chief  complaint.  In  a  case  under  our  observation  marked  tremor  was 
one  of  the  first  symptoms  of  the  disease.  It  may  become  so  violent  at  times  that 
there  are  even  spasmodic  twitchings  in  the  extremities  and  in  the  muscles  of  the 
face.  We  have  repeatedly  seen  lesser  degrees  of  tremor,  especially  in  the  handsi 
and  we  regard  it,  indeed,  as  quite  characteristic.  We  may  also  mention  among 
the  nervous  symptoms  which  are  sometimes  present,  headache,  vertigo,  weakness 
of  memory,  and  sleeplessness.  The  peculiar  nervous  anxiety  and  the  irritable  dis- 
position of  the  patient  are,  however,  very  frequent,  and  in  fact  very  characteristic, 
in  many  cases  of  the  disease.  The  anxiety  and  the  haste  in  all  movements,  in 
speaking,  etc.,  often  show  themselves,  even  during  the  physician's  examination,  in 
so  striking  a  way  that  they  must  be  regarded  as  not  unimportant  factors  in  diag- 
nosis. Exophthalmic  goitre  is  sometimes  complicated  with  other  neuroses — with 
actual  hysteria,  epilepsy,  chorea,  the  psychoses,  etc.  The  marked  subjective  feel- 
ing of  heat,  from  which  many  patients  suffer,  is  probably  due  to  vaso-motor  dis- 


EXOPHTHALMIC  GOITRE.  507 

turbances.  Objective  elevations  of  temperature  up  to  100°  or  101  '5°  (38°-38'8°  C.) 
have  also  been  repeatedly  confirmed  by  others  (Eulenburg)  and  by  ourselves.  A 
marked  increase  of  the  sweat  production,  which  in  rare  cases  is  only  unilateral, 
is  often  associated  with  the  feeling  of  heat.  On  the  other  hand,  one  of  our  patients 
complained  of  a  constant  dryness  in  the  mouth. 

Of  symptoms  which  are  referred  to  other  organs  we  must  first  consider  some 
disturbances  on  the  part  of  the  respiration.  The  respiration  is  usually  moderately 
accelerated,  and  many  patients  complain  of  dyspnoea  and  of  a  feeling  of  oppres- 
sion in  the  chest.  In  one  case  we  saw  at  times  deep  spasmodic  inspirations;  in 
other  cases  a  peculiar  dry,  "  nervous  cough  "  appears.  There  are  also  symptoms 
on  the  part  of  the  digestive  organs.  Vomiting  is  common,  and  in  severe  cases  it 
may  become  so  persistent,  distressing,  and  uncontrollable  as  to  constitute  one  of 
the  chief  dangers  of  the  disease.  It  is  sometimes  associated  with  peculiar  parox- 
ysmal sero-mucous  or  even  bloody  diarrhoea.  Icterus  may  also  develop.  Finally 
we  must  mention  certain  disturbances  in  the  skin :  vitiligo  has  often  been  ob- 
served, and  also  diffuse  brownish  pigmentation  of  the  skin  or  chloasma-like  pig- 
ment-spots and  urticaria.  A  very  rare  but  dangerous  occurrence,  of  which  we  our- 
selves have  seen  a  striking  example,  is  an  apparently  spontaneous  gangrene  of  the 
extremities.  In  our  case,  which  ended  fatally,  the  gangrene  affected  the  right  leg. 
Not  the  slightest  anomaly  could  be  made  out  in  the  vessels  at  the  autopsy.  This 
gangrene  in  exophthalmic  goitre  recalls  decidedly  the  so-called  "  spontaneous  sym- 
metrical gangrene  "  {vide  supra),  for  which  we  also  must  assume  a  neurotic  origin. 

The  general  nutrition  of  the  patient  siiffers  in  most  cases ;  a  certain  degree  of 
ansemia  and  emaciation  is  often  pi'esent.  In  severe  cases,  especially  in  those  of 
rapid  development,  there  is  often  in  a  very  short  time  a  high  degree  of  emaciation 
associated  with  much  general  weakness.  Muscular  atrophy  frequently  develops, 
chiefly  in  certain  regions — the  arm  or  leg  muscles.  [The  electrical  resistance  of 
the  body  is  said  to  be  diminished. — K.] 

Pathological  Anatomy  and  Pathogenesis. — Although  all  the  symptoms  of 
exophthalmic  goitre  point  to  an  affection  of  the  nervous  system  as  a  cause  of  the 
disease,  as  we  see  fi'om  the  symptomatology,  the  results  of  pathological  investiga- 
tions are  still  very  meager.  There  is  a  class  of  cases  in  which  changes  in  the  sym- 
pathetic, and  especially  in  the  lowest  cervical  ganglion,  are  said  to  have  been  pres- 
ent ;  but  the  pathological  significance  of  the  discovery  is  not  placed  beyond  all 
doubt;  and  in  other  cases  nothing  abnormal  at  all  could  be  found  in  the  sympa- 
thetic. The  theory  that  all  the  symptoms  of  exophthalmic  goitre  are  derived 
from  a  disturbance  of  the  sympathetic  also  meets  many  difficulties  and  contradic- 
tions. If  we  regard  only  the  three  cardinal  symptoms,  we  can  bring  the  accelera- 
tion of  the  pulse,  and  perhaps  the  exophthalmus,  into  harmony  with  the  theory  of 
irritation  of  the  sympathetic;  but  not  the  goitre,  which  is  due  to  a  dilatation  of  the 
vessels.  The  theory  of  a  paralysis  of  the  sympathetic  explains  the  goitre,  and  also 
the  exophthalmus — if  we  assume  as  the  cause  of  the  latter  a  dilatation  of  the  ves- 
sels in  the  back  of  the  orbit— but  again  the  acceleration  of  the  pulse  remains  unex- 
plained. The  experiments  by  Filehne,  interesting  in  themselves,  in  which  symp- 
toms similar  to  those  of  exophthalmic  goitre  were  produced  by  dividing  the  resti- 
form  bodies  in  young  rabbits,  have  had  up  to  the  present  time  no  bearing  upon 
human  pathology.  We  must  therefore  admit  that  the  cause  of  exophthalmic 
goitre  is  still  completely  unknown.  Possibly  the  recent  experiments  on  the  sig- 
nificance of  the  thyroid  gland  (vide  supra)  may  throw  some  light  on  the  origin  of 
this  remarkable  affection. 

Course  and  Diagnosis. — The  course  of  the  disease  is  in  most  cases  very  chronic, 
and  may  extend  over  years  and  years,  but  there  are  also  more  acute  cases  with  a 
rapid  development  of  all  the  symptoms  and  a  comparatively  unfavorable  course. 


59S  DISEASES  OF  THE  NERVOUS  SYSTEM. 

We  may  often  see  considerable  variation  in  the  intensity  of  the  symptoms.  All 
the  symptoms  of  the  disease  may  often  almost  wholly  disappear,  to  recur  after 
the  lapse  of  years.  In  general,  the  cases  beginning  in  youth  give  a  more  unfavor- 
able prognosis  than  those  arising  in  later  years.  Complete  recoveries  have  cer- 
tainly been  observed,  but  they  are  at  all  events  rare.  The  disease  sometimes 
terminates  fatally  with  the  signs  of  general  marasmus,  but  more  frequently  from 
complications  in  the  heart  or  lungs.  We  would  note  especially,  however,  that 
mild  and  to  some '  extent  rudimentary  cases  of  the  disease  are  not  rare,  and  that 
these  in  no  way  endanger  life;  and  even  in  severe  cases  we  sometimes  see  marked 
improvement,  or  at  least  an  arrest  of  the  disease.  The  diagnosis  of  undeveloped 
cases  is  difficult  at  times,  since  the  three  cardinal  symptoms  are  not  always  by  any 
means  fully  developed.  We  must  then  pay  careful  and  especial  attention  to  the 
other  symptoms  of  the  disease,  chiefly  to  the  general  nervous  irritability,  the  trem- 
or, the  subjective  feeling  of  heat,  and  the  tendency  to  sweating.  In  well- developed 
cases,  however,  the  diagnosis  is  almost  always  to  be  made  with  certainty  and  with- 
out difficulty.  The  peculiar  expression  of  the  face,  altered  by  the  emaciation  and 
the  exophthalmus,  often  permits  us  to  recognize  the  disease  at  the  first  glance. 

Treatment. — In  the  first  place  we  must  consider  the  general  treatment  of  the 
patient.  Physical  and  mental  rest,  good  food,  and  the  avoidance  of  all  stimulants 
— such  as  alcohol  or  strong  coffee — and  the  cautious  use  of  cold-water  cures,  espe- 
cially sponging,  may  cause  an  actual  improvement  of  the  condition.  For  anaemic 
patients  we  prescribe  iron,  alone  or  in  combination  with  small  doses  of  arsenic. 
A  course  at  the  springs  springs  at  Franzensbad,  Schwalbach,  Pyrmont,  Elster,  and 
Cudowa,  is  also  sometimes  attended  with  good  results.  Residence  in  mountainous 
regions  or  by  the  sea  often  seems  to  act  still  more  favorably. 

Of  other  remedies,  electricity  is  first  to  be  mentioned,  especially  the  application 
of  galvanism  to  the  neck — the  so-called  galvanization  of  the  sympathetic  at  the 
inner  border  of  the  sterno-mastoid.  The  slowing  of  the  pulse,  which  sometimes 
comes  on  at  once  (vagus  irritation?),  is  striking.  Vigouroux  praises  faradization 
of  the  sympathetic  and  of  the  goitre  as  the  best  method  of  treatment.  Among 
internal  remedies  we  may  recommend  atropine  or  tincture  of  belladonna,  and 
ergot  or  ergotine.  We  believe  we  have  repeatedly  seen  good  results  from  the 
latter.  Digitalis  has  often  been  prescribed  for  the  palpitation,  but  usually  without 
any  good  result.  The  use  of  iodine  preparations  against  the  goitre  is  also  almost 
always  unavailing.  With  great  exophthalmus  the  eyes  must  be  protected  from 
external  injuries.  The  occasional  severe  symptoms  on  the  part  of  the  digestive 
organs  (vomiting,  diarrhoea)  must  be  treated  symptomatically,  by  ice,  opium, 
and  champagne. 

In  some  cases  the  extirpation  of  the  goitre  has  been  practiced,  and  favorable 
results  have  been  claimed  for  it.  Should  the  above-mentioned  relation  of  the 
morbid  symptoms  to  the  functions  of  the  thyroid  gland  be  confirmed,  further 
advance  in  this  direction  would  perhaps  be  worthy  of  trial. 


DISEASES  OF  THE  SPINAL  MENINGES.  599 


III.— The  Diseases  of  the  Spinal  Cord. 


CHAPTER  I. 
DISEASES   OF   THE    SPINAL   MENINGES. 

1.  Acute  Inflammations  of  the  Spinal  Meninges. 

./Etiology  and  Pathology. — Isolated  acute  inflammation  of  the  spinal  meninges 
is  very  rarely  primary,  so  far  as  we  know,  but  inflammatory  processes  in  the 
neighborhood  quite  frequently  involve  the  meninges,  or  a  spinal  meningitis, 
occurs  as  one  symptom  of  a  general  cerebro-spinal  meningitis.  This  latter  con- 
dition is  seen  chiefly  in  the  idiopathic,  generally  epidemic,  cerebro-spinal  menin- 
gitis, which  is  a  specific  infectious  disease,  and  has  already  been  described  in 
detail  in  a  previous  chapter.  A  tubercular  spinal  meningitis  is  also  very  often 
combined  with  tubercular  inflammation  of  the  cerebral  meninges,  but,  since  the 
symptoms  of  the  latter  are  usually  in  the  foreground  of  the  picture,  we  will  treat 
of  tubercular  cerebro-spinal  meningitis  in  the  section  on  diseases  of  the  cerebral 
meninges.  Secondary  cerebro-spinal  meningitis  is  sometimes  seen  in  the  course 
of  certain  other  infectious  diseases,  and  is  then  probably  to  be  regarded  as  a 
special  localization  of  the  specific  poison  of  the  disease.  This  is  the  explanation 
of  the  occurrence  of  acute  spinal  and  cerebral  meningitis  as  a  sequel  of  croupous 
pneumonia,  and  also  of  its  occurrence  in  pyaemic  and  septic  diseases,  and,  very 
rarely,  in  typhoid  and  the  acute  exanthemata.  We  must  mention,  finally,  the 
occurrence  of  a  purulent  cerebro-spinal  meningitis  as  a  sequel  of  empyema,  pul- 
monary gangrene,  etc.,  which,  although  very  rare,  we  have  repeatedly  noticed.  In 
these  cases  the  infection  of  the  meninges  also  results  from  the  primary  foci  of 
disease,  but  the  channel  of  infection  is  not  yet  exactly  known.  Perhaps  the 
intercostal  nerves  are  the  media  of  communication. 

In  all  the  cases  so  far  mentioned  we  have  chiefly  an  inflammation  of  the  pia 
mater,  a  so-called  lepto-meningitis ;  the  dura  mater  is  not  implicated  in  the  dis- 
ease at  all,  or  only  to  a  slight  degree.  The  condition  is  different  in  those  inflam- 
matory processes  which  gradually  invade  the  meninges  from  the  neighboring 
parts  outside  the  cord.  Thus  we  very  often  see  circumscribed  inflammations  on 
the  outer  surface  of  the  dura  (pachymeningitis)  in  caries  of  the  vertebra?,  and 
these  inflammations  often  invade  the  inner  surface  of  the  dura,  or  more  rarely 
reach  the  pia  mater.  Acute  purulent  peripachymeningitis  is  a  very  rare  disease ; 
it  is  a  purulent  inflammation  of  the  connective  tissue  between  the  dura  mater 
and  the  vertebral  column,  which  in  almost  all  cases  is  of  secondary  origin.  We 
have  seen  a  very  characteristic  case  of  this  sort  in  the  course  of  a  puerperal 
pyaemia.  The  inflammation  had  spread  from  a  purulent  inflammation  of  the  pel- 
vic cellular  tissue,  through  the  foramina  of  the  vertebral  canal,  and  had  finally 
set  up  a  purulent  inflammation  on  the  outer  surface  of  the  dura,  extending  up  to 
the  cervical  cord.  We  meet  with  an  affection  of  the  pia  mater  from  an  extension 
of  the  inflammation,  chiefly  in  diseases  of  the  spinal  cord,  since  the  pia  takes  part 
in  the  process  to  a  greater  or  less  extent  in  many  cases  of  myelitis. 

We  do  not  know  with  certainty  whether  other  influences,  especially  injuries 
and  exposure  to  cold,  can  lead  directly,  as  has  oftenbeen  claimed,  to  inflammation 
of  the  spinal  meninges. 


GOO  DISEASES  OF  THE  NERVOUS  SYSTEM. 

We  need  to  say  but  little  in  regard  to  the  pathological  anatomy  of  acute  spinal 
meningitis.  The  changes  in  purulent  inflammation  of  the  pia  mater  have  been 
described  in  the  chapter  on  epidemic  meningitis.  Precisely  the  same  conditions 
are  found  in  the  other  forms  of  acute  leptomeningitis.  The  changes  in  pachy- 
meningitis are  completely  analogous.  The  dura  mater  is  traversed  by  dilated 
vessels,  and  therefore  is  reddened;  it  is  also  thickened,  and  on  its  internal  or  ex- 
ternal surface  {pachymeningitis  interna  or  externa,  or  peripachymeningitis) 
there  is  usually  found  a  purulent  or  a  sero-purulent  exudation. 

Symptoms. — An  accurate  distinction  between  acute  inflammations  of  the  pia 
mater  and  those  of  the  dura  mater  can  not  be  made  clinically.  The  symptoms 
of  the  disease  include  the  symptoms  of  any  primary  disease  present,  the  general 
symptoms,  such  as  fevei*,  etc.,  and  in  addition  the  necessary  consequences  which 
the  presence  of  a  disturbance  of  the  meningeal  circulation  and  of  the  meniugeal 
exudation  exerts  on  the  cord  and  nerve-roots.  These  consequences  are  due  both 
to  a  mechanical  compression  of  the  parts  named,  and  often  probably  to  an  inva- 
sion of  the  substance  of  the  cord  itself  by  the  inflammation.  To  these  is  added 
the  frequent  combination  of  spinal  symptoms  with  the  symptoms  of  a  co-existing 
cerebral  meningitis. 

Those  symptoms  which  occur  in  acute  spinal  meningitis,  and  are  especially 
referred  to  it,  are  all  of  them  already  known  to  us  from  the  description  of  epi- 
demic meningitis  (see  page  103).  Recapitulating  them  briefly,  we  may  mention 
chiefly  the  very  severe  pain  in  the  back,  the  great  sensitiveness  of  the  vertebral 
column,  and  its  stiffness.  To  these  may  be  added  usually  symptoms  of  irritation 
on  the  part  of  the  nerve-roots :  eccenü'ic  pains  in  the  trunk  and  the  extremities, 
hyperesthesia  of  the  skin  and  of  the  deeper  parts,  symptoms  of  direct  or  reflex 
motor  irritation,  muscular  tension,  contractions,  etc.  The  cutaneous  and  tendon 
reflexes  are  often,  but  not  always,  much  diminished  or  abolished  in  consequence 
of  the  lesion  of  the  nerve-roots.  There  are  at  times  disturbances  in  the  passage  of 
urine  and  faeces.  If,  in  the  later  course  of  the  disease,  there  are  actual  paralysis  and 
anaesthesia,  they  are  usually  a  sign  of  a  more  marked  implication  of  the  cord  itself. 

Diagnosis. — From  the  symptoms  named,  we  can  in  many  cases  make  a  diag- 
nosis of  spinal  meningitis.  Of  course  a  meningitis  is  found  often  enough  on  the 
autopsy -table  whose  symptoms  during  life  were  completely  obscured  by  other 
severe  general  symptoms,  while,  on  the  other  hand,  with  severe  constitutional 
symptoms  the  symptoms  of  meningitis  may  be  illusory,  as  in  typhoid  or  pyaemia. 
Fuller  information  as  to  the  seat  and  the  extent  of  the  inflammation  is  afforded 
by  considering  the  most  painful  parts  of  the  vertebral  column,  the  predominance 
of  pain  and  cutaneous  hyperaesthesia  in  the  arms  (cervical  region)  or  legs  (lumbar 
region),  etc.  When  the  meningitis  involves  the  upper  portion  of  the  cord  and  the 
medulla  there  may  also  be  disturbances  of  respiration,  symptoms  in  the  pupils, 
and  anomalies  in  the  innervation  of  the  heart.  We  can  decide  as  to  the  form  of 
the  meningitis,  whether  purulent  or  tubercular,  only  by  a  consideration  of  the 
history,  the  other  morbid  symptoms,  and  the  course  of  the  disease. 

Prognosis. — We  have  seen  an  undoubted  recovery,  in  severe  cases,  only  in  epi- 
demic cerebro-spinal  meningitis,  and  in  the  spoi'adic  cases  of  idiopathic  meningitis, 
which  are  probably  identical  in  aetiology.  In  all  other  cases  reported  with  a  favor- 
able termination  the  diagnosis  may  be  doubted,  for  in  general  the  rule  is  certain 
that,  in  extensive,  acute  purulent  leptomeningitis  and  pachymeningitis,  the  prog- 
nosis is  almost  absolutely  unfavorable,  whether  it  be  secondary  to  another  infec- 
tious disease  or  arise  from  propagation  from  some  neighboring  focus  of  inflamma- 
tion. We  may,  perhaps,  make  an  exception  of  certain  mild,  circumscribed  cases, 
which  do  not  come  to  suppuration,  but  these  are  always  uncertain  in  regard  to 
diagnosis. 


DISEASES  OF   THE  SPINAL  MENINGES.  601 

Treatment— In  regard  to  treatment  we  must  refer  entirely  to  what  has  been 
said  under  epidemic  and  tubercular  meningitis. 

2.  Chronic  Spinal  Leptomeningitis. 

Although  chronic  leptomeningitis  (usually  wrongly  termed  chronic  spinal 
meningitis)  once  played  quite  a  large  part  in  the  diagnosis  and  pathology  of  dis- 
eases of  the  spinal  cord,  we  must  at  present  assert  that  its  occurrence  as  an  inde- 
pendent disease  may  justly  be  doubted.  Almost  all  the  cases  reported  come  from 
a  time  when  the  diagnosis  of  many  diseases  of  the  cord  itself  was  still  perfectly 
impossible,  and  when  the  thickenings  and  opacities  of  the  meninges  were  much 
more  striking  at  the  autopsy  than  the  far  more  essential  changes  in  the  sub- 
stance of  the  cord  itself,  which  could  not  be  made  out  with  the  naked  eye,  but 
only  by  a  careful  microscopic  examination.  At  any  rate,  we  may  say  that  a  case 
of  primary  chronic  leptomeningitis,  which  can  be  surely  and  convincingly  proven 
clinically  and  anatomically,  does  not  exist,  and  that  our  present  clinical  experi- 
ence also  by  no  means  favors  the  assumption  of  the  existence  of  mild  and  curable 
forms  of  it.  Among  many  cases  of  spinal  disease  we  shall  scarcely  be  induced 
even  to  assume  the  probability  of  the  existence  of  primary  chronic  meningitis.  It 
goes  without  saying  that  we  can  not  dispute  the  possibility  of  its  occurrence, 
although  even  for  this  we  can  scarcely  find  an  analogy. 

The  case  is  different  with  secondary  chronic  leptomeningitis.  This,  in  the  first 
place,  in  rare  cases,  is  the  termination  of  an  acute  meningitis.  Secondary  lepto- 
meningitis may  be  certainly  made  out,  especially  in  epidemic  meningitis.  We 
also  find  chronic  meningitis  frequently  as  a  secondary  affection  in  primary  dis- 
eases of  the  cord  and  the  vertebrae.  Thus,  for  example,  in  old  cases  of  chronic 
spinal  disease,  associated  with  atrophy,  such  as  tabes  dorsalis,  progressive  muscu- 
lar atrophy,  etc.,  the  pia  is  almost  always  quite  opaque,  thickened,  and  often 
united  to  the  cord  and  the  dura  by  very  many  firm  adhesions,  while  a  cloudy 
sero-gelatinous  exudation  is  found  in  the  meshes  of  the  arachnoid.  All  these 
anomalies,  however,  are  of  a  secondary  nature,  and  have  no  clinical  significance, 
for  the  same  changes,  though  rarely  so  marked,  are  quite  often  found  in  old 
people,  where  they  are  analogous  to  the  equally  frequent  opacities  of  the  cerebral 
meninges,  the  pleuritic  adhesions,  etc.,  and  where,  during  life,  they  have  not 
caused  the  slightest  symptom  of  spinal  disease. 

The  s3rmptoms  which  have  been  set  down  as  characteristic  of  leptomeningitis 
correspond  precisely  to  those  of  acute  meningitis,  except,  of  course,  that  they  are 
relatively  less  intense,  and  that  the  course  of  the  disease  is  more  protracted.  Pain 
and  stiffness  in  the  back  and  neck,  abnormal  painful  sensations  and  parsesthesia 
in  the  extremities,  a  girdle  sensation,  and  finally  paresis,  anaesthesia,  and  vesical 
disturbances,  are  the  leading  features  of  the  type  of  disease  as  constructed,  in 
whose  fabrication  there  have  been,  at  any  rate,  many  confusions  with  myelitis, 
spondylitis,  beginning  tabes,  multiple  neuritis,  etc. 

It  is  clear  that  under  such  circumstances  no  special  rules  for  the  treatment  of 
chronic  spinal  meningitis  can  be  given.  Given  a  case,  we  would  try  local  applica- 
tions to  the  vertebral  column;  painting  with  iodine;  dry,  or,  exceptionally,  in 
strong  patients,  wet  cups;  also  protracted  tepid  baths,  90°  to  95°  (26°-28°  R),  or 
cautious  cold-water  treatment;  and  finally  the  use  of  the  galvanic  current.  Of 
internal  remedies,  iodide  of  potassium  would  be  most  indicated.  We  may  refer 
to  the  description  of  the  treatment  of  myelitis  in  regard  to  all  further  details. 


602  DISEASES  OF  THE  NERVOUS  SYSTEM. 

3.  Pachymeningitis  Cervicalis  Hypertrophica. 

Pachymeningitis  cervicalis  hypertrophica  was  first  fully  described,  as  a  spe- 
cial form  of  disease,  by  Charcot  in  1871,  and  later  by  bis  pupil  Joffroy.  Little  is 
known  as  to  its  origin ;  it  has  been  attributed  to  exposure  to  cold  and  the  abuse  of 
alcohol. 

Anatomically,  the  disease  is  characterized  by  a  chronic  and  often  very  con- 
siderable thickening  of  the  dura,  almost  always,  as  it  seems,  in  the  cervical  portion 
of  the  cord,  while  the  pia  takes  but  a  comparatively  small  part  in  the  affection. 
The  dura  may  attain  a  thickness  of  six  or  seven  millimetres,  and  usually  appears 
composed  of  a  number  of  concentric  layers.  Histologically,  the  hypertrophy  con- 
sists of  a  new  growth  of  dense  connective  tissue.  The  clinical  symptoms  of  the 
disease  arise  from  the  fact  that,  first,  the  penetrating  nerve-roots,  and  later  on  the 
cord  itself,  undergo  a  considerable  mechanical  compression.  If  this  is  of  high 
degree  and  persistent,  there  are,  as  a  necessary  result,  secondary  degenerations  of 
the  motor  nerves  and  muscles,  and  a  secondary  descending  degeneration  of  the 
pyramidal  tract  in  the  cord. 

The  clinical  symptoms  are  easily  understood  from  this.  The  disease  almost 
always  begins  with  severe  pain,  which  shoots  from  the  neck  into  the  occiput  and 
the  arms.  Besides  this,  there  are  paraesthesia  and  a  numb  feeling  in  the  arms  and 
hands.  Rarely  there  is  an  eruption  of  herpes.  All  these  symptoms  depend  upon 
tbe  irritation  of  the  posterior  roots. 

After  this  first  period  of  the  disease  (periode  doidourease  of  Charcot)  has 
lasted  some  two  or  three  months,  the  second  period  begins — the  period  of  paralysis. 
An  atrophic  paralysis  in  the  upper  extremities  gradually  develops,  mainly  as  a 
result  of  the  compression  of  the  anterior  motor  roots.  This  affects,  in  a  remark- 
able manner,  chiefly  the  distribution  of  the  ulnar  and  median  nerves,  while  the 
distribution  of  the  radial  on  both  sides  usually  remains  free.     The  hand,  therefore, 

assumes  a  characteristic  position 
(Fig.  81),  as  a  result  of  the  contract- 
ure of  the  antagonistic  extensors. 
The  paralyzed  muscles  rapidly  be- 
come atrophic  and  show  a  marked 
reaction  of  degeneration.  In  this 
stage  there  may  also  be  partial  anaes- 
thesia of  the  skin. 

If  the  compression  of  the  cord  ad- 
vances, the  motor  fibers  for  the  lower 
extremities,  which  pass  through  the 

Fig.  81.— Position  of  the  hand  in  pachymeningitis  „OT„7^ol     or.vc\     miKt     Tippp^arilv  it 

cervicalis  hypertrophica.    (From  Charcot.)  Cervical     cord,    must     necessailiy  at 

last  be  involved  sympathetically — 
the  third  period  of  the  disease.  The  result  of  this  is  a  spastic  paralysis  of  the 
lower  extremities— that  is,  a  paresis  or  paralysis  with  increased  tendon  reflexes, 
but  of  course  without  muscular  atrophy,  because  the  trophic  centers  for  the  mus- 
cles of  the  legs,  in  the  anterior  cornua  of  the  lumbar  cord,  remain  perfectly  in- 
tact. The  compression  of  the  cervical  cord,  however,  may  finally  lead  also  to  an- 
aesthesia of  the  lower  extremities,  to  paralysis  of  the  bladder,  and  bedsores, 
under  which  symptoms  death  ensues ;  but,  on  the  other  hand,  it  must  be  men- 
tioned that  probably  cases  of  recovery,  or  at  least  of  actual  improvement  in 
pachymeningitis  cervicalis  hypertrophica,  may  occur  even  after  it  has  lasted  for 
years. 

The  diagnosis  of  the  disease  is  based  first  upon  the  fact  that  the  affection  be- 
gins with  pains  in  the  arms,  and  upon  the  later  appearance  of  the  characteristic 


DISEASES  OF  THE  SPINAL  MENINGES.  603 

paralyses.  It  may  easily  be  confused  with  tumors  in  the  cervical  cord  and  with 
cervical  spondylitis.  Amyotrophic  lateral  sclerosis  is  distinguished,  however,  by 
the  absence  of  disturbances  of  sensibility,  by  the  final  appearance  of  atrophy  in  the 
lower  extremities,  by  the  bulbar  symptoms,  and  by  the  fact  that  the  functions  of 
the  bladder  remain  intact. 

Treatment  can  do  little  directly,  and  must  be  chiefly  symptomatic.  Baths, 
iodide  of  potassium,  and  electricity  are  most  used.  Joffroy  recommends  the  use 
of  the  hot  iron  to  the  neck. 

4.    HAEMORRHAGE   INTO   THE  SPINAL   MENINGES. 

(Ilaimatorrhachis.     Meningeal  Apoplexy.     Pachymeningitis  spinalis  hämorrhagica  interna.) 

Large  haemorrhages  into  and  between  the  spinal  meninges  are  of  rare  occur- 
rence. They  arise  chiefly  from  traumatic  influences,  from  concussion  or  fracture 
of  the  vertebral  column,  or  from  direct  injuries  of  the  meninges,  such  as  stabs  or 
gun-shot  wounds.  In  a  few  cases  great  physical  exertion  may  also  lead  to  a  men- 
ingeal apoplexy.  Diseases  of  the  vertebrae,  caries,  and  carcinoma,  may  also  lead  to 
a  haemorrhage  from  the  erosion  of  a  vessel.  The  frequent  little  meningeal  haemor- 
rhages which  appear  as  a  complication  of  meningitis,  in  haemorrhagic  diseases,  in 
the  course  of  severe  general  infectious  diseases,  septic  infections,  typhoid,  and 
small-pox,  and  as  a  result  of  severe  general  convulsions,  very  rarely  have  any 
clinical  significance.  Finally,  it  may  be  mentioned  that  aneurism  of  the  aorta  or 
its  branches  may  rupture  into  the  vertebral  canal. 

The  clinical  symptoms  of  meningeal  haemorrhage  are  almost  always  sudden 
and  "apoplectiform,"  but  are  unattended  by  any  disturbance  of  consciousness. 
Their  intensity  depends  entirely  upon  the  degree  of  compression  which  the  nerve- 
roots  and  the  cord  undergo  from  the  effused  blood.  The  symptoms  of  irritation 
usually  predominate — severe  pain  in  the  back,  paraesthesia,  and  neuralgic  pains  in 
the  extremities;  and  also  symptoms  in  the  motor  distribution,  tension,  tremors, 
and  contractures  of  the  muscles.  With  large  haemorrhages,  symptoms  of  paral- 
ysis, partial  anaesthesia,  disturbances  of  the  bladder,  symptoms  of  unilateral  lesion, 
etc.,  may  ensue.  Therefore  the  different  types  of  the  disease,  depending  upon  the 
seat  of  the  haemorrhage,  follow  the  same  general  rules  which  are  to  be  con- 
sidered in  judging  of  the  seat  of  any  other  affection  of  the  cord  {vide  infra).  On 
the  whole,  the  diagnosis  of  meningeal  haemorrhage  can  but  rarely  be  made  with 
any  certainty,  unless  suggestive  aetiological  factors  precede  and  the  symptoms  and 
manner  of  beginning  are  especially  characteristic. 

The  course  is  quite  favorable  in  many  cases  if  the  blood  be  rapidly  reabsorbed, 
but  sometimes  a  permanent  disturbance  of  function  is  left. 

In  regard  to  treatment,  complete  rest  and  the  energetic  local  use  of  ice  are 
chiefly  to  be  recommended,  and  also  local  bloodletting— dry  cups,  or  leeches, 
where  there  are  severe  initial  symptoms  of  irritation.  If  permanent  disturbances 
be  left,  they  should  be  treated  by  the  ordinary  methods — iodide  of  potassium, 
baths,  and  electricity.  [When  the  diagnosis  of  haemorrhage  into  the  meninges  is 
reasonably  certain,  an  attempt  should  be  made  to  relieve  the  condition  by  opening 
the  spinal  canal  and  removing  the  clot. — K.] 

We  must  here  speak  of  pachymeningitis  interna  hsemorrhagica  as  a  special 
form  of  disease,  which  usually  occurs  at  the  same  time  with  haematoma  of  the 
cerebral  dura  mater  {vide  infra),  and  is  precisely  analogous  to  it  in  its  aetiology 
and  pathological  anatomy.  Encapsulated  collections  of  blood  are  found  on  the 
inner  surface  of  the  dura ;  these  may  have  quite  a  considerable  circumference,  and 
contain  blood  already  disintegrated,  detritus,  haematoidin  crystals,  etc. ,  since  they 
are  usually  of  old  standing.     Besides  this,  there  are  also  the  signs  of  a  fibrinous 


604  DISEASES  OF  THE  NERVOUS  SYSTEM. 

inflammation— as  in  the  cerebral  dura — which,  according  to  the  opinion  of  most 
observers,  is  the  primary  process,  so  that  the  haemorrhages  into  the  newly  formed 
false  membrane  are  secondary.  The  symptoms  of  the  affection — which  has  been 
observed  chiefly  in  the  chronic  insane  (general  paralytics)  and  drunkards — are 
rarely  pronounced,  and  consist  chiefly  of  pain  in  the  back,  stiffness  of  the  vertebra?, 
and  some  signs  of  compression  on  the  part  of  the  nerve-roots  and  the  cord ;  but  we 
can  very  rarely  make  a  definite  diagnosis. 


CHAPTER  II. 


DISTURBANCES  OF  CIRCULATION,  HEMORRHAGES,  FUNCTIONAL 
DISTURBANCES,  AND  TRAUMATIC  LESIONS  OF  THE  SPINAL 
CORD. 

1.  Disturbances  of  Circulation.— Our  knowledge  as  to  the  occurrence  and  as  to 
the  clinical  significance  of  pure  disturbances  of  circulation  in  the  spinal  cord  is 
very  slight.  All  that  is  stated  in  regard  to  it  in  the  descriptions  of  the  pathology 
of  the  spinal  cord  corresponds  much  more  to  theoretical  hypotheses  than  to  the 
actual  objective  facts. 

It  goes  without  saying  that  a  complete  anaemia  of  the  spinal  cord  must  destroy 
its  function ;  this  fact  is  best  illustrated  by  the  well-known  experiment  of  Stenson: 
if  we  compress  the  abdominal  aorta  of  an  animal,  and  thus  cut  off  the  blood-sup- 
ply to  the  lumbar  cord  almost  completely,  a  paralysis  of  the  posterior  portion  of 
the  body  very  rapidly  ensues.  Some  precisely  analogous  observations  have  been 
made  in  man  in  the  rare  cases  of  obstruction  of  the  aorta  by  emboli  or  thrombi. 
Pronounced  spinal  symptoms  in  general  anaemia,  which  may  be  referred  to  a  co- 
existing anaemia  of  the  cord,  are  rare,  and  at  any  rate  are  of  much  less  clinical 
prominence  than  the  important  results  of  a  co-existing  cerebral  anaemia  (vide 
infra).  In  only  a  few  cases  has  paraplegia  been  seen  after  a  great  general  loss  of 
blood,  as  after  metrorrhagia  or  intestinal  haemorrhage. 

Any  statement  which  may  be  made  as  to  the  occurrence  of  hyperaemia  of  the 
spinal  cord  is  still  more  uncertain.  We  do  not  know  whether  active  hyperaemia 
of  the  cord  has  in  itself  any  clinical  significance.  The  hyperaemia  from  stasis,  in 
general  disturbances  of  the  circulation,  in  which  certainly  the  spinal  cord  often 
takes  part,  causes  no  especially  marked  symptoms. 

2.  Haemorrhage  into  the  Substance  of  the  Spinal  Cord— Spinal  Apoplexy— 
Heematomyelia. — Primary  haemorrhage  into  the  spinal  cord  is  as  rare  as  haemor- 
rhage into  the  brain  is  frequent.  In  some  cases  it  may  arise  from  traumatic  influ- 
ences, but  in  others  we  are  disposed  to  assume  a  primary  disease  of  the  spinal 
vessels.  Perhaps  there  are  occasionally  aneurismal  dilatations  in  the  cord,  similar 
to  those  found  in  the  smaller  vessels  in  the  brain,  and  these  may  give  rise  to 
haemorrhage.  Finally,  the  sudden  onset  of  spinal  paralysis  has  been  seen  after 
great  physical  exertion,  and  this  perhaps  is  due  to  a  spinal  apoplexy.  The  small 
spinal  haemorrhages  which  are  seen  as  a  complication  in  tumors  of  the  cord,  and 
in  inflammatory  affections  such  as  myelitis,  epidemic  meningitis,  etc.,  and  in  the 
general  baemorrhagic  diathesis,  as  in  scurvy  or  severe  general  infectious  diseases, 
but  rarely  have  any  special  significance. 

Anatomical  experience  in  regard  to  primary  spinal  apoplexy  is  still  extremely 
slight,  but  the  conditions  met  with  do  not  differ  matei'ially,  at  any  rate,  from  simi- 
lar processes  in  other  organs.  If  the  haemorrhage  be  abundant,  we  find  the  sub- 
stance of  the  cord  destroyed  to  a  great  extent.     The  apoplectic  center  usually 


DISTURBANCES  OF  CIRCULATION,   HAEMORRHAGES,   ETC.     605 

extends  principally  in  the  long  axis  of  the  cord.  The  blood  is  still  fluid  in  fi<  li 
cases.  Later  on  it  undergoes  all  those  changes  which  are  fully  described  in  the 
chapter  on  cerebral  apoplexy. 

The  symptoms  of  spinal  apoplexy  must  in  the  first  place  depend  entirely  upon 
the  seat  and  extent  of  the  haemorrhage.  The  sudden,  apoplectiform  beginning  of 
the  symptoms  is  always  characteristic.  Usually  in  a  very  short  time  a  more  or 
less  complete  paraly sis,  with  a  severe  pain  in  the  back,  comes  on;  the  paralysis 
being  usually  in  the  lower  extremities,  or  rarely  in  the  muscles  of  the  trunk  and 
the  upper  extremities  also.  There  are  usually  at  the  same  time  anaesthesia  and 
paralysis  of  the  bladder;  but  in  this  respect,  as  also  in  regard  to  the  condition  of 
the  reflexes,  there  are  of  course  many  variations  according  to  the  seat  of  the 
haemorrhage.  Haemorrhage  into  one  half  of  the  cord  sometimes  produces  the 
symptoms  of  unilateral  lesion.  We  need  not  go  into  a  precise  description  of  the 
details,  since  they  will  follow  of  themselves  from  the  general  rules  in  regard  to 
the  localization  of  affections  of  the  cord. 

The  course  of  haemorrhage  of  the  cord  may  in  many  cases  be  comparatively 
favorable.  If  the  blood  be  absorbed,  and  essential  paths  of  conduction  be  not  per- 
manently destroyed,  the  symptoms  of  paralysis  gradually  pass  away,  and  recovery 
or  at  least  improvement  and  an  arrest  of  the  symptoms  follow.  In  many  cases, 
of  course,  the  severe  type  of  spinal  paralysis  develops,  with  bedsores,  cystitis,  etc., 
and  this,  after  a  longer  or  shorter  time,  leads  to  death. 

We  must  always  be  very  guarded  in  making  a  diagnosis  of  spinal  haemorrhage. 
We  can  do  so  with  some  probability  only  when  the  symptoms  begin  in  a  pro- 
nounced apoplectiform  manner,  and  when  definite  aetiological  factors  are  to  be 
made  out;  but  we  should  never  forget  that  many  forms  of  multiple  neuritis  (vide 
supra),  acute  myelitis,  and  even  chronic  spinal  affections,  may  also  show  a  re- 
markably sudden  onset,  or  at  least  may  suddenly  become  worse.  The  distinction 
between  genuine  spinal  apoplexy  and  meningeal  haemorrhage  can  hardly  ever  be 
made  with  certainty. 

Treatment. — If  we  have  the  rare  opportunity  to  be  able  to  interfere  at  the 
beginning  of  the  symptoms,  we  should  prescribe  a  perfectly  quiet  position  in  bed, 
local  use  of  ice,  and  eventually  ergotine.  Later  on  the  treatment  should  be 
directed  according  to  the  methods  generally  in  use  in  spinal  paralysis. 

3.  Functional  Disturbances. — In  practice  we  very  often  see  cases  where  the 
patient  complains  of  a  set  of  symptoms  which  are  in  all  probability  of  spinal 
origin ;  but  since  all  the  objective  signs  of  a  severe  spinal  affection  are  entirely 
absent,  and  since  the  whole  development  and  further  course  of  these  cases  oppose 
the  theory  of  a  coarse  anatomical  disturbance  in  the  cord,  we  have  a  right  to 
regard  them  as  mere  ''  functional  disturbances,"  and  thus  to  express  their  rela- 
tion to  certain  injurious  aetiological  influences,  and  their  comparative  freedom 
from  clanger.  We  know  nothing  at  all  definite  as  to  whether  the  symptoms  are 
based  upon  unknown  disturbances  in  the  nervous  mechanism  itself,  or  whether 
circulatory  disturbances,  on  a  basis  of  abnormal  vaso-motor  influences,  play  a  part 
here ;  but  the  types  of  disease  met  with  clinically  are  very  characteristic,  are  usu- 
ally easy  to  be  recognized,  and,  on  account  of  their  frequency,  have  the  greatest 
practical  significance.  As  a  rule,  the  spinal  symptoms  are  joined  to  certain  cere- 
bral symptoms,  since  the  morbid  phenomena  present  are  an  expression  of  a  disturb- 
ance of  the  whole  central  nervous  system.  The  type  of  disease  which  is  briefly 
described  in  what  follows,  for  which  the  names  of  spinal  irritation  or  spinal  neur- 
asthenia are  most  in  use,  is  often,  then,  only  a  complication  of  a  general  neuras- 
thenia, to  the  description  of  which  we  must  therefore  refer  for  the  details. 

The  aetiology  of  the  disease  is  often  easy  to  discover.  We  have  to  do  with 
patients  upon  whom  one  or  more  of  those  injurious  influences  have  acted,  which 


006  DISEASES  OF  THE  NERVOUS  SYSTEM. 

have  an  undoubted  influence  in  the  development  of  almost  all  the  neuroses: 
severe  and  persistent  emotional  excitement,  mental  and  physical  overexertion, 
impi'oper  methods  of  living,  toxic  influences,  such  as  alcohol  and  nicotine,  sexual 
excesses,  such  as  onanism,  etc.  Beside  these  there  is  very  often  a  hereditary  pre- 
disposition, a  congenital  weak  resistance  of  the  nervous  system,  which  is  often 
increased  by  a  poor  state  of  the  general  nutrition.  Finally,  a  hypochondriacal 
disposition  is  of  great  etiological  significance,  as  it  causes  not  only  an  abnormally 
increased  attention  to  the  symptoms,  but  also  an  abnormal  hyperesthesia  to  all 
subjective  sensations.  The  constant  anxiety  about  the  dreaded  results  of  any 
excesses  committed  is  often  much  more  injurious  than  the  excesses  themselves. 
•  Hypochondriacal  dread,  too,  usually  plays  the  largest  part  in  the  neurasthenic 
conditions  frequent  among  physicians. 

The  symptoms  of  the  morbid  conditions  in  question  usually  begin  gradually. 
The  patient  begins  to  complain  of  weakness  and  fatigue  in  walking,  and  also  very 
often  of  pains  in  the  back  and  loins,  and  not  infrequently  in  the  extremities  also. 
In  spite  of  the  vivid  description  which  the  patients  give  of  their  pain,  they  usually 
have  to  admit,  if  questioned  about  it  closely,  that  the  intensity  of  the  pain  is 
really  not  very  great.  Besides  the  pain  there  are  usually  many  forms  of  pares- 
thesia— numbness,  formication,  cold  feelings,  etc.  The  more  the  patient  knows,  or 
at  least  believes  he  knows,  of  the  symptomatology  of  spinal  diseases  from  reading 
and  from  associating  with  other  patients,  the  more  detailed  are  his  complaints. 
Disturbances  of  the  bladder  are  usually  present  only  in  a  slight  degree,  but  still 
they  do  occur.  They  often  depend  merely  upon  the  disturbance  of  the  involuntary 
reflex  mechanism,  due  to  the  added  factor  of  increased  voluntary  attention.  There 
are  very  often  sexual  disturbances,  which  are  usually  to  be  referred  to  former 
excesses,  especially  to  onanism  or  to  the  hypochondriacal  condition  of  the 
patient. 

If  we  make  a  physical  examination  of  the  patient  we  can  not  discover  definite 
signs  of  a  spinal  affection.  In  some  of  the  cases  we  find  an  increased  sensitive- 
ness of  the  vertebrae  on  pressure,  which  may  be  limited  to  a  few  definite  spots, 
a  symptom  to  which  the  name  of  "spinal  irritation"  is  often  given;  but  we 
often  fail  to  find  this  tenderness  of  the  vertebra?.  Nothing  abnormal  is  to  be  dis- 
covered in  the  pupils  or  the  reflexes.  The  tendon  reflexes  are  sometimes  quite 
lively  and  sometimes  weak.  The  sensibility  is  objectively  perfectly  normal; 
neither  can  we  discover  actual  paresis  or  atrophy  of  the  muscles.  Vaso-motor 
disturbances,  however,  are  often  seen:  abnormal  coldness,  pallor  or  redness  of 
the  hands,  tendency  to  sweating,  etc.  The  manifold  cerebral  symptoms,  that  are 
usually  present  at  the  same  time,  will  be  mentioned  in  the  description  of  neuras- 
thenia. The  condition  of  the  general  nutrition  in  many  patients  remains  un- 
changed, but,  of  course,  some  become  pale,  thin,  and  weak. 

The  diagnosis  of  functional  disturbances  of  the  spinal  cord  is  usually  not  diffi- 
cult, as  we  have  said,  and  it  may  often  be  made  from  the  history,  from  the  patienfs 
whole  outward  behavior,  and  from  the  manner  of  his  complaints;  but  we  can 
not  lay  too  much  stress  upon  the  injunction  that  a  careful  physical  examination 
should  always  be  made,  in  order  to  avoid  confusion  with  an  incipient  serious  dis- 
ease. We  shall  repeatedly  call  attention  in  what  follows  to  the  symptoms  which 
must  chiefly  be  observed  for  this  purpose. 

In  regard  to  prognosis  and  treatment  we  will  refer  to  what  is  said  in  the  chap- 
ter on  neurasthenia. 

4.  Traumatic  Lesions  of  the  Spinal  Cord.* — In  spite  of  the  protected  position  of 

*  "  Spinal  concussion  "  (commotio  spinalis)  will  be  considered  later,  in  the  chapter  on  the  "  traumatic 
neuroses." 


DISTURBANCES  OF  CIRCULATION,  HEMORRHAGES,    ETC.    607 

the  spinal  cord,  it  is  often  the  seat  of  severe  acute  traumatic  lesions.  Fractures 
and  dislocations  of  the  vertebrae  are  the  most  frequent,  and  these  may  give  rise 
to  considerable  injury  of  the  spinal  cord  by  the  dislocation  of  the  vertebra;,  or 
by  the  projection  of  a  fragment  of  bone.  In  many  cases  the  cord  is  injured,  not 
by  the  affection  of  the  bones  directly,  but  by  the  occurrence  of  traumatic  haemor- 
rhage. Gun-shot  wounds  of  the  cord  are  quite  frequent,  in  which  tlie  bullet  either 
penetrates  the  cord  itself  or  produces  injury  of  the  vertebrae  and  haemorrhage, 
which  involve  the  cord  indirectly.  Stabs  and  incised  wounds  of  the  cord  have 
been  repeatedly  seen.  The  point  of  a  knife  or  sword  may  penetrate  the  spinal 
canal  through  the  intervertebral  disks  and  cause  a  partial  section  or  at  least  a  con- 
tusion of  the  cord.  As  in  all  other  traumatic  lesions  of  the  cord,  a  secondary 
"  traumatic  inflammation  "  {vide  infra),  with  its  results,  may  be  added  to  the  direct 
injury  in  such  cases. 

We  need  not  go  into  all  the  details  of  the  pathology  and  symptomatology  of 
the  traumatic  lesions  of  the  spinal  cord,  since  the  number  of  special  conditions 
is,  of  course,  almost  inexhaustible ;  but  it  is  usually  not  particularly  difficult  to 
judge  of  a  given  case,  if  we  follow  the  rules  which  generally  obtain  in  the  pathol- 
ogy of  the  cord.  We  can  easily  tell  when  the  cord  is  involved  in  injuries  in  its 
vicinity  by  the  appearance  of  pronounced  motor  and  sensory  disturbances,  which, 
however,  differ  very  much  according  to  the  seat  and  the  extent  of  the  affection  of 
the  cord.  There  is  usually  at  first  a  pronounced  and  often  complete  motor  paraly- 
sis of  the  lower  extremities,  and  sometimes,  when  the  cervical  vertebrae  are  injured, 
of  the  upper  extremities  also.  There  is  also  anaesthesia,  differing  very  much,  of 
coui^se,  in  extent  and  intensity  in  the  different  cases ;  and  there  is  very  often  vesi- 
cal and  rectal  paralysis.  In  many  severe  cases  the  secretion  of  urine  seems  at 
first  much  diminished  or  wholly  wanting.  If  the  spinal  roots  be  affected  there 
are  severe  shooting  pains  and  paraesthesia.  The  reflexes  are  usually  diminished 
at  first,  but,  later,  if  the  injury  be  above  the  reflex  arc,  they  are  increased ;  but  if 
the  arc  itself  be  broken,  they  are  permanently  absent.  We  often  see  in  men  a 
more  or  less  complete  and  persistent  erection  of  the  penis,  which  is  probably  due 
to  a  direct  or  reflex  irritation  of  the  nerves  of  erection.  In  injuries  of  the  cervical 
cord  we  often  see  a  great  and  general  increase  of  temperature,  up  to  110°  or  112° 
(43°-44°  C),  especially  in  severe  and  rapidly  fatal  cases;  this  is  of  physiological 
interest,  and  agrees  with  the  results  of  experiments.  On  the  other  hand,  there  are 
also,  especially  in  injuries  of  the  dorsal  cord,  as  it  seems,  great  falls  of  temperature, 
down  to  90°  or  86°  (32°-30°  C). 

The  further  course  of  the  affection  differs  very  much.  In  the  worst  cases  death 
ensues  in  a  few  hours  or  days.  In  other  cases  the  patients  recover  from  the  first 
"  shock,"  but  permanent  paralysis  remains,  which  may  sooner  or  later  lead  to 
death  from  the  ensuing  sequelae,  cystitis  and  bedsores ;  but  we  often  see  partial 
improvement  and  a  cessation  of  all  the  symptoms.  Although  certain  functional 
disturbances  remain  permanently,  life  is  not  further  endangered.  Finally,  in  one 
class  of  comparatively  mild  cases,  there  may  be  a  complete  recovery. 

The  treatment  of  the  primary  affections  belongs  to  the  domain  of  surgery; 
especially  any  attempt  to  trephine  the  vertebral  column,  in  order,  if  possible,  to 
relieve  the  existing  pressure  on  the  cord  by  reducing  the  dislocation  of  the  verte- 
brae or  the  splintei'S  of  bone.  In  most  cases  we  have  to  confine  ourselves  to  putting 
the  patient  in  a  proper  position  on  a  water-bed,  and  guarding  as  carefully  as  pos- 
sible against  bedsores  and  cystitis.  Locally,  the  constant  application  of  ice  is 
most  to  be  recommended.  We  can  expect  but  little  from  local  blood-letting, 
inunctions  with  mercurial  ointment,  etc.  If  the  first  acute  stage  pass  off  favor- 
ably, the  treatment  of  any  paralytic  symptoms  remaining  follows  the  ordinary 
rules  (baths  and  electricity). 


608  DISEASES  OF  THE  NERVOUS  SYSTEM. 

5.  Diseases  of  the  Spinal  Cord  after  a  sudden  Reduction  of  the  Atmospheric 
Pressure  [Caisson  Disease].— In  bridge-builders  and  others,  who  have  worked  for 
hours  under  water  in  the  so-called  "  caissons,"  uuder  an  external  pressure  of  two 
or  three  atmospheres,  we  sometimes  see  the  appearance  of  peculiar  symptoms  after 
leaving  the  caisson — that  is,  on  the  sudden  reduction  of  the  atmospheric  pressure. 
Besides  the  frequent  mild  symptoms  of  pain  in  the  ears  and  haemorrhage  from 
the  ears,  articular  and  muscular  pains  in  the  back  and  the  extremities,  slowing  of 
the  pulse  and  vomiting,  there  are  also  severe  disturbances  of  motility  and  sensi- 
bility, which  point  unequivocally  to  an  affection  of  the  spinal  cord.  Usually  the 
lower  half  of  the  body  is  alone  affected.  The  legs  are  more  or  less  completely 
paralyzed,  the  skin  is  usually  anaesthetic  up  to  the  trunk,  and  there  is  genei^ally 
retention  of  urine.  The  patient  sometimes  recovers  in  a  few  weeks,  but  in  other 
cases  the  condition  terminates  fatally  iu  a  comparatively  short  time — in  a  few 
weeks  or  months.  The  first  special  anatomical  investigations  in  question  (Ley- 
den,  F.  Schultze)  gave  in  such  cases  a  disseminated  but  extensive  affection  in  the 
dorsal  cord,  chiefly  in  the  posterior  columns  and  the  posterior  portions  of  the 
lateral  columns.  The  nervous  tissue  in  the  diseased  parts  was  completely  de- 
stroyed, and  instead  of  it  was  found  detritus  and  a  collection  of  large,  round,  finely 
granular  cells  (fatty  granular  cells  ?).  Haemorrhages  into  the  cord,  which  might 
perhaps  be  expected,  have  up  to  the  present  time  not  been  found. 

Nothing  definite  is  known  as  to  the  precise  process  in  this  form  of  spinal  dis- 
ease. Ley  den  suspected  that  there  was  a  development  of  gas  from  the  blood 
which  caused  a  rupture  of  the  surrounding  tissue,  under  the  influence  of  the  rap- 
idly diminished  barometric  pressure,  as  Hoppe-Seyler  and  P.  Bert  have  discovered 
by  experiment;  but  the  circumscribed  limitation  of  the  affection  to  the  dorsal  cord, 
and  the  lack  of  any  signs  of  vascular  haemorrhage,  speak  against  this  theory. 

The  treatment  is  the  same  as  in  acute  myelitis. 


CHAPTER  III. 

THE   PRESSURE   PARALYSES  OF   THE   SPINAL  CORD. 

(Slow  Compression  of  the  Spinal  Cord,  especially  in  Caries  and  Carcinoma  of  the  Vertebra.) 

iEtiology. — Many  pathological  processes  which  develop  in  the  vicinity  of  the 
spinal  cord  may  exert  a  gradually  increasing  pressure  upon  it,  and  thus,  on  the 
one  hand,  inhibit  the  conduction  of  nervous  irritation,  and,  on  the  other,  cause 
coarse  mechanical  injuries  in  the  substance  of  the  coi'd.  The  seat  of  such  affec- 
tions is  in  the  first  place  in  the  membranes  of  the  spinal  cord.  In  the  chapter 
on  meningitis  we  have  already  mentioned  the  compressing  action  of  the  masses  of 
inflammatory  exudation  on  the  nerve-roots  and  the  cord,  and  we  have  learned  to 
recognize,  especially  in  pachymeningitis  cervicalis  hypertrophica,  a  characteristic 
example  of  a  gradually  increasing  compression  of  the  cervical  cord.  Precisely 
similar  conditions  are  found  in  the  rare  meningeal  tumors,  "whose  special  pathol- 
ogy will  be  described  in  connection  with  the  tumors  of  the  cord  itself. 

By  far  the  most  frequent  pressure  paralyses  of  the  spinal  cord,  and  hence  the 
most  important  practically,  are  caused  by  certain  diseases  of  the  vertebrae,  and 
first  of  all  by  chronic  caries  of  the  vertebrae  (spondylitis,  Pott's  disease,  spondyl- 
arthrocace).*    There  is  no  longer  any  doubt  at  present  that  certainly  the  greatest 

*In  the  kyphoscolioses  of  the  vertebral  column,  not  due  to  spondylitis,  there  are  practically  never 
any  symptoms  of  compression  in  the  cord,  even  in  very  pronounced  cases.  In  these  cases  the  cord 
manifestly  shows  quite  a  great  adaptability. 


THE  PRESSURE  PARALYSES  OF  THE  SPINAL  CORD.  009 


part,  if  not  all,  of  the  cases  of  vertebral  caries  are  of  tubercular  origin,  that  verte- 
bral caries  is  a  local  tuberculosis  of  the  vertebrae.  Although  these  facts  were  for- 
merly rendered  very  probable  by  the  histological  conditions  of  the  process,  and  by 
its  frequent  relation  to  other  unquestionable  tubercular  diseases,  such  as  phthisis, 
miliary  tuberculosis,  and  tubercular  meningitis,  they  have  of  late  been  confirmed 
beyond  a  doubt  by  the  discovery,  which  can  usually  be  made,  of  tubercle  bacilli  in 
the  cheesy  nodules  of  the  vertebral  caries.  Tubercular  spondylitis  occurs  at 
almost  any  age ;  it  is  rare  only  in  old  people.  It  often  develops  in  children,  but 
it  is  almost  as  frequent  in  adults.  The  ^etiological  significance  of  injuries,  such  as 
a  fall  or  a  blow,  which  are  often  mentioned  by  the  patients  themselves  or  their 
parents,  is  in  most  cases  doubtful ;  but  we  can  very  often  succeed  in  finding  aetio- 
logical  factors  for  the  onset  of  tubercular  disease  in  general— the  tubercular  habit, 
hereditary  tendency,  or  tubercular  disease  elsewhere,  such  as  phthisis,  pleurisy, 
other  affections  of  the  bones,  etc. 

Cancer  of  the  vertebrae,  as  well  as  caries,  leads  to  pressure  paralyses  of  the  spinal 
cord;  but  it  is  relatively  much  rarer  than  caries,  it  develops  chiefly  in  older  per- 
sons, and  it  occurs  both  as  a  primary  new  growth  and  also  as  secondary  to  cancer 
of  other  organs— the  breast,  the  stomach,  or  the  oesophagus. 

We  must  mention  here  briefly,  as  very  rare  causes  of  compression  of  the  spinal 
cord,  aneurism  of  the  aorta,  which  gradually  erodes  the  vertebrae,  echinococci  in 
the  vertebral  canal,  exostoses  of  the  vertebrae,  and  syphilitic  new  growths. 

Pathological  Anatomy. — Vertebral  caries  is  most  common  in  the  dorsal  portion 
of  the  vertebral  column  (dorsal  spondylitis),  somewhat  rarer  in  the  cervical  por- 
tion (cervical  spondylitis),  and  rarest  in  the  lumbar  portion  (lumbar  spondylitis) 
and  in  the  sacrum  (sacral  spondylitis).  It  usually  extends  over  several  adjacent 
vertebrae,  or  more  rarely  two  separate  foci  of  disease  are  seen.  The  process  itself, 
the  details  of  which  can  not  be  discussed  here,  probably  always  begins  in  the 
spongy  substance  of  the  bodies  of  the  vertebrae.  We  see  here,  on  section,  in 
incipient  cases,  roundish,  pale  reddish,  or  yellowish  nodules,  which  consist  of 
newly  formed  fungous  tissue — that  is,  tubercular  granulation-tissue.  The  bony 
substances  become  more  and  move  destroyed  by  the  invasion  of  the  new  growth, 
which  itself  shows  the  characteristic  tendency  of  all  tubercular  new  growths  to 
cheesy  degeneration.  Thus  there  is  often  an  extensive  destruction  of  the  bodies 
of  the  vertebrae,  which  later  on  also  involves  the  vertebral  processes,  the  inter- 
vertebral disks,  and  the  other  articular  connections  between 
the  different  vertebrae. 

There  are  essentially  two  factors  to  be  considered  in  re- 
gard to  the  question  which  chiefly  interests  us  here — that  is, 
in  regard  to  the  occurrence  of  compression  of  the  spinal  cord. 
In  the  first  place,  it  is  clear  that  the  complete  or  partial  de- 
struction of  the  bodies  of  one  or  even  more  vertebrae,  and  of 
their  articular  connections,  can  not  remain  without  influ- 
ence upon  the  position  of  the  other  adjacent  vertebrae.  In 
fact,  we  very  often  see  dislocations  of  the  vertebrae  as  a  result 
of  it,  usually  by  the  pushing  backward  of  the  partly  de- 
stroyed vertebra  by  the  movements  of  the  vertebrae  above 
and  below  the  diseased  portion  on  one  another  (see  Fig.  82). 
There  arises,  on  the  one  hand,  a  contraction  of  the  vertebral 
canal,  and  with  it  often  a  very  considerable  limitation  of  the 
space  for  the  cord;  and,  on  the  other  hand,  that  characteris- 
tic projection  of  the  spinous  processes  in  the  region  of  the 
diseased  portion  of  the  vertebral  column  which  forms  the  so-called  Pott's  boss — 
the  angular  kyphosis.  In  very  slight  degrees  of  the  disease  there  is  only  a  slighc 
39 


Fig.  82.— Schematic  rep- 
resentation of  verte- 
bral displacement  in 
spondylitis.  The  point 
of  compression  of  the 
cord,  at  the  level  of 
the  second  dorsal  ver- 
tebra, is  at  C. 


610  DISEASES  OF  THE  NERVOUS  SYSTEM. 

projection  of  one  or  more  spinous  processes,  but  in  other  cases  it  gradually  be- 
comes an  extensive  deformity  of  the  vertebral  column,  which  strikes  us  at  the 
first  glance.  It  goes  without  saying  that,  under  some  circumstances,  the  Pott's 
boss  may  be  entirely  absent  in  vertebral  caries. 

The  second  factor,  which  is  often  to  be  considered  in  the  mechanism  of  com- 
pression of  the  cord,  is  the  formation  of  foci  of  cheesy  pus  on  the  posterior  surface 
of  the  bodies  of  the  vertebrae.  Since  the  inflammatory  tubercular  new  growth  in- 
volves the  periosteum,  there  are  often  formed  here  large  collections  of  cheesy  pus, 
which  are  situated  beneath  the  periosteum,  raise  it,  and  push  it  out  far  into  the 
vertebral  canal.  In  other  cases,  the  tubercular  new  growth  still  further  directly 
involves  the  outer  surface  of  the  dura,  and  forms  here  extensive  cheesy  masses 
which  of  course  may  also  cause  a  compression  of  the  cord.  The  inner  surface  of 
the  dura  at  the  corresponding  parts  is  usually  markedly  injected,  but  a  direct  in- 
vasion of  the  pia  by  the  tubercular  process  through  the  dura  is  rare. 

If  now  a  considerable  contraction  of  the  vertebral  canal  have  arisen  from  dislo- 
cation of  the  vertebrae,  or  from  the  projection  inward  of  the  cheesy  purulent 
masses  into  the  canal,  the  necessary  mechanical  consequences  in  the  spinal  cord 
itself  are  usually  to  be  recognized  with  ease.  The  cord  appears  smaller  at  the 
point  of  compression.  If  the  narrow  part  correspond  to  a  bend  in  the  vertebral 
column,  we  can  very  often  see  a  marked  angle  of  bending  on  the  anterior  surface 
of  the  cord.  The  consistency  of  the  cord  at  the  part  affected,  the  extent  of  which 
seldom  exceeds  a  few  centimetres,  is  usually  diminished ;  the  cord  is  soft  and  may 
be  easily  bent.  In  old  cases  only  do  we  find  the  cord  itself  harder  than  normal 
and  sclerosed  (vide  infra).  It  is  very  remarkable,  however,  that  often,  as  we  have 
repeatedly  seen,  marked  symptoms  of  compression  may  be  present  during  life  with- 
out finding  any  coarse  mechanical  lesion  of  the  cord  in  the  cadaver,  so  tbat  the 
cord  may  show  an  almost  perfectly  normal  appearance.  As  in  the  peripheral 
nerves,  so  in  the  spinal  cord,  a  moderate  pressure  is  manifestly  enough  to  excite  a 
partial  break  in  the  conduction,  without  being  at  the  same  time  necessarily  associ- 
ated with  an  actual  mechanical  destruction  of  nervous  elements.  On  careful 
microscopic  examination  of  the  cord,  we  find  in  such  cases,  in  spite  of  the  existence 
of  a  complete  paraplegia  during  life,  that  most  of  the  nerve-fibers  are  still  com- 
pletely preserved,  and  that  there  are  only  hei'e  and  there  a  few  lacunae,  corre- 
sponding to  single  fibers,  which  have  been  destroyed.  This  discovery  is  especially 
interesting  because  it  makes  us  understand  the  possibility  of  recovery,  even  in 
apparently  severe  cases  (vide  infra). 

Even  where  we  can  find  considerable  histological  changes  in  the  spinal  cord, 
however,  where  the  softness  of  the  cord  points  to  a  coarse  lesion  of  it,  and  where 
the  microscope  shows  the  destruction  of  a  great  part  of  the  normal  tissue  at  the 
point  of  compression,  all  these  changes  are  merely  the  necessary  results  of  the 
purely  mechanical  pressure  on  the  spinal  cord.  As  we  must  maintain,  against  the 
theory  generally  received  at  present,  on  the  ground  of  many  of  our  own  investi- 
gations, we  have  not  the  slightest  reason  to  refer  the  occurrence  of  paralysis  in 
spondylitis  to  a  secondary  myelitis.  Such  a  "  compression  myelitis  " — that  is,  an 
inflammation  of  the  spinal  cord  arising  from  the  pressure  as  such — is  to  be  rejected 
from  general  pathological  reasons ;  and  the  microscopic  examination  of  the  cord 
also  shows  nothing  which  points  to  an  inflammation,  or  which  may  not  be 
entirely  the  result  of  mechanical  compression.  If  we  take  a  portion  from  the 
soft  place  of  compression  for  fresh  examination,  we  find  sometimes  many,  some- 
times only  a  few,  granular  cells,  according  to  the  amount  of  disintegrated  nerve- 
medulla,  the  remains  of  which  are  taken  up  by  the  white  blood-corpuscles — the 
wandering  cells.  If  we  make  stained  cross-sections  of  the  hardened  cord,  we  see 
under  the  microscope  no  signs  of  vascular  changes,  of  hyperaernia,  of  accumula- 


THE  PRESSURE  PARALYSES  OF  THE  SPINAL  CORD.  611 

tion  of  cells  about  the  vessels,  antl  only  exceptionally  a  little  traumatic  haemor- 
rhage; but  we  do  find,  besides  many  still  preserved  nerve-fibers,  other  fibers,  which 
are  involved  in  the  disintegration  or  are  already  destroyed.  Very  commonly  the 
changes  are  distributed  in  the  form  of  nodules.  We  find  groups  of  greatly 
swollen  axis-cylinders,  which  have  wholly,  or  almost  wholly,  lost  their  medullary 
sheaths,  and  in  other  places  we  notice  already  the  signs  of  their  disintegration,  or 
the  already  empty  lacunae  in  the  meshes  of  the  neuroglia.  If  the  destruction  of 
the  nervous  tissue  have  advanced  to  a  certain  degree,  there  is  in  the  later  stages,  as 
in  all  analogous  processes,  a  secondary  implication  of  the  neuroglia.  Now  fol- 
lows an  increase  of  the  interstitial  connective  tissue.  Its  proliferations,  which 
take  the  place  of  the  destroyed  nervous  tissue,  seem  diffuse— at  first  loose,  but  later 
firm  and  fibrillary.  Thus  it  happens  that  in  old  cases  we  find  nothing  at  the 
point  of  compression  but  a  loss  of  nerve-fibers  in  the  cord,  and  instead  of  it  there 
is  a  firm  fibrous  tissue.  All  the  changes  mentioned  are  always  much  more  devel- 
oped in  the  white  matter  of  the  cord  than  in  the  gray. 

Finally,  after  a  more  protracted  compression  of  the  cord  we  find  an  ascending 
and  descending  secondary  degeneration  of  certain  systems  of  fibers  in  the  cord 
(vide  infra). 

We  need  not  go  more  fully  into  the  details  of  compression  of  the  cord  from 
other  causes,  since  the  results,  as  far  as  they  are  of  a  purely  mechanical  nature, 
are  precisely  the  same.  In  cancer  of  the  vertebra?  there  may  also  be  dislocations 
of  the  vertebral  column  after  the  destruction  of  some  of  the  vertebra?,  but  usually 
the  compression  depends  upon  the  direct  growth  of  the  newly  formed  tissue  into 
the  dura.  In  these  cases  the  compression  of  the  nerve-roots  in  the  intervertebral 
foramina  is  also  of  importance. 

Clinical  History. — Many  cases  of  spondylitis  run  their  course  without  involving 
the  cord,  or  at  least  involving  it  only  in  quite  a  subordinate  fashion.  In  other 
cases  the  symptoms  of  disease  of  the  vertebra?  exist  for  a  long  time  alone,  until  at 
last,  slowly  or  suddenly,  the  signs  of  compression  of  the  cord  are  added  to  them. 
Finally,  in  a  third  group  of  cases,  the  vertebral  disease  is  so  latent  that  only  the 
cord  symptoms  are  prominent  in  the  type  of  the  disease,  and  the  disease  of  the 
vertebra?  may  easily  be  entirely  overlooked. 

Usually  the  symptoms  of  the  developing  primary  disease,  the  affection  of  the 
vertebra?,  precede  the  appearance  of  the  first  cord  symptoms  by  some  time.  The 
patient  feels  a  dull  pain  at  a  definite  part  of  the  spine,  which  is  increased  by 
movements  of  the  trunk,  by  bending  or  straightening  up.  Many  patients  notice 
the  stiffness  of  the  vertebral  column  of  themselves,  and  sometimes  even  a  begin- 
ning deformity.  The  first  cord  symptoms  usually  consist  of  painful  sensations, 
which  are  not  confined  to  the  place  of  the  disease,  but  shoot  out  approximately 
along  the  course  of  the  nerve-paths.  These  pains,  which  are  due  chiefly  to  an 
irritation  of  the  nerve-roots  caused  by  the  compression,  extend,  according  to  the 
seat  of  the  affection,  into  the  shoulders  and  arms,  into  the  lateral  portions  of  the 
trunk,  or  into  the  lower  extremities.  They  are  sometimes  very  severe,  and  then 
they  usually  have  a  pronounced  neuralgiform  character,  or  they  may  be  more  dull 
and  dragging.  Besides  the  special  pains,  there  are  also  many  forms  of  paresthe- 
sia, such  as  formication  and  cold  feeliugs. 

The  disturbances  of  motility  begin  to  appear  at  the  same  time  with  these  symp- 
toms or  soon  after  them.  A  stiffness  and  weakness  arise  which  impede  the  gait, 
usually  not  in  both  legs  at  once,  but  first  in  one  and  then  in  the  other.  This 
paresis  increases  rapidly  or  slowly,  and  it  may  finally  go  on  to  a  complete  motor 
paralysis.  If  the  seat  of  the  affection  be  in  the  dorsal  vertebra?,  as  it  usually  is,  or 
if  it  be  in  the  lumbar  vertebra?,  the  paralysis  affects  the  lower  extremities  only, 
and  the  arms,  of  course,  remain  intact;  but  in  cervical  spondylitis  the  arms  are 


612  DISEASES  OF  THE  NERVOUS  SYSTEM. 

usually  first  and  chiefly  affected.  Only  on  great  compression  of  the  cervical  cord 
is  the  conduction  of  the  fibers  passing  through  it  for  the  lower  extremities 
impaired,  and  then  there  are  also  disturbances  of  function  in  these. 

Disturbances  of  sensibility  are  often  found,  independently  of  the  pains  and 
paresthesia?  above  mentioned,  but  in  many  cases  of  pressure  paralysis  they  are 
present  in  only  a  comparatively  slight  degree.  It  seems  that  the  sensory  nerves 
resist  pressure  more  than  the  motor  nerves,  just  as  in  the  pressure  paralyses  of 
peripheral  nerves ;  but  possibly  their  position  in  the  gray  matter  of  the  posterior 
cornua  protects  them  better  from  mechanical  attack  than  is  the  case,  for  example, 
with  the  motor  fibers  in  the  pyramidal  tract  (see  Figs.  66  and  67).  The  fact  is 
that  often,  even  in  complete  motor  paraplegia,  there  is  little  if  any  diminution  of 
sensibility,  and  that  marked  anaesthesia  is  rare,  and  is  seen  only  in  the  last  stages 
of  the  disease.  We  find  most  frequently  a  slight  blunting  of  sensibility  equally 
to  all  forms  of  sensation,  especially  to  the  sense  of  pain.  The  different  parts  of 
the  skin  not  infrequently  act  differently,  so  that  we  find  portions  with  quite  nor- 
mal sensibility,  as  well  as  very  anaesthetic  portions. 

The  condition  of  the  reflexes  is  interesting.  If  the  seat  of  the  compression  be 
above  the  reflex  arc,  which  we  must  assume  to  be  in  the  lumbar  cord  for  the 
reflexes  of  the  lower  extremities,  we  should  expect  that  the  reflexes  would  persist, 
and  in  many  cases  even  be  increased,  corresponding  to  the  decline  in  the  inhibi- 
tory influences  coming  from  above.  The  latter  takes  place  invariably  with  the  ten- 
don reflexes,  which  are  always  increased  in  the  lower  extremities  in  the  pressure 
paralyses  arising  from  the  cervical  or  dorsal  cord.  The  increase  of  the  tendon 
reflexes  may  reach  so  great  a  degree  as  to  show  in  the  lower  extremities  the  pro- 
nounced type  of  spastic  paralysis  (vide  infra).  The  limbs  are  then  found  in  a 
rigid  tonic  extension,  they  can  only  with  difficulty  be  flexed  passively  on  account 
of  the  muscular  resistance,  and  they  show  a  very  vigorous  ankle  clonus,  sometimes 
degenerating  into  a  general  tremor  of  the  leg,  and  also  marked  patellar  reflex, 
adductor  reflex,  etc. ;  but  even  in  flaccid  paraplegia  the  tendon  reflexes  may  be 
quite  vigorous.  In  cervical  spondylitis  the  tendon  and  periosteal  reflexes  in  the 
arms  are  also  increased  sometimes,  but  in  other  cases,  if  the  reflex  arc  be  injured, 
they  are  absent.  Where  the  seat  of  the  compression  is  above  the  lumbar  cord,  the 
cutaneous  reflexes  sometimes  show  considerable  vigor,  but  their  increase  is  much 
less  frequently  as  marked  as  is  the  increase  of  the  tendon  reflexes.  In  severe 
pressure  paralyses  in  the  dorsal  cord  the  cutaneous  reflexes  are  even  frequently 
diminished.  They  are  probably  never  entirely  absent,  but  one  must  understand 
testing  them,  and  must  employ  long-continued  cutaneous  irritation,  such  as  pinch- 
ing and  pricking,  in  different  parts  of  the  skin  in  order  to  provoke  them. 

Trophic  disturbances  are  often  found  in  the  paralyzed  parts.  If  there  be 
severe  symptoms  of  sensory  irritation  there  may  sometimes  be  eruptions  of  her- 
pes, corresponding  to  the  course  of  the  nerves.  More  frequently  there  are  chronic 
disturbances  in  the  nutrition  of  the  skin  in  severe  and  long-continued  cases.  It 
becomes  dry,  the  epidermis  scales  off,  and  the  nails  become  brittle.  Bedsores 
form  very  easily  in  severe  cases  on  the  sacrum,  on  the  buttocks,  on  the  inner  side 
of  the  knees,  and  on  the  heels,  especially  when  the  patient  has  insufficient  care. 
The  muscles  retain  their  normal  volume  and  their  normal  electrical  excitability 
in  many  cases  as  long  as  their  trophic  center  remains  uninjured;  but  sometimes, 
even  when  the  point  of  compression  is  above  the  lumbar  cord,  there  is  a  great 
atrophy  of  the  muscles  of  the  legs,  although  the  electrical  reaction  of  the  nerves 
is  normal,  or  at  most  a  little  reduced  in  quantity.  If  the  lesion  involve  the  lum- 
bar cord  itself,  or  the  fibers  of  the  cauda  equina,  in  caries  of  the  sacrum,  there 
must,  of  course,  be  an  atrophic  paralysis  in  the  legs,  with  reaction  of  degeneration. 
There  may  also  be  an  atrophic  paralysis  in  the  arms  in  cervical  spondylitis. 


THE  PRESSURE  PARALYSES  OF  THE  SPINAL  CORD.         613 

Disturbances  of  the  rectum  and  bladder  occur  in  almost  all  severe  cases  of 
pressure  paralysis.  The  difficulty  of  micturition  is  often  an  early  symptom  of  the 
disease ;  later  on  there  is  complete  retention  of  urine,  and,  in  the  more  advanced 
stages  of  the  disease,  there  is  usually  incontinence.  With  this  the  danger  of  the 
development  of  cystitis  becomes  very  great.  The  bowels  are  usually  constipated, 
but  sometimes  there  is  also  incontinence  of  faeces. 

Thus  we  see,  under  some  circumstances,  in  compression  of  the  cord  the  whole 
group  of  symptoms  arising  which  are  the  necessary  consequence  of  the  break 
in  conduction  in  the  spinal  cord,  and  which  we  shall  likewise  meet  again  in  vari- 
ous other  spinal  affections,  especially  in  myelitis  and  in  tumors.  The  intensity 
and  selection  of  the  symptoms  must,  of  course,  vary  very  much  in  the  different 
cases.  If  the  compression  be  quite  slight,  there  are  only  mild  symptoms  of  sensory 
irritation  and  slight  paresis.  One  of  the  earliest  and  most  constant  signs  of  a 
compression  of  the  cord,  in  the  dorsal  or  cervical  region,  is  a  decided  increase  of 
the  patellar  reflex.  We  sometimes  find  it  at  a  time  when  there  is  scarcely  a  single 
other  cord  symptom  present.  If  the  compression  increases,  the  paresis  becomes 
more  marked,  the  disturbance  of  sensibility  is  greater,  and  vesical  disturbances 
arise,  until  finally  the  complete  type  of  an  entire  transverse  interruption  of  con- 
duction in  the  cord  is  developed ;  but  the  latter  is  but  rarely  the  case,  since,  as  we 
have  said,  the  conduction  of  sensory  impressions  is  usually  not  wholly  abolished. 
The  time  required  for  the  development  of  the  symptoms  of  spinal  compression 
differs  very  much.  They  sometimes  attain  a  considerable  height  in  a  short  time, 
and  sometimes  they  develop  only  after  a  course  of  months.  Variations  in  the 
intensity  of  the  symptoms  are  frequent,  and  they  point  perhaps  to  a  corresponding 
variation  in  the  severity  of  the  compression. 

In  regard  to  the  result  of  pressure  paralyses,  it,  of  course,  depends  first  upon 
the  nature  of  "the  primary  disease.  In  tumors,  especially  in  cancer  of  the  verte- 
brae, recovery  is  not  to  be  thought  of,  but  spondylitic  processes  without  doubt  can 
recover,  which  is  by  no  means  in  contradiction  to  their  character  as  a  local  tuber- 
cular process.  In  this  connection  the  fact  i,3  of  great  practical  importance  that 
even  the  pressure  paralyses  may  be  completely  restored,  as  far  as  the  cause  of  the 
compression  can  be  removed  by  the  absorption  of  inflammatory  and  tubercular 
new  growths,  so  that  a  complete  and  permanent  recovery  may  take  place  even 
after  the  paralysis  has  lasted  for  some  months,  or  a  year,  or  even  a  year  and  a  half. 
Such  recoveries  have  been  seen  in  great  numbers  by  others  and  also  by  ourselves. 

Although,  according  to  this,  the  prognosis  in  a  part  of  the  cases  of  pressure 
paralysis  from  spondylitis  is  comparatively  good,  still  many  other  cases  terminate 
unfavorably.  The  cause  of  this  lies  either  in  the  occurrence  of  dangerous  sequela? 
of  the  paralysis,  such  as  bedsores,  cystitis,  or  pyelo-nephritis,  with  fever  and  in- 
creasing general  weakness;  or  in  the  development  of  other  tubercular  diseases, 
especially  phthisis,  or  more  rarely  miliary  tuberculosis  or  tubercular  meningitis, 
which  prove  fatal. 

Diagnosis. — The  frequency  of  the  pressure  paralyses  of  the  spinal  cord  admon- 
ishes us  to  examine  the  vertebral  column  carefully  in  every  case  of  spinal  disease, 
especially  if  the  case  can  not  be  put  under  one  of  the  special  types  of  systemic  dis- 
eases (vide  infra).  We  should  look  especially  for  the  stiffness  of  special  parts  of 
the  vertebral  column  on  movements  of  the  head  or  trunk,  and  also  for  the  pro- 
nounced tenderness  of  single  vertebrae  to  pressure,  and,  finally,  as  a  most  impor- 
tant and  most  certain  sign,  for  the  deformity  of  the  vertebral  column,  the  marked 
projection  of  a  single  spinous  process,  or  the  formation  of  an  evident  angular 
kyphosis.  If  we  find  such  a  Pott's  boss  the  diagnosis  is  easy,  and  we  can  then 
at  any  rate  refer  the  existing  cord  symptoms  to  a  compression  of  the  cord  caused 
by  a  disease  of  the  vertebrae. 


614  DISEASES  OF  THE  NERVOUS  SYSTEM. 

The  diagnosis  is  more  difficult  if  the  signs  of  an  affection  of  the  vertebrae  be 
not  evident.  It  must  once  for  all  be  stated  that  vertebral  caries  does  not  inva- 
riably and  necessarily  result  in  a  manifest  Pott's  boss,  and  that  even  the  tender- 
ness of  the  vertebrae  to  pressure  is  sometimes  very  slight  in  spondylitis.  In  such 
cases  the  examination  of  the  vertebral  column  must  be  repeated  more  frequently, 
since  even  slight  anomalies  obtain  a  diagnostic  value  if  constantly  present ;  and 
the  whole  course  of  the  disease  is  also  to  be  considered.  The  most  characteristic 
features  of  a  compression  of  the  cord  are  its  beginning  with  symptoms  of  sensory 
irritation,  the  preponderance  of  symptoms  of  motor  paralysis  with  comparatively 
little  disturbance  of  sensibility,  and  finally  the  frequent  asymmetry  of  the  symp- 
toms on  the  two  sides,  which  may  even  recall  the  type  of  the  so-called  "  unilateral 
lesion  "  of  the  spinal  cord  (vide  infra).  Sometimes  the  cause  of  the  spinal  symp- 
toms is  at  first  obscure,  and  later  on  in  the  disease  a  marked  anomaly  of  the  verte- 
bral column  develops. 

If  the  diagnosis  of  an  affection  of  the  vertebrae  be  certain,  the  next  question  is 
as  to  the  nature  of  it,  especially  whether  we  have  to  do  with  a  spondylitis,  or  with 
a  cancer  of  the  vertebra?.  Since  spondylitis  is  by  far  the  more  frequent  disease, 
we  must  always  think  of  that  first,  especially  in  young  people,  and  where  we  have 
the  formation  of  a  pronounced  angular  kyphosis.  In  cancer  of  the  vertebrae  the 
coarser  changes  in  the  form  of  the  vertebral  column  are  generally  less  marked. 
This  develops  usually  in  older  people,  after  the  age  of  forty,  and  is  manifested  by 
the  great  intensity  of  the  initial  symptoms  of  sensory  irritation.  The  "paraplegia 
dolorosa"  the  paralysis  of  the  lower  extremities  associated  with  severe  pains,  is 
the  most  characteristic  symptom  of  cancer  of  the  vertebrae.  The  discovery  of  a 
primary  nodule  of  cancer,  as  in  the  breast,  or,  as  we  ourselves  have  seen,  the 
appearance  of  a  swelling  of  the  inguinal  glands,  may  serve  to  support  the  diag- 
nosis. Finally,  a  certain  stress  is  to  be  laid  on  the  well-known  general  habit  of 
patients  with  cancer,  and  on  the  peculiar  cancerous  cachexia. 

The  place  of  compression  is,  in  the  majority  of  cases,  to  be  recognized  by  the 
evident  localization  of  the  disease  of  the  vertebrae.  In  other  respects  the  same 
rules  hold  for  localization  which  we  shall  discuss  more  fully  in  the  description  of 
myelitis  in  the  following  chapter. 

Treatment. — In  regard  to  the  special  treatment  of  spondylitis,  especially  the 
orthopaedic  treatment,  we  must  refer  to  the  text-books  of  surgery.  In  general,  we 
have  not  thus  far  gained  the  impression  that  a  particularly  favorable  influence 
can  be  exerted  on  the  symptoms  of  spinal  compression  by  contrivances  for  exten- 
sion of  the  vertebral  column.  These  are  often  injudicious  where  there  is  para- 
plegia, since  they  increase  the  pain  and  make  it  harder  to  guard  against  bedsores. 
We  would  not  deny,  however,  that  in  many  cases  certain  supports  for  the  verte- 
bral column,  and  contrivances  for  extension,  may  be  used  to  advantage.  Perma- 
nent rest  in  bed  is,  at  any  rate,  always  of  the  greatest  importance.  Local  applica- 
tions to  the  vertebral  column  are  much  used— dry  cups,  painting  with  iodine,  and 
especially  the  hot  iron.  The  use  of  the  latter  in  spondylitis  has  even  to-day  warm 
advocates,  and,  in  fact,  deserves  to  be  tried,  the  procedure  with  Paquelin's  thermo- 
cautery being  especially  easy ;  we  make  some  three  or  four  eschars  on  each  side 
of  the  diseased  vertebrae. 

Among  other  remedies  we  may  mention  stabile  galvanization  at  the  point  of 
pressure,  and  the  electrical  treatment  of  the  paralyzed  extremities;  also  the  use  of 
baths,  especially  salt  baths,  and,  finally,  the  internal  use  of  compounds  of  iodine- 
iodide  of  potassium  and  iodide  of  iron.  In  regard  to  the  symptomatic  treatment 
we  will  refer  to  the  following  chapter. 

[In  a  few  cases  great  benefit  has  been  derived  from  trephining  the  vertebrae  and 
removing  the  inflammatory  products  which  have  compressed  the  cord.     In  some 


ACUTE  AND  CHRONIC  MYELITIS.  615 

cases  a  patient  who  was  completely  paraplegic  has  regained  considerable  use  of  the 
legs.  It  is  obvious  that  the  operation  should  not  be  too  long  delayed  after  symp- 
toms of  pressure  have  once  developed. — K.J 


CHAPTER  IV. 

ACUTE    AND   CHRONIC   MYELITIS. 

{Diffuse  Myelitis.     Transverse  Myelitis.) 

Preliminary  Remarks. — The  pathological  processes  in  the  spinal  cord  known 
to  us  at  the  present  time  may  be  divided  into  two  groups.  In  the  first  group  we 
find  this  peculiarity,  that  the  pathological  changes  are  confined,  with  a  remarkable 
constancy,  to  certain  definite  parts  of  the  spinal  cord,  so  that  consequently  the 
clinical  symptoms  of  the  disease  may  be  quite  exactly  defined.  To  this  group 
belongs  the  disease  known  as  anterior  poliomyelitis  (noXiös,  gray),  which  is  local- 
ized almost  exclusively  in  the  anterior  cornua  of  the  gray  matter  of  the  spinal 
cord,  and  also  a  class  of  affections,  such  as  tabes  dorsalis,  amyotrophic  lateral  scle- 
rosis, etc.,  in  which  perfectly  definite  fasciculi  in  the  cord  are  diseased.  From  the 
comparison  of  the  anatomical  lesions  in  these  cases  with  our  other  knowledge  as 
to  the  structure  and  functions  of  the  spinal  cord,  it  has  been  shown  that  the  dis- 
eased portions  occupy  a  distinct  position,  even  in  their  anatomical  and  physiologi- 
cal relations.  Hence  we  are  justified  in  terming  these  affections  of  the  cord  sys- 
temic diseases.  We  can  not  at  present  give  a  correct  explanation  of  the  remark- 
able fact  that  such  isolated  diseases  may  occur  in  parts  of  the  cord  which  have 
perfectly  definite  functions,  in  "  systems  of  fibers."  We  must  imagine  that  the 
factors  which  cause  the  disease,  in  such  cases,  do  not  exert  their  influence  upon 
the  whole  cord,  but  only  upon  the  fibers  and  cells  of  a  definite  system ;  an  idea 
which  finds  a  fitting  analogy  in  the  action  of  many  poisons,  such  as  curare,  strych- 
nine, lead,  etc. 

Besides  the  systemic  diseases  there  is  a  second  group  of  affections  of  the  cord 
in  which  there  is  not,  by  any  means,  such  a  limitation  of  the  process  to  definite 
portions  of  the  cord.  In  these  cases  the  disease  extends  more  or  less  widely  over 
the  cross-section  or  the  length  of  the  cord,  and  forms  either  one  large  focus,  or 
several  single  smaller  foci,  separate  from  one  another.  To  this  group,  to  the  un- 
systemic,  diffuse  diseases  of  the  spinal  corcl,  belong  the  haemorrhages  and  trau- 
matic lesions  already  described,  and  the  new  growths,  the  acute  and  chronic 
"inflammations  "  of  the  cord  (diffuse  myelitis),  multiple  sclerosis,  etc. 

Since  in  the  diffuse  diseases  of  the  spiual  cord  all  those  portions  may  be 
affected  whose  isolated  affections  form  the  systemic  diseases,  of  course  all  the 
clinical  symptoms  of  the  latter  may  also  be  found  in  the  diffuse  affections ;  for  the 
individual  symptoms  of  spinal  disease,  as  such,  never  depend  upon  the  form  of  the 
pathological  process,  but  only  upon  its  situation,  and  upon  the  irritation  or  inter- 
ruption of  conduction  in  certain  nerve-tracts  caused  by  it.  The  diagnosis  of  spinal 
diseases,  therefore,  is,  in  the  first  place,  always  a  topical  diagnosis.  We  seek  to 
recognize,  from  the  functional  disturbances  prominent  in  the  different  cases,  the 
place  in  the  cord  in  which  the  affection  must  be  situated,  which  has  as  a  conse- 
quence these  disturbances.  By  comparing  all  the  existing  morbid  symptoms,  and 
by  attending  to  the  functions  which  are  still  normal,  we  can  decide  whether 
the  affection  is  limited  in  a  systemic  fashion  to  a  special  physiological  region,  or 
whether  it  extends  in  a  diffuse,  irregular  fashion  over  a  greater  portion  of  the 
cord.     In  the  former  case  we  usually  have  no  difficulty  in  finding  a  connection 


616  DISEASES  OF  THE  NERVOUS  SYSTEM. 

with  the  different  well-known  typical  forms  of  disease;  in  the  latter  case  we  can 
at  least  decide  the  main  point,  as  to  the  extent  and  seat  of  the  disease,  and  then, 
from  the  whole  course  and  the  combination  of  the  morbid  symptoms,  we  can  also 
draw  our  conclusions,  as  far  as  it  is  possible,  as  to  the  form  of  the  affection. 

After  these  general  remarks  we  will  pass  on  to  the  description  of  myelitis. 

iEtiology. — Hardly  anything  certain  is  known  as  to  the  causes  of  diffuse  mye- 
litis, in  the  same  way  as  little  is  known  in  regard  to  the  aetiology  of  diseases  of 
the  spinal  cord  in  general.  We  often  see  the  disease  develop  in  men  previously 
healthy,  without  being  able  to  discover  any  influence  which  may  act  as  a  cause  of 
the  disease.  In  those  cases,  too,  where  we  may  at  least  ascribe  a  possible  aetiolog- 
ical  significance  to  certain  conditions,  we  are  still  completely  in  the  dark  as  to  the 
manner  in  which  they  act. 

The  factors  which  seem  to  be  most  frequently  i*elated  to  the  development  of 
myelitis  are  as  follows :  Exposure  to  cold,  especially  repeated  wettings,  and  work- 
ing in  the  open  air  under  unfavorable  conditions ;  bodily  fatigue  and  overexer- 
tion, especially  when  combined  with  the  factors  first  named,  as  in  the  hardships 
of  war,  etc.  The  aetiological  significance  of  profound  emotions  and  sexual  ex- 
cesses, which  formerly  were  often  mentioned  in  the  aetiology  of  myelitis,  is  ex- 
tremely doubtful  as  far  as  the  development  of  anatomical  changes  in  the  cord  is 
concerned. 

The  occasional  appearance  of  spinal  disease  after  certain  acute  infectious  dis- 
eases, such  as  typhoid,  small-pox,  or  puerperal  affections,  favors  the  possibility  of 
infectious  causes;  but  these  cases  are  very  rare  in  comparison  with  the  great 
number  of  cases  of  primary  myelitis,  and  their  anatomy  is  also  but  little  known. 
Syphilis  probably  has  a  greater  importance,  although  our  knowledge  on  this 
point  is  not  so  broad  that  we  can  give  a  definite  descriptiou  of  k<  syphilis  of  the 
spinal  cord " ;  but,  at  any  rate,  it  is  quite  striking  that  in  the  history  of  patients 
with  diffuse  myelitis,  especially  in  myelitis  in  the  upper  dorsal  region,  we  quite 
often  get,  as  it  seems  to  us,  an  account  of  a  former  syphilitic  infection.  Of  course, 
in  any  individual  case,  the  actual  connection  between  the  two  diseases  can  hardly 
ever  be  proven  with  certainty. 

It  is  proven  with  regard  to  purulent  spinal  meningitis  that  inflammations  of 
neighboring  organs  may  invade  the  spinal  cord.  In  most  of  the  other  cases  which 
are  usually  cited  in  regard  to  this  point,  we  have  to  do  with  confusions  between 
lesions  of  the  cord  from  mechanical  pressure  and  actual  myelitis,  as  we  have 
explained  in  detail  in  the  previous  chapter  on  compression  of  the  cord.  Hence 
we  consider  it  unjustifiable  to  speak  of  a  "  traumatic  myelitis  "  except  in  very  rare 
cases.  If  spinal  symptoms  develop  after  an  injury,  we  usually  have  to  do  either 
with  the  type  of  symptoms  described  above  under  spinal  concussion,  or  with  genu- 
ine traumatic  lesions  of  the  vertebrae,  or  sometimes  perhaps  with  traumatic  haemor- 
rhages, etc.,  which  always  excite  disturbances  in  the  functions  of  the  spinal  cord 
by  mechanical  conditions  alone.  Finally,  in  regard  to  the  theory  of  an  "  ascend- 
ing neuritis  ''—that  is.  the  supposed  extension  of  an  inflammation  from  the  nerves 
to  the  cord— it  is  a  hypothesis  that  is  still  very  much  in  need  of  further  con- 
firmation. 

Pathological  Anatomy. — Macroscopic  examination  of  the  cord  in  its  fresh  con- 
dition shows  no  marked  pathological  changes  except  in  a  small  number  of  cases. 
At  the  first  glance,  the  spinal  cord  often  seems  almost  completely  normal,  even  if 
there  have  been  severe  spinal  symptoms  during  life,  and  sometimes  the  opacities 
and  adhesions  of  the  pia,  which  often  strike  us  at  first,  have  no  practical  importance. 
If  we  test  the  consistency  of  the  cord  carefully  by  touching  it,  of  course  a  change 
in  it  often  strikes  the  practiced  examiner,  since  the  cord  over  a  definite  extent  is 
either  softer  and  more  flexible,  or,  on  the  other  hand,  harder  and  firmer.     If  we 


ACUTE  AND  CHRONIC  MYELITIS.  617 

now  make  a  number  of  cross-sections  through  the  cord,  we  notice  that  the  sub- 
stance of  the  cord  rises  up  more  on  section,  that  the  outline  of  the  gray  matter  is 
less  distinct,  and  especially  that  the  white  matter  is  of  a  reddish-gray  color,  and 
that  sometimes  there  is  also  a  reddish,  hyperaemic  coloring  of  the  gray  matter.  In 
some  cases  we  can  recognize  small  capillary  haemorrhages  with  the  naked  eye, 
but  the  macroscopic  examination  of  the  fresh  cord  is  never  sufficient  for  the  pre- 
cise determination  of  the  extent  and  intensity  of  the  disease. 

The  changes  are  much  more  plainly  visible  if  we  harden  the  cord  in  chromic 
acid,  or  Müller's  fluid,*  for  at  least  eight  or  ten  weeks.  All  the  normal  parts  of 
the  white  matter  of  the  cord  assume  a  dark-green  color  from  the  acid,  which  is 
really  due  to  the  staining  of  the  medullary  sheaths.  The  diseased  portions,  in 
which  the  medullary  sheaths  are  mainly  if  not  entirely  absent,  are  thus  often 
very  sharply  distinguished  from  the  healthy,  dark-green  portions.  Since  similar 
differences  in  color  between  healthy  and  diseased  tissue  are  also  noticed  in  the 
gray  matter,  although  less  sharply  defined,  the  cross-section  of  the  cord,  well 
hardened  in  chromic  acid,  usually  gives  quite  a  correct  idea  of  the  extent  of  the 
disease. 

We  obtain  more  precise  disclosures,  however,  as  to  the  form  of  the  anatomical 
changes  by  microscopical  examination.  When  made  on  the  fresh,  unhardened 
cord,  it  affords  little  information.  The  presence  of  numerous  granular  cells  (vide 
infra)  in  fresh  teased-out  preparations  is  the  only  thing  that  is  important,  since 
they  show  with  certainty  the  existence  of  a  pathological  change.  If,  however,  we 
make  fine  cross-sections  of  the  hardened  cord,  and  stain  them  with  carmine  or 
some  similar  staining  fluid,  even  the  naked  eye  notices  at  first  a  marked  difference 
between  the  diseased  and  the  healthy  tissue,  since  the  former,  which  is  almost 
always  richer  in  connective  tissue,  has  a  much  darker  staining,  and  thus  is  distin- 
guished from  the  brighter  normal  tissue.  The  microscopic  examination  now  shows 
that  in  the  diseased  parts  the  normal  nerve-tissue  has  been  almost  wholly  or  at 
least  partly  destroyed.  Only  occasionally  do  we  see  nerve-fibers  of  normal  appear- 
ance remaining  here  and  there.  In  other  places  the  fibers  that  are  still  visible 
are  smaller  and  atrophied,  and  the  axis-cylinders  have  in  part  lost  their  medullary 
sheaths,  or  are  swollen.  The  changes  in  the  ganglion-cells  are  harder  to  follow, 
but  in  more  advanced  cases  they  also  show  marked  signs  of  destruction ;  they  are 
contracted,  rounder,  and  have  lost  their  processes.  The  increase  of  the  connective 
tissue  corresponds  to  the  destruction  of  the  nerve-substance.  The  meshes  of  the 
neuroglia  extend  and  swell,  so  that  the  space  formed  by  the  destruction  of  the 
nerve-tissue  is  in  great  measure  taken  up  by  connective  tissue.  The  older  the 
process,  the  firmer  and  more  fibrous  is  the  connective  tissue.  The  nuclei  of  the 
neuroglia  increase  in  number,  and  we  often  find  a  very  great  increase  in  those 
peculiar,  flat,  connective-tissue  cells  with  many  processes,  first  described  by  Dei- 
ters, and  named  after  him— the  so-called  "Deiters'  spider-cells."  The  fatty  granu- 
lar cells  are  also  easily  recognized  in  hardened  preparations,  so  long  as  they  are 
not  treated  with  alcohol.  They  lie  in  the  interstices  between  the  meshes  of  the 
neuroglia,  and  are  especially  numerous  about  the  vessels.  They  are  to  be  regarded 
either  as  white  blood-corpuscles,  or  as  endothelial  cells  from  the  sheaths  of  the 
vessels,  which  have  taken  up  the  fat  from  the  disintegrated  nerve-substance.  If, 
therefore,  the  process  be  still  fresh,  or  if  it  be  still  advancing,  the  fatty  granular 
globules  are  to  be  met  with  in  great  numbers,  while  in  old,  sclerosed  nodules,  only 
a  few  of  them,  or  scarcely  any,  are  to  be  found.  The  changes  in  the  vessels  are 
usually  very  striking.     They  are  often  dilated  and  congested.     Here  and  there 

[*  The  formula  for  Müller's  fluid  is  as  follows :  Two  and  a  half  parts  of  potassic  bichromate,  one 
part  of  sodic  sulphate,  and  one  hundred  parts  of  water. — Tkans.] 


618  DISEASES  OF  THE  NERVOUS  SYSTEM. 

there  may  be  haemorrhages.  The  vascular  walls  are  thickened,  especially  in  old 
cases,  and  sometimes  have  become  peculiarly  homogeneous — "  hyaline  degenera- 
tion " ;  and  a  large  accumulation  of  nuclei  may  be  found  about  the  vessels.  The 
so-called  corpora  amylacea  are  sometimes  present  in  great  numbers,  and  some- 
times they  are  only  scanty.  Their  significance  and  their  genesis  are  still  un- 
known. 

The  extent  of  the  whole  process  values  very  much  in  different  cases.  We 
usually  find  one  main  focus  of  myelitis,  which  extends  in  a  diffuse  manner 
over  the  greatest  part  of  the  transverse  section  of  the  spinal  cord,  and  may  reach 
upward  and  downward  for  a  space  of  five  to  ten  centimetres  or  more.  The  dor- 
sal portion  of  the  cord  is  most  frequently  affected  (dorsal  myelitis),  the  upper  half 
being  usually  most  involved,  but  in  some  cases  the  lower  half  is  chiefly  affected. 
Nearly  the  whole  of  the  dorsal  cord  is  often  the  seat  of  a  diffuse  inflammatory 
affection,  which,  of  course,  differs  in  extent  at  different  levels.  In  other  cases  the 
chief  focus  of  disease  is  in  the  cervical  cord  (cervical  myelitis),  while  it  is  most  rare 
in  the  lumbar  cord  (lumbar  myelitis).  We  often  find  small,  distinct  foci  in  the 
vicinity  of  the  main  focus.  In  all  severe  cases  there  develops  later  on  a  systemic 
ascending  and  descending  secondary  degeneration  (vide  infra). 

We  have  intentionally  avoided  any  division  of  the  process  into  different  stages, 
because,  according  to  our  present  knowledge,  this  can  be  only  artificial.  As  a 
general  rule,  the  cases  where  the  cord  is  soft  and  has  more  of  a  reddish-gray  color, 
where  the  fatty  granular  cells  are  still  abundant,  and  the  meshes  of  the  neuroglia 
are  not  yet  fibrous,  may  be  considered  as  belonging  ,to  the  comparatively  more 
acute  and  fresher  stages ;  while  in  the  older  cases  the  cord  has  become  firmer, 
"  sclerosed,"  in  the  affected  part,  through  the  formation  of  a  denser  fibrillary  con- 
nective tissue,  and  it  has  more  of  a  gray  appearance ;  but  we  can  not  draw  a  sharp 
distinction  between  acute  and  chronic  myelitis  in  regard  to  their  pathological 
anatomy.  Genuine  transverse  myelitis  always  shows  a  chronic  course,  and  many 
cases  deserve  the  name  of  "  acute  myelitis  "  in  their  clinical  aspect  only  in  so  far 
as  the  beginning  of  the  morbid  symptoms  is  acute  and  rapid.  We  may  entirely 
disregard  actual  abscess  of  the  cord,  because  it  is  so  rare  that  it  very  seldom 
comes  into  question  as  an  independent  disease.  It  is  still  undecided  whether  there 
is  a  softening  of  the  cord  analogous  to  the  foci  of  softening  in  the  brain— that  is, 
as  a  result  of  an  obstruction  of  the  vessels  by  a  thrombus  or  embolus.  At  any 
rate,  an  actual  softening  of  the  cord  is  quite  rare— that  is,  a  change  of  the  substance 
of  the  cord  into  a  soft  pulp,  which  contains  nothing  but  the  remains  of  the  nerve- 
tissue  and  some  fatty  granular  cells.  We  have  seen  ourselves  only  one  such  case, 
in  the  lower  dorsal  region,  which  lasted  two  years  as  a  chronic  transverse  myelitis, 
and  ended  fatally. 

The  Individual  Symptoms  of  Myelitis.— The  course  of  transverse  myelitis  differs 
so  much  in  the  different  cases  that  it  is  impossible  to  give  a  picture  of  the  disease 
which  will  be  generally  applicable.  According  as  one  or  another  part  of  the  cord 
is  involved,  the  clinical  symptoms  will  affect  chiefly  the  sensibility  or  the  motility, 
the  trophic  functions  or  the  reflexes,  and  will  be  present  in  the  upper  or  the  lower 
extremities,  or  in  both  at  once.  The  following  description  will,  therefore,  be 
devoted  first  to  the  single  symptoms,  and  will  give  the  inferences  which,  accord- 
ing to  the  present  state  of  our  knowledge,  may  be  drawn  from  their  presence  as  to 
the  seat  and  the  extent  of  the  anatomical  process. 

1.  Symptoms  of  Motor  Paralysis  are  not  only  the  chief  symptoms,  as  a  rule, 
in  well-developed  myelitis,  but  are  often  the  first  sign  of  the  beginning  of  the  dis- 
ease. The  patient  feels  at  first  only  a  slight  weakness  in  one  or  both  legs ;  he  gets 
tired  more  easily  in  walking,  and  begins  to  "  drag  "  his  legs  after  him.  The  motor 
weakness  gradually  becomes^greater  and  increases  to  complete  paralysis.     The 


ACUTE  AND  CHRONIC  MYELITIS.  010 

patient  is  then  bed-ridden,  and,  finally,  can  not  make  the  least  active  movement 
with  his  legs.     The  symptoms  of  paralysis  in  the  arms  are  analogous. 

Since  the  chief  paths  for  the  conduction  of  voluntary  motion  are  situated,  as 
we  have  seen,  in  the  lateral  columns  of  the  spinal  cord,  and  especially  in  the 
lateral  pyramidal  tract,  we  conclude,  in  every  spinal  disease  where  symptoms  of 
paralysis  are  present,  that  there  is  an  interruption  of  this  tract — that  is,  an 
implication  of  the  posterior  portions  of  the  lateral  columns.  Since  in  transverse 
myelitis  the  whole  cross-section  of  the  cord  is  more  or  less  involved,  the  paralysis 
also  extends  to  the  two  halves  of  the  body:  motor  paraplegia  is  the  characteristic 
form  of  paralysis  for  transverse  myelitis.  Paraplegia  of  the  lower  extremities 
may  of  course  arise  wherever  the  myelitis  is  situated,  whether  in  the  lumbar, 
dorsal,  or  cervical  region;  but  the  upper  extremities  necessarily  remain  entirely 
free  in  every  doi'sal  or  lumbar  myelitis.  The  occurrence  of  paretic  symptoms 
here,  and  the  final  development  of  a  brachial  paraplegia,  point  with  certainty  to 
an  implication  of  the  cervical  region,  to  a  cervical  myelitis.  If  the  symptoms  of 
paralysis  are  not  alike  in  the  two  corresponding  extremities,  but  are  more  marked 
on  one  side  than  on  the  other,  the  anatomical  affection  must  also  be  more  intense 
on  that  side  of  the  cord  than  on  the  opposite  side. 

2.  Symptoms  of  Motor  Irritation  of  various  sorts  are  often  seen,  both  at  the 
beginning  and  during  the  whole  course  of  myelitis.  Single  twitchings  come  on 
spontaneously  in  the  limbs,  which  are  at  the  same  time  paralyzed,  or  at  least 
paretic,  and  these  twitchings  are  short  and  rapid  or  slow  and  persistent.  The 
thighs  are  drawn  up  on  the  abdomen,  or  there  are  severe  spasms  of  the  extensors. 
The  interpretation  of  these  symptoms  is  not  always  easy.  It  is  often  particularly 
hard  to  decide  whether  they  are  the  result  of  a  direct  irritation  of  motor  fibers 
in  the  cord,  or  whether  they  represent  reflexes  {vide  infra).  The  value  of  the 
symptoms  of  motor  irritation  for  the  localisation  of  the  disease  is  accordingly 
slight,  but,  of  course,  in  these  cases  we  must  chiefly  consider  the  motor  tracts  in 
the  lateral  columns. 

Ataxia  and  intention  tremor  are  comparatively  rare,  but  they  are  most  frequent 
in  the  upper  extremities.  They  are  also  seen  in  the  stage  of  convalescence  in 
acute  cases. 

3.  Disturbances  of  Sensibility. — The  disturbances  of  sensibility  usually 
appear  to  a  marked  degree  only  in  the  later  stages  of  the  disease.  At  the  outset 
we  usually  notice  merely  mild  symptoms  of  sensory  irritation,  such  as  formication, 
prickling,  numbness,  a  woolly  feeling,  etc.,  while  severe  pain  is  hardly  ever 
present  in  transverse  myelitis,  and  hence  it  always  points  to  some  affection  of  the 
vertebrae  or  the  meninges.  Slight  diminution  of  sensibility  is  often  to  be  made 
out  early  on  careful  examination,  but,  in  many  cases,  the  sensibility  remains  for  a 
long  time  wholly,  or  almost  wholly,  intact,  either  because  the  localization  of  the 
disease  spares  the  sensory  portions  of  the  cord,  or  because  the  sensory  paths  of 
conduction  are  more  resistant,  or  can  act  vicariously  for  one  another  to  a  higher 
degree.  In  the  further  course  of  the  disease,  however,  there  are  almost  always 
more  marked  disturbances  of  sensibility:  at  first  a  simple  diminution  in  the  sensi- 
tiveness of  the  skin,  sometimes  partial  paralyses  of  sensation,  analgesia,  paralysis 
of  the  sense  of  pressure,  and  finally  frequently  a  complete  anaesthesia.  On  the 
other  hand,  we  see  in  many  cases  a  striking  hyperesthesia  to  painful  stimuli, 
such  as  a  pin-prick. 

From  the  presence  of  marked  disturbances  of  sensibility  we  can  conclude  with 
certainty  that  there  is  an  affection  of  the  posterior  columns,  and  especially  of  the 
posterior  cornua  of  the  gray  matter.  With  marked  anaesthesia  the  latter  are 
always  involved.  It  is  still  very  doubtful  whether  the  statement  made  by  Schiff, 
that  the  conduction  of  painful  sensations  is  chiefly  in  the  gray  matter,  and  the 


020  DISEASES  OF  THE  NERVOUS  SYSTEM. 

conduction  of  tactile  sensations  is  chiefly  in  the  white  matter,  holds  in  man.  The 
pathological  facts,  as  we  have  said  hefore,  also  give  no  support  at  all  to  the  theory 
that  there  are  sensory  fibers  in  the  lateral  columns  in  man. 

The  disturbance  of  sensibility  gives  important  service  in  estimating  the  height 
at  which  the  affection  in  the  cord  is  situated.  If  we  search  on  the  trunk  for  the 
line  where  the  cutaneous  sensibility  becomes  normal,  we  may  place  the  upper 
boundary  of  the  myelitis,  as  far  as  it  disturbs  the  sensibility,  at  approximately  the 
same  level.  In  myelitis  in  the  lumbar  region  the  disturbance  of  sensibility 
reaches  to  the  umbilicus,  or  even  a  little  higher ;  in  myelitis  in  the  lower  dor- 
sal region  it  reaches  about  to  the  lower  end  of  the  sternum;  in  myelitis  in  the 
upper  dorsal  region  to  the  level  of  the  axillae ;  and  in  cervical  myelitis  the  sen- 
sibility of  the  upper  extremities  is  also  impaired,  but  complete  anaesthesia  is  very 
rare. 

4.  Cutaneous  Reflexes. — As  is  well  known,  the  reflex  arcs  in  the  cord  are 
found  at  about  the  same  level  as  the  centripetal  sensory  and  the  centrifugal  motor 
fibers.  They  are  also  connected  with  fibers  which  come  from  above,  and  to  which 
must  be  ascribed  the  property  of  reflex  inhibition.  If  these  fibers  above  the  reflex 
arc  are  put  into  a  state  of  irritation,  the  reflex  is  thereby  impaired ;  but  if  the  con- 
duction be  broken  in  these  fibers,  the  reflex  activity  appears  increased,  the  reflex 
comes  on  at  a  weaker  irritation,  and  the  contraction  is  more  vigorous.  If  the 
reflex  arc  itself  be  broken  at  any  point,  the  reflex  must  disappear. 

The  data  from  the  examination  of  the  patient  may  generally  be  harmonized 
with  this  scheme,  although,  of  course,  the  reality  probably  shows  more  complicated 
conditions.  In  extensive  lumbar  myelitis,  by  which  the  reflex  path  in  the  lum- 
bar cord  is  broken,  the  cutaneous  reflexes  in  the  lower  extremities  must  be  dimin- 
ished or  absent.  In  these  cases  the  loss  of  sensibility  runs  about  parallel  to  the 
diminution  of  the  reflexes.  In  dorsal  and  cervical  myelitis,  however,  the  reflex 
arc  in  the  lumbar  cord  remains  unimpaired,  but  the  conduction  of  sensory  impres- 
sions to  the  brain  may  very  well  be  interrupted.  In  these  cases  the  cutaneous 
reflexes  are  retained,  even  when  there  is  anaesthesia;  or,  if  the  reflex  inhibitory 
influences  be  removed,  they  are  decidedly  increased.  The  cutaneous  reflexes  in 
the  legs,  however,  may  be  diminished,  even  in  disease  above  the  lumbar  cord,  in 
which  case  we  must  imagine  a  loss  of  irritability  in.  the  fibers  which  take  part  in 
the  reflex,  or  an  irritation  of  the  reflex  inhibitory  fibers.  The  cremaster  reflex 
has  its  reflex  arc  about  at  the  point  of  exit  of  the  first  lumbar  nerves ;  diseases  of 
the  cord  at  this  point  must  therefore,  under  some  circumstances,  cause  a  disappear- 
ance of  the  reflex.  Of  the  abdominal  reflexes  the  upper,  epigastric,  corresponds 
about  to  the  level  of  the  fourth  to  the  seventh  dorsal  nerves,  and  the  lower 
abdominal  reflex  proper  to  the  lower  portion  of  the  dorsal  cord. 

5.  Tendon  Reflexes. — The  same  rules  generally  hold  in  judging  of  the  ten- 
don reflexes  as  are  to  be  considered  in  judging  of  the  condition  of  the  cutaneous 
reflexes.  We  know  comparatively  little  of  the  course  of  the  reflex  arc  of  the 
patellar  reflex  in  the  lumbar  cord.  It  lies  about  at  the  levels  of  exit  of  the  second 
to  the  fourth  lumbar  nerves.  We  know,  also,  that  the  reflex  fails  as  soon  as  the 
middle  part  of  the  posterior  columns  (see  the  chapter  on  tabes  dorsalis)  or  the 
anterior  cornua  of  the  gray  matter  of  the  lumbar  cord  are  much  diseased.  The 
Achilles'  tendon  reflex,  or  the  ankle  clonus,  has  its  reflex  arc  at  the  level  of 
the  first  sacral  nerves.  It  is  always  absent  in  extensive  disease  of  the  posterior 
columns  and  of  the  gray  matter  in  the  corresponding  portion  of  the  lumbar  cord, 
so  that,  besides  the  other  symptoms,  the  absence  of  the  tendon  reflexes  in  the  lower 
extremities  is  one  of  the  most  important  points  for  the  diagnosis  of  a  myelitis  of 
the  lumbar  cord.  In  almost  all  inflammations  above  the  lumbar  cord — that  is,  in 
dorsal  and  cervical  myelitis — there  is,  however,  a  very  decided  increase  of  the 


ACUTE  AND  CHRONIC  MYELITIS.  021 

tendon  reflexes,  the  result,  as  we  must  suppose,  of  the  loss  of  the  reflex  inhibitory- 
influences.  We  have  a  certain  right  to  assume  that  the  fibers  which  influence 
the  condition  of  the  tendon  reflexes  run  chiefly  in  the  lateral  columns  of  the 
spinal  cord,  but  that  they  are  not  identical  with  the  fibers  of  the  lateral  pyramidal 
tracts  which  serve  for  voluntary  motion  (see  the  chapter  on  spastic  spinal  paraly- 
sis). We  may  therefore  assert  that,  with  a  considerable  increase  of  the  tendon 
reflexes  in  the  lower  extremities,  the  seat  of  the  myelitis  must  be  above  the 
lumbar  cord — that  is,  in  the  cervical  or  dorsal  cord — and  that  in  these  cases  we 
have  to  suppose  that  the  lateral  columns  are  chiefly  implicated.  In  cervical 
myelitis  the  tendon  reflexes  in  the  upper  extremities  are  often  considerably  in- 
creased. 

We  have  already  said,  on  page  544  et  seq.,  what  is  necessary  in  regard  to  the 
different  signs  of  the  increased  tendon  reflexes,  the  exaggerated  patellar  reflex, 
ankle  clonus,  the  periosteal  reflexes,  etc.  The  peculiar  character  which  the 
paralysis  of  the  legs  assumes  from  a  considerable  increase  of  the  tendon  reflexes 
at  the  same  time  will  be  described  more  fully  in  the  chapter  on  "  spastic  spinal 
paralysis  "  (vide  infra). 

6.  Disturbances  in  the  Bladder  and  Rectum. — Disturbances  in  micturition 
are  one  of  the  commonest  symptoms  of  myelitis.  The  first  manifestation  is  usu- 
ally a  difficulty  in  micturition ;  the  patient  has  to  strain  and  to  wait  longer  before 
urinating.  There  may  finally  be  a  complete  retention  of  urine  from  paralysis  of 
the  detrusor  urinae.  In  the  later  stages  of  the  disease,  however,  there  is  usually  a 
paralysis  of  the  sphincter  vesicas,  and  consequently  incontinence  of  urine.  The 
disturbances  of  the  bladder  give  no  points  for  the  localization  of  myelitis,  since 
they  may  occur  with  disease  at  any  level  of  the  spinal  cord ;  but  we  believe  we 
are  right  in  assuming  that  they  always  permit  us  to  decide  that  the  posterior 
columns  of  the  cord  are  involved. 

The  clinical  significance  of  disturbances  of  the  bladder  in  myelitis,  and  in 
many  other  diseases  of  the  cord,  apart  from  the  great  distress  and  discomfort  for 
the  patient,  lies  in  the  fact  that  they  very  often — almost  always  in  severe  cases — 
give  rise  to  the  development  of  cystitis.  In  retention  of  urine  the  use  of  the 
catheter,  by  which  inflammatory  irritants  are  often  brought  into  the  bladder,  in 
spite  of  all  attempts  at  disinfection,  leads  to  decomposition  of  the  urine  and  to  cys- 
titis ;  but  where  there  is  also  incontinence,  the  imperfect  closure  of  the  sphincter 
and  the  constant  presence  of  stagnating  and  decomposing  urine  in  the  urethra  are 
the  causes  of  the  entrance  of  these  irritants  into  the  bladder.  If  cystitis  have 
developed,  it  may  be  followed  under  some  circumstances  by  pyelitis  and  puru- 
lent pyelo-nephritis  (vide  infra),  which  conditions  are  often  the  immediate  cause 
of  death  from  the  sequelae  connected  with  them,  such  as  fever,  which  is  sometimes 
associated  with  chills,  general  weakness,  and  emaciation. 

Defecation  is  also  disturbed  in  many  cases  of  myelitis.  There  is  usually  con- 
stipation at  first,  which  may  depend  either  upon  weakness  of  the  intestinal  peri- 
stalsis, or  upon  paresis  of  the  abdominal  muscles.  Sometimes  the  constipation 
reaches  such  a  degree  that  the  bowels  move  only  at  intervals  of  one  or  two  weeks. 
In  many  severe  cases  there  is  finally  incontinence  of  faeces,  as  a  result  of  paralysis 
of  the  sphincter  ani.  We  can  give  no  details  as  to  the  localization  of  the  nerve- 
tracts  in  the  cord  which  take  part  in  defecation. 

We  have  yet  to  note  that  micturition  and  defecation  are  often  aroused  reflexiv 
in  an  abnormal  fashion  where  there  is  increased  reflex  irritability.  On  irritation 
of  the  skin  over  the  thighs,  the  perineum,  the  gluteal  region,  etc.,  there  is  often 
an  involuntary  contraction  of  the  bladder,  associated  with  loss  of  urine. 

In  conclusion,  we  may  mention,  as  an  addendum,  that  the  sexual  functions  are 
often  considerably  disturbed  in  many  cases  of  myelitis,  and  finally  may  be  wholly 


622 


DISEASES  OF  THE  NERVOUS  SYSTEM. 


ret. 


D. 


lost.     The  tracts  involved  here  lie  probably  chiefly  in  the  upper  lumbar  cord,  but 

their  precise  localization  (posterior  columns  ?)  is  still  unknown. 

7.  Trophic  Disturbances. — The  trophic  condition  of  the  paralyzed  muscles 

affords  extremely  important  points  for  diagnosis.     In  cervical  and  dorsal  myelitis 

the  trophic  centers  in  the  lumbar  cord  for  the  mus- 
cles of  the  legs  remain  intact ;  the  paralyzed  muscles, 
therefore,  retain  essentially  their  normal  volume, 
and  especially  their  normal  electrical  excitability. 
Even  in  such  cases  the  muscles  are  sometimes  flab- 
bier and  of  lesser  girth  than  under  normal  condi- 
tions, but  this  depends  partly  on  the  decline  in  the 
general  nutrition,  and  partly  perhaps  on  the  lack  of 
movement,  the  "atrophy  of  inactivity."  Only  occa- 
sionally do  we  find  more  marked  muscular  atrophy, 
but  it  is  of  a  simple  character  and  not  degenerative, 
and  hence  without  reaction  of  degeneration;  but  if 
we  find  in  myelitis  a  genuine  degenerative  atrophy, 
with  reaction  of  degeneration  in  the  muscles  of  the 
lower  extremities,  we  can  from  this  draw  a  definite 
conclusion  that  the  anterior  gray  cornua  or  the  fibers 
of  the  anterior  roots  in  the  lumbar  cord  are  affected 
(see  page  538).  In  an  analogous  fashion  degenera- 
tive atrophy  with  reaction  of  degeneration  in  the 
muscles  of  the  upper  extremities  points  to  an  affec- 
tion of  the  anterior  gray  matter  in  the  cervical  cord. 
Trophic  disturbances  in  the  skin  are  also  frequent, 
but  they  have  no  definite  diagnostic  significance. 
We  often  find  the  skin  dry,  hard,  with  a  scaly  epi- 
dermis, and  the  nails  thickened  and  brittle.  Excep- 
tionally there  are  eruptions  of  herpes,  urticaria,  etc. 
Vaso- motor  disturbances  also  occur.  Sometimes 
the  paralyzed  extremities  show  a  mottled,  cyanotic 
reddening,  and  feel  cold.  Slight  oedema  is  quite  fre- 
quently present  in  the  paralyzed  parts.  Disturb- 
ances of  the  s^seat  secretion  are  not  infrequent.  We 
find  either  that  it  is  absent  or  that  there  is  a  great 
increase  in  it,  so  that  the  paralyzed  parts  are  con- 
stantly moist.  All  these  symptoms  have  no  value  at 
present  for  the  special  topical  diagnosis. 

The  frequent  occurrence  of  bedsores  in  the  sacral 
region,  over  the  glutaei,  or  more  rarely  on  the  feet 
or  the  inner  side  of  the  knees,  is  of  great  practical 
importance.  Although  trophic  and  vaso-motor  in- 
fluences may  play  a  part  in  their  origin,  still  their 
ultimate  cause  is  always  to  be  found  in  external 
conditions,  pressure,  uncleanliness,  etc.  The  more 
faulty  the  care  of  the  patient  is,  the  easier  bedsores 
arise.  With  completely  paralyzed  and  anaesthetic 
patients,  with  incontinence  of  urine  and  faeces,  of 
course  they  sometimes  can  not  be  wholly  and  per- 
manently avoided,  even  with  the  most  careful  man- 

Fig.  83.— A  diagram  designed  to    agement.     The  extent  to  which  a  bedsore  may  reach 

show  the  relations  of  the  verte-      .  ,.  -,       ■,    ,   i        a  •    -,  ,  n   ■,  at  j 

bra?  to  ths  spinal  segments.  is    sometimes    absolutely   frightful.      A  large   part 


10 

11 
!2 


M 


m 


1  L 


t 


J 


_     1  S 


-  ■  3 


ACUTE  AND   CHRONIC  MYELITIS. 


023 


of  the  sacrum  may  be  laid  bare,  after  the  overlying  soft  parts  and  the  periosteum 
have  become  gangrenous  and  been  thrown  off. 

8.  Disturbances  in  the  Region  op  the  Cerebral  Nerves  are  entirely  absent 
in  most  cases  of  transverse  myelitis.  In  rare  cases  of  cervical  myelitis  the  process 
may  gradually  extend  up- 
ward and  give  rise  to  bulbar 
symptoms.  We  sometimes 
see  changes  in  the  pupils 
also  in  cervical  myelitis,  such 
as  inequality  and  spinal  my- 
osis ;  and  finally  myelitis  has 
been  repeatedly  found  com- 
bined with  an  optic  neuritis. 

Different  Forms  of  Mye- 
litis, Course  of  the  Disease, 
and  Diagnosis.— The  whole 
picture  of  transverse  myeli- 
tis in  its  different  forms  may 
be  constructed  from  the 
symptoms  described  in  detail 
in  the  preceding  paragraphs. 
We  can  usually  determine 
without  difficulty,  at  least 
approximately,  the  seat  and 
extent  of  the  disease.  If  we 
group  the  chief  symptoms  of 
the  different  forms  of  mye- 
litis together,  they  are  as 
follows : 

Cervical  Myelitis. — Par- 
aplegia of  the  legs,  combined 
with  more  or  less  extensive 
disturbances  in  the  upper 
extremities,  and  eventually 
disturbances  of  sensibility 
over  a  like  extent.  At  times  atrophy  of  single  muscular  regions  in  the  arms. 
Muscles  of  the  legs  not  materially  atrophied.  Increased  tendon  reflexes  and  spas- 
tic symptoms  in  the  legs  and  often  in  the  arms.  Cutaneous  reflexes  in  the  legs 
retained,  and  sometimes  even  increased.  Disturbances  of  the  bladder  and  rectum. 
Sometimes  changes  in  the  pupils. 

Dorsal  Myelitis. — Upper  extremities  free.  Motor,  and  eventually  sensory, 
paraplegia  of  the  legs,  without  degenerative  atrophy.  Increased  tendon  reflexes, 
especially  strong  in  myelitis  in  the  upper  dorsal  cord ;  cutaneous  reflexes  retained, 
rarely  increased.     Disturbances  of  the  bladder  and  rectum. 

Lumbar  Myelitis. — Upper  extremities  free.  Motor,  and  eventually  sensory 
paraplegia  of  the  legs.  Cutaneous  and  tendon  reflexes  in  the  legs  diminished  or 
absent.  Under  some  circumstances  degenerative  muscular  atrophy,  with  reaction 
of  degeneration.     Disturbances  of  the  bladder  and  rectum. 

[In  view  of  the  increasing  importance  of  exact  localization  of  lesions  of  the 
spinal  cord  with  regard  to  surgical  interference  we  have  thought  it  best  to  add 
Starr's  tables,  as  modified  by  Herter,  showing  the  functions  of  the  segments  of  the 
spinal  cord  at  the  level  of  the  various  nerve-roots,  and  Starr's  recent  diagrams 
which  show  the  sensory  distribution  of  the  different  lumbar  and  sacral  roots  (see 


Fig.  84.—  Areas  of  anaesthesia  in  lesions  at  various  levels  of  the  spi- 
nal cord  from  sacral  v.  to  lumbar  n.  I,  Sacral  v.  II,  Sacral  iv. 
III.  Sacral  in.  IV,  Sacral  i.  V,  Lumbar  v.  VI,  Lumbar  in. 
VII,  Lumbar  u. 


624 


DISEASES  OF  THE  NERVOUS  SYSTEM. 


Fig.  84).  These,  with  the  accompanying  illustration  (Fig.  83),  showing  the  rela- 
tion of  the  vertebra?  to  the  nerve-roots,  will  serve  as  a  guide  to  the  exact  locali- 
zation of  the  lesion  in  cases  which  may  require  surgical  interference,  such  as  cases 
of  meningeal  hasmorrhage,  fracture,  caries,  or  new  growths. — K.] 

LOCALIZATION  OF  THE  FUNCTIONS  OF  THE  SEGMENTS  OF  THE  SPINAL  CORD. 


Segment 
of  Cord. 


Second 
and  third 
cervical. 


Fourth 
cervical, 


Fifth 
cervical. 


Sixth 
cervical. 


Seventh 
cervical. 


Eighth 
cervical. 


First 
dorsal. 


Second 
dorsal. 

Second 

to  twelfth 

dorsal. 


First 
lumbar. 


Second 
lumbar. 


Third 
lumbar. 


Occipitalis  major  and 

minor. 
Auricularis  magnus. 
Superficialis  colli. 
Supra-clavicular. 

Supra-clavicular. 
Circumflex. 
Musculocutaneous. 
Musculo  -  spiral     (ra- 
dial). 

Supra-clavicular. 
Circumflex. 
External  cutaneous. 
Internal  cutaneous. 
Post,  spinal  branches. 


External  and  internal 

cutaneous. 
Radial. 


External  and  internal 

cutaneous. 
Radial. 
Median. 
Post,  spinal  branches. 


Internal  cutaneous. 
Ulnar. 


Internal     cutaneous 
nerve  of  Wrisberg. 


Intercosto-humeral. 


Intercostals  and  dor- 
sal posterior  nerves. 


Ilio-hypogastric. 
Ilioinguinal. 

Genito-crural. 
External  cutaneous. 

Anterior. 

Crural. 

Internal  cutaneous. 

Long  saphenous. 

Obturator. 


Muscles. 


Sterno-mastoid. 
Trapezius. 

Scaleni  and  neck  mus- 
cles. 
Diaphragm. 

Diaphragm. 
Supra-  and  infraspina- 
tus. 
Deltoid. 

Supinator  longus. 
Rhomboidei. 

Deltoid. 

Biceps  and  coraco- 
brachialis. 

Supinator  longus  and 
brevis. 

Rhomboidei. 

Deep  muscles  of  shoul- 
der-blade. 

Pectoralis  (clavicular 
part). 

Teres  minor. 

Serratus  magnus. 

Brachialis  anticus. 

Biceps. 

Brachialis  anticus. 
Pectoralis      (clavicular 

part). 
Subscapular. 
Serratus  magnus. 
Triceps. 
Extensors  of  wrist  and 

fingers. 
Pronators. 

Triceps  (long  head). 
Extensors  of  wrist  and 

fingers. 
Pronators. 
Flexors  of  wrist. 
Subscapular. 
Pectoralis  (costal  part). 
Serratus  magnus. 
Latissimus  dorsi. 
Teres  major. 

Triceps  (long  head). 
Flexors    of    wrist    and 

fingers. 
Small  muscles  of  hand. 

Extensors  of  thumb. 
Small  muscles  of  hand. 
Thenar  and  hypothenar 
muscles. 


Muscles  of  back  and  ab- 
domen. 
Erectores  spina?. 


Ilio-psoas. 
Sartorius. 
Rectus. 

Ilio-psoas. 
Sartorius. 

Quadriceps  femoris. 
Quadriceps  femoris. 
Anterior  part  of  biceps. 
Inner  rotators  of  thigh. 
Adductors  of  thigh. 


Sensory  Areas. 


Reflexes. 


Neck    and 
head. 


Neck. 


back    of 


Superior    surface    of 

shoulder. 
Outer  surface  of  arm. 


Back  of  shoulder  and 

arm. 
Outer  side  of  arm  and 

forearm. 


Outer  side  and  front 

of  forearm. 
Back  of  hand  (radial 

distribution). 


Radial    and     median 
distribution. 


Inner  side  of  arm  and 

forearm. 
Ulnar  area  of  hand. 

Inner  side  of  arm  and 
forearm. 


Inner  side  of  arm  near 
axilla. 

Skin  of  back  and  up- 
per glutseal  region, 
and  of  breast  and 
abdomen,  in  bands 
running  downward 
and  forward. 

Skin  over  groin  and 
front  of  scrotum. 

Outer  surface  of  thigh. 


Anterior    surface    of 
thigh. 


Hypochondrium  (?). 


Cilio  -  spinal  (fourth 
cervical  to  second 
dorsal). 


Scapular  (fifth  cervical 

to  first  dorsal). 
Biceps  jerk. 
Supinator  jerk. 


Elbow  jerk  (triceps). 
Wrist  jerk. 


Palmar   (seventh  cer- 
vical to  first  dorsal). 


Epigastric  (fourth  to 
seventh  dorsal). 

Abdominal  (seventh  to 
eleventh  dorsal). 


Cremasteric    (first    to 
third  lumbar). 


Knee  jerk. 


ACUTE  AND   CHRONIC   MYELITUS. 


625 


Segment 
of  Cord. 

Nerves. 

Muscles.                     Sensory  Areas. 

Reflexes. 

Fourth 
lumbar. 

Internal  cutaneous. 
Long  saphenous. 
Obturator. 

Adductors  of  thigh. 
Abductors  of  thigh. 
Flexors  of  knee. 
Tibialis  anticus. 
Peroneus  longus. 

Inner  si<l<-  of  thigh, 
leg,  and  foot. 

GHutaeal  (fourth  to  fifth 

lumbar). 

Fifth 
lumbar. 

External  popliteal. 
External  saphenous. 
Musculocutaneous. 
Plantar. 

Outward     rotators     of 

thigh. 
Flexors  of  knee. 
Flexors  of  ankle. 
Extensors  of  toes. 
Peronei. 

Outer  and  back  side 

of  leg  .'iinl  root. 
Sole  of  foot. 

Ankle  clonus. 

First  and 
second 
sacral. 

Same  as  fifth  lumbar. 

Flexors    and   extensors 

of  ankle. 
Long  flexor  of  toes. 
Small  foot  muscles. 

Same  as  fifth  lumbar. 

Plantar  (fifth  lumbar 
to  second  sacral;. 

Third, 

fourth, 

and  fifth 

sacral. 

Small  sciatic. 

Pudic. 

Inferior  hemorrhoidal 

Inferior  pudendal. 

Perineal. 

Muscles  of  bladder,  rec- 
tum,    and     external 
genitals. 

Back  of  thigh,  anus, 
perineum,  and  gen- 
ital organs. 

Vesical  and  anal  cen- 
ters. 

Fifth  sa- 
cral and 
coccyg- 
eal. 

Coccygeal. 

Coccygeus. 

Skin  about  anus  and 
coccyx. 

The  whole  course  of  myelitis  is  almost  always  chronic.  We  consider  it  im- 
possible, as  we  have  said,  to  make  a  sharp  distinction  between  acute  and  chronic 
myelitis.  Many  cases,  of  course,  show  quite  a  rapid  beginning,  so  that  severe 
spinal  symptoms  develop  in  a  few  weeks.  Such  cases  may  be  termed  acute  mye- 
litis, but  their  further  course  is  almost  always  chronic.  In  only  a  few  cases  do 
the  morbid  symptoms  come  on  suddenly,  progress  rapidly,  and  speedily  prove 
fatal.  In  such  cases  the  autopsy  shows  a  true  acute  inflammation  of  the  spinal 
cord  which  is  often  disseminated.  Sometimes  the  severe  initial  symptoms  may 
after  a  certain  time  subside.  There  then  remains  a  more  or  less  severe,  quite 
pronounced  stationary  type  of  spinal  disease.  In  such  cases  the  acute  myelitis 
has  healed,  but  the  resultant  cicatrization  (contraction)  is  the  cause  of  the  per- 
manent symptoms. 

True  chronic  myelitis  begins  very  gradually  from  the  start,  and  in  some  cases 
only  after  years  results  in  complete  paraplegia. 

As  a  rule,  the  disease  begins  with  motor  symptoms,  either  in  one  leg  or  in  both 
at  about  the  same  time.  The  paresis  gradually  increases  more  and  more,  spastic 
symptoms  set  in,  and  symptoms  of  sensory  irritation,  such  as  formication,  and  also 
disturbances  of  the  bladder,  etc.  The  sensibility  is  sometimes  a  little  blunted 
quite  early,  but  it  is  almost  always  retained  for  a  longer  time  than  the  motility. 
Only  in  the  last  stages  is  complete  ansesthesia  common.  The  whole  duration  of 
the  disease  is  seldom  under  a  year,  and  it  often  lasts  two  or  three  years,  or  even 
longer.  Remissions,  apparent  halts,  and  improvements  are  not  infrequent,  and 
the  condition  often  becomes  rapidly  worse.  Recoveries  are  not  impossible,  but 
they  are  rare,  at  any  rate.  We  know  of  no  case  that  recovered  where  the  diag- 
nosis could  be  made  with  certainty.  The  cases  reported  where  a  recovery  is 
claimed  are  usually  cases  of  pressure  paralysis,  multiple  neuritis,  poliomyelitis, 
etc.  The  fatal  termination  is  the  result  of  the  general  weakness  which  finally  sets 
in ;  or  it  comes  from  cystitis  or  pyelo-nephritis,  both  of  which  are  often  combined 
with  pyaemic  conditions ;  or  from  extensive  bedsores ;  or  finally  from  some  com- 
plications, such  as  tuberculosis  or  acute  diseases. 

The  diagnosis  of  diffuse  transverse  myelitis  is  always  made  by  considering  the 
whole  group  of  symptoms  prominent  in  the  individual  case.  The  possibility  of  a 
compression  of  the  cord  must  be  excluded  by  a  careful  examination  of  the  verte- 
bral column,  and  by  consideration  of  the  course  of  the  disease.  We  must  also  be 
sure  that  the  existing  symptoms  do  not  correspond  to  a  definite  typical  disease,  or 
40 


026  DISEASES  OF  THE  NERVOUS  SYSTEM. 

a  systemic  disease,  but  that  they  can  agree  only  with  the  assumption  of  an  ex- 
tensive diffuse  disease  at  a  certain  point  in  the  cord,  to  be  made  out  accurately 
according  to  the  symptoms.  The  further  distinction,  as  to  whether  this  diffuse 
disease  js  a  myelitis,  can  of  course  hardly  ever  be  made  with  absolute  certainty, 
since  diffuse  new  growths  and  the  formation  of  cavities  in  the  spinal  cord  must 
cause  precisely  the  same  symptoms.  In  these  cases  the  decision  can  be  made  only 
by  considering  the  whole  course  of  the  disease,  and  by  the  physician's  individual 
acuteness  in  diagnosis.  It  is  also  still  impossible  at  present  to  formulate  with 
certainty  the  differential  diagnosis  between  diffuse  myelitis  and  certain  combined 
fascicular  or  systemic  diseases  of  the  spinal  cord  (vide  infra). 

Treatment. — Although  our  therapeutic  endeavors  may  rarely  hope  for  a  per- 
manent and  complete  success,  still  in  many  cases  the  treatment  can  relieve  the 
suffering  and  delay  the  end. 

We  can  try  to  meet  the  causal  indication  in  cases  where  the  history  or  the 
examination  shows  syphilis.  Even  if  the  connection  between  this  and  myelitis 
can  not  be  assumed  with  certainty,  which  is  usually  the  case,  still  we  must  always 
try  inunction  thoroughly,  using  half  a  drachm  to  a  drachm  (grm.  2-5)  of  mercurial 
ointment  a  day.  We  give  twenty  to  thirty  grains  (grm.  1*5-2)  of  iodide  of  po- 
tassium daily  at  the  same  time.  We  sometimes  see  decided  improvement  from 
this;  but  in  some  cases,  of  course,  the  result  is  uncertain,  or  the  treatment  seems 
to  exert  even  an  unfavorable  influence  upon  the  disease.  In  the  latter  case  we 
must  stop  it  at  once. 

Of  the  other  methods  of  treatment  the  chief  are  electricity,  baths,  and  cold- 
water  cures.  We  alternate  with  these.  New  attempts  at  cure  raise  the  patient's 
courage  and  hope  afresh. 

Electricity  may  give  improvement  in  many  cases,  but  of  course  it  causes  recov- 
ery only  exceptionally,  at  most.  In  severe  and  hopeless  cases,  however,  it  is  at 
least  the  best  means  of  consoling  the  patient.  The  constant  current  has  the  great- 
est therapeutic  value.  We  use  large  electrodes  placed  on  the  vertebral  column, 
and  pass  not  too  strong  a  stabile  or  slowly  labile  current  through  the  cord  for 
about  four  or  five  minutes,  chiefly  through  the  region  where  we  suppose  the  seat 
of  the  disease  to  be.  We  usually  take  the  ascending  current,  and  alternate  with 
the  two  poles  on  the  diseased  part.  We  should  avoid  changes  and  great  varia- 
tions in  the  current.  We  associate  with  this  peripheral  galvanization,  and  often 
faradization  of  the  muscles  and  nerves  of  the  paralyzed  extremities.  Single 
symptoms  sometimes  deserve  special  attention — faradization  of  the  skin  in  anaes- 
thesia, galvanization  of  the  bladder  in  vesical  weakness,  etc.  The  sittings  should 
take  place  daily  or  every  other  day.  If  we  would  be  successful,  the  treatment 
must  be  kept  up  persistently  for  months. 

The  treatment  of  myelitis  by  baths,  if  prudently  used,  may  also  be  of  evident 
service.  Even  simple  tub-baths,  such  as  can  be  had  in  almost  every  household, 
do  good  service  under  some  circumstances.  The  chief  rules  are  never  to  make  the 
baths  too  warm — about  85°  or  90°  at  most  (24°-26°  R) — to  limit  them  at  first  to  ten 
or  fifteen  minutes,  and  to  give  them  at  first  not  offener  than  three  or  four  times 
a  week.  If  the  baths  are  well  borne,  they  can  be  employed  daily.  We  should 
be  most  cautious  in  incipient  and  still  advancing  cases.  The  best  action  of  the 
simple  warm  bath  is  seen  in  chronic  myelitis  with  predominant  spastic  symptoms. 
In  these  cases  the  duration  of  the  baths  may  be  increased  to  an  hour  or  more. 
Sometimes  the  baths  work  still  better  than  baths  of  simple  water  when  certain 
substances  are  added,  especially  salt  baths,  which  are  made  by  the  addition  of  five 
or  ten  pounds  of  common  salt  (Stassfurt  salt),  or  four  to  six  pounds  of  brine  salt, 
or  one  to  three  quarts  of  brine  to  the  water.  By  bringing  carbonic  acid  into  the 
water  by  a  perforated  tube  in  the  floor  of  the  tub  we  can  easily  make  "  artificial 


MULTIPLE  SCLEROSIS  OF  THE  BRAIN   AND  SPINAL  CORD.  027 

Rehme  baths,"  which  were  formerly  often  used  with  good  success  in   the  clinique 
in  Leipsic. 

If  we  can  send  patients  in  easy  circumstances  to  a  health  resort,  the  carbonic 
acid  thermal  salt  springs  at  Rehme  and  Nauheim  are  most  suitable  for  this  pur- 
pose, and  also  sometimes  mud-baths  such  as  Marienbad  and  Elster,  and  the  ther- 
mal baths  of  Ragatz,  Teplitz,  Wildbacl,  Gastein,  or  Wiesbaden. 

A  methodical  cold-water  treatment  sometimes  gives  quite  good  results;  but  in 
these  cases  we  should  wholly  avoid  all  the  more  heroic  treatment  such  as  douches, 
violent  rubbing,  and  very  cold  baths,  and  employ  only  short,  cool,  full  or  balf 
baths,  or  mild  cold  sponging.  Hydrotherapeutics  are  usually  combined  with  elec- 
tricity. 

We  can  expect  but  little  success  from  internal  treatment,  but  it  can  not  be  dis- 
pensed with  in  practice.  Ergotine,  strychnine  (also  given  subcutaneously),  iodide 
of  potassium,  and  nitrate  of  silver  are  most  to  be  recommended. 

The  general  hygienic  and  symptomatic  treatment  is  very  important.  If  the 
first  symptoms  of  a  beginning  spinal  disease  show  themselves,  we  should  urgently 
advise  the  patient  to  take  the  best  possible  physical  care  of  himself,  and  recom- 
mend mental  rest.  The  diet  should  be  strengthening  but  easily  digestible.  Large 
amounts  of  spirits,  much  smoking,  much  tea  and  coffee,  etc.,  are  to  be  avoided.  If 
the  patient  becomes  bedridden,  we  must  first  employ  the  utmost  care  to  get  a  good 
bed  in  order  to  guard  against  bedsores.  In  severe  cases,  especially  where  there 
are  disturbances  of  sensibility,  a  water-cushion  is  most  desirable.  The  patient's 
position  must  also  be  frequently  changed,  and  the  sacral  region  must  often  be 
washed  and  rubbed.  Every  incipient  bedsore  must  be  very  carefully  treated  by 
Peruvian-balsam  ointment  (1  to  30)  or  iodoform,  in  order  to  prevent  its  spreading. 
When  the  bedsore  is  very  extensive  the  continuous  bath  is  the  best  remedy. 

If  there  is  retention  of  urine  and  the  patient  has  to  be  catheterized,  the  most 
extreme  care  must  be  employed  in  cleaning  and  disinfecting  the  catheter,  or  else 
cystitis  will  develop  in  a  few  days.  If  it  does,  it  is  best  in  severe  cases  to  wash  out 
the  bladder  regularly  with  acetate  of  lead  (1  to  1,000)  and  like  remedies.  In  milder 
cases  we  may  try  chlorate  of  potassium  internally,  fifty  to  seventy-five  grains  a 
day  (grm.  3-5),  astringents,  or  balsams.  If  there  is  complete  incontinence  it  is 
advisable  to  introduce  a  permanent  catheter  (sonde  ä  demeure)  into  the  bladder — 
that  is,  a  Nelaton's  catheter,  which  lies  in  the  bladder  and  is  fastened  to  the  thighs 
by  strips  of  plaster.  The  urine  runs  away  through  a  rubber  tube,  and  we  avoid 
the  constant  wetting  of  the  skin  and  linen. 

Constipation  must  be  met  according  to  the  general  rules.  We  should  be  as 
sparing  as  possible  with  cathartics  at  first,  and  try  to  make  an  appropriate  diet  and 
enemata  suffice.  If  there  is  sevei^e  pain,  subcutaneous  injections  of  morphine  are 
unavoidable,  but  we  always  delay  this  as  long  as  possible,  although  finally  we  let 
the  dose  of  morphine  be  unlimited  in  hopeless  cases. 


CHAPTER  V. 

MULTIPLE    SCLEROSIS  OF   THE    BRAIN  AND   SPINAL   CORD. 

(Disseminated  Nodular  Sclerosis.     Sclerose  en  plaques.) 

iEtiology  and  Pathology. — Multiple  sclerosis  of  the  central  nervous  system  is  a 
special  chronic  form  of  disease,  whose  anatomical  basis  consists  in  the  develop- 
ment of  numerous  disseminated  "  sclerotic  nodules  "  (vide  infra)  in  the  brain  and 


628 


DISEASES  OF  THE  NERVOUS  SYSTEM. 


cord.  We  know  practically  nothing  as  to  its  aetiology,  for  the  significance  of 
exposure  to  cold,  overexertion,  and  mental  emotions,  sometimes  given  as  causes  of 
the  disease,  is  wholly  doubtful.  It  is  also  still  undecided  whether  syphilis  plays 
any  part  in  the  aetiology  of  multiple  sclerosis.  A  hereditary  predisposition  seems 
to  be  prominent  in  some  cases.  [Marie  lays  stress  upon  acute  infectious  disease  as 
a  possible  cause. — K.]  The  affection  occurs  chiefly  in  youth,  somewhere  between 
the  ages  of  eighteen  and  thirty-five,  but  we  have  ourselves  seen 
one  case,  which  came  to  an  autopsy,  in  a  man  of  sixty.  The 
disease  also  occurs  in  children.  No  material  distinction  has 
been  made  out  as  to  sex. 

In  regard  to  the  development  of  the  different  sclerotic  nod- 
ules, nothing  definite  has  been  established  at  present  as  to  their 
genesis.  Various  reasons  lead  us  to  favor  the  theory  that  the 
disease  depends  upon  anomalies  in  the  vessels,  but  the  proof  of 
this  can  not  yet  be  given.  The  nodules  are  in  part  easy  to  rec- 
ognize with  the  naked  eye,  from  their  gray  color,  and  we  can 
also  feel  an  increased  resistance.  They  are  scattered  over  the 
whole  central  nervous  system.  Their  favorite  seats  in  the  brain 
are  the  centrum  ovale,  the  walls  of  the  lateral  ventricles,  and 
the  corpus  callosum ;  the  nodules  are  also  quite  abundant  in  the 
pons,  less  frequent  in  the  medulla,  and  very  abundant  and 
variously  distributed  in  the  cord  (see  Figs.  85  and  86),  and  chiefly 
in  its  white  substance.  Examined  microscopically,  the  nodules 
consist  of  an  abundant,  reticulated,  fibrillary  connective  tissue, 
which  is  traversed  only  by  comparatively  few  nerve-fibers  that 
are  preserved.  In  the  vessels  we  notice  first  an  increase  in  nu- 
clei, and  later  usually  a  thickening  of  the  walls.  Fatty  granu 
lar  cells  are  always  present  in  fresh  cases.  Charcot  first  made 
the  statement,  since  confirmed  by  other  observers,  that  the  axis- 


Fig.  85.— Example  of 
disease  of  the  cord 
in  multiple  sclero- 
sis. The  dark  por- 
l  ions  are  the  parts 
diseased. 


Fig.  86.— Distribution  of  the  sclerosed  nodules  on  the  surface  of  the  pons. 
(From  Leube.; 


cylinders  are  preserved  in  the  nodules  for  a  remarkably  long  time,  even  after  the 
destruction  of  the  medullary  sheaths.  Perhaps  this  is  connected  with  the  fact  that 
secondary  degeneration  in  the  cord  is  strikingly  absent. 

Clinical  History. — From  the  variations  which  the  number  and  the  localization 
of  the  nodules  show,  it  may  be  understood  from  the  outset  that  a  type  of  the  dis- 


MULTIPLE  SCLEROSIS  OF  THE  BRAIN  AND  SPINAL  CORD.  629 

ease  which  represents  all  cases  can  not  exist;  but  a  comparison  of  a  number  of 
cases  taken  together  always  shows  so  characteristic  a  group  of  symptoms  that  the 
diagnosis  can  often  be  made  with  quite  great  certainty.  We  will  first  describe 
this  typical  form  of  disease,  for  the  knowledge  of  which  we  must  thank  Charcot 
chiefly,  and  to  that  we  will  add  some  remarks  upon  the  cases  which  differ  from 
this  type  ("  formes  frustes  "),  which  are  by  no  means  very  rare. 

The  symptom  of  the  typical  cases  of  nodular  sclerosis  which  we  must  first 
mention  is  tremor.  This  has  been  the  reason  why  multiple  sclerosis  has  formerly 
been  repeatedly  confounded  with  paralysis  agitans,  although  the  tremor  in  the  two 
diseases  shows  entirely  different  peculiarities.  In  distinction  from  the  constant 
rhythmical  oscillations  of  the  limbs  in  paralysis  agitans  (vide  infra),  the  tremor  in 
multiple  sclerosis  comes  on  only  with  intended  movements— "intention  tremor" — 
and  usually  does  not  show  a  perfectly  regular  rhythmical  character,  but  is  unequal 
and  jerking,  although  the  intended  direction  of  the  motion  is,  on  the  whole, 
always  retained.  The  tremor  is  most  marked  in  the  upper  extremities,  as  shown 
when  the  patient  tries  to  take  hold  of  a  certain  object,  to  bring  a  glass  of  water  to 
his  mouth,  to  bring  the  tips  of  the  forefingers  together,  etc. ;  but  the  tremor  also 
occurs  in  the  head,  in  the  trunk,  and  in  the  lower  extremities.  When  the  patient 
is  perfectly  quiet  the  tremor  ceases  entirely.  Only  a  few  exceptions  to  this  rule 
have  been  known.  If  the  patient  be  mentally  excited  the  tremor  usually  becomes 
more  marked.  We  know  nothing  as  to  its  peculiar  cause.  We  are  ourselves 
most  disposed  to  assume  that  it  is  due  to  an  abnormal  cross-conduction  of  irrita- 
tion from  one  fiber  to  neighboring  fibers.  The  possibility  of  such  an  abnormal 
cross-conduction  seems  to  us  to  be  due  to  the  loss  of  medullary  sheaths  in  the 
sclerotic  nodules,  with  persistence  of  the  axis-cylinders  (vide  supra).  At  any  rate, 
the  anatomical  fact  of  the  persistence  of  the  axis-cylinders  in  the  sclerotic  nodules 
seems  to  have  some  relation  to  the  clinical  symptom  that,  as  a  rule,  in  multiple 
sclerosis  we  do  not  see  real  paralyses  but  other  motor  disturbances,  especially  the 
pronounced  intention  tremor. 

Two  other  symptoms  which  often  occur  in  nodular  sclerosis  are  to  a  certain 
degree  analogous  to  the  tremor — a  peculiar  disturbance  of  speech,  and  nystagmus. 
The  disturbance  of  speech  depends  upon  disturbances  in  the  motor  innervation  of 
the  organs  of  speech,  the  tongue  and  larynx,  and  may  probably  be  referred  to  the 
presence  of  sclerotic  nodules  in  the  pons  and  medulla.  The  speech  is  slow,  "  scan- 
ning," obscure,  and  finally  sometimes  almost  incomprehensible.  The  equality  in 
the  pitch  is  often  very  striking.  We  often  notice  tremulous  movements  in  the 
tongue  and  the  lips  on  speaking:  Nystagmus  shows  itself  in  the  form  of  slight 
and  usually  lateral  twitchings  of  the  eyeballs  on  fixation,  or  on  intended  ocular 
movements. 

Other  motor  disturbances  are  usually  present  besides  the  symptoms  thus  far  de- 
scribed. 

In  many  cases  the  crude  strength  of  the  muscles  is  for  a  long  time  completely 
normal,  but  in  other  cases  there  is  a  marked  paresis,  which  sometimes  increases  to 
complete  paralysis.  The  "  spastic  symptoms,"  however,  are  far  more  characteristic 
and  more  frequent  (see  the  chapter  on  "spastic  spinal  paralysis").  These  depend, 
in  great  part  at  least,  upon  the  very  considerable  increase  in  the  tendon  reflexes, 
which  is  almost  always  present.  In  the  upper  extremities  the  spastic  symptoms 
are  less  prominent,  but  even  here  we  almost  always  find  very  vigorous  tendon 
and  periosteal  reflexes  on  striking  the  lower  ends  of  the  bones  of  the  forearm  or 
the  tendon  of  the  biceps  or  triceps.  In  the  lower  extremities  we  see  not  only 
marked  patellar  reflex  and  a  very  intense  and  persistent  ankle  clonus  (formerly 
given  the  unsuitable  name  of  "  spinal  epilepsy  "),  but  very  often  a  pronounced  tonic 
rigidity  of  the  two  legs.     Passive  motion  is  difficult,  and  the  gait  is  completely 


030  DISEASES  OF  THE  NERVOUS  SYSTEM. 

spastic.  If  there  is  at  the  same  time  a  marked  paresis  in  the  legs,  the  gait,  although 
stiff,  is  also  dragging— a  paretic-spastic  gait.  The  disturbances  of  sensibility  are 
usually  remarkably  subordinate  in  multiple  sclerosis.  Only  rarely  do  we  find  a 
blunting  of  sensation,  and  quite  exceptionally  marked  anaesthesia.  The  cutaneous 
reflexes  usually  remain  completely  normal.  Of  the  disturbances  of  the  organs  of 
the  special  senses  we  have  still  to  mention  that  optic  atrophy  has  often  been  seen, 
associated  with  considerable  disturbance  of  vision,  such  as  amblyopia  or  achroma- 
topsia, or  even  with  complete  blindness.  Optic  neuritis  with  a  subsequent  atrophy 
also  occurs,  especially  in  the  temporal  halves  of  the  papillae,  according  to  Gnauck. 
Finally,  we  sometimes  see  anomalies  in  the  innervation  of  the  ocular  muscles,  and 
diplopia  caused  by  these  anomalies. 

In  one  class  of  cases  there  are  certain  cerebral  symptoms  which  may  be  impor- 
tant with  regard  to  diagnosis.  In  the  course  of  the  disease  there  often  appears  a 
certain  mental  weakness,  an  imbecility,  which  sometimes  increases  to  marked 
dementia.  Conditions  of  melancholy  or  exaltation  are  much  rarer.  We  must 
also  mention  the  occurrence  of  apoplectiform  attacks.  After  slight  prodromal 
symptoms,  such  as  headache  and  vertigo,  loss  of  consciousness  and  hemiplegia  come 
on  quite  suddenly.  With  this  the  face  is  usually  red,  the  pulse  is  frequent,  and 
the  temperature  may  rise  to  104°  or  106°  (40°-41°  C).  After  a  day  or  two  the  con- 
sciousness gradually  returns,  and  the  hemiplegia  soon  disappears.  Epileptiform 
attacks  are  much  rarer.  We  saw  these  repeatedly  in  a  typical  case ;  they  were 
mainly  unilateral,  and  were  followed  by  a  hemiplegia  which  soon  passed  away. 
The  precise  cause  of  these  attacks  is  still  wholly  unknowu.  Vertigo  or  giddiness 
is  a  frequent  cerebral  symptom,  which  may  develop  even  in  the  earlier  stages  of 
the  disease,  and  often  comes  on  paroxysmally. 

Symptoms  on  the  part  of  the  bladder,  the  rectum,  or  the  genital  organs,  are 
usually  entirely  absent  in  the  typical  cases,  or  they  appear  only  toward  the  close 
of  the  disease.     Trophic  disturbances,  such  as  muscular  atrophy,  are  also  rare. 

In  regard  to  the  general  course  of  typical  cases,  the  disease  develops  very  slowly 
and  gradually.  Motor  symptoms,  tremor,  paresis,  and  disturbances  in  gait,  usually 
appear  in  the  lower  extremities  first.  The  patient  often  complains  at  the  same 
time  of  occasional  headache  and  vertigo.  The  speech  gradually  becomes  more 
indistinct,  the  intelligence  weaker,  and  the  other  symptoms  of  the  disease  described 
above  develop.  The  affection  almost  always  lasts  for  years  and  years.  Variations, 
cessations,  and  remissions  are  common.  We  often  see  the  condition  rapidly  grow 
worse,  especially  after  the  above-mentioned  apoplectiform  attacks.  The  last  stage 
is  characterized  by  the  gradually  increasing  disturbance  of  the  general  nutrition, 
and,  finally,  by  paralysis  and  bedsores.  Death  ensues  from  intercurrent  diseases, 
from  the  increasing  weakness,  or  sometimes  in  an  apoplectiform  attack. 

Anomalous  Cases. — Besides  the  typical  form  of  multiple  sclerosis  described, 
there  are  often,  as  we  have  said,  cases  that  vary  from  the  type.  We  will  mention 
briefly  the  following  possibilities : 

1.  The  disease  may  be  very  latent.  We  saw  one  case  in  which,  for  a  long  time, 
the  only  symptom  was  a  complaint  of  slight  headache  and  vertigo.  Finally,  there 
was  a  transitory  apoplectiform  attack,  several  months  later  an  epileptiform  attack, 
and  a  few  days  after  that  death  took  place.  The  autopsy  showed  a  completely 
developed  multiple  sclerosis. 

2.  Sometimes  the  disease  appears  under  the  exact  type  of  a  chronic  myelitis. 
The  cerebral  nodules  cause  no  symptoms,  they  are  present,  perhaps,  only  in  small 
numbers,  and  the  spinal  nodules  cause  a  gradually  increasing  paraplegia  of  the 
legs,  with  vesical  disturbance,  loss  of  sensibility,  etc.  We  have  notes  of  two  cases 
of  multiple  sclerosis,  with  autopsies,  in  which,  during  life,  the  diagnosis  of  a  simple 
transverse  myelitis  had  been  made. 


MULTIPLE  SCLEROSIS  OP  THE   BRAIN   AND   SPINAL  CORD.  631 

3.  Cases  have  been  repeatedly  known  where  multiple  sclerosis  lias  appeared 
under  almost  the  exact  type  of  a  spastic  spinal  paralysis  (vide  infra).  In  the» 
cases  many  nodules  were  situated  in  the  lateral  columns  of  the  cord.  If  the  spas- 
tic symptoms  be  combined  with  muscular  atrophy  (nodules  in  the  anterior  gray 
cornua),  the  disease  may  even  simulate  the  type  of  an  amyotrophic  lateral  scle- 
rosis, with  at  times  co-existing  bulbar  symptoms  (vide  infra).  If  multiple  sclerosis 
be  localized  to  an  unusual  extent  in  the  pons  and  medulla,  the  symptoms  of  a 
chronic  bulbar  paralysis  may  be  prominent. 

4.  Symptoms  like  those  of  tabes  dorsalis,  pain  and  ataxia,  are  less  frequently 
of  chief  prominence.  Combinations  of  multiple  sclerosis  and  gray  degeneration 
of  the  posterior  columns  have,  however,  also  been  observed. 

5.  It  sometimes  happens  that  multiple  sclerosis  is  the  reason  for  a  slowly  devel- 
oping hemiplegia,  which  may  then  be  falsely  regained  as  cerebral,  while  the 
autopsy  shows  several  nodules  in  the  corresponding  side  of  the  cord  and  pons. 

6.  In  many  cases  the  mental  disturbance,  dementia,  is  so  prominent  that  there 
is  the  pronounced  picture  of  paralytic  dementia  (general  paralysis),  with  disturb- 
ances of  speech,  etc. 

7.  Finally,  we  must  mention  here  that  Westphal  has  of  late  described  some 
very  chronic  cases  which  have  closely  resembled  multiple  sclerosis  in  their  type, 
although  the  autopsy  usually  showed  no  discoverable  anatomical  lesion  of  the 
nervous  system  at  all.  In  these  cases  the  symptoms  consisted  chiefly  of  muscular 
paresis,  tremor  on  voluntary  motion,  paretic-spastic  gait,  disturbance  of  speech, 
difficulty  in  moving  the  eyes,  rigid  expression  of  the  face,  and  of  the  presence  of 
the  so-called  paradoxical  contraction  in  the  muscles  of  the  legs  (see  page  546).  A 
hereditary  predisposition  to  nervous  disease  was  probably  of  significance  in  their 
aetiology.     Westphal  proposes  to  call  such  cases  provisionally  "pseudo-sclerosis." 

The  diagnosis  of  multiple  sclerosis  in  atypical  cases  is  sometimes  quite  impossi- 
ble, or  at  best  it  can  be  made  with  a  fair  amount  of  probability  only  when  some, 
at  least,  of  the  characteristic  symptoms  of  the  disease  are  present  besides  the  anom- 
alous symptoms.  The  circumstance,  indeed,  that  the  anomalous  cases  will  not 
properly  fit  the  molds  of  any  other  form  of  disease,  should  make  us  think  of  the 
possibility  of  a  multiple  sclerosis;  for  in  these  anomalous  cases,  of  course,  there 
may  be  all  possible  combinations  of  symptoms. 

The  diagnosis  is  usually  not  difficult  in  the  typical  cases.  The  intention  tre- 
mor, the  spastic  symptoms,  the  disturbance  of  speech,  the  nystagmus,  the  gradual 
manifestation  of  mental  weakness,  and  eventually  the  apoplectiform  attacks,  are 
the  most  valuable  signs  in  diagnosis.  The  distinction  from  paralysis  agitans 
(vide  infra)  is  almost  always  easy,  if  we  remember  that  in  this  latter  disease,  in  dis- 
tinction from  all  others,  the  tremor  is  chiefly  during  rest,  and  the  oscillations  are 
much  more  equal.  The  diagnosis  of  "  pseudo-sclerosis  "  can  scarcely  be  made  with 
certainty  at  present. 

The  prognosis  of  multiple  sclerosis  is  utterly  unfavorable.  A  case  of  recovery 
has  never  yet  been  seen  with  certainty.  The  disease  may,  of  course,  last  for  a 
very  long  time,  as  was  said  above. 

The  treatment  adopts  the  same  remedies  that  have  been  mentioned  in  the  de- 
scription of  chronic  myelitis.  The  galvanic  current,  tepid  baths  and  sponging, 
and  perhaps  the  internal  use  of  nitrate  of  silver,  may  give  the  best  promise  of  a 
temporary  benefit. 


632  DISEASES  OF  THE  NERVOUS  SYSTEM. 


CHAPTER  VI. 

TABES    DORSALIS. 

{Locomotor  Ataxia.     Gray  Degeneration  of  the  Posterior  Column«.     Posterior  Spinal  Sclerosis.) 

We  give  at  present  the  old  name  of  tabes  dorsalis,  "  consumption  of  the  spinal 
cord,"  to  a  perfectly  definite  chronic  disease  of  the  central  nervous  system,  whose 
chief  anatomical- basis  is  regarded  as  a  typical  degeneration  of  the  posterior  col- 
umns of  the  spinal  cord.  The  disease  has  not  been  accurately  known  for  a  very 
long  time.  The  first  description,  which,  of  course,  is  defective  in  many  respects, 
is  found  in  a  work  of  W.  Horn  in  1827.  We  must  thank  especially  the  investiga- 
tions of  Romberg  in  Germany,  in  1851,  and  of  Duchenne  in  France,  in  1858,  for  a 
more  comprehensive  knowledge  of  the  disease,  and  for  a  precise  distinction  between 
it  and  the  other  chronic  diseases  of  the  spiual  cord. 

iEtiology. — But  little  that  is  definite  was  known  until  lately  as  to  the  cause  of 
tabes  dorsalis.  Hereditary  conditions  play  a  very  slight  part  in  genuine  cases, 
and  even  a  general  "  neuropathic  taint "  can  only  rarely  be  made  out  in  ataxic 
patients.  Much  weight  in  regard  to  aetiology  was  formerly  laid  upon  previous 
exposure  to  cold.  It  can  not  be  denied  that  sometimes  the  first  symptoms  of  the 
disease  follow  some  pronounced  exposure  to  wet  or  cold,  but  much  more  fre- 
quently nothing  of  the  sort  can  be  made  out.  The  case  is  similar  with  regard  to 
physical  and  mental  overexertion,  which  were  formerly  made  answerable  for  the 
origin  of  tabes.  It  is  an  utterly  ungrounded  assertion  that  sexual  excesses  may  be 
the  cause  of  tabes.  Some  observers  report  that  tabes  may  develop  as  a  result  of 
acute  diseases  or  of  injuries,  such  as  a  broken  leg,  etc.  In  these  rare  cases,  too,  it 
is  hard  to  confirm  the  connection.  The  earlier  teaching  that  tabes  develops  after 
"  suppression  of  the  foot-sweat "  is  manifestly  due  to  a  confusion  of  cause  and 
effect.  The  absence  of  foot-sweat  is  not  the  cause,  but  a  symptom,  of  incipient 
tabes. 

The  only  aetiological  fact  which  in  our  opinion  is  beyond  any  doubt  is  the 
relation  of  tabes  to  a  previous  syphilitic  infection.  This  relation  of  the  two  dis- 
eases to  each  other  was  first  confirmed  in  France  by  Fournier  and  in  Germany  by 
Erb,  and  in  spite  of  the  vigorous  contradiction  which  the  views  of  these  observers 
at  first  met  with  on  many  sides,  this  theory  of  tabes  is  constantly  acquiring  more 
and  more  disciples. 

In  the  first  place,  the  connection  between  tabes  and  syphilis  can  be  confirmed 
by  statistics.  Erb  was  able  to  find  a  history  of  syphilis,  with  secondary  symptoms, 
in  about  62  per  cent,  of  his  patients;  and  Fournier,  in  103  cases,  found  syphilitic 
antecedents  as  many  as  94  times.  Our  own  observations  agree  exactly  with  Erb's 
data,  since  61  per  cent,  of  our  patients  stated  definitely  that  they  had  formerly 
suffered  from  syphilis.  If  we  also  reckon  the  cases  where  the  patients  admit  a 
former  sore  but  no  secondary  symptoms,  the  percentage  becomes  much  greater — 
90  per  cent.  In  general  it  is  worthy  of  note  that,  as  a  rule,  in  most  cases  of  tabes 
the  previous  syphilis  has  not  had  a  great  intensity.  Only  quite  infrequently  do 
we  find  tertiary  syphilitic  symptoms  as  well  as  tabes;  we  have  seen,  for  example, 
severe  ulcers  of  the  skin,  gummous  periostitis,  etc.  The  time  between  the  infec- 
tion and  the  beginning  of  the  first  symptoms  of  tabes  varies  very  much ;  it  may 
be  from  two  to  twenty  years. 

The  connection  between  tabes  and  syphilis  becomes  especially  striking  and 
convincing  when  we  consider  certain  peculiar  cases.  Thus  we  sometimes  see 
tabes  in  perfectly  irreproachable  women;  here  we  can  almost  always  detect  pre- 
vious syphilis  in  the  husband  which  has  been  transmitted  to  the  wife.  We  have 
ourselves  seen  tabes  arise  in  this  way  in  both  persons.     We  may  also  find  tabes 


TABES   DORS  ALIS.  ,;:;;; 

in  very  young  or  very  old  persons,  and  then  we  can  discover  that  syphilis  was 
acquired  at  a  very  early  or  a  very  advanced  age.  Some  cases  of  tahes  observed  in 
children  were  in  all  probability  to  be  referred  to  hereditary  syphilis. 

Although  we  thus  recognize  the  great  probability  of  the  connection  between 
tabes  and  syphilis,  we  can  not,  on  the  other  hand,  conceal  the  fact  that  the  per- 
ception of  the  precise  nature  of  this  connection  causes  no  slight  difficulty  at  pres- 
ent. The  anatomical  changes  in  tabes  {vide  infra)  do  not  correspond  at  all  to  the 
other  well-known  anatomical  products  of  constitutional  syphilis,  gummatous  new 
growths;  and  thus  they  require  an  entirely  separate  classification.  We  are  most 
disposed  to  assume  that  a  chemical  poison  is  formed  by  the  action  of  the  syphilitic 
infection,  which  has  a  special  deleterious  action  on  the  affected  system  of  fibers, 
these  fibers  being  usually  centripetal.  Tabes  accordingly  stands  in  the  same  rela- 
tion to  syphilis  as  a  u  post-syphilitic  disease,"  as  diphtheritic  paralysis  and  ataxia 
do  to  previous  pharyngeal  diphtheria.  Whether  the  same  disturbance  of  nutri- 
tion as  in  ordinary  tabes  can  not  also  be  provoked  by  other  agents  such  as  crgo- 
tine,  can  at  present  neither  be  affirmed  nor  denied.  At  least  provisionally  it  can 
not  be  questioned  that  there  are  also  cases  of  tabes  where  we  can  not  discover  a 
former  syphilitic  infection.  We  might  state  here,  in  opposition  to  statements  that 
several  authors  have  made,  that  the  theory  that  syphilis  excites  merely  an  in- 
creased predisposition  to  the  disease  seems  to  us  to  mean  absolutely  nothing. 

Finally,  we  must  mention  here  the  interesting  fact  discovered  by  Tuczek,  that 
in  chronic  ergot  poisoning— "  ergotism" — symptoms  may  develop  which  are  pre- 
cisely analogous  to  tabes,  and  which  depend  upon  a  corresponding  affection  of  the 
posterior  columns  of  the  cord  that  can  be  made  out  anatomically. 

Tabes  dorsalis  is  chiefly  a  disease  of  middle  life.  Most  of  the  cases  begin  at  the 
age  of  thirty-five  or  forty-five.  The  disease  is  decidedly  more  frequent  in  the  male 
sex  than  in  the  female ;  but  it  is  not  especially  rare  in  women,  and  here  we  can 
usually  make  out,  with  remarkable  frequency,  a  previous  syphilitic  infection. 

Pathological  Anatomy. — If  we  examine  the  spinal  cord  of  a  patient  who  has 
died  in  the  advanced  stage  of  tabes,  the  smallness  and  thinness  of  the  cord  usu- 
ally strike  us  first.  The  pia  mater  is  thickened  and  opaque,  especially  on  the 
posterior  surface.  We  often  see  the  posterior  columns  appearing  through  the 
pia  as  a  gray  band  extending  the  whole  length  of  the  spinal  cord.  On  cross- 
section  we  notice  that  the  smallness  Qf  the  cord  is  due  chiefly  to  the  atrophy  of  the 
posterior  columns,  which  is  often  very  considerable.  These  have  wholly  lost  their 
normal  backward  prominence,  and  seem  flat  and  sunken.  From  their  pronounced 
gray  color  they  are  very  plainly  distinguished  on  cross-section  from  the  rest  of 
the  white  matter  of  the  cord.  The  posterior  cornua  of  the  gray  matter,  and  the 
posterior  nexwe-roots,  show  exceptionally  a  considerable  atrophy,  and  appear  very 
small  and  thin  and  also  of  a  gray  color. 

Microscopic  examination  gives  more  exact  information  as  to  the  extent  and 
form  of  the  degeneration.  This  shows  that  all  portions  of  the  posterior  columns 
are  not  affected  in  like  manner.  The  degeneration  is  always  most  intense  in  the 
lumbar  cord  ;  here  it  affects  chiefly  the  middle  and  posterior  portions  of  the 
posterior  columns,  while  the  most  anterior  portion  remains  intact  in  all  cases  (see 
Fig.  87).  In  the  dorsal  cord  the  posterior  cohmins  are  almost  completely  degen- 
erated. There  are  usually  small  normal  areas  still  preserved  in  the  posterior 
external  and  the  most  anterior  portions.  In  the  cervical  cord  (see  Fig.  SS)  the 
so-called  columns  of  Goll  are  chiefly  affected,  together  with  the  prolongation  of 
the  fibers  from  the  root-zones  of  the  lumbar  cord,  and  also  the  "  lateral  root- 
areas  " — that  is,  those  portions  in  the  columns  of  Burdach  where  fibers  enter 
directly  from  the  posterior  nerve-roots,  and  from  which  fibers  may  be  traced 
farther  into  the  gray  matter  of  the  posterior  cornua ;  but  the  so-called  posterior 


084 


DISEASES  OF  THE  NERVOUS  SYSTEM. 


external  areas,  and  also  two  little  antero-lateral  areas,  remain  entirely,  or  at  least 
for  a  long  time,  free  from  the  disease.     Figures  89  and  90  show  how  the  first 


Fig.  87. — Transverse  section  through  the  lum- 
bar region  in  locomotor  ataxia.  The  dis- 
eased portions  of  the  posterior  columns  are 
shaded. 


Fig.  88.— Transverse  section  through  the  cervi- 
cal region  in  locomotor  ataxia.  G.  Col- 
umns of  Goll.     Wz.  Root-zones. 


beginnings  of  the  disease  are  localized  in  the  posterior  columns.  These  were 
drawn  from  preparations  from  a  case  examined  by  us  in  the  very  first  stage  of  the 
disease.  A  system  of  very  fine  fibers,  entering  through  the  posterior  roots,  is  also 
frequently  affected,  even  very  early.     They  branch  outward  immediately  after 


Fig.  89.  Dorsal  region.  Fig.  90r  Lumbar  region. 

Transverse  section  through  the  posterior  columns  of  the  cord  in  beginning  locomotor  ataxia. 

the  entrance  of  the  roots,  and  here  occupy  a  small  but  very  sharply  defined 
territory  at  the  point  of  the  posterior  cornua,  between  the  posterior  and  lateral 
columns  (Lissauer). 

We  must  state,  with  reference  to  the  participation  of  the  gray  matter  in  the 
disease,  that  the  posterior  cornua,  as  we  have  already  said,  are  also  found  con- 
siderably affected,  which  is  explained  mainly  by  the  atrophy  of  the  posterior  root- 
fibers  wbich  enter  them  directly.  It  also  can  not  appear  strange  that  the  medul- 
lated  fibers  found  in  Clarke's  columns  seem  very  much  reduced  in  number,  since 
they  are  also  direct  processes  of  the  posterior  root-fibei's.  The  cells  of  the  columns 
of  Clarke  remain  normal. 

On  the  other  hand,  the  peripheral  processes  of  the  posterior  root-fibers  are  not 
wholly  spared.  At  any  rate,  in  advanced  tabes  we  can  also  make  out  in  the 
larger  peripheral  nerve  trunks,  such  as  the  sciatic,  and  probably  still  more  in 
the  finer  branches  of  the  sensory  nerves,  a  number  of  degenerated  fibers,  at  least 
of  centripetal  fibers  (Dejerine,  Oppenheim  and  Siemerling,  and  others).  At  pres- 
ent we  can  make  no  definite  statement  as  to  which  part  of  the  conducting  tract 
the  degeneration  here  begins  in,  or  how  far  primary  and  secondary  atrophies  are 
to  be  separated ;  but  it  now  seems  most  probable  that  the  peripheral  degenerations 
in  tabes  occupy  an  independent  position,  since,  besides  the  changes  in  the  periphe- 
ral sensory  nerves,  pronounced  degenerative  conditions  sometimes  occur  in  the 
trunks  of  certain  cranial  nerves,  notably  in  the  optic  and  oculomotor  nerves,  and 
more  rarely  in  the  vagus,  acoustic,  etc. 


TABES  DORSALIS.  635 

It  is  most  remarkable  that  the  changes  described  are  found  in  almost  precisely 
the  same  manner  in  all  cases,  that  the  same  portions  of  the  spinal  cord  are  always 
chiefly  affected,  while  certain  other  portions  constantly  remain  free;  that  tbe  dis- 
ease is  very  exactly  limited,  and  is  precisely  symmetrical  in  the  two  halves  of  the 
cord.  This  condition  is  explained  only  by  the  assumption  that  in  tabes  certain 
systems  of  fibers  are  always  affected — that  is,  fibers  which  belong  together  in  their 
anatomical  and  physiological  aspect.  Since  fibers  of  different  functions  are  mani- 
festly diseased,  as  the  symptoms  of  tabes  show,  we  must  regard  the  trouble  not  as 
a  simple  affection  but  as  a  combined  sytemic  disease,  the  more  so  as  we  often  find 
certain  cerebral  nerves,  as  above  stated,  affected  at  the  same  time  (vide  infra). 

The  form  of  the  disease  consists  of  a  primary  degenerative  atrophy  of  the 
nerve-fibers,  and  a  corresponding  secondary  increase  of  the  connective  tissue. 
The  gray  color  of  the  posterior  columns  is  due  to  the  loss  of  the  medullary 
sheaths.  Since  the  destruction  of  the  nerve-fibers  advances  but  very  slowly,  we 
never  find  more  than  a  few  fatty  granular  cells  (see  page  617).  In  old  cases  we 
find  numerous  corpora  amylacea,  whose  origin  and  significance  are  still  un- 
known. The  thickening  of  the  pia  mater  is  a  secondary  and  insignificant  phe- 
nomenon. 

We  will  state  below  the  little  that  we  know  as  to  the  precise  relations  between 
the  anatomical  lesions  and  the  clinical  symptoms  of  tabes,  and  we  will  also  men- 
tion some  other  rarer  anatomical  changes  in  the  disease. 

Clinical  History. — A  disease  which  has  as  its  basis  so  definite  and  strictly  lim- 
ited an  anatomical  change  as  is  the  case  with  tabes  dorsalis  would  also  be  ex- 
pected to  give  a  very  characteristic  clinical  picture.  This  supposition  is  entirely 
correct,  and  there  are  few  diseases  which  can  be  diagnosticated,  even  in  their 
earliest  stages,  with  as  much  certainty  as  tabes.  This  fact  is  explained  only  by 
regarding  tabes  as  a  systemic  disease,  in  which  certain  systems  of  fibers  are  always 
affected,  while  others  are  as  constantly  spared  by  the  disease.  The  difference 
between  individual  cases  of  tabes  lies,  therefore,  less  in  the  symptoms  themselves 
than  in  their  intensity,  their  duration,  and  the  order  of  their  occurrence.  In  this 
regard,  however,  the  differences  in  the  clinical  pictures  are  extremely  varied,  so 
that,  even  with  a  comparatively  great  personal  experience,  we  often  see  new  com- 
binations of  symptoms  and  also  peculiarities  in  their  course. 

For  the  majority  of  cases  we  may  sketch  the  following  general  description  of 
the  disease,  in  which  it  is  better  to  divide  the  whole  course  into  several  stages; 
but,  of  course,  this  division  can  have  only  a  schematic  value. 

Tabes  dorsalis  begins,  as  a  rule,  with  a  stage  of  initial  symptoms,  which  de- 
velop very  gradually  and  insidiously,  and  which  may  be  of  a  very  varying  dura- 
tion. The  most  characteristic  symptoms  of  this  stage  are  those  of  sensory  irrita- 
tion, most  frequently  in  the  form  of  the  so-called  lightning-like,  "lancinating" 
pains  in  the  lower  extremities.  They  are  sometimes  very  severe,  but  at  other 
times  only  of  slight  intensity,  and  are  comparatively  little  noticed  by  the  patient, 
who  regards  them  as  "rheumatism."  Many  patients  have  a  feeling  of  numbness 
and  tingling  in  the  tips  of  the  fingers,  especially  of  the  ring  and  little  fingers,  and 
there  is  often  a  pronounced  girdle  sensation  in  the  trunk.  In  some  cases,  too, 
neuralgic  and  migraine-like  pains  in  the  head  may  appear  in  the  early  stages. 

Besides  these  symptoms  of  sensory  irritation,  which  may  often  be  for  years 
the  only  symptoms  of  which  the  patient  complains,  two  objective  symptoms  ap- 
pear very  early,  which  are  of  the  greatest  importance  in  the  diagnosis  of  incipient 
tabes :  the  disappearance  of  the  patellar  reflex,  first  discovered  by  Westphal,  and 
the  reflex  immobility  of  the  pupils  (Argyll  Robertson).  The  absence  of  the  patel- 
lar reflex  is  the  most  constant  of  all  the  known  symptoms  of  tabes,  and  it  is  found 
so  early  that  we  can  hardly  ever  decide  with  exactness  upon  the  time  of  its  occur- 


C36  DISEASES  OF  THE  NERVOUS  SYSTEM. 

rence.  The  reflex  immobility  of  the  pupil — that  is,  the  failure  of  the  pupil  to  con- 
tract to  light,  while  the  changes  on  accommodation  may  he  perfectly  retained — 
is,  indeed,  not  so  constant  as  the  failure  of  the  patellar  reflex,  but  still  it  is  quite 
frequent.  If  all  three  symptoms — lancinating  pains,  absence  of  patellar  reflex, 
and  immobility  of  the  pupils — are  present  at  the  same  time,  the  diagnosis  of  tabes 
is  absolutely  certain,  even  if  all  other  symptoms  are  wanting,  because  this  pecul- 
iar combination  of  three  such  apparently  heterogeneous  symptoms  is  seen  in  this 
disease  alone. 

Among  the  rarer  initial  symptoms  we  shall  also  learn  to  recognize  diplopia, 
caused  by  paralysis  of  certain  ocular  muscles,  loss  of  vision,  from  optic  atrophy, 
and  certain  disturbances  of  cutaneous  sensibility,  such  as  analgesia.  Sometimes 
disturbances  in  micturition  appear  quite  early,  while  in  other  cases,  however,  gas- 
tric crises  {vide  infra)  are  the  first  symptom  which  the  patient  notices. 

After  this  first  stage  of  the  disease  has  lasted  for  a  very  varying  period,  from 
a  few  months  to  two  or  five  or  even  twenty  years,  the  second  stage  begins ;  this 
we  usually  term  the  ataxic  stage  of  tabes. 

The  beginning  of  this  stage  is  recognized  by  the  appearance  of  disturbances  of 
gait.  The  gait  becomes  more  difficult  and  more  uncertain,  and  there  are  certain 
peculiarities  which  we  will  describe  more  fully  later.  Careful  examination  shows 
that  the  disturbance  in  gait  is  due  not  to  a  paresis  of  the  muscles  but  to  a  disturb- 
ance of  co-ordination,  ataxia  of  the  lower  extremities.  This  symptom  usually 
increases  very  slowly,  until  it  reaches  a  degree  where  the  patient  can  walk  only 
with  effort,  and  finally  can  not  walk  at  all.  There  is  often  later,  but  almost 
always  not  for  years,  ataxia  of  the  upper  extremities. 

Besides  the  persisting  symptoms  of  the  first  stage,  there  are  often  now  more 
marked  disturbances  of  sensibility,  as  well  as  ataxia.  The  patient  has  a  feeling  as 
if  he  were  walking  on  wool,  felt,  or  similar  substances.  If  he  closes  his  eyes  there 
is  great  swaying  of  the  whole  body — "Romberg's  symptom."  Physical  examina- 
tion of  the  sensibility  often  shows  a  marked  loss  of  tactile  sense,  of  sensibility  to 
pain,  or  other  disturbances  (vide  infra).  A  loss  of  muscular  sense  is  especially 
frequent.  The  disturbances  of  micturition,  such  as  incontinence,  gradually  be- 
come more  marked,  and  very  often  cystitis  gradually  develops.  This  stage  may 
also  last  for  years.  Sometimes  the  disease  seems  to  stand  still,  frequently  even 
manifest  improvement  is  seen,  but  then  the  condition  becomes  worse  again. 

The  third  stage,  the  terminal  stage  of  the  disease,  develops  if  the  patient  has 
not  previously  succumbed  to  an  intercurrent  disease.  The  symptoms  are  the 
same  as  in  most  of  the  other  chronic  diseases  of  the  spinal  cord.  The  patient 
gradually  becomes  more  and  more  wretched  and  helpless,  and  finally  is  confined 
almost  wholly  to  his  bed.  The  ataxia  is  very  marked,  and  sometimes  even  paresis 
develops,  which  may  increase  to  an  actual  paralysis  of  the  legs.  In  these  cases, 
which  are  by  no  means  frequent,  we  are  right  in  calling  the  third  stage  of  tabes 
the  "paralytic  stage."  A  severe  pyelo-cystitis  usually  develops,  bedsores  appear, 
and  death  finally  frees  the  patient  from  his  lamentable  condition. 

We  must  now  complete  this  briefly  sketched  picture  of  the  disease  by  a  more 
careful  description  of  the  single  symptoms. 

1.  Disturbances  of  Motility  in  the  Extremities.— The  typical  motor  symp- 
tom of  developed  tabes  dorsalis  is  the  disturbance  of  co-ordination,  the  ataxia 
(see  page  542).  This  is  almost  always  seen  in  the  lower  extremities  first.  If  we 
have  the  patient  describe  a  circle  in  the  air  with  his  foot,  while  lying  on  his  back 
we  notice  the  irregularity,  the  "  excursion  "  of  the  movement.  It  is  still  better  to 
tell  the  patient  to  touch  the  knee  of  one  leg  with  the  heel  of  the  other  foot.  We 
see  then  that  the  leg  moved  is  often  carried  beyond  the  point  designated  several 
times  before  it  reaches  it.     The  ataxia  is  often  noticeable,  even  in  throwing  one 


TABES  DORSALIS.  037 

leg  over  the  other,  as  the  leg  raised  makes  much  too  great  and  too  "  throwing"  a 
movement. 

The  alteration  of  the  gait  is  very  characteristic — the  ataxic  gait,  from  which  we 
can  often  perceive  the  patient's  disease  at  the  first  glance.  If  the  patient  sits  down 
and  tries  to  get  up  again  to  walk,  there  is  difficulty  in  rising.  He  separates  his 
legs  to  find  a  firm  point  of  support,  he  takes  a  stick  to  help  himself  if  he  can,  and 
he  often  gets  the  proper  balance  to  keep  himself  erect  only  after  several  attempts. 
The  gait  itself  is  straddling,  and  the  legs  are  raised  abnormally  high  and  set  down 
with  a  stamp.  If  we  have  the  patient  turn  rapidly  or  make  a  proper  military 
''about  face,"  the  uncertainty  of  movement  is  still  more  marked.  These  methods 
of  testing  are  therefore  especially  suitable  for  ascertaining  the  first  beginnings  of 
ataxia.  Most  patients  always  walk  with  a  stick  and  control  the  movements  of 
their  legs  by  keeping  their  eyes  fixed  on  the  floor  as  they  walk.  This  control  is 
particularly  necessary  when  the  sensibility  of  the  legs,  especially  the  muscular 
sensibility,  is  diminished  at  the  same  time. 

The  disturbances  of  sensibility  are  also  the  sole  reason  for  Eomberg's  symptom 
mentioned  above — namely,  the  swaying  with  the  eyes  shut,  especially  when  the 
patient  puts  his  feet  together.  This  phenomenon  has  often  been  classed  with 
ataxia,  but  it  depends  merely  upon  the  defective  control  of  the  muscular  move- 
ments, which  are  necessary  to  preserve  the  equilibrium,  as  a  result  of  the  impaired 
sensibility  of  the  slrin  of  the  soles  of  the  feet  and  that  of  the  muscles  themselves. 
If  this  control  be  supplied  by  the  eyes,  the  swaying  is  insignificant,  but  it  at  once 
becomes  more  marked  if  the  control  by  the  eyes  is  lost.  From  a  like  reason  it  is 
much  harder  for  most  ataxics  to  walk  in  the  dark  than  by  daylight. 

If  the  ataxia  be  very  marked,  the  patient  can  finally  keep  on  his  legs  no  longer. 
Walking  is  wholly  impossible.  The  ataxia  can  then  be  made  out  very  plainly 
from  the  different  movements  of  the  legs  in  bed.  The  throwing  movement,  the 
excess  of  innervation,  is  almost  always  most  prominent. 

If  ataxia  of  the  upper  extremities  occur  in  the  course  of  the  disease,  it  is  easily 
recognized  if  the  patient  tries  to  take  hold  of  some  definite  object,  such  as  his  ears, 
or  if  he  brings  the  tips  of  his  two  forefingers  together  from  a  certain  distance,  or  if 
he  does  fine  work  with  his  hands,  such  as  writing  or  sewing.  The  movements  are 
irregular  and  uncertain,  and  the  excursions  are  marked.  If  there  be  at  the  same 
time  any  sensory  disturbance  in  the  arms,  the  anomaly  in  their  movements  is  still 
greater  with  the  eyes  shut. 

There  has  been  much  written  and  much  dispute  as  to  the  cause  of  the  ataxia  in 
tabes  dorsalis,  although  at  present  we  have  not  attained  perfect  clearness  and 
unity.  There  are  three  principal  theories,  or,  more  properly,  groups  of  theories, 
which  have  been  advanced  up  to  the  present  time  to  explain  the  ataxia.  Accord- 
ing to  the  first  theory  (Jaccoud,  Cyon,  Benedikt),  ataxia  depends  upon  a  disturb- 
ance in  the  reflex  activity  of  the  spinal  cord.  According  to  the  second  theory 
(Leyden  and  others),  ataxia  is  the  result  of  the  sensory  disturbance  in  tabes, 
"  sensory  ataxia  " ;  and  finally,  according  to  a  third  theory  (Friedreich,  Erb),  in 
ataxia  we  have  a  lesion  of  definite  "  co-ordinatory  fibers,"  which  run  centrifugally, 
and  preside  over  the  co-ordination  of  motion.  The  exact  place  where  these  fibers 
run  is  not  definitely  asserted.  If  Charcot  places  these  fibers  in  the  external  por- 
tions of  the  posterior  columns,  in  the  "  cuneate  fasciculi,"  it  does  not  agree  with 
the  above  theory,  because  centrifugal  fibers  probably  do  not  pass  through  this 
part  at  all. 

It  would  be  an  impossible  task  for  us  to  try  here  to  estimate  these  theories 
exactly  and  critically.  The  main  reason  why  it  is  at  present  impossible  to  give 
an  incontrovertible  explanation  of  the  occurrence  of  ataxia  lies  in  the  fact  that  we 
are  not  yet  in  a  condition  to  know  and  to  analyze  exactly  the  process  of  normal 


638  DISEASES  OF  THE  NEEVOUS  SYSTEM. 

co-ordination  of  motion ;  for  manifestly  every  theory  as  to  the  causes  of  ataxia 
must  begin  with  the  processes  involved  in  the  co-ordination  of  normal  movements. 
If  we  try  to  get  a  clear  idea  of  this,  the  most  essential  point  seems  to  us  to  be  that 
co-ordination  of  motion  is  not  a  congenital  function,  but  a  power  of  our  organs  of 
motion  learned  by  practice.  The  movements  of  little  children  who  are  learning  to 
walk  are  ataxic,  and  even  in  later  life  it  often  happens  that  we  have  to  leam  how 
to  perform  certain  complicated  and  difficult  movements.  We  can  get  no  other 
idea  of  this  learning  how  to  co-ordinate  than  that  it  takes  place  by  the  aid  of  the 
constant  action  of  controlling  and  correcting  impressions  coming  from  the 
periphery — that  is,  centripetal — but  we  must  bear  in  mind  that  these  actions  are 
mainly  iinconscious.  The  surer  we  become  in  the  execution  of  the  movements, 
the  more  the  regulatory  influence  of  the  centripetal  irritations  falls  into  the  back- 
ground, without  ever  wholly  disappearing.  In  these  cases  we  must  not  consider, 
by  any  means,  merely  the  irritations  which  are  brought  to  the  central  organs 
from  the  skin  of  the  parts  moved;  but  we  should  consider,  just  as  much  or  even 
more,  those  irritations  which  are  due  to  the  varying  tension  and  position  of  the 
deeper  parts,  the  muscles,  the  fasciae,  the  ligaments,  and  the  articular  surfaces. 
Even  the  special  organs  of  sense,  particularly  the  eye,  under  some  circumstances, 
assist  materially  in  regulating  motion. 

According  to  this,  a  disturbance  of  co-ordination  must  take  place  when  the 
regulating  influences  themselves  either  are  absent  or  have  lost  their  activity — that 
is,  when  the  possibility  of  a  successful  transmission  of  these  influences  to  the 
motor  apparatus  is  absent.  We  do  not  know  exactly  which  of  these  two  condi- 
tions is  realized  in  tabes.  Perhaps  both  are  concerned.  Several  circumstances 
may  be  cited  to  favor  the  theory  of  a  loss  of  centripetal  irritations  in  tabes :  the 
disturbances  of  sensibility  that  can  often  be  made  out,  the  absence  of  the  tendon 
reflexes,  the  undoubtedly  diminished  muscular  tonus,  etc.  All  these  symptoms 
are  certainly  not  in  themselves  the  causes  of  ataxia,  but  still  they  are  noteworthy 
facts,  because  they  generally  point  to  the  actual  loss  of  centripetal  irritations.  A 
second  theory  has  perhaps  still  more  support.  According  to  this,  the  transmis- 
sion of  the  regulatory  centripetal  irritations  to  the  motor  apparatus  is  disturbed 
in  tabes.  It  harmonizes  completely  with  the  fact  that  the  degree  of  ataxia  in 
tabes  does  not  run  at  all  parallel  to  the  disturbance  of  conscious  sensibility. 
There  are  doubtless  cases  where  there  is  a  good  deal  of  ataxia,  while  the  sensi- 
bility—that is,  the  conscious  perception  of  sensory  impressions— is  practically 
undisturbed.  On  the  other  hand,  there  are  several  cases  recorded  in  literature 
in  which,  in  spite  of  marked  anaesthesia,  there  was  no  ataxia.  In  these  cases 
the  regulatory  influence  of  the  irritations  from  the  anaesthetic  parts  was  certainly 
absent,  but  it  could  be  replaced  by  the  control  of  the  organs  of  the  other  senses, 
especially  the  eye;  for  as  long  as  the  completely  anaesthetic  patient  has  his  eyes 
open  he  can  walk  well,  but  as  soon  as  he  shuts  his  eyes  he  can  no  longer  stand 
a  moment,  and  falls  at  once.  In  these  cases,  then,  a  regulation  of  motion  by 
the  eyes  is  still  possible ;  there  is  no  special  ataxia.  In  genuine  ataxia,  motion 
remains  unco-ordinated  in  spite  of  the  control  sought  from  the  sensations  of 
sight;  which  can  be  explained  by  the  fact  that  the  influences  coming  from  the 
eyes,  which  regulate  motion,  are  no  longer  of  value,  because  their  transmission  to 
the  motor  apparatus  has  become  impossible.  Nevertheless,  the  eye  has  a  certain 
unmistakable  influence  on  the  movements  of  ataxics.  As  soon  as  the  patient 
shuts  his  eyes  all  the  movements  become  much  more  uncertain  and  lack  any  con- 
trol, so  that  the  patient's  judgment  as  to  the  degree  of  his  movements,  when  there 
is  at  the  same  time  cutaneous  and  muscular  anaesthesia,  is  entirely  lost. 

We  may  suppose  that  the  point  where  the  transmission  of  centripetal  impres- 
sions to  the  motor  apparatus  for  the  purpose  of  co-ordination  of  motion  takes  place 


TABES  DORS  ALIS.  639 

is  only  in  the  gray  rnatter,  and  that  it  takes  place  only  by  the  interposition  of  the 
ganglion  cells.  We  must  thus  assume  that  ataxia,  so  far  as  it  depends  upon  any 
disturbance  of  transmission,  is  due  anatomically  to  a  lesion  of  the  gray  matter 
(posterior  cornua  ?) ;  although,  of  course,  we  do  not  exclude  the  idea  that  the  loss 
of  centripetal,  unconscious  irritations,  independently  of  a  lesion  of  the  centripetal 
fibers  running  in  the  posterior  roots  into  the  cord  itself,  may  have  an  influence 
upon  the  occurrence  of  ataxia. 

These  brief  glances  at  the  conditions  to  be  considered  in  the  question  as  to  the 
origin  of  ataxia  may  suffice  to  give  the  reader  a  preliminary  survey  of  the  most 
important  points,  and  an  incitement  to  further  reflection  upon  this  interesting 
subject. 

Ataxia  is  the  chief  motor  disturbance  in  tabes.  The  crude  strength  of  the 
muscles  may  be  perfectly  normal,  and  it  is  chiefly  a  service  of  Duchenne's  to  have 
made  clear  for  the  first  time  the  principal  distinction  between  ataxia  and  paralysis. 
He  showed  that  ataxics,  who  can  no  longer  walk  a  step  alone,  can  nevertheless 
exert  the  greatest  strength  with  their  legs.  We  have  ourselves  treated  a  teacher 
of  gymnastics  who,  in  spite  of  the  most  marked  ataxia  of  the  arms,  had  still  so 
much  strength  in  them  that  he  could  support  himself  in  bed  on  his  arms  and  keep 
his  whole  body,  with  his  legs  extended,  in  the  air. 

It  sometimes  happens,  however,  that  even  the  crude  strength  disappears  in  tabes, 
and  that  the  muscles  become  paretic.  We  have  stated  above  that  even  a  complete 
paraplegia  may  finally  develop  in  the  course  of  the  disease.  In  these  cases  we  find, 
on  anatomical  examination,  that  the  process  is  no  longer  confined  to  the  posterior 
columns,  but  that  there  is  also  a  systemic  degeneration  of  the  lateral  pyramidal 
motor  tracts  in  the  lumbar  cord.  The  rare  paralyses  of  certain  motor  nerves  have 
another  significance.  They  have  usually  been  noted  at  the  beginning  of  the  dis- 
ease, and  affect  the  radial,  peroneal,  accessory,  etc.  They  are  probably  due  to 
changes  in  the  affected  peripheral  nerves,  but  as  a  rule  they  are  transitory,  and,  in 
our  opinion,  are  to  be  put  in  the  same  category  with  tabetic  oculomotor  paralyses 
(vide  infra) . 

We  may  add,  finally,  that  slight  symptoms  of  motor  irritation,  slight  twitch- 
ings  in  the  muscles,  especially  in  the  fingers,  are  not  uncommon,  but  they  are 
noticed  only  when  the  attention  is  especially  directed  to  them.  It  is  not  certainly 
known  how  they  arise ;  in  our  opinion,  they  are  of  reflex  origin. 

The  condition  of  the  muscles  on  passive  motion  is  very  characteristic.  We 
notice  in  most  cases  a  very  striking  flaccidity  of  the  limbs,  so  that  there  is  hardly 
any  muscular  resistance  to  be  felt.  We  have  to  do,  as  it  seems,  with  a  diminution 
of  muscular  tonus,  whose  cause  is  not  yet  quite  clear;  but  since  there  are  many 
reasons  for  believing  that  the  normal  muscular  tonus  is  of  reflex  origin,  we  are 
led  to  think  of  a  connection  between  the  absence  of  muscular  tonus  and  the  other 
reflex  disturbances  in  tabes,  such  as  the  absence  of  the  tendon  reflexes. 

The  electrical  excitability  of  the  nerves  and  muscles,  as  we  may  also  note  here, 
remain  perfectly  normal  in  uncomplicated  tabes. 

2.  Disturbances  of  the  Cutaneous  and  Muscular  Sensibility.— As  we 
have  already  said,  tabes  begins,  in  the  great  majority  of  cases,  with  symptoms  of 
sensory  irritation,  which  usually  persist  in  the  later  course  of  the  disease  also.  Be- 
sides the  simple  paresthesia— the  feeling  of  tingling  and  numbness  in  the  legs,  and 
sometimes,  too,  a  similar  feeling  which  appears  quite  early  in  the  upper  extremi- 
ties (especially  often,  as  we  have  said,  in  the  ulnar  region)— the  tabetic  pains  are 
remarkably  characteristic  of  the  disease. 

The  intensity  of  the  pains  differs  very  much  in  different  cases ;  but  we  see  a 
complete  absence  of  them  extremely  rarely.  The  patient's  attention  is  often  first 
called  to  his  slight  and  infrequent  pains  by  direct  questioning;  btit  in  some  cases 


6^0  DISEASES  OF  THE  NEEVOUS  SYSTEM. 

the  severe  pains  are  a  constant  distress  to  him.  The  pains  most  characteristic  of 
tabes  are  the  lightning-like,  "  lancinating  "  pains,  which  shoot  like  neuralgic  pains 
for  some  distance  along  the  course  of  the  nerves.  They  often  come  on  in  very 
severe  paroxysms,  and  are  absent  at  other  times.  There  are  also  boring,  stabbing 
pains,  which  are  fixed  at  one  point  and  have  their  seat  especially  in  the  vicinity  of 
the  joints;  and  finally  "constricting  pains,"  which  are  felt  most  frequently  in  the 
back  and  loins.  The  well-known  "  girdle  feeling  "  of  tabetics — that  is,  the  sensa- 
tion of  a  band  tightly  encircling  the  trunk,  or  a  tight,  "  drawn-together  "  pressure 
on  the  lateral  portions  of  the  trunk— belongs  to  the  latter  form  of  symptoms  of 
sensory  irritation.  The  girdle  feeling  is  manifestly  due  to  irritative  processes  in 
the  region  of  the  lower  dorsal  or  upper  lumbar  nerves.  Since  it  is  comparatively 
frequent,  and  often  appears  quite  early,  it  also  has  a  certain  diagnostic  significance. 

The  tabetic  pains  also  begin  in  the  legs,  corresponding  to  the  almost  constant 
beginning  of  the  symptoms  of  the  disease  in  the  lower  extremities ;  btit  later  on 
quite  analogous  pains  sometimes  appear  in  the  arms,  and  in  very  advanced  cases 
we  have  also  observed  pains  in  the  region  of  the  occipital  nerves  and  of  the 
trigeminus.  On  the  other  hand,  neuralgic  pains  in  the  face,  especially  in  the 
region  of  the  frontal  nerve,  or  in  the  occiput,  or  even  migraine-like  attacks,  also 
occur,  even  in  the  initial  stage  of  tabes,  as  we  have  ourselves  observed.  In  some 
cases  the  lancinating  pains  in  tabes  may  be  accompanied  by  the  appearance  of  an 
eruption  of  herpes— a  condition  which  at  any  rate  is  extremely  rare. 

Usually  much  later  than  the  pains  appears  also  a  diminution  of  sensibility 
which  can  be  made  out  objectively.  As  a  rule,  it  may  be  stated  that  in  most,  but 
not  in  all,  cases  of  tabes  the  sensibility  does  not  remain  normal ;  although  more 
marked  anaesthesia  never  appears  until  the  more  advanced  stages  of  the  disease. 

The  form  of  the  disturbances  of  sensibility  varies  extremely,  and  no  disease 
furnishes  so  many  opportunities  for  the  study  of  interesting  details  in  the  region 
of  anomalies  of  sensation  as  tabes  dorsalis.  Our  knowledge  of  the  occurrence  of 
partial  paralyses  of  sensation  especially  is  very  largely  based  on  the  examination 
of  tabetic  patients.  The  tactile  sense  suffers  in  most  cases  of  tabes,  but  we  can 
usually  make  out  only  a  certain  blunting  of  it.  Only  when  the  disease  is  far  ad- 
vanced does  the  patient  cease  to  feel  a  light  touch  on  the  skin.  The  sense  of  pain 
is  also  often  abnormal.  We  sometimes  see  a  pronounced  analgesia,  but  in  other 
cases  there  is  a  very  decided  sensibility  to  pain,  in  spite  of  a  defective  tactile  sensi- 
bility. It  is  a  very  frequent  symptom  that,  at  a  pin-prick,  the  patient  has  at  first 
only  a  slight  and  not  a  painful  sensation,  and  that  a  few  seconds  later,  especially 
if  the  prick  persist,  he  suddenly  winces  and  says  he  feels  a  decided  pain.  With  it 
there  is  usually  a  reflex  contraction  in  the  affected  leg.  We  generally  speak  of 
this  symptom  as  a  "  delayed  conduction  of  painful  sensations  "  or  "  delayed  reflex  " ; 
but  it  seems  to  us  that  the  symptom  has  not  yet  been  analyzed  carefully  enough, 
and  especially  that  it  has  not  been  properly  separated  from  the  after-sensations, 
which  are  also  very  common  in  tabes.  It  often  happens  that  after  a  single  prick, 
tabetic  patients  report  at  varying  intervals  five  or  six  or  more  painful  after-sen- 
sations.* 

If  the  first  sensation  is  not  painful  in  these  cases,  it  may  happen  that  the 
patient  may  first  say  "  Now"  at  a  prick,  and  soon  after  "  Ow,"  when  he  first  feels 
the  pain  (the  "double  sensation"  of  Naunyn,  Remak,  and  others).  Fischer  has 
termed  a  peculiar  disturbance  of  sensibility  occurring  in  tabes,  polyaesthesia ;  the 

*  If,  while  the  patient's  eyes  are  shut,  we  prick  the  leg  and  the  arm  or  neck  as  nearly  as  possible  at 
the  same  time,  the  prick  on  the  leg' would  necessarily  be  felt  much  later  than  that  on  the  arm,  if  there 
is  a  delayed  conduction  of  sensory  impressions  from  the  leg;  but  we  have  never  as  yet  been  able  to 
make  out  this  condition  with  certainty. 


TABES   DORSALIS.  641 

patient  asserts,  when  examined  with  an  aesthesiometer,  that  he  feels  several  (four 
or  five)  points,  although  he  was  touched  with  but  one. 

Disturbances  of  the  sense  of  pressure,  and  still  more  that  of  temperature,  are 
also  quite  frequently  found,  especially  as  partial  paralyses  of  sensation,  when  the 
sensibility  is  otherwise  well  preserved.  We  should  note  particularly  the  occur- 
rence of  partial  anaesthesia  of  the  sensibility  to  heat  or  cold.  On  the  other  hand, 
the  special  sensations  of  temperature  may  sometimes  be  pretty  well  defined,  while 
in  other  respects  there  is  quite  a  high  degree  of  anaesthesia. 

The  considerable  anomalies  of  the  muscular  sense,  which  are  often  to  be  made 
out  in  more  advanced  cases,  have  a  special  interest  (see  page  509).  If  the  patient 
shuts  his  eyes,  he  is  often  entirely  unaware  of  the  situation  and  position  of  his 
limbs.  He  makes  a  false  report  as  to  the  direction  and  extent  of  passive  motions.* 
If  the  muscular  sense  in  the  arms  be  disturbed,  and  we  put  the  arms  into  any 
unusual  position,  the  patient  has  considerable  trouble  in  bringing  the  hands 
together  with  his  eyes  shut.  He  gropes  about  in  the  air  with  his  arms  until  he 
accidentally  touches  one  arm  with  the  other  hand,  and  then  he  feels  down  this  to 
the  hand.  The  action  of  ataxia  and  muscular  anaesthesia  are  accordingly  com- 
bined in  these  cases,  but  we  can  not  possibly  consider  the  foi'mer  as  a  result  of  the 
latter ;  for  there  are  doubtless  cases  of  ataxia— we  have  ourselves  carefully  exam- 
ined such  with  regard  to  this  question — in  which  the  perception  of  motion  and 
position  is  perfectly  normal  in  spite  of  the  existence  of  ataxia.  The  disturbance 
of  movements  willed,  by  the  loss  of  muscular  sense,  is  noticed  only  when  the  eyes 
are  shut.  With  the  eyes  open  the  control  by  the  sense  of  sight  supplies  the  lack 
of  muscular  sensibility.  Pitres  has  lately  described  peculiar  attacks  of  muscular 
rigidity,  and  attacks  of  a  decided  feeling  of  fatigue  in  the  muscles,  apparently 
coming  on  spontaneously  in  incipient  tabes  (" crises  de  courbature  musculaire"). 

Only  in  rare  and  far-advanced  cases  is  there  finally  a  complete  anaesthesia  of 
the  lower,  and  exceptionally  of  the  upper  extremities.  We  then  see  also  at  times 
disturbances  of  sensibility  in  the  region  of  the  trigeminus,  in  the  skin  of  the  face. 
These  disturbances  are  probably  connected  with  a  degeneration  of  the  sensory 
ascending  root  of  the  trigeminus,  which  degeneration  has  already  been  observed 
several  times  at  the  autopsy  (Westphal). 

It  is  very  hard  to  judge  as  to  the  dependence  of  all  these  sensory  disturbances 
mentioned  upon  the  anatomical  changes  of  tabes.  In  many  cases  both  the  initial 
pains,  and  in  part  the  anaesthesias,  especially  if  they  have  their  chief  seat  in  a  single 
nerve  territory  (ulnar,  etc.),  are  to  be  referred  to  disease  of  the  sensory  peripheral 
nerves.  The  severer  pains,  however,  are  perhaps  due  chiefly  to  morbid  processes 
in  the  posterior  roots,  while  with  a  high  degree  of  anaesthesia  we  are  usually  right 
in  assuming  that  there  is  a  pronounced  atrophy  in  the  posterior  cornua. 

3.  Disturbances  of  the  Reflexes. — The  cutaneous  reflexes  show  no  constant 
changes  in  tabes.  They  are  usually  approximately  normal,  but  sometimes  they 
are  diminished,  especially  if  there  be  at  the  same  time  a  marked  disturbance  of 
sensibility. 

The  absence  of  the  tendon  reflexes,  especially  of  the  patellar  reflex,  is,  how- 
ever, an  almost  constant  sign  of  tabes,  and  is  a  sign  of  the  highest  diagnostic  value. 
As  we  have  already  said,  the  disappearance  of  this  reflex  is  one  of  the  earliest  symp- 
toms of  the  disease,  and  is  therefore  of  the  greatest  significance  in  the  diagnosis  of 
initial  tabes.  There  are  certainly  cases  of  tabes  in  which  the  patellar  reflex  may 
persist  for  a  long  time,  in  spite  of  the  development  of  many  other  morbid  symp- 
toms.    These,  however,  are  only  very  rare  exceptions,  which  do  not  disprove  the 


*  We  can  describe  different  letters  and  figures  in  the  air  with  the  patient's  extremities,  and  try 
whether  they  can  be  correctly  recognized  with  the  eyes  shut. 
41 


642  DISEASES  OF  THE  NERVOUS  SYSTEM. 

rule,  and  do  not  at  all  contradict  our  general  views  as  to  tabes.  In  individual 
cases  the  affected  fibers,  which  serve  to  set  free  the  reflex,  may  be  spared  for  a  long 
time,  just  as  any  other  characteristic  symptom  of  the  disease  may  under  some  cir- 
cumstances occasionally  be  absent.  Concerning  the  precise  anatomical  cause  of 
the  disappearance  of  the  patellar  reflex,  it  can  be  due  only  to  a  degeneration  in 
the  centripetal  portion  of  the  affected  reflex  arc— that  is,  only  in  the  fibers  which 
belong  to  the  territory  of  the  posterior  roots.  It  is  in  accordance  with  this  that 
disease  of  the  middle  portion  of  the  posterior  columns  in  the  lumbar  cord  (that  is, 
the  root-zones,  see  Fig.  89)  always  seems  to  be  accompanied  by  a  failure  of  the 
patellar  reflex.  The  direct  mechanical  irritability  of  the  muscles,  especially  of  the 
quadriceps,  is  almost  always  retained  in  tabes.* 

4.  Disturbances  in  the  Eye  and  the  other  Organs  op  Special  Sense. — 
The  authority  for  regarding  tabes  as  a  combined  systemic  disease  arises  from  the 
frequency  with  which  certain  cerebral  symptoms,  as  well  as  the  spinal,  are  found 
in  it. 

The  symptoms  in  the  eyes  deserve  the  first  attention.  We  find  disturbances  in 
the  pupils,  of  course  not  in  all  cases,  but  still  in  the  great  majority  of  them.  The 
pupils  are  often  very  much  contracted — "  spinal  myosis"— and  show  no  trace  of  con- 
traction to  light,  although  the  well-known  changes  in  the  pupils  are  very  manifest 
upon  any  variation  of  the  accommodation — dilatation  of  the  pupils  with  approxi- 
mately parallel  axes  of  vision  on  looking  at  distant  objects,  and  contraction  of  the 
pupils  with  the  most  marked  convergence  of  the  eyeballs  on  fixing  a  near  object. 
We  give  this  phenomenon,  whose  precise  anatomical  cause  is  not  yet  known,  the 
name  of  reflex  immobility  of  the  pupils  with  retained  mobility  on  accommodation 
(Argyll  Eobertson  pupils).  It  is  not  at  all  necessary,  however,  that  there  should 
also  be  a  myosis,  for  we  not  very  infrequently  find  the  pupils  quite  dilated  or 
unequal,  although  we  find  there  is  reflex  immobility.  As  we  have  already  said, 
the  immobility  of  the  pupils  is  often  a  very  early  symptom,  so  that  it  also  has  a 
diagnostic  importance.  In  other  cases  we  find  inequality  of  the  pupils  and,  as  a 
rare  symptom,  a  striking  change  in  the  size  of  the  pupils,  so  that  first  one  and  then 
the  other  pupil  is  the  larger. 

The  paralyses  of  the  ocular  muscles  in  tabes  are  also  very  interesting.  They 
are  usually  unilateral,  but  sometimes  bilateral,  and  often  appear  even  at  the  be- 
ginning of  the  disease,  so  that  diplopia  may  be  the  first  subjective  symptom  of 
which  the  patient  complains.  In  every  sudden  oculomotor  or  abducens  paralysis, 
coming  on  without  any  other  cause,  we  must  think  of  the  possibility  of  an  incipi- 
ent tabes.  It  is  remarkable  that  these  paralyses  in  many  cases  disappear  perma- 
nently and  entirely  after  some  time;  but  sometimes  they  remain,  as  we  have  re- 
peatedly seen,  especially  in  a  case  with  bilateral  abducens  and  unilateral  oculo- 
motor paralysis,  and  also  in  a  case  with  almost  complete  bilateral  oculomotor 
paralysis.  In  the  autopsies  on  such  cases  we  find  the  trunks  of  the  affected  nerves 
and  their  nuclei  markedly  atrophic.  It  seems  to  us  very  probable,  however,  that 
the  temporary  ocular  paralyses  in  tabetic  patients  depend  upon  changes  in  the 
peripheral  nerves  of  the  ocular  muscles. 

The  third  complication  in  the  eyes  in  tabes  is  optic  atrophy.  It  occurs  in 
about  ten  or  fifteen  per  cent,  of  all  cases,  and  is  usually  an  initial  symptom,  at 
a  time  when  the  absence  of  the  tendon  reflexes,  which   may  usually  also  be 

*[From  autopsies  on  cases  of  combined  sclerosis,  where  the  symptoms  very  closely  resembled  those 
of  tabes,  but  where  the  patellar  reflex  persisted  until  near  the  close  of  life,  Westphal  thinks  that  the 
patellar  reflex  disappears  only  when  a  special  region  in  the  posterior  columns  is  involved  in  the  dis- 
ease. This  region  lies  at  the  junction  of  the  dorsal  and  lumbar  cords,  between  the  posterior  cornu 
and  a  line  running  parallel  with  the  posterior  fissure,  and  starting  from  the  angle  seen  in  the  posterior 
cornu  at  the  site  of  the  substantia  gelatinosa. — Tbans.] 


TABES  DORSALIS.  643 

noticed,  is  the  only  thing,  except  this,  to  render  the  diagnosis  of  the  disease  pos- 
sible. The  patient  complains  of  diminution  of  vision,  and  the  power  to  distin- 
guish colors,  especially  green,  disappears  quite  early.  On  objective  examination, 
we  find,  besides  this  anomaly  in  the  color  sense,  usually  a  limitation  of  the  field  of 
vision,  and  the  beginning  gray  degeneration  of  the  optic  nerve  can  easily  be  made 
out  on  ophthalmoscopic  examination.  The  affection  sometimes  makes  little  baits 
and  slight  apparent  improvements,  but  it  usually  ends  with  complete  blindness. 
The  optic  atrophy  more  rarely  first  appears  in  the  later  stages  of  the  disease,  when 
all  the  other  symptoms  are  already  fully  developed. 

Auditory  disturbances  are  much  rai-er  than  those  of  sight,  but  they  also  occur. 
The  cause,  in  at  least  a  part  of  the  cases,  is  an  atrophy  of  the  acoustic  nerve. 
Symptoms  are  also  frequently  seen  which  resemble  those  of  Meniere's  disease — 
tinnitus,  vertigo,  and  deafness. 

Changes  in  the  senses  of  taste  and  smell  have  been  observed  only  in  a  few 
cases. 

5.  Disturbances  in  the  Bladder,  the  Rectum,  and  the  Sexual  Organs. — 
Difficulty  in  emptying  the  bladder  is  an  almost  constant  symptom  in  the  later 
stages  of  tabes.  It  sometimes,  indeed,  appears  very  early.  The  patient  feels  the 
desire  to  urinate  more  frequently,  there  is  often  a  slight  involuntary  micturition, 
and  at  other  times  there  is  retention  of  urine,  sometimes  coming  on  quite  sud- 
denly ;  in  advanced  stages  there  is  frequently  complete  incontinence.  A  cystitis 
very  often  develops  as  a  result  of  all  these  disturbances,  which  may  be  the  starting- 
point  of  severe  cysto-pyelitis  and  pyelo-nephritis,  and  thus  be  the  cause  of  death. 

Persistent  constipation  is  also  a  very  frequent  symptom  of  tabes,  the  reason 
for  which  is  perhaps  to  be  sought  in  the  defective  reflex  excitation  of  intestinal 
peristalsis.  The  constipation  may  in  many  cases  give  rise  to  great  distress  to  the 
patient,  since  it  sometimes  provokes  very  painful  sensations  in  the  loins  and  abdo- 
men. The  coccyodynia,  which  sometimes  occurs  in  tabes,  has  already  been  men- 
tioned (see  page  528).  Incontinence  of  faeces  occurs  quite  rarely  in  the  last  stages 
of  the  disease. 

A  diminution  in  the  sexual  functions  is  found  almost  constantly  in  advanced 
cases.     The  loss  in  power  is  also  often  one  of  the  initial  symptoms. 

6.  Symptoms  in  the  Internal  Organs. — We  see,  not  very  infrequently,  in 
tabes  certain  symptoms  in  the  internal  organs  which  are  in  part  very  character- 
istic, and  which,  at  any  rate,  are  based  upon  disturbances  of  innervation.  The 
most  important  and  the  most  frequent  are  the  so-called  "gastric  crises."  These 
almost  always  come  on  suddenly  and  paroxysmally,  and  consist  of  an  extremely 
severe  cardialgic  pain,  which  is  accompanied  by  violent  vomiting.  The  patient 
also  feels  very  wretched,  and  there  is  often  at  the  same  time  palpitation,  accel- 
eration of  the  pulse,  vertigo,  etc.  The  attacks  last  about  two  or  three  days.  In 
many  patients  they  are  repeated  every  few  months.  As  we  have  said,  the  gastric 
crises  may  appear  very  early.  We  ourselves  know  cases  where,  in  consequence 
of  severe  gastric  crises,  a  severe  gastric  affection  has  been  falsely  diagnosticated, 
in  the  beginning  of  the  disease.  Attacks  of  diarrhoea,  "  intestinal  crises,"  usually 
not  associated  with  pain,  have  also  been  repeatedly  observed. 

We  term  attacks  of  severe  dyspnoea  "laryngeal  crises."  These  probably 
depend  upon  a  (reflex  ?)  spasm  of  the  glottis,  and  may  attain  a  very  alarming 
degree.  They  are  also  associated  with  a  severe  spasmodic  nervous  cough.  Paraly- 
sis of  the  laryngeal  muscles  (crico-arytsenoids)  has  also  been  observed.  We  may 
assume  changes  in  the  vagus-accessory  nucleus,  or  in  the  vagus  or  recurrent  itself 
(Oppenheim)^  as  the  anatomical  cause  of  all  these  symptoms. 

In  a  few  cases  "  renal  crises  "  ("  crises  nephritiques  ")  have  also  been  described. 
They  consist  of  severe   attacks   of  pain,  like  renal  colic.     French  authors  also 


6±4 


DISEASES  OF  THE  NERVOUS  SYSTEM. 


describe  " urethral  crises "  and " crises  clitoruliennes" the  paroxysmal  appearance 
of  voluptuous  feelings  with  a  vaginal  secretion  in  women,  in  the  beginning  of 
the  disease. 

We  may  mention,  finally,  that  we  sometimes  see  in  tabetic  patients  a  constant 
and  very  great  frequency  of  the  pulse,  100  to  120  a  minute.  We  also  frequently 
see  the  combination  of  tabes  with  aortic  insufficiency  which  has  been  mentioned 
by  some  authors.  The  precise  connection  between  the  two  affections  is  probably 
dependent  upon  previous  syphilis. 

7.  Trophic  Disturbances. — In  many  cases  of  tabes  trophic  disturbances  are 
entirely  absent.  We  have  already  spoken  of  the  occasional  appearance  of  an 
eruption  of  herpes,  with  severe  lancinating  pains.  In  some  cases  a  marked  exfolia- 
tion of  the  epidermis  has  been  seen,  and  also  a  falling  out  of  the  hair  and  nails. 
Sometimes  there  are  small  haemorrhages,  apparently  spontaneous,  into  the  skin 
or  into  the  visible  mucous  membranes,  especially  into  the  conjunctiva,  as  we  have 
seen  in  several  cases. 

The  peculiar  joint  affections  which  occur  in  tabes,  and  were  first  accurately 
described  by  Charcot  as  "  arthropathies  tabetiques"  have  a  greater  interest.  (See 
Fig.  91.)     The  affection  is  situated  most  frequently  in  the  knee-  and  hip-joints, 

more  rarely  in  the  ankle-  and  shoulder-joints. 
It  is  usually  bilateral,  even  if  it  be  more 
marked  on  one  side  than  on  the  other.  We 
sometimes  find  abundant  serous  effusions,  so 
that  the  knee-joint  in  particular  may  swell  up 
in  monstrous  fashion ;  but  we  find  especially 
a  high  degree  of  arthritis  deformans,  with 
marked  atrophy  of  the  ends  of  the  bones,  and 
with  the  formation  of  many  osteophytes. 
Spontaneous  dislocations  and  fractures  also 
occur.  An  affection  of  the  anterior  gray  cor- 
nua,  which  Charcot  suspected  to  be  a  cause  of 
the  articular  affection,  could  not  be  made  out 
in  a  case  examined  by  us  anatomically.  We 
do  not  believe  that  the  theory  of  an  exclusive 
''nervous-trophic  disturbance"  can  explain 
the  origin  of  the  tabetic  joint  affections.  Per- 
haps we  have  to  do  with  syphilitic  joint  affec- 
tions, and  perhaps  with  those  of  some  other 
more  fortuitous  (traumatic  ?)  origin,  which  are 
rather  a  complication  than  a  symptom  of 
tabes.  We  believe,  however,  that  the  unus- 
ual intensity  and  the  peculiar  form  of  the 
anatomical  lesion  are  indeed  directly  connected  with  tabes,  and  are  due  chiefly  to 
the  anaesthesia  of  the  articular  surfaces.  We  saw  a  case,  a  short  time  ago,  where 
an  affection  of  the  knee-joint  developed  in  a  comparatively  very  early  stage  of 
tabes,  which  up  to  that  time  had  not  been  diagnosticated  at  all.  As  the  patient 
felt  no  pain  at  all  in  his  knee,  he  nevertheless  hunted  most  vigorously  through  a 
whole  autumn,  until  finally  an  extremely  severe  swelling  of  the  knee-joint  and 
an  actual  dislocation  of  the  leg  ensued. 

The  muscles  preserve  their  normal  state  of  nutrition,  except  as  they  take  part 
in  a  general  emaciation.  Charcot  described  a  case  of  a  combination  of  tabes  with 
genuine  progressive  muscular  atrophy,  in  which  the  autopsy  showed  a  degenera- 
tion of  the  anterior  gray  cornua  in  the  spinal  cord  besides  the  atrophy  of  the  pos- 
terior columns.      The  first  report  upon  a  unilateral  atrophy  of  the  tongue,  which 


Fig.   91.— Tabetic  arthropathy  of    the  right 
kuee  and  left  ankle.    Personal  observation. 


TABES  DORS  ALIS.  r,45 

sometimes  develops  quite  early  in  tabes,  is  due  to  the  same  observer.  Nothing 
definite  is  known  at  present  as  to  the  origin  of  this  peculiar  complication. 

In  conclusion,  it  is  worthy  of  note  that  cases  of  " mal  perforant  dupied" 
(ulcerations  on  the  heels  or  between  the  toes)  have  been  repeatedly  observed  in 
tabes. 

8.  Cerebral  Symptoms. — Besides  the  frequent  important  disturbances  on  the 
part  of  certain  cerebral  nerves,  such  as  the  optic  and  oculomotor,  which  have 
already  been  mentioned,  we  must  mention  here  the  relation  between  tabes  and 
progressive  general  paralysis  (q.  v.).  On  the  one  hand,  the  symptoms  of  tabes 
are  often  present  in  the  course  of  general  paralysis,  so  that  the  autopsy  shows  a 
typical  degeneration  of  the  posterior  columns  (Westphal) ;  and,  on  the  other  hand, 
it  also  happens  that  the  whole  process  begins  with  a  tabes,  which  may  exist  alone 
for  years  without  any  mental  symptoms,  and  then  only  at  the  close  do  the  symp- 
toms of  paralytic  dementia,  delusions  of  grandeur,  dementia,  etc.,  appear. 

The  complication  of  tabes  with  hemiplegia  repeatedly  occurs.  The  latter  de- 
pends upon  a  cerebral  haemorrhage  or  an  embolic  or  thrombotic  softening,  so  that 
it  is  doubtful  whether  the  two  affections  have  a  real  connection  or  are  merely  a 
chance  combination.  It  seems  to  us  worthy  of  note  that  in  two  such  cases  we  saw 
scarcely  any  contracture  develop  in  the  paralyzed  limbs. 

Course  and  Prognosis. — Although  most  of  the  characteristic  symptoms  of  tabes 
develop  in  almost  all  cases,  still  the  order  and  the  intensity  of  their  onset  vary 
greatly.  We  have  already  briefly  described  the  general  type  of  the  disease  which 
most  frequently  comes  under  observation,  and  many  other  peculiarities  in  its 
course  have  been  mentioned  from  time  to  time. 

We  have  stated  that  the  initial  period  is  usually  characterized,  apart  from  the 
symptoms  that  can  be  made  out  only  objectively,  such  as  absence  of  the  patellar 
reflex  and  reflex  immobility  of  the  pupils,  by  the  lancinating  pains ;  that  these  may 
differ  very  much  in  intensity ;  and  that  the  duration  of  this  first  stage  may  vary 
between  a  few  months  and  ten  or  twenty  years.  The  optic  atrophy,  the  ocular 
paralyses,  gastric  crises,  vesical  disturbances,  etc.,  were  mentioned  as  rarer  initial 
symptoms.  The  passage  from  the  first  stage  to  the  second — the  stage  of  ataxia — is 
sometimes  very  gradual,  but  in  some  cases  very  rapid  and  sudden.  We  have 
repeatedly  seen  such  changes,  with  a  sudden  change  for  the  worse  in  the  condition. 
If  the  previous  symptoms  were  slight,  the  patient  dates  his  disease  from  this  point, 
and  says  that  he  was  quite  suddenly  broken  down  by  some  cause,  and  that  since 
then  he  has  not  been  able  to  walk  at  all,  or  else  only  with  difficulty.  In  such  cases 
there  is  often  slow  improvement  following  the  sudden  change  for  the  worse  in  the 
condition,  which,  of  course,  is  not  permanent. 

No  rules  of  general  value  can  be  given  as  to  the  further  advance  of  the  disease, 
the  invasion  of  the  arms  by  the  ataxia,  or  the  occurrence  of  the  rarer  symptoms, 
such  as  the  joint  affections,  etc.  Almost  every  individual  case  affords  its  idiosyn- 
crasies, since  one  group  of  symptoms  is  often  especially  prominent,  while  another 
is  entirely  absent  or  developed  only  to  a  slight  degree.  On  the  whole,  however,  we 
can  almost  always  make  out  a  gradual,  even  if  a  very  slow,  advance  in  the  disease. 
New  symptoms  appear,  the  old  ones  increase,  the  general  condition  becomes  worse, 
until  finally  the  last  stage  of  the  disease  comes  on. 

Recovery  from  tabes  occurs  only  very  rarely,  if  at  all.  The  treatment  of  the 
affection  may  indeed  cause  improvement,  delay  the  course  of  the  disease,  and  alle- 
viate single  symptoms,  but  the  prognosis  is  always  to  be  regarded  as  unfavorable, 
although  many  patients,  especially  under  favorable  external  conditions,  may  lead 
a  tolerable  existence  for  years.        * 

Diagnosis. — There  is  scarcely  any  other  disease  of  the  spinal  cord  whose  diag- 
nosis can  in  most  cases  be  made  with  so  great  certainty  and  such  comparative 


6±6  DISEASES  OF  THE  NERVOUS  SYSTEM. 

ease.  Since  tabes  is  a  combined  systemic  disease,  it  affords  a  definite  combination 
of  symptoms  such  as  can  occur  under  no  other  conditions.  The  diagnosis,  there- 
fore, is  to  be  made  not  from  any  one  single  symptom,  but  only  from  the  combina- 
tion of  all  and  from  the  whole  course  of  the  disease. 

The  diagnosis  of  initial  tabes  is  especially  important.  In  every  case  of  obsti- 
nate "  rheumatic  "  pains,  or  similar  pains  in  the  lower  extremities,  we  should  think 
of  the  possibility  of  tabes,  and  examine  the  tendon  reflexes  and  the  pupils.  The 
combination  of  characteristic  pains,  absence  of  the  patellar  reflex  on  the  two  sides, 
and  reflex  immobility  of  the  pupils,  usually  makes  the  diagnosis  almost  perfectly 
certain;  two  of  these  symptoms,  especially  if  the  reflex  immobility  of  the  pupils 
be  one,  make  it  at  least  very  probable.  Ocular  paralyses,  temporary  ptosis,  or 
temporary  diplopia,  may  be  very  important  for  the  diagnosis.  With  these  symp- 
toms, too,  we  should  never  forget  to  think  of  the  possibility  of  tabes,  and  to  look 
for  the  other  characteristic  symptoms.  Finally,  we  may  recall  the  fact  here  that 
the  disease  may  begin  with  an  optic  atrophy,  and  that  early  gastric  crises  may 
simulate  a  gastric  affection,  early  disturbance  in  mictui'ition  a  vesical  trouble,  or 
swelling  of  the  joints  a  joint  disease,  until  careful  examination  of  the  other  symp- 
toms explains  the  true  nature  of  the  disease. 

In  the  fully  developed  ataxic  stage  of  tabes  the  diagnosis  is  almost  always  easy, 
and  often  cau  be  made  at  the  first  glance.  The  history,  the  characteristic  ataxic 
gait,  the  swaying  with  the  eyes  shut,  the  absence  of  the  reflexes,  etc.,  make  the 
diagnosis  certain.  The  diagnosis  may  be  more  difficult  if  we  happen  to  see  the 
patient  for  the  first  time  in  the  final  stage,  when  actual  paralysis  has  set  in,  when 
a  complicating  hemiplegia  has  arisen,  etc.  In  such  cases  we  must  lay  stress  on 
the  development  of  the  disease  and  find  out  what  characteristic  tabetic  symptoms 
— pupillary  symptoms,  absence  of  patellar  reflex,  remains  of  ataxia,  or  pains — can 
now  be  discovered.  With  proper  attention  and  knowledge  of  the  case,  the  diag- 
nosis can  eveu  then  almost  always  be  made  correctly. 

Vertebral  affections  are  to  be  mentioned  first  of  the  diseases  which  may  be  con- 
fused with  tabes.  These  also  cause,  under  some  circumstances,  lancinating  pains 
and  an  absence  of  the  patellar  reflex,  as  a  result  of  compression  of  the  spinal  roots ; 
but  in  these  cases  the  later  course  of  the  disease  is  entirely  different,  apart  from  the 
changes  in  the  vertebral  column  and  the  absence  of  other  characteristic  symptoms 
of  tabes.  The  same  holds  true  of  certain  deep-seated  tumors  in  the  neighborhood 
of  the  spinal  cord.  We  have  already  said  that  in  rare  cases  a  multiple  sclerosis 
may  offer  symptoms  similar  to  those  of  tabes.  In  these  cases  the  chief  stress  in 
regard  to  diagnosis  is  to  be  laid  on  the  ensemble  of  symptoms  and  their  develop- 
ment. It  is  of  greater  practical  importance  that  certain  toxic  nervous  diseases 
may  have  a  great  similarity  to  tabes.  Chronic  alcoholic  neuritis  has  already 
been  spoken  of  in  this  connection  (see  page  583).  In  these  cases,  however,  the 
reflex  immobility  of  the  pupils  and  the  disturbances  of  the  bladder  ai'e  usually 
absent,  while  atrophic  paralysis  may  develop  later,  which  never  happens  in  tabes. 
The  serological  factors  are  also,  of  course,  to  be  taken  into  account. 

Finally,  it  may  be  mentioned  here  that  we  have  twice  seen  a  group  of  nervous 
symptoms  in  workmen  who  have  worked  many  years  in  tobacco  factories,  which 
resembled  tabes  in  so  many  points  that  we  might  term  it  "  nicotine  tabes."  The 
morbid  symptoms,  which  resemble  tabes,  consist  of  painful  sensations,  absence  of 
the  patellar  reflex,  contracted  pupils  with  reflex  immobility,  and  uncertainty  of 
gait ;  but  the  whole  type  of  the  disease  is  distinguished  from  tabes  by  a  peculiar 
tremor,  by  a  marked  increase  of  the  cutaneous  reflexes,  especially  in  the  lower 
extremities,  etc. 

Treatment. — The  tedious  course  of  tabes  demands  that  the  physician  have  at 
hand  a  choice  of  remedies  and  methods  of  treatment  which  he  can  vary  according 


TABES  DORSALIS.  047 

to  the  predominating  circumstances,  either  to  obtain  a  certain  amount  of  improve- 
ment by  a  new  way  of  attacking  the  disease,  or  at  least  constantly  to  kindle  tin- 
patient's  hope  and  courage  anew. 

If  syphilis  be  a  possible  etiological  factor,  we  regard  it  as  entirely  justifiable 
to  prescribe  first  an  antisyphilitic  treatment:  inunction  of  fifty  to  seventy-livo 
grains  (grm.  3-5)  of  mercurial  ointment  a  day,  with  iodide  of  potassium  inter- 
nally. In  very  many  cases  this,  of  course,  does  no  brilliant  service — at  times  the 
disease  has  even  been  noticed  to  grow  worse  under  inunction— but  sometimes  we 
see  distinct  improvement.  The  earlier  the  treatment  is  begun,  the  more  is  to  be 
expected  of  it.  At  any  rate,  we  should  try  whether  we  can  not  check  the  further 
advance  of  the  disease  by  a  methodical  and  continuous  antisyphilitic  treatment. 
When  symptoms  implying  loss  of  function  {Ausfallssymptome)  have  already 
appeared,  we  can  not,  of  course,  cause  them  to  disappear,  for  iodine  and  mer- 
cury can  not  restore  fibers  in  the  posterior  columns  that  have  already  been 
destroyed. 

If  the  antisyphilitic  treatment  be  not  indicated,  or  have  been  unsuccessful,  elec- 
tricity and  balneo-therapeutics  or  hydro-therapeutics  deserve  the  most  confidence. 

The  electrical  treatment  consists  chiefly  of  the  passage  of  the  ascending  con- 
stant current  through  the  spinal  cord.  The  cm-rents  must  not  be  too  strong,  and 
the  sittings  should  take  place  daily,  or  every  other  day.  Erb  recommends  placing 
the  medium-sized  cathode  in  the  vicinity  of  the  sympathetic,  and  the  large  anode 
close  to  the  spinous  processes  on  the  other  side  of  the  vertebral  column,  moving  it 
at  intervals  from  above  downward.  This  procedure  lasts  about  four  or  five  min- 
utes for  each  side.  We  also  obtain  good  results  symptomatically  when  there  are 
severe  pains,  vesical  weakness,  etc.,  by  peripheral  galvanization.  If  we  find  pain- 
ful points  on  the  vertebral  column,  as  is  rarely  the  case,  they  should  be  especially 
treated  with  the  stabile  anode.  Lately,  the  treatment  recommended  by  Rumpf 
with  the  faradic  bimsh  has  been  used  several  times  with  good  results.  This  con- 
sists in  brushing  the  skin  of  the  back  and  the  extremities  with  a  strong  current 
for  five  or  ten  minutes.  Every  form  of  electrical  treatment,  in  order  to  obtain 
results,  must  be  kept  up  for  months. 

Hydro-therapeutics,  used  rationally,  have  often  resulted  in  considerable  im- 
provement in  tabes,  although  they  may  cause  much  mischief.  Hot  baths,  espe- 
cially vapor-baths,  are  often  followed  by  a  rapid  change  for  the  worse — a  fact 
which,  unfortunately,  we  can  often  observe  where  vapor-baths  have  been  pre- 
scribed for  patients  at  the  beginning  of  their  disease  "for  rheumatism."  Con- 
tinuous wet  packs  and  severe  rubbings  are  also  often  accompanied  by  unfavorable 
results.  Tepid  half  or  full  baths,  however,  of  75°  to  86°  at  most  (20°-24°  R.), 
associated  with  gentle  rubbing  of  the  skin,  often  do  good  seiwice.  Wet  com- 
presses, laid  about  the  abdomen  or  the  legs  at  night,  often  have  a  favorable  influ- 
ence on  the  pains.  In  general,  it  is  a  good  plan  to  send  well-to-do  patients  in 
summer  to  a  water-cure  establishment  which  is  conducted  by  an  experienced 
director  and  well  managed,  but  the  necessary  procedures  may  also  be  undertaken 
at  home. 

Of  the  baths  whose  use  is  recommended  in  tabes,  Oeynhausen-Rehme  has 
the  greatest  reputation,  and  the  best  results  to  show.  Many  tabetics,  of  course, 
come  back  from  Rehme  just  as  they  went;  but,  in  advising  a  bath,  Rehme  is 
always  the  first  to  be  considered.  We  may  refer  to  what  was  said  on  page  626 
as  to  the  establishment  of  artificial  Rehme  baths.  The  baths  in  Nauheim  have  a 
very  singular  composition.  The  indifferent  thermal  baths,  Teplitz,  Wildbad.  and 
Ragatz,  formerly  much  in  favor,  have  at  present  lost  their  reputation  in  tabes. 
Mud  baths  and  iron  baths — Pyrmont,  Driburg,  Cudowa,  Elster,  Fx*anzensbad — may 
sometimes  act  favorably. 


648  DISEASES  OF  THE  NERVOUS  SYSTEM. 

Besides  the  methods  of  treatment  so  far  mentioned,  there  are  still  a  number  of 
internal  remedies,  the  use  of  which  seems  sometimes  to  be  of  advantage.  The 
chief  ones  to  be  mentioned  are  nitrate  of  silver,  first  recommended  by  Wunderlich, 
one-sixth-of-a-grain  pills  (grm.  O'Ol),  at  first  three,  gradually  increasing  to  six  a 
day,  before  meals;  and  ergotine,*  one-grain  pills  (grm.  0#05),  three  to  six  a  day; 
we  may  also,  try  iodide  of  potassium,  phosphorus,  arsenic  [chloride  of  aluminium, 
two  to  four  grains.(grm.  0'l-0-25),  thrice  daily],  etc.  All  these  remedies,  especially 
the  two  first  named,  may  be  used  for  a  long  time,  and,  with  interruptions,  even 
for  years. 

Finally,  we  must  mention  here  nerve-stretching,  usually  stretching  of  the 
sciatics,  which  for  a  short  time  was  practiced  on  many  tabetic  patients  as  a  result 
of  a  somewhat  too  sanguine  recommendation  on  the  part  of  Langenbuch.  Since, 
however,  experience  has  taught  us  that  nerve-stretching,  in  spite  of  some  apparent 
successes,  scarcely  ever  exerts  a  permanent  favorable  action,  and  is  also  not  wholly 
without  danger,  the  operation  has  been  almost  entirely  given  up  in  tabes.  It  may 
still  be  tried  in  those  cases  where  we  have  unusually  severe  attacks  of  pain  in  the 
region  of  definite  nerves. 

[Of  late  years  Charcot  has  advocated  suspension  in  the  treatment  of  tabes. 
The  patient  is  suspended  in  a  Sayre  apparatus  from  one  to  three  minutes  daily  or 
every  other  day.  It  is  not  without  danger,  and  it  should  not  be  employed  if  any 
spastic  symptoms  be  present.  It  has  not  met  with  the  success  at  first  claimed  for 
it,  but  in  a  few  cases  it  seems  to  relieve  the  pain  and  the  ataxic  gait. — K.] 

Symptomatically,  the  same  remedies  are  to  be  considered  as  were  mentioned  in 
the  treatment  of  chronic  myelitis.  We  try  to  alleviate  the  pains  by  narcotic 
embrocations  and  bandaging  the  legs.  Of  internal  remedies,  sodic  salicylate  and 
antipyrine  sometimes  undoubtedly  alleviate  and  shorten  the  pains.  In  bad  cases 
morphine  is  indispensable.  We  try  to  remove  the  constipation  by  prescriptions 
as  to  diet,  or  by  mild  cathartics,  such  as  the  bitter  waters,  tamarinds,  and  rhubarb, 
and  by  enemata.  Morphine  is  the  best  remedy  in  the  gastric  and  laryngeal  crises. 
Cystitis  and  bedsores  must  be  treated  according  to  the  rules  in  general  use. 

In  regard  to  the  patient's  general  manner  of  life,  we  must  warn  him  against 
any  physical  or  mental  overexertion,  prescribe  a  prudent  but  strengthening  diet, 
and  enjoin  good  air,  a  country  residence  in  summer,  or  perhaps  the  Alps  or  sea 
air.  The  earlier  we  get  the  patient  under  treatment,  the  more  persevering  and 
careful  should  we  be  in  our  treatment,  because  then  we  can  still  hope  for  success. 
In  old  and  far-advanced  cases  we  must  confine  ourselves  to  a  purely  symptomatic 
treatment. 

APPENDIX. 

HEREDITARY  ATAXIA.      FRIEDREICH'S  FORM  OF  TABES. 

A  peculiar  and  rare  disease,  which  has  a  certain  similarity  to  tabes,  was  first 
described  by  Friedreich  under  the  name  of  "hereditary  ataxia."  The  affection 
almost  always  occurs  in  several  children  of  the  same  family,  and  develops  in 
youth,  somewhere  between  twelve  and  eighteen  years  of  age.  The  female  mem- 
bers of  the  family  are  decidedly  more  often  affected  than  the  male.  A  stage  of 
initial  pains  is  usually  absent.  The  disease  begins  with  a  pronounced  ataxia  of 
the  legs,  which  usually  very  soon  passes  to  the  arms.     The  tendon  reflexes  disap- 

*  There  is  only  an  apparent  contradiction  in  the  fact  that,  in  spite  of  the  occurrence  of  an  "  ergotine 
tabes  "  {vide  supra),  ergotine  is  also  used  as  a  remedy  against  tabes.  It  may  very  well  be  that  the 
same  remedy,  which  in  large  doses  causes  certain  systems  of  fibers  to  atrophy,  may  in  smaller  doses 
have  some  favorable  (irritating)  action  on  the  same  system  of  fibers ;  but  we  must  always  be  cautious 
in  the  use  of  ergotine. 


ATAXIC  PARAPLEGIA.  649 

pear  in  most  cases,  but  the  sensibility  of  the  skin  and  muscles  remains  perfectly 
intact,  a  fact  which  may  properly  be  regarded  as  evidence  for  the  independence 
of  ataxic  disturbances  from  anomalies  of  sensibility.  The  vesical  functions  also 
remain  completely  normal  for  a  long  time.  Disturbances  of  vision  have  not  been 
observed  up  to  the  present  time,  but  in  the  further  course  of  the  disease  a  peculiar 
disturbance  of  speech  arises,  which  is  probably  due  to  a  disturbance  of  co-ordina- 
tion in  the  muscular  movements  of  the  lips  and  tongue  necessary  in  speaking. 
Friedreich  has  also  sought  to  interpret  the  nystagmus  which  appears  by  the  hypo- 
thesis of  an  "  ataxic  nystagmus."  The  disease  lasts  for  a  very  long  time,  for  many 
years,  and  finally  leads  to  complete  paralysis,  contractures,  and  atrophy  of  the 
paralyzed  muscles. 

The  anatomical  examination  of  the  spinal  cord  has  so  far  shown  in  all  cases  a 
combined  fascicular  disease  of  the  posterior  and  lateral  columns.  In  the  case  re- 
ported by  Kahler  and  Pick  this  disease  could  be  demonstrated  as  a  combined 
systemic  disease.  It  affected  the  lateral  pyramidal  tracts,  the  lateral  cerebellar 
tracts,  the  fundamental  bundle  of  the  posterior  columns,  and  the  columns  of 
Goll.  F.  Schultze  has  lately  taken  the  same  views  in  regard  to  the  anatomical 
lesion. 

The  disease  is  incurable;  at  least  all  the  attempts  at  treatment  up  to  the  pres- 
ent time  have  been  unsuccessful. 

Ataxic  Paraplegia. 

( Combined  Postero-lateral  Sclerosis.) 

[This  name  has  been  given  by  Gowers  to  a  chronic  degenerative  disease  of  the 
spinal  cord  which  involves  both  the  posterior  and  lateral  columns.  It  differs 
from  Friedreich's  ataxia  in  that  it  is  not  a  family  disease,  and  that  it  usually  at- 
tacks persons  in  middle  life,  men  being  affected  more  frequently  than  women. 
Unlike  true  tabes,  syphilis  is  only  rarely  a  factor  in  the  aetiology.  The  various 
alleged  causes  of  chronic  myelitis  have  been  supposed  to  have  an  influence  in  pro- 
ducing this  affection,  especially  exposure  to  cold,  trauma,  and  sexual  excess.  In 
Italy,  pellagra  has  been  known  to  produce  it.  Chronic  lead  poisoning  may  be  of 
influence. 

As  has  been  said,  the  pyramidal  tracts  and  the  postero-median  columns  are 
chiefly  affected,  but  the  degeneration  is  not  limited  absolutely  to  these  systems  of 
fibers. 

The  symptoms,  as  may  be  inferred  from  the  distribution  of  the  sclerosis,  are  a 
combination  of  those  of  spastic  paraplegia  and  true  tabes.  There  is  weakness  of 
the  legs  combined  with  ataxia.  Rigidity  is  a  late  symptom.  Pain  is  occasionally 
present,  but  it  is  much  less  marked  than  in  true  tabes.  Sensory  disturbances 
are  rarely  met  with.  The  knee-jerk  is  usually  exaggerated,  and  there  may  be 
ankle  clonus.  If,  however,  Westphal's  tract  be  involved  (vide  supra),  the  knee- 
jerk  is  lost.  The  bladder  and  rectum  may  become  affected  later.  Eye  symptoms 
are  not  common.     The  affection  may  be  associated  with  general  paralysis  (q.  v.). 

The  affection  is  slowly  progressive.  The  diagnosis  is  based  on  the  co-existence 
of  ataxia  and  paraplegia,  and  the  absence  of  sensory  and  ocular  symptoms. 
Transition  forms  more  closely  resembling  chronic  myelitis  may  also  occur.  The 
treatment  is  that  of  chronic  myelitis. — K.] 


650  DISEASES  OF  THE  NERVOUS  SYSTEM. 

CHAPTER  VII. 
AMYOTROPHIC   LATERAL   SCLEROSIS. 

Amyotrophic  lateral  sclerosis  is  a  disease  perfectly  sharply  defined  both  in  its 
clinical  and  its  pathological  aspects,  and  in  the  majority  of  cases  it  may  be  diag- 
nosticated with  great  certainty,  even  during  the  patient's  life.  For  the  first  accu- 
rate knowledge  of  it  we  must  thank  Charcot,  who  published  in  1869,  in  company 
with  Joffroy,  his  first  observations  upon  such  cases,  and  who  in  1874  was  able  to 
give  quite  a  complete  description  of  the  disease ;  but  an  exact  knowledge  of  amyo- 
trophic lateral  sclerosis  was  first  made  possible  by  Flechsig's  investigations  upon 
the  course  of  the  paths  of  conduction  in  the  spinal  cord.  According  to  these,  it 
may  be  stated  with  perfect  certainty  that  the  affection  is  to  be  regarded  as  a  sys- 
temic degeneration  of  the  pyramidal  tract  throughout  its  whole  extent,  or  at  least 
in  certain  portions  of  it,  combined  with  atrophy  of  certain  nerve-nuclei  in  the 
medulla  oblongata.  It  is  still  entirely  unknown  to  us  what  causes  bring  on  the 
disease  of  these  nerve-fibers  and  the  cells  belonging  to  them.  In  individual  cases 
we  can  not  usually  make  out  any  definite  aetiological  factor  at  all.  Severe  physi- 
cal exertion  is  sometimes  claimed  to  be  a  cause  for  the  disease.  It  occurs  chiefly 
in  persons  in  youth  and  middle  life,  between  twenty-five  and  forty-five.  The  male 
sex  seems  to  be  decidedly  more  prone  to  the  disease  than  the  female. 

Pathological  Anatomy. — In  the  typical  cases  of  amyotrophic  lateral  sclerosis, 
which  come  to  autopsy  in  the  last  stage  of  the  disease  (initial  cases  have  not  yet 
been  examined  anatomically),  we  find  in  the  spinal  cord  a  degeneration  or  "  sclero- 
sis "of  both  pyramidal  tracts,  and  a  considerable  atrophy  of  the  corresponding 
large  ganglion-cells  in  the  anterior  gray  cornua,  especially  in  the  external  portion. 
The  degeneration  of  the  pyramidal  tract  is  to  be  made  out  either  in  the  two  lateral 
columns  alone,  or,  if  there  be  an  anterior  pyramidal  tract  also,  in  one  or  both 
anterior  columns  (see  page  535  and  Figs.  66  and  67).  It  occupies  mainly  the  same 
area  on  cross-section  of  the  cord  as  the  region  of  the  pyramidal  tract ;  the  boundaries 
of  which  tract  have  been  determined  by  the  distribution  of  secondary  descending 
degeneration  {vide  infra),  and  by  the  results  of  the  history  of  development.  Begin- 
ning in  the  lowest  part  of  the  lumbar  cord,  it  may  be  traced  upward  to  the  pyra- 
mids of  the  medulla,  and  sometimes,  but  not  always,  still  farther  through  the  pons 
and  the  crura  to  the  internal  capsule.  In  some  cases  examined  recently  by  Char- 
cot and  Marie  the  degeneration  extended  even  to  the  central  convolutions,  whose 
large  motor  ganglion-cells  also  showed  a  pronounced  atrophy.  Toward  the  lateral 
cerebellar  tract  the  disease  of  the  pyramidal  tract  in  the  cord  is  very  sharply  de- 
fined, but  in  the  anterior  portions  of  the  lateral  columns  other  bundles  of  fibers 
are  often  affected.  The  whole  extent  of  the  disease  in  the  lateral  columns  is 
therefore  usually  greater  in  amyotrophic  lateral  sclerosis  than  in  secondary  de- 
scending degeneration.  Of  the  greatest  clinical  importance,  however,  is  the  al- 
ready-mentioned co-existing  disease  of  the  motor  ganglion-cells  in  the  anterior 
cornua  of  the  spinal  cord  and  the  disease  of  certain  nerve-nuclei  in  the  medulla 
oblongata,  especially  the  hypoglossus  nucleus,  the  vagus-accessory  nucleus,  etc. 
From  these  cells,  which  are  inserted  into  the  motor  tract,  the  degeneration  passes 
on  toward  the  periphery,  in  the  affected  nerve-trunks  (hypoglossus,  etc.),  or  in 
the  anterior  roots  belonging  to  them.  It  is  difficult  to  make  out  atrophied 
fibers  in  the  peripheral  nerves,  and  up  to  the  present  time  they  have  not  always 
been  looked  for  with  sufficient  care,  but  it  can  scarcely  be  doubted  that  the 
affected  motor  fibers,  which  are  processes  of  the  atrophied  ganglion-cells,  are 
likewise  to  be  found  in  a  condition  of  degeneration.  Finally,  the  muscles  show 
a  considerable  atrophy,   as  is  plainly  manifest  even  during  the  life-time  of  the 


AMYOTROPHIC  LATERAL  SCLEROSIS.  <;:,! 

patient.  Their  volume  is  much  diminished;  many  muscles  (for  details  vide  in- 
fra) finally  almost  wholly  disappear,  so  that  in  their  place  there  is  little  left 
but  connective  tissue  and  fat.  In  the  other  muscles  we  find,  besides  a  number 
of  normal  fibers  still  preserved,  many  very  small  fibers,  and  also  some  which 
have  lost  their  tran verse  striation  and  show  a  granular  or  fatty  degeneration. 
The  nuclei  of  the  sarcolemma  are  usually  increased,  and  the  interstitial  fat  tissue 
is  often,  but  not  always,  abundantly  developed. 

We  accordingly  see  that  the  anatomical  basis  of  amyotrophic  lateral  sclero- 
sis is  a  more  or  less  completely  isolated  disease  of  the  great  motor  cortico-mus- 
cular  conducting  tract  from  the  center  to  the  periphery.  The  process  is  to  be 
regarded  as  a  simple  degenerative  atrophy.  Fiber  after  fiber  becomes  diseased  and 
atrophies.  We  do  not  know  where  the  process  begins,  whether  at  one  definite  spot, 
whence  it  extends  upward  and  downward,  or  whether  the  fibers  throughout  their 
whole  extent,  with  the  corresponding  ganglion-cells  and  muscular  fibers,  are  at- 
tacked at  the  same  time.  Perhaps  different  possibilities  are  to  be  regarded  in  these 
cases,  which  may  explain  the  many  variations  in  the  clinical  course.  At  any  rate, 
the  different  portions  of  the  system  may  become  diseased  in  a  varying  order,  and 
the  further  extension  of  the  disease  may  vary  in  its  rapidity.  The  spinal  and  the 
bulbar  diseases  are  perfectly  analogous  to  each  other  and  are  co-ordinated.  Both 
affect  portions  of  the  same  system ;  one  belongs  to  the  muscles  of  the  extremities, 
the  other  to  the  muscles  of  the  face,  tongue,  etc.  The  nerve-nuclei  in  the  medulla 
are  to  be  regarded  as  precisely  analogous  to  the  anterior  gray  cornua.  The  destruc- 
tion of  the  nerve-fibers  is  always  the  primary  process,  the  increase  of  the  intersti- 
tial connective  tissue  and  the  slight  changes  in  the  vessels  are  a  secondary,  acci- 
dental process. 

Besides  the  typical  cases  of  amyotrophic  lateral  sclerosis,  there  are  also,  quite 
rarely,  combined  and  transitional  forms.  Besides  the  degeneration  of  the  pyram- 
idal tract,  an  affection  of  the  posterior  columns  and  a  degeneration  of  the  lateral 
cerebellar  tract  have  also  occasionally  been  found. 

Clinical  History. — In  all  typical  cases  the  clinical  symptoms  give  a  perfectly 
characteristic  type  of  disease,  limited  strictly  to  the  motor  sphere,  corresponding 
to  the  perfectly  systemic  anatomical  lesions  just  described. 

The  first  signs  of  the  disease  almost  always  begin  in  the  arm.  The  patient 
notices  a  difficulty  in  working,  and  becomes  easily  tired.  The  weakness  of  the 
arm  gradually  increases,  and  finally,  usually  some  months  later,  involves  the 
other  arm.  A  wasting  of  certain  muscles,  which  gradually  increases  and  be- 
comes more  extensive,  is  now  often  noticed  by  the  patient.  About  six  months 
or  a  year  later,  symptoms  appear  in  the  lower  extremities.  The  gait  becomes 
stiff  and  uncertain,  the  patient  gets  tired  more  easily,  and  quite  a  marked  tremor 
of  the  legs  often  comes  on,  apparently  spontaneously. 

If  we  now  examine  the  patient  carefully,  the  type  of  the  disease  is  usually 
perfectly  plain.  We  notice,  first  in  the  upper  extremities,  a  very  pronounced 
and  more  or  less  extensive  muscular  atrophy.  This  is  usually  most  marked 
where  it  begins — namely,  at  the  thenar  and  hypothenar  eminences.  The  inter- 
ossei  are  also  plainly  atrophied,  and  the  muscles  on  the  extensor  side  of  the 
forearms.  The  flexors  of  the  hand  and  the  fingers  remain  intact  longer.  In 
the  upper  arm  the  triceps  and  the  deltoid  are  usually  the  most  atrophied,  and 
later,  and  to  a  less  degree,  the  biceps  and  the  muscles  of  the  shoulder.  We  find 
a  functional  disturbance  of  the  muscles — a  paresis — corresponding  to  the  degree 
of  atrophy.  The  functional  capacity  depends  upon  how  much  muscle  is  left, 
and  only  with  a  complete  disappearance  of  the  muscle  is  there  a  complete  loss 
of  the  corresponding  motion,  but  a  marked  paresis  can  sometimes  be  noticed  in 
muscles  which  are  not  yet  much  atrophied.      The   electrical  excitability  in  the 


652  DISEASES  OF  THE  NERVOUS  SYSTEM. 

muscular  fibers  still  preserved  is  normal.  The  strength  of  contraction  of  the 
muscle  irritated  by  the  faradic  current  is  therefore  proportional  to  the  amount 
of  muscular  substance  still  present.  In  the  much-atrophied  muscles  the  effects 
of  irritation  are  finally  very  slight,  and  then  we  can  always  make  out  a  distinct 
reaction  of  degeneration  in  the  degenerated  muscular  fibers  that  are  still  left,  es- 
pecially in  the  bail  of  the  thumb.  We  can  scarcely  ever  make  out  with  certainty 
a  loss  of  excitability  in  the  nerve- trunk,  probably  because  here  a  greater  number 
of  normal  fibers  are  always  preserved. 

The  examination  of  the  tendon  reflexes  is  very  important.  They  are  invari- 
ably much  increased,  even  from  the  early  stages  of  the  disease.  We  obtain  vigor- 
ous reflex  contractions  from  a  gentle  blow  on  the  tendons  of  the  biceps  and  the 
triceps,  and  on  the  lower  ends  of  the  bones  of  the  forearm.  These  are  of  diag- 
nostic importance,  because  they  never  occur  in  this  way  in  ordinary  "  progress- 
ive muscular  atrophy" — that  is,  that  disease  in  which  the  degeneration  extends 
merely  from  the  muscles  to  the  motor  ganglion-cells  in  the  anterior  cornua,  while 
the  lateral  motor-tracts  remain  free  (vide  infra).  In  the  later  stages  of  the  dis- 
ease marked  contractures  in  the  arms  and  hands  sometimes,  but  not  always,  de- 
velop. The  sensibility  of  the  skin  and  deeper  parts,  however,  remains  absolutely 
normal. 

The  first  morbid  symptoms  usually  develop  in  the  lower  extremities  some 
months  later  tban  in  the  arms.  The  pure  spastic  symptoms  are  here  remarkably 
prominent,  while  the  muscular  atrophy  is  late  in  its  development,  and  is  but 
slight.  The  legs  become  stiff,  and  oppose  considerable  muscular  resistance  to 
attempts  at  passive  motion,  but  the  crude  strength  of  the  muscles  is  decidedly 
below  the  normal.  There  is  an  obvious  paresis,  although  there  is,  as  it  seems, 
hardly  ever  a  complete  paralysis  of  the  legs;  and  the  disturbance  of  motion,  at 
any  rate,  is  considerably  increased  by  the  spastic  symptoms  (see  a  later  chapter). 
These  symptoms  depend  mainly  upon  the  great  increase  of  the  tendon  reflexes. 
The  patellar  reflex  is  very  vigorous,  and  we  often  find  a  marked  and  persistent 
ankle  clonus.  The  patient  can  still  walk  quite  a  distance,  but  the  gait  is,  of  course, 
difficult  and  laborious.  The  patient  walks  with  short,  slow,  dragging  steps — the 
spastic-paretic  gait.  The  sensibility  also  remains  absolutely  normal  in  the  legs. 
The  cutaneous  reflexes  show  no  striking  changes.  Disturbances  in  micturition 
are  also  entirely  absent.  The  bowels  may  be  somewhat  costive,  but  are  otherwise 
normal. 

After  the  condition  has  lasted  for  some  time  (a  year  or  two)  in  this  form- 
muscular  atrophy  and  increased  tendon  reflexes  in  the  upper  extremities  and 
spastic  paresis  in  the  lower— and  has  slowly  grown  worse,  bulbar  symptoms  come 
on  in  the  third  and  last  stage  of  the  disease.  The  speech  gradually  becomes  more 
indistinct,  and  there  is  difficulty  in  swallowing.  If  we  examine  closely  we  find 
the  lips  atrophied,  so  that  puckering  the  mouth,  whistling,  etc.,  are  difficult.  We 
also  notice  a  decided  atrophy  of  the  tongue.  Its  surface  is  uneven,  and  we  notice 
more  or  less  marked  fibrillary  twitchings  of  single  muscular  bundles.  The  sensi- 
bility is  also  normal  here.  We  sometimes  find  a  vigorous  masseter  reflex  (jaw- 
jerk)  on  striking  the  lower  jaw,  analogous  to  the  increased  tendon  reflexes  in  the 
extremities.  If  the  patient  have  trouble  in  taking  food,  from  difficulty  in  swal- 
lowing, the  state  of  the  general  nutrition  soon  becomes  worse.  Respiratory  dis- 
turbances are  usually  the  final  immediate  cause  of  death,  if  an  intercurrent  disease, 
such  as  inhalation  pneumonia,  etc.,  does  not  previously  put  an  end  to  the  patient's 
melancholy  condition. 

The  picture  of  amyotrophic  lateral  sclerosis  just  sketched  accords  very  well 
with  the  pathological  lesions.  As  the  degeneration  affects  the  main  motor  tract 
exclusively,  the  clinical  symptoms  are  also  limited  entirely  to  the  domain  of 


PROGRESSIVE   (SPINAL)   MUSCULAR  ATROPHY.  653 

motility.  The  associated  affection  of  the  antei'ior  gray  cornua  explains  the  occur- 
rence of  muscular  atrophy,  while  the  degeneration  of  the  lateral  columns  must 
be  made  answerable  for  the  paresis,  independent  of  the  atrojmy,  and  for  the 
spastic  symptoms.  The  increase  of  the  tendon  reflexes,  whose  reflex  arc  passes 
through  the  anterior  cornua,  forces  us  to  suppose  that  the  disease  in  the  lateral 
columns  precedes  the  degeneration  in  the  anterior  cornua,  as  this  increase  is  seen 
especially  in  the  lower  extremities;  for  manifestly  there  can  be  no  longer  any 
reflex  in  muscular  fibers  whose  special  ganglion-cells  are  already  atrophied.  The 
increased  reflexes  are  seen  only  in  muscles  which  are  composed,  at  least  in  part,  of 
normal  fibers.  The  bulbar  symptoms  are  dependent  upon  the  degeneration  of  the 
nerve-nuclei  in  the  medulla. 

The  diagnosis  of  the  disease  is  usually  easily  made.  Its  typical  course,  the 
muscular  atrophy  with  co-existing  increased  tendon  reflexes,  the  complete  absence 
of  sensory  or  vesical  disturbances,  and  the  final  appearance  of  bulbar  symptoms, 
are  chiefly  to  be  considered  in  diagnosis.  Confusion  may  arise  from  the  fact  that 
tumors  or  myelitis  may  for  a  long  time  have  a  similar  localization,  as  in  the  gray 
matter  of  the  cervical  cord,  and  therefore  provoke  analogous  symptoms ;  but  in 
such  cases  the  later  course  is  almost  always  different,  and  thus  a  subsequent  diag- 
nosis can  be  made  correctly. 

The  prognosis  of  amyotrophic  lateral  sclerosis  must  be  regarded  as  absolutely 
unfavorable.  The  disease  advances  slowly  but  unceasingly,  and  usually  leads  to 
death  in  a  few  years.  Only  in  a  few  cases,  occurring  in  early  youth  (Seeligmüller), 
does  the  disease  seem  to  come  to  a  standstill. 

We  can  therefore  expect  but  slight  results  from  treatment.  At  most  we  can 
perhaps  check  the  advance  of  the  disease  by  an  electrical  treatment,  kept  up  with 
very  great  patience  and  perseverance. 


CHAPTER  VIII. 
PROGRESSIVE   (SPINAL)   MUSCULAR  ATROPHY. 

Preliminary  Remarks  and  Pathological  Anatomy.— Few  diseases  of  the  spinal 
cord  have  undergone  such  different  conceptions  and  significations  in  the  course 
of  time  as  progressive  muscular  atrophy.  The  reason  for  this  lies  chiefly  in  the 
fact  that  its  main  symptom,  the  progressive  atrophy  of  the  voluntary  muscles, 
may  be  found  in  many  totally  distinct  diseases,  and  hence  has  given  rise  to  con- 
stant confusion  and  mistakes.  If,  at  the  present  time,  we  read  the  older  and  even 
a  part  of  the  newer  literature  on  this  subject,  we  find  everywhere  a  mixture  of 
different  cases,  not  at  all  of  the  same  disease,  and  only  the  latest  accurate  clinical 
and  anatomical  methods  of  investigation  have  enabled  us  to  bring  at  least  some 
order  out  of  this  chaos. 

Except  for  a  few  earlier  observations,  Duchenne  and  Aran,  in  1849  and  1850, 
gave  the  first  good  description  of  progressive  muscular  atrophy.  The  French 
observers,  therefore,  at  present  speak  of  the  disease,  in  distinction  from  other 
similar  affections,  as  " atrophie  musculaire  progressive,  type  Duchenne- Aran.'" 
A  short  time  after,  in  1855,  Cruveilhier,  on  the  ground  of  a  positive  lesion  on 
autopsy,  first  pronounced  the  opinion  that  a  disease  of  the  gray  matter  in  the 
spinal  cord  was  to  be  regarded  as  the  special  anatomical  cause  of  the  disease. 
Since  then  a  tedious  dispute  has  been  carried  on,  and  even  in  part  kept  up  to  the 
present  time,  as  to  whether,  in  fact,  the  disease  has  its  seat  in  the  spinal  cord,  or 
rather  in  the  muscles  themselves — a  dispute  which  was  necessarily  without  results 


654  DISEASES  OF  THE  NERVOUS  SYSTEM. 

for  a  long  time ;  the  more  because  the  actual  pathological  basis  was  very  scanty, 
and  because  the  data  of  examinations  completely  contradicted  one  another,  owing 
to  the  confusion  between  different  forms  of  morbid  processes  which  did  not  belong 
together  at  all.  Tbe  spinal  nature  of  the  disease  was  proven  especially  by  the  in- 
vestigations of  Lockhart  Clarke,  and  Charcot,  while  in  Germany  Friedreich  in 
particular  has  of  late  asserted  its  myopathic  origin. 

In  our  opinion  there  can  no  longer  be  any  doubt*  of  the  fact  that  there  is 
a  perfectly  clearly  defined  disease,  whose  chief  clinical  symptom  consists  of  a 
very  slow  but  constantly  progressing  atrophy  of  the  muscles,  following  a  certain 
type,  while  anatomical  examination  shows  a  degenerative  atropby,  not  only  of 
the  affected  muscles,  but  also  of  the  corresponding  peripheral  nerve-fibers,  an- 
terior root-fibers,  and  motor  ganglion-cells  in  the  anterior  cornua  of  the  spinal 
cord.  We  are  therefore  right  in  separating  this  disease,  as  a  "  spinal  form  of 
progressive  muscular  atrophy,"  from  those  cases  where  there  is  also  the  develop- 
ment of  an  independent  progressive  atrophy  of  the  muscles,  but  where  the  affec- 
tion always  remains  to  the  last  confined  to  the  muscles,  and  never  invades  the 
motor  nerves  and  the  spinal  cord.  These  last-named  cases  form  the  pure  muscu- 
lar atrophies,  which  correspond  to  the  types  of  the  "  hereditary  or  juvenile  muscu- 
lar atrophy  or  pseudo-hypertrophy  "  (see  the  appendix  to  this  chapter).  The  spi- 
nal form  of  progressive  muscular  atrophy,  with  which  we  have  to  do  here,  is 
undoubtedly  nearly  allied  to  "  amyotrophic  lateral  sclerosis,"  described  in  the  pre- 
vious chapter;  but  although  in  the  latter  the  whole  pyramidal  motor  tract  may  be 
degenerated,  and  the  lateral  pyramidal  tracts  in  the  cord  are  in  particular  always 
affected,  in  "  progressive  muscular  atrophy  "  the  degeneration,  as  we  have  said,  is 
confined  to  that  portion  of  the  motor  conducting  tract  which'  extends  from  the 
ganglion-cells  of  the  anterior  cornua  to  the  muscular  fibers  themselves.  The 
further  central  prolongation  of  this  tract,  however— that  is,  the  lateral  pyramidal 
tract — remains  perfectly  normal.  It  is  very  improbable  that  this  difference  in  the 
extent  of  the  anatomical  localization  is  the  principal  distinction  between  the  two 
diseases  named.  In  their  serological  relations  the  two  diseases,  and  also  progress- 
ive bulbar  paralysis  (vide  infra),  are  identical.  The  clinical  distinctions  due  to 
the  different  anatomical  localization  are,  however,  of  sufficiently  marked  promi- 
nence to  justify,  at  least  provisionally,  a  special  description  of  progressive  muscular 
atrophy  and  of  amyotrophic  lateral  sclerosis.  [In  the  great  majority  of  cases 
which  have  come  to  autopsy,  changes  have  been  found  in  the  lateral  columns,  so 
that  an  anatomical  distinction  between  the  three  affections  can  hardly  be  main- 
tained. Hence  Schultze  suggests  the  name  of  motor  tabes  as  a  general  term  for 
the  three. — K.] 

The  precise  anatomical  lesion  in  progressive  (spinal)  muscular  atrophy  is  as 
follows : 

In  the  spinal  cord,  most  marked  usually  in  the  cervical  cord,  we  find  the  ante- 
rior gray  cornua  very  small ;  the  ganglion-cells  have  wholly  or  largely  disap- 
peared, and  those  remaining  are  atrophied;  and  the  neuroglia  is  changed  to  a  fine 
fibrous  tissue,  sometimes  studded  with  spider-cells;  but  the  lateral  columns,  espe- 
cially the  pyramidal  tracts— that  is,  the  portion  of  the  motor  conducting  tract  cen- 
tral to  the  ganglion-cells  of  the  anterior  cornua — are  perfectly  normal.  The 
anterior  roots  and  the  affected  motor  fibers  in  the  peripheral  nerves  are  also  atro- 
phied, although  in  the  nerve-trunks  the  discovery  of  degenerated  fibers  mixed 

*  To  the  cases  already  published  we  can  add  a  recent  observation  of  our  own,  on  a  case  of  progress- 
ive muscular  atrophy,  involving  the  upper  extremities  chiefly,  with  almost  complete  atrophy  of  the 
ganglion-cells  in  the  anterior  cornua,  although  it  was  not  followed  by  a  corresponding  co-existing 
degeneration  of  the  lateral  pyramidal  tracts. 


PROGRESSIVE   (SPINAL)   MUSCULAR  ATROPHY.  655 

with  many  other  normal  fibers  is  not  perfectly  easy.  In  the  muscles  the  atrophy 
is,  of  course,  still  more  noticeable  on  a  post-mortem  examination  than  on  examina- 
tion during  life.  The  muscles  most  affected  are  reduced  to  small,  pale,  and  flabby 
bundles,  in  which  fat  and  connective  tissue  outweigh  the  proper  muscular  tissue. 
On  histological  examination,  we  find  in  many  fibers  a  simple  atrophy — that  is  a 
very  considerable  diminution,  but  with  the  transverse  striation  still  retained ;  but 
in  many  other  fibers  we  run  across  the  signs  of  a  degenerative  atrophy — fatty  and 
waxy  degeneration  of  the  muscular  fibers,  a  splitting  longitudinally  or  trans- 
versely, etc.  The  interstitial  connective  tissue  is  always  increased,  the  muscular 
nuclei  are  increased  in  number,  and  we  often  find  quite  a  deposit  of  fat  between 
the  fibers  which  are  still  preserved. 

So  far  the  actual  lesion.  In  comprehending  it,  the  only  difficulties  arise  from 
the  questions  as  to  the  mode  of  development,  and  as  to  the  reciprocal  dependence 
of  the  different  disturbances.  Is  the  atrophy  of  the  anterior  comua  to  be  regarded 
as  primary,  and  the  atrophy  of  the  nerves  and  muscles  as  a  secondary  descending 
degeneration;  or  does  the  process  begin  in  the  muscles,  and  extend  upward  from 
them  to  the  spinal  cord ;  or,  finally,  do  we  have  to  do  with  an  approximately 
simultaneous  degeneration  of  the  whole  motor  portion  affected  ?  These  are 
questions  to  which  at  present  no  definite  answer  can  be  given.  Many  reasons  seem 
to  us  to  favor  the  belief  that  the  degenerative  process  begins  in  the  last  terminal 
branches  of  the  motor  nerves,  and  from  these  ascends  gradually  to  the  spinal  cord. 
This,  however,  is  not  yet  proven,  and  possibly  the  starting-point  of  the  disease  and 
its  further  extent  may  differ  in  different  cases. 

iEtiology  and  Clinical  History.— Progressive  muscular  atrophy  is  an  extremely 
slow  and  chronic  disease  from  the  beginning.  We  often  can  not  find  any  eetio- 
logical  factors  which  seem  to  favor  its  development,  but  in  a  good  many  cases  the 
first  symptoms  follow  an  immoderate  muscular  exertion.  Thus  we  see  the  first 
signs  of  muscular  weakness  coming  on,  for  example,  after  continued  thrashing, 
hard  washing,  and  similar  severe  physical  toil.  A  hereditary  predisposition  is 
reported  as  common  by  most  observers,  but  it  is  at  present  certain  that  most  cases 
of  this  "  hereditary  muscular  atrophy  "  belong,  not  to  the  spinal,  but  to  the  myo- 
pathic form  {vide  infra).  It  also  seems  to  us  to  be  very  probable  that  of  most  of 
the  other  etiological  factors  reported  their  number  is  to  be  explained,  for  the 
most  part,  only  by  erroneously  reckoning  other  forms  of  atrophic  processes  with 
genuine  progressive  muscular  atrophy.  We  refer  especially  to  the  alleged  origin 
of  this  disease  from  injuries,  from  acute  diseases,  such  as  typhoid  and  diphtheria, 
or  from  syphilis. 

The  disease  begins,  by  far  the  most  frequently,  in  the  upper  extremities,  and 
especially,  as  it  seems,  in  the  right  arm,  but  sometimes  in  the  left,  or  in  both  arms 
at  once.  As  a  rule,  it  begins  with  an  atrophy  of  the  short  muscles  of  the  thumb 
and  of  the  hypothenar  eminence,  which  is  accompanied  by  a  corresponding  dis- 
turbance of  function.  Any  other  symptoms,  especially  disturbances  of  sensibility, 
paresthesia,  or  pain,  are  usually  entirely  absent.  The  atrophy  usually  affects  the 
abductor  pollicis  brevis  first,  and  then  the  opponens  and  the  adductor.  We  notice 
very  early  the  characteristic  sinking  in  and  flattening  of  the  ball  of  the  thumb, 
and  the  abnormal  position  of  the  thumb,  which  is  persistently  approximated  to 
the  second  metacarpal  bone — the  "ape  hand."  At  the  same  time,  or  a  little 
earlier  or  later,  the  interossei  begin  to  atrophy,  which  is  recognized  by  the  sink- 
ing in  of  the  interosseous  spaces  and  the  increasing  incomplete  extension  of  the 
terminal  phalanges  of  the  fingers.  The  atrophy  of  the  lumbricales  causes  a 
visible  flattening  of  the  hollow  of  the  hand.  If  the  disturbance  in  the  function 
of  the  interossei  have  reached  a  certain  degree,  the  same  claw-like  position  of  the 
fingers  appears,  as  we  have  already  learned  to  recognize  in  ulnar  paralysis  (see 


656  DISEASES  OF  THE  NERVOUS  SYSTEM. 

Fig.  78),  due  to  the  contracture  of  the  antagonist  of  the  interossei,  the  extensor 
communis  digitorum. 

In  the  further  progress  of  the  disease  the  atrophy  extends  either  to  the  muscles 
of  the  forearm,  or,  what  is  not  at  all  rare,  it  jumps  over  these  and  attacks  the 
muscles  of  the  shoulder,  usually  the  deltoid  first.  In  the  forearm  it  is  usually  the 
muscles  on  the  extensor  side  which  are  first  attacked,  the  abductor  and  extensor 
lougus  pollicis,  and  only  later  the  supinators,  flexors,  etc.  In  the  upper  arm  the 
deltoid  almost  always  atrophies  first,  and  then  the  biceps,  while  the  triceps  may 
remain  intact  for  a  comparatively  long  time.  Sooner  or  later  the  muscles  of  the 
trunk  are  often  added  to  the  list,  the  trapezius  first  usually,  then  the  pectorals, 
the  rhomboidei,  and  the  latissimus  dorsi.  The  disturbance  of  function  caused 
by  the  atrophy  of  all  these  muscles  is  readily  apparent  from  what  was  said  in 
the  chapter  on  the  different  forms  of  paralysis.  In  advanced  cases  the  arms  hang 
down  laxly  by  the  two  sides  of  the  trunk.  Only  with  the  greatest  difficulty,  if  at 
all,  can  the  patient  do  anything  with  them,  either  dress  or  undress;  but  he  some- 
times learns  to  help  himself,  at  least  in  some  degree,  by  throwing  movements,  by 
bending  his  body  to  meet  anything,  by  using  his  mouth  in  taking  hold  of  things* 
etc.  Quite  rarely  the  atrophy  finally  attacks  the  muscles  of  the  neck.  The 
severest  respiratory  disturbances  may  be  excited  by  an  implication  of  the  dia- 
phragm and  the  other  muscles  of  respiration. 

The  time  which  elapses  before  the  gradual  appearance  of  the  more  marked 
disturbances  of  function  is  almost  always  very  long.  Years  may  elapse  before 
the  atrophy  extends  from  the  little  muscles  of  the  hand  to  the  other  muscles  of 
the  arm.  In  the  muscles  of  the  legs  the  first  signs  of  atrophy  almost  always 
develop  very  late  if  at  all.  The  arms  are  often  perfectly  useless  when  the  patient 
can  still  walk  for  hours.  Of  course  there  are  some  exceptions  to  this  rule.  In 
the  arms  themselves,  too,  the  process  does  not  always  develop  in  the  way  described 
above.  Thus  we  not  very  rarely  see  the  affection  begin  in  the  scapular  muscles  or 
the  deltoid,  and  from  this  point  the  atrophy  involves  the  muscles  of  the  hand  or 
of  the  upper  arm.  The  muscles  of  the  trunk,  the  pectorals,  and  the  muscles  of 
the  back,  are  much  more  rarely  the  starting-point  of  the  disease,  and  in  only  a 
very  few  cases  have  we  been  able  to  make  out  that  the  disease  began  in  the  legs. 
It  is  worthy  of  note  that  in  such  abnormal  cases  the  muscles  first  affected  were 
sometimes,  but  not  always,  subjected  to  extraordinary  demands  in  camwing 
loads,  etc. 

Besides  the  atrophy,  and  the  loss  of  function  that  runs  parallel  to  it,  we  must 
mention  some  other  changes  in  the  muscles.  The  fibrillary  muscular  twitchings 
are  often  very  striking.  A  constant  tremor  and  wave  of  the  muscle  may  be  pro- 
voked by  them.  In  some  cases  they  are  weak  and  only  rarely  noticed.  They 
usually  become  vigorous  if  one  irritates  the  muscle  mechanically  by  a  blow. 
The  electrical  excitability  of  the  diseased  muscles  varies,  inasmuch  as  it  depends 
entirely  upon  the  number  of  normal  fibers  still  preserved  in  the  muscle.  Since 
the  atrophy  affects  only  one  fiber  after  another,  the  faradic  and  galvanic  excita- 
bility decrease  gradually,  and  are  lost  completely  only  when  the  greatest  part  of 
the  muscle  is  destroyed.  On  careful  testing,  we  can  then,  however,  almost  always 
make  out  a  decided  reaction  of  degeneration  in  single  muscles  that  are  much  dis- 
eased, especially  in  the  form  of  the  so-called  partial  reaction  of  degeneration :  the 
excitability  of  the  nerves  is  retained,  but  the  contractions  in  the  muscles  them- 
selves seem  very  slow,  and  the  anodic  closure  contractions  (AnSZ)  predominate 
(see  page  552). 

In  many  cases  there  is  an  increase  of  the  fatty  tissue  at  the  same  time  with 
the  atrophy  of  the  muscular  substance,  which  often  makes  it  very  hard  to  judge 
of  the  atrophy ;  but  the  loss  of  function  in  the  muscles,  the  diminished  electrical 


PROGRESSIVE  (SPINAL)   MUSCULAR  ATROPHY.  057 

excitability,  and  the  peculiar  soft  feeling  which  atrophied  muscles  have  when 
covered  with  fat,  reveal  the  true  condition  of  things.  Other  trophic  disturbances 
in  the  skin  are  usually  entirely  absent,  but  they  are  sometimes  seen.  In  a  few 
cases  a  spontaneous  pemphigoid  formation  of  bullae  has  been  observed,  especially 
in  the  hands.  The  skin  sometimes  becomes  thick  and  fissured,  and  the  nails 
become  brittle,  grooved,  and  greatly  curved.  The  coldness  and  cyanosis  of  the 
skin  sometimes  seen  are  due  perhaps  to  vaso-motor  disturbances,  but  at  any  rate 
we  must  also  consider  the  disturbance  of  circulation  which  is  due  to  the  lack  of 
muscular  movements. 

The  examination  of  the  tendon  reflexes  is  of  great  diagnostic  importance.  While 
they  are  invariably  decidedly  increased  in  the  upper  extremities  in  amyotrophic  lat- 
eral sclerosis,  they  are  entirely  absent  in  genuine  progressive  muscular  atrophy,  a 
condition  which  is  easily  explained  by  the  atrophy  of  the  motor  ganglion-cells 
belonging  to  the  reflex  arc,  or  by  the  atrophy  of  the  centrifugal  motor  fibers. 
Since  no  degeneration  of  the  lateral  pyramidal  tract  precedes  this  atrophy,  it  goes 
without  saying  that  the  preceding  increase  of  the  tendon  reflexes,  characteristic 
of  amyotrophic  lateral  sclerosis,  is  also  absent.  In  the  lower  extremities  the  patel- 
lar reflex  is  retained  as  long  as  the  disease  spares  the  legs,  but  it  is  not  increased. 
If  the  atrophy  involve  the  legs,  the  patellar  reflex  is  usually  lost. 

In  distinction  from  all  these  manifest  disturbances  in  the  motor  region,  the 
sensibility  of  the  skin  and  deeper  parts  remains  perfectly  preserved.  There  are 
also  never  any  morbid  symptoms  on  the  part  of  the  bladder  or  rectum. 

In  many  cases  the  affection  finally  invades  the  muscular  region  innervated 
from  the  medulla ;  the  symptoms  of  "  progressive  bulbar  paralysis  "  (vide  infra) 
are  added  to  those  of  progressive  muscular  atrophy.  This  combination  of  spinal 
and  bulbar  disease  appears,  as  we  have  previously  shown,  as  a  rule,  in  amyotro- 
phic lateral  sclerosis,  and  even  after  the  disease  has  lasted  a  comparatively  short 
time.  In  genuine  progressive  muscular  atrophy  the  bulbar  symptoms  usually 
develop,  if  at  all,  only  after  the  disease  has  gone  on  for  years.  Then  the  speech 
begins  to  become  indistinct,  from  the  atrophy  of  the  tongue,  swallowing  is  difficult, 
and  the  patient  finally  succumbs  to  increasing  inanition  or  to  respiratory  disturb- 
ances. In  their  principal  characteristics  the  muscular  atrophy  of  the  extremities 
and  the  bulbar  symptoms  are  precisely  analogous  phenomena,  inasmuch  as  the 
nerve  nuclei  in  the  medulla  have  pi'ecisely  the  same  significance  for  the  muscles 
of  the  tongue,  the  pharynx,  and  the  face,  as  the  anterior  gray  cornua  of  the  cord 
have  for  the  muscles  of  the  trunk  and  the  extremities.  In  many  cases,  however, 
bulbar  symptoms  do  not  develop  at  all,  since  the  patients  die  before  then  of  some 
intercurrent  disease. 

Diagnosis.— The  diagnosis  of  progressive  muscular  atrophy  can  easily  be  made 
if  we  confine  ourselves  strictly  to  the  definition  of  the  disease,  and  do  not  confuse 
it  with  other  affections  in  which  the  muscular  atrophy  is  only  a  symptom  which 
under  some  circumstances  may  have  an  entirely  different  origin:  muscular  atro- 
phies in  extensive  diffuse  myelitis,  in  tumors,  and  in  the  formation  of  cavities  in 
the  cord,  in  multiple  neuritis,  as  a  result  of  articular  affections  (see  the  chapters 
on  acute  and  chronic  inflammations  of  the  joints),  etc.  We  should  consider  espe- 
cially the  typical  course  of  the  affection  in  most  cases  of  genuine  progressive  mus- 
cular atrophy,  its  beginning  in  the  upper  extremities,  the  small  muscles  of  the 
hand,  or  more  rarely  the  muscles  of  the  shoulder  and  upper  arm,  its  slow  advance, 
the  peculiar  "individualization"  of  the  atrophy— that  is,  the  affection  of  some 
muscles  while  other  neighboring  muscles  remain  completely  normal;  and,  finally, 
the  absence  of  all  disturbances  of  sensibility  or  of  the  sphincters.  Progressive 
muscular  atrophy  is  doubtless  nearly  allied  to  amyotrophic  lateral  sclerosis,  but  the 
latter  is  distinguished  by  its  more  rapid  course,  and  especially  by  the  increase  of 
42 


658  DISEASES  OF  THE  NERVOUS  SYSTEM. 

the  tendon  reflexes  due  to  the  affection  of  the  lateral  columns,  and  the  correspond- 
ing appearance  of  spastic  symptoms  in  the  legs.  The  differential  diagnosis  between 
the  spinal  and  the  myopathic,  juvenile  muscular  atrophy,  will  be  described  in  the 
appendix  to  this  chapter. 

The  prognosis  of  progressive  muscular  atrophy  is  to  be  regarded  as  absolutely 
unfavorable.  The  disease  appears  comparatively  benign  only  in  its  frequently 
very  slow  advance,  since  it  may  last  for  ten  or  fifteen  years,  or  even  longer.  As 
we  have  already  said,  the  fatal  termination  at  last  appears  from  some  intercurrent 
disease,  or  as  a  result  of  the  final  appearance  of  dangerous  bulbar  symptoms, 
paralysis  of  deglutition  and  respiration. 

The  results  of  treatment  are  accordingly  very  slight.  An  electrical  treatment, 
continued  for  months  and  years  with  very  great  persistence,  can  alone  produce 
a  little  improvement  or  check  the  advance  of  the  atrophy  somewhat.  Temporary 
improvement  may  also  sometimes  be  attained  by  a  methodical  massage  of  the 
muscles  and  a  rationally  conducted  gymnastic  treatment.  In  other  respects,  the 
treatment  must  be  symptomatic.  [Gowers  claims  that  daily  subcutaneous  injec- 
tions of  stiwchnine,  gr.  y^  to  ^  (grm.  0  0005-0 -002)  often  arrests  the  disease.— K.] 


APPENDIX. 

THE  PRIMARY  MYOPATHIC  FORMS  OF  MUSCULAR  ATROPHY. 

(Hereditary  or  Juvenile  Forms  of  Muscular  Atrophy.     Pseudo-hypertrophy  of  the  Muscles.     Pseudo- 
hypertrophic Muscular  Paralysis.) 

Besides  the  spinal  form  of  progressive  muscular  atrophy,  just  described,  there 
are  also  morbid  conditions  of  the  muscles,  which  develop  exclusively  in  the  mus- 
cles themselves,  independently  of  any  discoverable  affection  of  the  spinal  or 
peripheral  motor  nerve-tracts,  and  which  also  lead  to  a  very  considerable  atrophy 
and  a  corresponding  disturbance  of  function  in  them.  Besides  this  anatomical 
distinction,  which  is  still  more  sharply  pronounced  in  the  special  form  of  the  dis- 
ease of  the  muscles  {vide  infra),  an  essential  clinical  distinction  between  the  spinal 
and  the  myopathic  forms  of  muscular  atrophy  is  shown  by  the  fact  that,  with  few 
exceptions,  the  myopathic  form  appears  in  youth,  and  often  even  in  childhood,  and 
that  it  very  often  attacks  several  members  of  the  same  family.  We  may  there- 
fore imagine  that  a  congenital  defective  predisposition  of  the  muscular  system  is 
the  chief  cause  of  myopathic  muscular  atrophy. 

The  form  of  this  class  of  muscular  diseases  longest  known  is  the  so-called 
pseudo-hypertrophy  of  the  muscles,  a  disease  in  which  the  actual  atrophy  of  the 
muscular  fibers  is  in  part  so  concealed  by  an  increase  of  the  interstitial  fatty  tissue 
that  the  atrophied  muscles  show  even  an  increase  of  volume.  Griesinger  in  1864 
gave  the  first  accurate  description  of  this  condition  in  Germany,  while  Duchenne 
first  called  attention  to  the  disease  in  France,  and  in  1868  was  able  to  give  a  very 
complete  description  of  the  clinical  aspect  of  the  disease.  M.  Eulenburg  and  Cohn- 
heim,  by  the  first  careful  anatomical  examination  of  the  nervous  system,  had 
already  before  this  (in  1866)  made  out  that  its  condition  was  perfectly  normal. 

Of  late,  however,  we  have  reached  the  opinion  that  juvenile  myopathic  mus- 
cular atrophy  need  not  always  appear  wholly  in  the  form  of  lipomatous  pseudo- 
hypertrophy, but  that  it  may  develop  partly,  if  not  exclusively,  as  simple  muscular 
atrophy  with  a  considerable  loss  of  volume  in  the  muscles.  Erb  in  particular  has 
lately  described  a  number  of  cases,  which  have  led  him  to  establish  a  second 
special  form  of  juvenile  muscular  atrophy.  In  fact,  we  can  not  deny  that  we  can 
establish  different  "  types  "  of  myopathic  muscular  atrophy  on  the  ground  of  cer- 


PRIMARY  MYOPATHIC   FORMS   OF  MUSCULAR  ATROPHY.    659 


tain  peculiarities;  but  it  is  shown  by  increasing1  experience,  as  Erb  himself  has 
already  stated,  that  the  individual  types  do  not  differ  in  principle,  but  that  they 
may  run  into  one  another  in  various  ways.  In  what  follows,  the  separate  descrip- 
tion of  the  chief  types  known  at  present  is  to  be  regarded  as  separate  only  in  a 
clinical  sense.  We  hold  firmly,  however,  to  the  general  distinction  between  these 
types  and  the  spinal  form  of  muscular  atrophy.  The  constant  confusion  of 
these  two  forms  of  disease  has  been  the  main  cause  of  the  errors  that  obtain'*  I 
until  a  short  time  ago  in  regard  to  all  the  questions  with  reference  to  this  subject. 
It  is  still  advisable  at  present,  however,  especially  from  didactic  reasons,  to  describe 
the  myopathic  forms  directly  after  the  spinal  forms. 

I.  Pseudo-hypertrophy  op  the  Muscles  {Lipomatosis  luxurians  muscu- 
laris  progressiva  of  Heller;  Atrophia  musculorum  lipomatosa  of  Seidel). — 
Pseudo-hypertrophy  develops  almost  invariably  in  childhood,  somewhere  between 
the  ages  of  five  and  eight  years.     It  very  often  depends  upon  a  pronounced  heredi- 


Fig.  92.— Positions  of  a  child  with  hereditary  (pseudohypertrophic)  muscular  atrophy,  on  rising  to  an 

erect  attitude.    (.From  Gowers.) 

tary  predisposition,  since  several  children  of  the  family  are  affected  by  the  disease 
in  the  greater  part  of  the  cases.  More  rarely  we  can  make  out  the  same  disease 
in  the  patient's  antecedents.  The  male  sex  is  decidedly  more  disposed  to  the  dis- 
ease than  the  female.  Sometimes,  but  not  always,  we  also  find  in  the  affected 
families  some  disposition  to  a  nervous  taint,  such  as  hysteria,  epilepsy,  feeble- 
mindedness, anomalies  of  the  skull,  etc. 

The  disease  begins  gradually  and  almost  always  without  a  special  exciting 
cause.  The  parents  notice  that  the  child,  who  had  been  previously  perfectly 
well  and  strong,  becomes  insecure  on  his  legs,  so  that  he  can  no  longer  jump  or 
go  up-stairs  as  well  as  he  used  to  do.  This  points  to  the  first  characteristic  pecul- 
iarity wherein  pseudo-hypertrophy  differs  from  progressive  muscular  atrophy.  It 
begins,  with  rare  exceptions,  in  the  muscles  of  the  trunk,  especially  in  the  muscles 
of  the  back  and  loins,  and  in  the  muscles  of  the  lower  extremities,  especially  in 
those  oi  the  thigh.  While  the  arms  and  hands  are  still  perfectly  normal,  walking 
constantly  grows  more  and  more  difficult,  and  the  gait  very  soon  assumes  so  char- 
acteristic a  type  that  from  this  alone  the  diagnosis  can  often  be  made  at  the  first 
glance.  The  gait  becomes  waddling,  the  belly  appears  very  prominent,  the  verte- 
bral column  is  arched  forward  in  the  lumbar  region  in  marked  lordosis,  and  the 


(560 


DISEASES  OF  THE  NERVOUS  SYSTEM. 


whole  upper  part  of  the  body  is  balanced  on  the  legs.  The  legs  are  raised  slowly 
and  with  difficulty,  and  the  toes  usually  droop  from  paresis  of  the  dorsal  extensors. 
The  child's  movements,  when  he  tries  to  raise  himself  from  the  floor  or  pick  up 
any  object,  are  very  characteristic,  and  are  alike  in  almost  all  cases.  Since  it  is 
impossible  to  raise  the  trunk,  the  child  usually  gets  on  all  fours  first,  and  then 
gradually  straightens  himself  up  by  leaning  his  arms  on  his  knees  (see  Fig.  92). 
Later  on  disturbances  of  motion  appear  in  the  upper  extremities  also,  and  in  gen- 
eral they  are  very  similar  to  those  to  be  described  more  fully  in  the  next  type. 

If  we  examine  the  patient  more  closely  we  shall  usually 
find  at  the  first  glance  an  extraordinary  increase  in  the  vol- 
ume of  single  muscles  (see  Fig.  93).  The  calves  are  dis- 
proportionately thick,  and  sometimes  the  thighs  also;  the 
arms  are  affected  later,  especially  the  deltoids,  the  triceps, 
etc.  This  inci'ease  of  volume  is  caused  by  an  abnormal  in- 
terstitial development  of  fat,  ''pseudo-hypertrophy."  Hence 
the  muscles  do  not  feel  firm,  but  soft  and  spongy.  It  is  by 
no  means  rare,  however,  that,  besides  the  pseudo-hypertro- 
phy in  some  muscles,  a  genuine  atrophy  develops  in  others, 
with  a  pronounced  loss  of  substance  and  without  any  co- 
existing development  of  fat.  This  is  seen  especially  in  the 
upper  extremities.  Finally,  there  seems  to  be  in  addition 
even  a  genuine  muscular  hypertrophy.  In  several  cases  we 
have  seen  a  marked  increase  in  volume  in  the  muscles  of 
the  calves,  which  were  capable  of  quite  an  extraordinary 
display  of  strength.  In  such  cases,  however,  there  is,  prob- 
ably, in  our  opinion,  a  sort  of  compensatory  hypertrophy, 
since  the  muscles  that  are  still  able  to  work  are  exerted  im- 
moderately. 

Fibrillary  twitchings  of  the  muscles  can  only  very  rarely 
be  plainly  noticed,  which  is  probably  connected  with  the 
form  of  atrophy  (vide  infra) .  Electrical  examination  shows 
a  diminution  of  excitability  corresponding  to  the  atrophy 
and  to  the  increased  deposit  of  fat,  but  never  reaction  of  de- 
generation. This  is  a  fact  of  great  importance  because  it 
agrees  with  the  anatomical  condition  of  the  diseased  mus- 
cles, and  is  in  remarkable  contrast  to  the  occurrence  of 
reaction  of  degeneration  in  spinal  muscular  atrophy.  The 
sensibility  remains  perfectly  normal,  and  also  micturition 
and  defecation;  the  patellar  reflex  was  absent  in  some  of 
the  cases  examined  by  us.  It  is  noticeable  that  the  skin,  especially  in  the  legs, 
very  often  shows  a  peculiar  bluish  marbled  coloring.  Bulbar  symptoms  probably 
never  occur.  The  intelligence  in  most  cases  is  perfectly  normal,  but  it  sometimes 
happens  that  children  with  hereditary  muscular  atrophy  at  the  same  time  show 
manifest  signs  of  mental  or  even  of  moral  weakness. 

The  disease  advances  very  slowly  but  without  remissions.  Finally  the  patient 
can  not  walk  at  all;  he  is  confined  to  the  bed,  and  becomes  more  and  more  help- 
less. Death  usually  ensues  from  some  intercurrent  disease,  but  sometimes  from 
insufficiency  of  the  respiratory  muscles. 

The  anatomical  lesions  in  all  cases  of  genuine  pseudo-hypertrophy,  whether 
hereditary  or  arising  in  childhood,  which  have  thus  far  been  carefully  examined 
(Charcot,  F.  Schultze,  Berger,  and  others),  have  been  completely  negative  with 
regard  to  the  nervous  system.  Except  for  accidental  and  insignificant  complica- 
tions, the  spinal  cord,  and  especially  its  anterior  gray  matter,  have  been  perfectly 


Fig.  93.— Pseudo-hypertro 
phy  of  the  muscles, 
(From  Duchenne.) 


PRIMARY  MYOPATHIC   FORMS  OF   MUSCULAR  ATROPHY.     661 

normal.  In  the  muscles  microscopic  examination  shows  a  very  considerable  in- 
crease of  the  interstitial  connective  tissue,  and  especially  of  the  fatty  tissue  between 
the  single  fibers  of  the  muscle.  This  may  sometimes  be  seen,  even  during  the 
patient's  life,  by  harpooning  or  excising  little  pieces  of  muscle.  The  fibers  them- 
selves have  not  undergone  fatty  degeneration,  and  they  show  but  very  little  de- 
generative atrophy,  but  everywhere  their,  transverse  striation  is  manifest.  Some 
of  them  are  perfectly  normal  in  volume,  others  decidedly  smaller,  and  some  are 
even  actually  hypertrophied  (compensatory  hypertrophy  ?).  We  see,  then,  that 
the  anatomical  lesions  of  the  muscular  disease  are  essentially  different  from  the 
purely  degenerative  changes  in  the  muscles  in  spinal  muscular  atrophy. 

2.  Erb's  Form  op  Juvenile  or  Hereditary  Muscular  Atrophy. — This  form 
also  begins  almost  always  in  youth,  before  the  age  of  twenty,  but,  as  a  rule,  some- 
what later  than  the  form  associated  with  pseudo-hypertrophy.  It  is  occasionally 
or  even  very  often  hereditary  or  generic  (that  is,  occurring  in  families),  and  the 
female  members  of  the  family  are  often  attacked  by  this  form,  while  pseudo- 
hypertrophy is  seen  especially  in  boys.  The  disease  is  also,  like  pseudo-hyper- 
trophy, sometimes  seen  to  begin  in  the  back  and  legs,  but  quite  frequently  the 
shoulders  and  tipper  extremities  are  first  attacked.  There  is  also  a  remarkable 
regularity  in  the  choice  of  the  muscles  attacked.  According  to  Erb,  the  following 
muscles  are  almost  constantly  diseased  in  the  trunk  and  the  upper  extremities: 
the  pectoralis  major  and  minor,  the  trapezius,  the  latissimus  dorsi,  the  serratus 
magnus,  the  rhomboidei  the  sacro-lumbalis  and  longissimus  dorsi,  and  later  the 
triceps.  The  following,  however,  almost  always  remain  normal:  the  sterno-mas- 
toid,  the  levator  anguli  scapulae,  the  coraco-brachialis,  the  teres  major  and  minor, 
the  deltoid,  the  supra-spinatus  and  infra-spinatus,  and,  in  distinction  from  what 
was  especially  stated  in  regard  to  spinal  muscular  atrophy,  the  small  muscles  of 
the  hand.  The  muscles  of  the  forearm,  too,  except  the  supinator  longus,  remain 
intact  for  a  long  time,  if  not  entirely.  In  the  lower  extremities  the  atrophy 
attacks  chiefly  the  glutsei,  the  quadriceps,  the  peronei,  and  the  tibialis  anticus, 
while  the  sartorius  and  the  muscles  of  the  calf  are  usually  spared  for  a  long  time. 
Fibrillary  twitchings  in  the  affected  muscles  are  generally  absent,  and  there  is 
never  any  reaction  of  degeneration. 

The  disturbances  of  function  due  to  this  condition  are  self-evident,  so  that  a 
full  description  of  them  may  be  omitted.  The  arms  usually  suffer  first,  as  we 
have  said.  The  marked  projection  of  the  scapulae,  from  the  paralysis  of  the  ser- 
ratus, is  especially  characteristic.  The  gait  soon  becomes  waddling,  as  in  pseudo- 
hypertrophy, and,  finally,  walking  is  utterly  impossible.  The  whole  course  of  the 
disease  is  always  very  chronic.  Erb  describes  cases  in  which  the  disease  has 
existed  from  twenty -three  to  thirty-eight  years.  Bulbar  symptoms  are  as  rare  as 
in  muscular  pseudo  hypertrophy.  It  is  of  significance  that  the  diaphragm  may 
atrophy,  and  the  consequent  respiratory  disturbance  may  be  the  cause  of  death. 

If  we  have  an  opportunity  to  examine  the  diseased  muscles  anatomically,  we  find 
that  the  interstitial  development  of  fat  is  entirely  absent.  The  connective  tissue 
is  somewhat  increased,  and  its  nuclei  are  more  numerous  than  in  healthy  muscles. 
In  the  beginning  of  the  disease  some  of  the  muscular  fibers  are  hypertrophied,  but 
simply  atrophied  fibers  predominate.  The  number  of  muscular  nuclei  is  con- 
siderably increased.  We  often  see  vacuoles  in  the  individual  fibers.  The  more 
the  muscular  substance  wastes  the  more  abundant  becomes  the  connective  tissue. 

3.  The  Infantile,  usually  Generic  Form  op  Myopathic  Muscular  Atrophy 
with  Implication  op  the  Facial  Muscles.  (Duchenne,  Landouzy  and  Dejerine ; 
see  Fig.  94.) — Duchenne  had  already  observed  that  in  children  there  is  a  form  of 
muscular  atrophy  which  begins  in  the  muscles  of  the  face:  but  his  statements 
were  almost  forgotten  until,  a  few  years  ago,  Landouzy  and  Dejerine  called  atten- 


662 


DISEASES  OF  THE  NERVOUS  SYSTEM. 


\ 


\ 


tion  anew  to  this  subject,  and  demonstrated,  contrary  to  previous  belief,  that  im- 
plication of  the  facial  muscles  is  by  no  means  an  unusual  symptom.     Indeed,  tbe 

disease  very  often  begins  in 
the  facial  muscles;  the  eyes 
can  no  longer  be  completely 
closed,  and  the  movements  of 
the  mouth  in  whistling,  laugh- 
ing, and  talking  become  im- 
paired. From  the  sinking  in 
of  the  cheeks,  the  drooping  of 
the  under  lip,  etc. ,  there  devel- 
ops a  very  characteristic  type 
of  countenance  ("fades  myo- 
pathique  "),  by  which  the  prac- 
ticed eye  can  recognize  the 
affection  at  once.  As  the  dis- 
ease advances  the  muscles  of 
the  shoulder  and  upper  arm 
are  usually  first  affected,  some- 
times the  muscles  of  the  back, 
the  thigh,  etc.  The  muscles  of 
mastication,  the  internal  ocu- 
lar muscles,  and  the  muscles 
of  the  forearm  and  hand  al- 
most always  remain  normal. 
A  slight  permanent  contrac- 
ture of  the  biceps  is  often  pres- 
ent and  is  characteristic.  The 
selection  of  muscles  usually 
affected  is  almost  precisely  the 
same  as  in  the  previously  de- 
scribed juvenile  muscular  atro- 
phy. Fibrillary  contractions 
and  reaction  of  degeneration 
are  almost  always  absent.  We  therefore  believe  that  the  two  forms  are  not  sharp- 
ly to  be  separated,  but  that  they  are  closely  allied  to  each  other.  The  implication 
of  the  facial  muscles  was  in  former  times  probably  often  overlooked.  In  order  to 
detect  it  it  is  the  best  plan  to  have  the  patient  close  his  eyes  when  the  head  is 
bent  backward ;  we  can  then  readily  detect  the  fissure  left  between  the  eyelids 
(insufficiency  of  the  orbicularis  oculi).  Sometimes  the  defective  development  and 
functions  of  the  facial  muscles  seem  to  be  a  congenital  condition,  which  may  re- 
main as  such,  or  to  which  sooner  or  later  an  actual  progressive  muscular  atrophy 
is  added.  We  have  ourselves  recently  made  the  especially  interesting  observation 
that  sometimes  we  find  in  the  relatives  (brothers  or  sisters)  of  patients  with  pro- 
nounced myopathic  muscular  atrophy,  signs  of  a  congenital  weakness  of  develop- 
ment of  the  facial  muscles,  such  as  incomplete  closure  of  the  lids,  inability  to 
whistle,  etc.,  without  any  disease  which  progresses  further. 

That  all  three  of  the  forms  just  described  of  juvenile  atrophy  and  pseudo-hyper- 
trophy are,  at  bottom,  probably  identical  diseases,  follows  not  only  from  all  the 
other  similarities  mentioned,  but  also  from  the  fact  that  sometimes  one  of  the 
children  affected  in  the  family  displays  rather  the  type  of  pseudo-hypertrophy, 
another  the  type  of  simple  juvenile  atrophy.  We  also  find  various  transitions 
between  the  different  forms.     Thus,  for  example,  pseudo-hypertrophy  in  the  legs 


Fiq.  94. — Juvenile  myopathic  muscular  atrophy  in  a  ten-year- 
old  child,  with  marked  implication  of  the  facial  muscles. 
Inability  to  close  the  eyes  or  move  the  lips.  Atrophy  of  the 
pectorals,  etc.    (From  the  Erlangen  Medical  Clinique.) 


THE  SO-CALLED  SPASTIC  SPINAL  PARALYSIS.  603 

may  be  associated  with  simple  atrophy  of  the  arms.  The  affection  may  also 
begin  in  the  arms,  while  later  the  facial  muscles  are  also  affected.  We  do  not 
know  what  causes  produce  the  great  increase  of  fat-tissue  in  a  part  of  the  cases. 
Even  in  the  cases  without  the  interstitial  development  of  fat  the  atrophy  of  the 
muscles  is  essentially  simple,  not  degenerative,  and  the  motor  nerves  and  spinal 
cord  remain  normal,  at  least  according  to  all  present  experience.  Erb  groups 
the  two  forms  together,  under  the  name  of  "  dystrophia  muscularis  jjrogres- 
swa." 

The  differential  diagnosis  between  the  myopathic  and  the  spinal  muscular 
atrophies  is  not  difficult,  if  we  pay  attention  to  the  juvenile  or  generic  character  of 
the  former,  and  also  to  its  characteristic  localization,  affecting  the  extensors  of  the 
spine  and  leaving  free  the  small  muscles  of  the  hand,  etc.,  and  to  the  absence  of 
fibrillary  twitchings  and  of  reaction  of  degeneration  in  the  muscles. 

The  treatment  can  scarcely  ever  be  expected  to  give  permanent  results,  but 
sometimes,  even  in  juvenile  muscular  atrophies,  some  considerable  improvement 
has  been  obtained  by  a  very  persistent  electrical  treatment  and  massage  of  the 
muscles. 

[Charcot  and  Marie,  and,  independently  of  them,  Tooth,  have  described  a  form 
of  progressive  atrophy,  the  tk  peroneal  type,"  which  begins  in  the  peroneal  mus- 
cles, or  perhaps  in  the  intrinsic  muscles  of  the  foot.  It  occurs  usually  in  families, 
and  begins  in  the  second  half  of  childhood,  seldom  after  the  age  of  twenty.  Males 
are  most  frequently  affected.  There  is  some  fibrillary  twitching  of  the  affected 
muscles,  and  reaction  of  degeneration  may  occur.  The  muscular  atrophy  may 
lead  to  club-foot.  Vasomotor  and  sensory  disturbances  have  been  noted.  It  is 
rather  apt  to  follow  acute  diseases,  especially  measles.  The  pathology  is  still  ob- 
scure, but  many  writers  are  disposed  to  think  it  due  to  a  peculiar  form  of  chronic 
peripheral  neuritis.  Hence  it  is  sometimes  spoken  of  as  progressive  neuritic 
atrophy. — K.] 


CHAPTEE  IX. 

THE   SO-CALLED   SPASTIC   SPINAL  PARALYSIS. 

{Primary  Lateral  Sclerosis.    Spasmodic  Tabes  Dorsalis.) 

In  the  year  1875  Erb,  and  soon  after  Charcot,  called  attention  to  a  clinical  form 
of  spinal  paralysis  by  no  means  rare,  which  is  characterized  "by  a  gradually 
increasing  paresis  and  paralysis,  usually  advancing  slowly  from  below  upward, 
with  muscular  tension,  reflex  contractions  and  contractures,  with  a  marked  increase 
of  the  tendon  reflexes,  with  complete  absence  of  sensory  and  trophic  disturbances, 
of  vesical  and  sexual  weakness,  and  of  any  cerebral  disturbance."  Both  observers 
agreed  in  assuming  a  "  primary  symmetrical  sclerosis  of  the  lateral  columns  "  as 
the  anatomical  cause  of  this  condition. 

The  numerous  observations  published  in  the  following  years  have  shown  that 
the  type  of  disease  just  briefly  described  is,  in  fact,  often  to  be  met  with,  and  may 
easily  be  distinguished  from  the  other  forms  of  spinal  paralysis.  The  hypothesis 
as  to  its  anatomical  basis  has  not  yet  been  confirmed,  however,  since,  in  all  the 
cases  that  have  come  to  autopsy  so  far,  other  anatomical  changes  were  found 
instead  of  the  primary  lateral  sclerosis  supposed  to  be  the  only  lesion ;  but  it  can 
not  be  denied  that,  besides  other  lesions,  of  course,  a  disease  of  the  lateral  columns 
has  been  repeatedly  made  out  in  such  cases;  and  that  this  was  certainly  not  with- 
out significance  for  the  occurrence  of  the  group  of  symptoms  in  question.     It  is 


06 ±  DISEASES  OF  THE  NERVOUS  SYSTEM. 

also  not  at  all  impossible  that  there  may  be  an  isolated  systemic  disease  of  the 
lateral  columns,  especially  of  the  pyramidal  tracts,  without  any  disease  of  the  gray 
matter  or  of  other  portions  of  the  cord  at  the  same  time,  which  disease  is  closely 
connected  with  amyotrophic  lateral  sclerosis  in  particular,  and  is  a  further  link 
in  the  chain  of  primary  diseases  of  the  motor  conducting  tract;  but,  as  we  have 
said,  a  definite  case  of  isolated  disease  of  the  spinal  pyramidal  tracts,  without 
invasion  of  the  anterior  gray  corn.ua,  has  not  yet  been  known. 

In  what  follows  we  will  first  describe  the  clinical  peculiarities  of  spastic  spinal 
paralysis,  and  then  add  the  enumeration  of  its  anatomical  causes,  as  far  as  they 
are  known  at  present.  Hence  we  mean  by  "  spastic  spinal  paralysis  "  only  a  group 
of  symptoms  which  is  so  often  observed  that,  from  practical  reasons,  it  is  advis- 
able to  give  it  a  short  and  unprejudiced  name. 

Type  of  Spastic  Spinal  Paralysis.— Two  symptoms  predominate  in  the  picture 
of  spastic  spinal  paralysis:  motor  paresis,  and  the  increase  of  the  tendon  reflexes — 
the  patellar  reflex,  and  the  ankle  clonus.  The  former—  we  are  speaking  at  present 
only  of  the  spastic  paralysis  of  the  legs,  which  is  by  far  the  most  frequent  and  the 
most  clearly  marked  —is  found  in  various  degrees,  from  a  simple  weakness  of 
movement  to  a  complete  and  more  or  less  extensive  paralysis.  It  is  the  second 
symptom,  however,  which  gives  to  the  disturbance  of  motion  its  characteristic 
feature  of  spastic  paralysis.  If  the  increase  of  the  tendon  reflexes  be  very  consid- 
erable, the  reflex  contractions  come  on  even  upon  the  stretching  and  pulling  of  the 
tendons,  which  is  excited  by  the  weight  of  the  limbs  or  by  any  active  or  passive 
movements.  The  reflex  muscular  tension  opposes  any  attempt  at  motion.  The 
muscles  feel  rigid  and  firm,  and  the  legs  are  often  found  in  almost  permanent 
contracture  and  extended,  with  the  feet  in  plantar  flexion.  If  we  try  to  flex  the 
leg  passively  at  the  knee,  or  if  we  try  to  extend  the  foot  dorsally,  we  find  it  almost 
impossible  to  do  so.  The  more  rapidly  and  suddenly  we  try  to  produce  the  motion, 
the  more  marked  is  the  muscular  resistance,  which  can  scarcely  be  overcome.  If, 
however,  we  go  to  work  very  slowly  and  cautiously,  and  avoid  any  sudden  ten- 
sion of  the  tendons,  we  can  almost  always  flex  the  leg  without  special  trouble. 
If  we  put  the  patient  on  the  edge  of  the  bed,  the  legs  do  not  hang  down  laxly,  but 
they  usually  fall  at  once  into  a  vigorous  extensor  tetanus,  since  the  weight  of  the 
leg  puts  the  quadriceps  into  contraction  by  the  tension  on  the  ligamentum  patella?. 
A  convulsive,  reflex  tremor  of  the  whole  leg  often  comes  on  at  once,  similar  to 
ankle  clonus.  If  we  examine  the  patient  while  in  the  bath  we  find  the  spasms 
decidedly  less,  because  in  the  water  the  influence  of  the  weight  of  the  limb  is 
absent. 

Active  motion,  as  is  easily  explained,  must  also  be  impaired  from  the  inhibi- 
tory action  of  the  reflex  spasms.  The  degree  of  disturbance  of  motion  is  thus 
increased,  and  the  paresis  often  seems  greater  than  is  really  the  case.  The  influ- 
ence of  the  muscular  tension  is  especially  manifest  in  the  gait  of  the  patient.  As 
long  as  walking  is  still  possible,  we  notice  very  plainly  that  it  is  rendered  difficult, 
not  only  by  the  muscular  paresis,  but  also  by  the  stiffness  of  the  legs.  The 
patient  walks  with  short  and  difficult  steps,  the  legs  are  scarcely  flexed  at  the 
knee,  and  the  feet  are  scarcely  raised  at  all.  The  feet  "stick  to  the  floor"  and 
are  slowly  slid  forward,  and  there  is  a  marked  tendency  to  walk  on  the  toes  from 
the  contraction  in  the  muscles  of  the  calves.  The  weight  of  the  body  alone  presses 
the  feet  downward.  We  term  this  very  characteristic  form  of  gait  the  spastic- 
paretic  gait. 

The  increase  in  the  tendon  reflexes  may  also  exist  without  the  jiresence  of  ary 
special  motor  paresis  of  the  muscles  at  the  same  time.  Since,  however,  in  this 
case,  the  motion  is  not  a  little  influenced  by  the  constant  spasms,  a  disturbance  of 
motility  may  be  counterfeited,  which  might  be  called  "  spastic  pseudo-paralysis," 


THE  SO-CALLED  SPASTIC  SPINAL  PARALYSIS.  665 

or,  more  properly,  pseudo-paresis.  In  these  cases  the  muscular  strength  is  almost 
normal,  and  the  patient  can  walk  for  quite  a  long  time.  Nevertheless,  all  his 
movements  are  stiff  and  difficult,  and  the  gait  shows  all  the  peculiarities  of  the 
pure  spastic  gait.  The  steps  are  not  very  short  and  they  follow  one  another  quite 
rapidly,  hut  the  legs  remain  perfectly  stiff  and  are  scarcely  raised  from  the 
ground,  and  the  patient  walks  almost  entirely  on  his  toes.  In  the  house  the 
patient  walks  with  a  noisy  shuffle,  and  in  soft  sand  we  can  see  the  furrows  drawn 
by  the  feet  as  they  slide  along  the  ground. 

Although  we  are  doubtless  justified  in  referring  the  spastic  condition  mainly 
to  the  increase  in  the  tendon  reflexes,  we  must  also  add  that  sometimes  symptoms 
of  direct  motor  irritation  may  occur — single  rapid  or  slow  contractions,  for  which 
we  can  not  make  out  a  reflex  origin.  In  some  muscles  there  seems  sometimes  to 
be  a  state  of  constant  tonic  irritation ;  thus  we  often  see  the  great  toes  in  a  perma- 
nent state  of  marked  dorsal  extension.  If  the  patient  bend  his  knee,  a  marked 
dorsal  extension  of  the  foot  is  added  as  an  associated  movement.  Although  the 
symptoms  mentioned  are  the  characteristic  positive  features  of  "  spastic  spinal 
paralysis,"  yet,  in  the  original  sense  of  the  word,  the  affection  is  also  character- 
ized by  the  fact  that  certain  other  spinal  symptoms,  especially  disturbances  of 
sensibility,  disturbances  in  micturition  and  defecation,  ataxia,  muscular  atrophy, 
and  other  trophic  symptoms,  are  entirely  absent.  Only  when  such  was  the  case 
have  Erb  and  Charcot  claimed  that  a  special  anatomical  cause  must  lie  at  the  bot- 
tom of  the  peculiar  group  of  symptoms.  In  fact,  the  cases  in  which  we  happen 
to  see  the  type  of  genuine  spastic  spinal  paralysis  without  any  other  symptoms  are 
not  very  rare.  It  develops  slowly  and  gradually,  without  known  cause,  and  usu- 
ally in  patients  in  youth  and  middle  life.  One  leg  is  first  affected  and  then  the 
other.  The  muscles  of  the  trunk  and  of  the  arms  are  sometimes  added  to  the  list 
later  on,  and  in  the  arms  we  find  a  paresis  with  a  decided  increase  of  the  tendon 
reflexes  and  without  any  disturbance  of  sensibility  or  any  muscular  atrophy. 
This  type  of  disease,  however,  only  very  rarely  remains  in  its  purity — at  least, 
according  to  present  experience.  Sooner  or  later  other  symptoms  are  mixed 
with  it,  and  in  those  cases,  which  so  far  have  come  to  autopsy,  the  anatomical 
lesions  are  by  no  means  always  of  the  same  sort. 

Pathological  Lesions. — As  we  have  already  said,  Erb  and  Charcot  originally 
advanced  the  hypothesis  that  the  anatomical  basis  of  spastic  spinal  paralysis  is 
to  be  found  in  a  sclerosis  of  the  lateral  columns.  This  opinion  is  well-founded, 
inasmuch  as  the  picture  of  the  symptoms  of  spastic  spinal  paralysis  manifestly 
recalls  amyotrophic  lateral  sclerosis  in  many  of  its  relations.  In  both  diseases  we 
find  symptoms  limited  exclusively  to  the  motor  sphere,  and  an  increase  of  the 
tendon  reflexes.  The  only  distinction  is  in  the  muscular  atrophy,  whose  anatomi- 
cal cause  is  undoubtedly  to  be  found  in  the  atrophy  of  the  anterior  gray  cornua. 
If  we  imagine  the  pyramidal  tract  exclusively  affected,  without  co-existing  disease 
of  the  gray  matter,  the  result  must  be  the  picture  of  "spastic  spinal  paralysis." 
This  line  of  reasoning,  the  justification  of  which  must  to-day  be  acknowledged, 
has,  however,  not  yet  been  entirely  confirmed  by  facts;  but  we  have  learned  to 
recognize  a  chain  of  circumstances  under  which,  at  least  at  times,  the  symptoms 
of  spastic  spinal  paralysis  may  arise. 

We  must  first  mention  that  cerebral  changes,  especially  chronic  hydrocephalus, 
may  sometimes  simulate  the  type  of  spastic  spinal  paralysis.  Except  for  some 
anomalies  in  the  skull,  special  cerebral  symptoms  may  be  entirely  absent,  while 
the  motility  of  the  legs  (and  arms)  is  diminished,  and  the  tendon  reflexes  are  so 
decidedly  increased  that  the  symptoms  of  spastic  paralysis  may  result.  E.  Schulz 
and  we  ourselves  have  made  such  observations. 

The  followiiiG:  chanares  are  also  to  be  considered  : 


Q6Q  •  DISEASES  OF  THE  NERVOUS  SYSTEM. 

1.  Transverse  myelitis  in  the  upper  dorsal  or  the  cervical  cord.  This  some- 
times shows  a  remarkable  symmetry  in  its  distribution  for  some  time,  and  a 
predominant  localization  in  the  lateral  columns,  while  the  posterior  columns 
remain  comparatively  free.  Hence,  as  we  can  easily  understand,  the  result  is 
a  paralysis  of  tbe  legs  with  greatly  increased  tendon  reflexes,  but  with  normal 
sensibility.  Tumors  of  the  cervical  cord  may  moi*e  rarely  cause  similar  appear- 
ances. 

2.  Compression  of  the  Spinal  Cord. — A  gentle  compression  of  the  cord  in  the 
cervical  or  dorsal  region  is  followed,  as  we  have  seen,  by  paresis  and  increase  of 
the  reflexes,  but  not  by  sensory  disturbance.  We  can  understand  that,  if  no 
manifest  cause  of  compression  can  be  made  out,  a  primary  affection  of  the  cord 
may  simulate  the  symptoms  of  spastic  spinal  paralysis. 

3.  Multiple  sclerosis  may  also  frequently  show  such  a  localization  of  its  nodules 
as  to  be  followed  by  paresis  and  spastic  symptoms  without  sensory  disturbances. 
The  case  diagnosticated  by  Charcot  himself  as  "  spasmodic  tabes  dorsalis  "  turned 
out  on  autopsy  to  be  multiple  sclerosis. 

4.  In  a  case  observed  by  us,  with  almost  the  entire  and  pure  type  of  symptoms 
of  spastic  spinal  paralysis,  the  autopsy  showed  a  hydromyelus  with  co-existing 
degeneration  of  the  lateral  columns. 

5.  Spastic  paralysis  has  been  sometimes  observed  to  come  on  after  acute  dis- 
eases, but  the  reports  of  autopsies  in  such  cases  are  at  present  wanting. 

6.  Finally,  we  will  here  briefly  mention  the  combined  systemic  disease  of  the 
pyramidal  tract,  the  lateral  cerebellar  tract,  and  the  columns  of  Goll,  in  adults, 
described  by  us.  In  these  cases  we  find  a  gradually  increasing  paralysis  of  the 
legs,  and  later  of  the  arms,  with  increased  tendon  reflexes,  spastic  symptoms,  and 
sensibility  almost  perfectly  normal.  Later  on,  however,  vesical  disturbances  arise, 
which  are  probably  to  be  referred  to  the  disease  of  the  columns  of  Goll.  The 
occurrence  of  true  ataxia  in  the  legs,  with  weakness  and  increased  tendon  reflexes, 
seems  to  be  not  unusual;  but  lancinating  paius,  marked  disturbances  of  sensi- 
bility, and  pupillary  changes  are  always  absent,  so  that  the  moi'bid  picture  is 
always  very  materially  different  from  that  of  tabes  dorsalis.  Further  observa- 
tions must  give  us  more  definite  knowledge  as  to  the  frequency  and  the  possibility 
of  diagnosis  of  this  apparently  especially  limited  form  of  spinal  disease.  Min- 
kowsky has  also  recently  reported  a  case  in  which  anatomical  examination 
showed  nothing  but  primary  degeneration  of  the  pyramidal  and  cerebellar  tracts 
in  the  two  lateral  columns  as  the  cause  of  a  spastic  spinal  paralysis.  In  this  and 
in  some  similar  cases,  which  come  very  close  to  Ei'b's  and  Charcot's  theoretical 
postulate,  syphilis  was  perhaps  to  be  regarded  as  the  special  cause  of  the  disease. 

Diagnosis. — The  symptomatic  diagnosis  of  spastic  spinal  paralysis  is  easy  to 
make,  with  attention  to  the  description  given  above.  We  must  always,  however, 
be  very  cautious  at  present  in  our  anatomical  diagnosis.  Only  the  further  course 
of  the  disease  can  give  us  data  whereby  we  can  first  consider  the  morbid  condi- 
tions mentioned  above. 

Prognosis. — The  prognosis  of  most  cases  which  show  the  symptoms  of  spastic 
spinal  paralysis  is  just  as  unfavorable  as  most  of  the  other  diseases  of  the  spinal 
cord,  but  we  must  always  bear  in  mind  that  many  of  these  cases  run  a  very  slow 
course.  The  disease  seems  to  stand  perfectly  still  for  a  long  time,  the  symptoms 
are  less  severe  than  in  other  spinal  diseases,  there  are  no  pain  and  no  incontinence, 
and  sometimes  we  have  seen  manifest  improvement  and  even  a  few  recoveries, 
but  such  cases  at  present  lack  definite  anatomical  proof. 

Treatment. — The  treatment  of  spastic  spinal  paralysis  in  general  agrees  with 
that  of  chronic  myelitis  {vide  supra).  Galvanic  treatment  usually  gives  compara- 
tively the  best  results.     We  must  also  mention  especially  that  prolonged  warm 


ACUTE  AND  CHRONIC  POLIOMYELITIS. 


007 


baths  often  act  well  against  the  spastic  symptoms.  They  may  last  for  half  an 
hour  to  an  hour  and  a  half,  and  should  be  of  a  temperature  of  90°,  or  at  most  05° 
(26°-28°  R.).  The  legs  are  more  flexible  and  more  movable  after  them.  Among 
internal  remedies  we  may  try  nitrate  of  silver  and  ergotine.  If  there  be  a  suspicion 
of  syphilis,  for  which  we  should  always  look  carefully,  it  is  an  absolute  necessity 
to  employ  inunction,  and  to  prescribe  iodide  of  potassium  internally. 


CHAPTER  X. 
ACUTE   AND   CHRONIC  POLIOMYELITIS. 

1.  Spinal  Paralysis  op  Children. 

(Acute  Poliomyelitis  in  Children.) 

JEtiology  and  Pathological  Anatomy. — In  children  there  is  quite  frequently  a 
definite  and  well-characterized  form  of  paralysis,  for  the  first  accurate  knowledge 
of  which  we  must  thank  Jac.  von  Heine  in  1840.  Although  Heine  later,  in  1860, 
expressed  the  opinion  that  a  disease  of  the  spinal  cord  formed  the  basis  of  the 
paralysis,  the  first  actual  confirmation  of  this  opinion  was  furnished  later  by  Pre- 
vost  and  Vulpian,  Charcot  and  Joffroy,  and  others,  so  that  at  present  we  are  justi- 
fied in  exchanging  the  old  term  "  essential  paralysis  of  children ''  for  the  name  of 
"spinal  paralysis  of  children." 

As  the  name  indicates,  the  affection  occurs  chiefly,  if  not  exclusively  (vide 
infra),  in  children,  and  is  most  frequent  in  the  earlier  years,  somewhere  between 
one  and  four.  An  exciting  cause,  such  as  taking  cold,  has  hardly  ever  been  made 
out.  The  children  are  almost  always  perfectly  healthy  *  previously,  and  come  of 
healthy  families  without  any 
neuropathic  predisposition. 
The  whole  course  of  the  dis- 
ease makes  the  hypothesis  very 
probable  that  we  have  to  do 
with  an  acute  infectious  dis- 
ease— with  an  infectious  pro- 
cess, which  first  causes  a  gen- 
eral infection  of  the  body,  and 
then  is  localized  chiefly  in  a 
circumscribed  portion  of  the 
spinal  cord.  It  also,  perhaps, 
bears  some  relation  to  the  na- 
ture of  the  disease  as  just  sig- 
nified that  most  of  the  cases  oc- 
cur in  w7arm  weather.  With 
regard  to  this,  it  is  worth  men- 
tioning that  a  short  time  ago 
we  observed  that  in  a  little  vil- 
lage within  a  few  days  three  children  fell  ill  with  acute  poliomyelitis. 

With  reference  to  its  anatomy,  the  disease  may  be  defined  as  an  acute  inflam- 
mation, which  affects  chiefly  a  definite  extent  of  the  anterior  gray  matter  of  the 


Fig.  95 Section  through  the  cervical  enlargment  in  anterior 

poliomyelitis:  the  left  anterior  column  is  very  much  con- 
tracted and  is  without  ganglion-cells.  (From  Charcot  and 
Joffroy.) 


*  The  paralyses  arising  after  acute  diseases — such  as  measles,  scarlet  fever,  smallpox,  etc. — are  per- 
haps partly  of  spinal  origin,  but  they  can  not  be  identified  with  the  idiopathic  spinal  paralysis  of  chil- 
dren. 


668  DISEASES  OF  THE  NERVOUS  SYSTEM. 

spinal  cord,  usually  attacking  only  the  anterior  gray  comu  of  one  side ;  yet  it  does 
not  always  limit  itself  strictly  to  this,  but  it  may  involve  the  white  matter  in  the 
vicinity  somewhat,  although,  of  course,  to  a  lesser  extent  than  the  gray  matter. 
Although  fresh  cases  have  so  far  been  examined  in  very  scanty  numbers,  still  we 
can  sometimes  make  out  clearly  the  remains  of  inflammation  in  the  older  centers 
of  disease.  The  ordinary  lesion  in  old  cases,  which  is  most  frequently  found,  con- 
sists of  a  considerable  atrophy  of  one  anterior  cornu,  which  is  changed  to  a  dense 
sclerosed  tissue,  often  pierced  by  dilated  and  thickened  vessels,  and  which  con- 
tains scarcely  a  single  normal  ganglion-cell.  If  the  paralysis  affect  one  arm,  the 
corresponding  anterior  cornu  in  the  cervical  enlargement  is  atrophied  (see  Fig. 
95) ;  if  the  leg  be  paralyzed,  the  process  is  seated  in  the  lumbar  enlargement.  In 
bilateral  paralysis  we  must  think  of  an  affection  of  both  anterior  cornua  at  the 
corresponding  level  of  the  cord. 

This  inflammation  of  the  anterior  cornu,  the  poliomyelitis,  is  to  be  regarded  as 
the  primary  center  of  disease.  From  this  point,  as  in  every  severe  lesion  of  the 
motor  ganglion-cells  there  situated,  there  develops  a  secondary  degeneration, 
which,  extending  to  the  periphery,  affects  the  corresponding  anterior  roots,  and 
later  their  appropriate  motor  nerves  and  the  muscles  supplied  by  them.  In  the 
paralyzed  muscles  and  nerves  we  accordingly  find  a  marked  pure  degenerative 
atrophy,  such  as  we  have  learned  to  recognize  in  severe  peripheral  paralyses. 

Although  at  present  the  spinal  origin  of  the  atrophic  paralysis  of  children  is 
regarded  as  sufficiently  certain,  we  would  not  deny  that  some  authors,  especially 
Leyden,  have  assumed  a  peripheral  origin  for  some  cases — that  is,  a  primary  neu- 
ritis, without  a  material  implication  of  the  spinal  cord.  In  fact,  it  does  not  seem 
impossible  that  the  same  morbid  setiological  factor,  which  we  have  supposed  to  be 
infectious,  may  exceptionally  be  localised  chiefly  in  a  peripheral  motor  nerve.  In 
the  chapter  on  cerebral  paralysis  of  children,  which  is  by  no  means  very  rare,  we 
shall  see  that  a  manifestly  closely  allied  acute  process  in  children — one,  perhaps, 
even  aetiologically  identical — may  also  develop  in  the  motor  regions  of  the  cortex 
cerebri. 

Clinical  History. — The  disease  almost  always  begins  suddenly.  A  child  who 
was  previously  perfectly  well  and  lively  is  all  at  once  attacked  with  severe  fever, 
often  reaching  105°  or  106°  (40°-41°  O),  which  is  associated  with  quite  severe  gen- 
eral symptoms  even  from  the  beginning.  The  child  complains  of  headache,  and 
sometimes  of  pain  in  the  loins  and  in  the  limbs,  and  is  decidedly  stupid  and  som- 
nolent. Very  often  still  more  marked  cerebral  symptoms  develop :  complete  loss 
of  consciousness,  single  twitchings  in  the  face  or  the  extremities,  or  general  con- 
vulsions. The  eclamptic  attacks,  turning  of  the  eyes,  and  clonic  contractions  in 
the  face  and  the  extremities,  often  appear  even  at  the  beginning  of  the  disease. 
The  whole  of  the  initial  symptoms,  whose  intensity  varies  very  much  in  the  dif- 
ferent cases,  sometimes  last  only  a  very  short  time — a  day  or  two — although  they 
often  continue  for  a  week  or  two.  Indeed,  we  even  know  cases  in  which,  as  the 
mothers  have  assured  us,  the  children  are  said  to  have  "  lain  in  spasms,"  almost 
uninterruptedly,  even  for  four  or  five  weeks  before  the  beginning  of  the  paralysis 
—that  is,  before  it  became  noticeable.  On  the  other  hand,  however,  it  may  hap- 
pen that  the  initial  symptoms,  especially  the  severe  cerebral  symptoms,  are  en- 
tirely absent  or  only  intimated. 

After  the  initial  period  of  the  disease  just  described  has  passed  away,  the 
parents  usually  notice  that  the  child  is  attacked  by  a  more  or  less  extensive  paraly- 
sis. If  its  development  can  be  followed  more  closely,  we  always  find  that  it 
spreads  rapidly,  often  in  single  spurts  which  rapidly  follow  one  another,  so  that 
it  usually  reaches  quite  a  great  extent  in  a  short  time.  Either  both  legs,  or  the 
legs  and  one  arm,  or  all  the  extremities,  and  even  the  muscles  of  the  trunk,  are 


ACUTE  AND  CHRONIC  POLIOMYELITIS.  669 

affected;  but  the  paralysis  scarcely  ever  remains  permanently  as  extensively  dis- 
tributed as  at  first;  it  is  reduced  much  more  rapidly,  and  soon  draws  back  to  a 
definite  muscular  region,  which  remains  permanently  paralyzed.  In  gome  cases 
the  paralysis  may  even  entirely  disappear,  but  as  a  rule  a  complete  paralysis  is 
left  in  one  extremity,  or  at  least  in  a  portion  of  it;  most  frequently  in  one  leg, 
especially  in  the  peroneal  muscles;  somewhat  more  rarely  in  the  arm,  chiefly  in 
the  deltoid;  sometimes  in  both  legs;  or,  very  rarely  in  spinal  paralysis,  in  one 
arm  and  leg  on  the  same  side  or  on  opposite  sides.  Meantime  the  child's  general 
health  has  been  completely  restored.  He  is  well  and  vigorous,  has  an  excellent 
appetite,  never  shows  any  permanent  cerebral  disturbance — only  the  painless,  flac- 
cid paralysis,  the  inability  to  use  the  affected  extremity,  is  left  behind.  In  the 
following  weeks  and  months  a  further,  slower  advance  in  the  improvement  iu  the 
power  of  motion  often  becomes  noticeable,  but,  as  a  rule,  a  permanent  and  more 
or  less  complete  paralysis  of  certain  muscles  remains. 

In  regard  to  the  more  intimate  peculiarities  of  this  remaining  paralysis,  it  may 
invariably  be  characterized  as  a  flaccid  atrophic  paralysis.  A  marked  atrophy  of 
the  paralyzed  muscles  shows  itself  a  few  weeks  after  the  beginning  of  the  paralysis. 
This  atrophy  gradually  advances  further  and  may  finally  attaiu  the  highest  degree. 
The  atrophy  is  often,  but  not  always,  partly  concealed  by  a  more  abundant  devel- 
opment of  fat  tissue.  The  changes  in  the  electrical  excitability  of  the  paralyzed 
nerves  and  muscles  come  on  still  more  rapidly  than  the  visible  atrophy.  Since 
we  have  to  do  with  a  pure  degenerative  atrophy  of  nerve  and  muscle,  as  follows 
from  the  anatomical  basis  of  the  disease,  a  pronounced  reaction  of  degeneration 
must  necessarily  develop  in  the  affected  parts.  Duchenne  found  that  usually  the 
faradic  excitability  of  the  nerves  and  muscles  is  completely  lost  after  a  week  or  two. 
On  galvanic  examination,  we  can  at  first  detect  an  increase  of  excitability  in  the 
muscles  with  a  predominance  of  slow  anodic  closure  contractions  (AnSZ),  while 
later,  after  two  or  three  months,  the  galvanic  excitability  also  sinks  very  consider- 
ably;  but  the  muscular  contractions  preserve  their  qualitative  peculiarities  charac- 
teristic of  reaction  of  degeneration  (see  page  551).  Very  often  the  whole  affected 
extremity  remains  backward  in  its  growth,  so  that  later  the  bones  may  show  a 
shortening  of  several  centimetres.  The  parallel  between  the  muscular  atrophy 
and  the  stunted  growth  is  not,  however,  pi'esent  in  all  cases,  as  Volkmann,  in 
particular,  has  stated. 

Passive  motion  of  the  paralyzed  extremity  is  at  first,  and  even  later,  perfectly 
free,  except  for  the  contractures  that  finally  set  in  (vide  infra).  Many  joints  are 
so  flaccid  that  we  can  actually  make  flapping  movements  with  the  paralyzed  limbs 
and  give  them  the  most  extraordinary  positions.  The  tendon  reflexes  are  invaria- 
bly completely  absent  in  the  paralyzed  extremities,  and  so  almost  always  are  the 
cutaneous  reflexes — a  condition  which  may  sometimes  be  of  diagnostic  significance. 
The  skin  often  shows  certain  trophic  disturbances;  it  feels  cool  and  has  a  cyanotic 
appearance.  Its  sensibility,  however,  is  completely  retained  in  all  cases.  Micturi- 
tion is  sometimes  a  little  disturbed  at  the  beginning  of  the  disease,  but  in  most 
cases  this  disturbance  completely  disappears  later. 

After  the  paralysis  has  existed  for  a  long  time,  certain  secondary  contrac- 
tures almost  always  develop  in  the  paralyzed  parts,  which  are  in  part  of  a  very 
characteristic  type.  In  the  legs  especially  the  "paralytic  club-foot"  (talijjes 
varo-equinus)  is  a  condition  long  known.  It  is  due  to  the  fact  that,  from  the 
paralysis  of  the  peronei  muscles  and  of  the  tibialis  anticus,  the  point  of  the  foot 
constantly  droops,  and  that  a  contracture  is  gradually  developed  in  the  antago- 
nistic muscles  of  the  calf,  whose  points  of  insertion  are  permanently  approxi- 
mated. In  paralysis  of  the  muscles  of  the  calf  there  arises,  on  the  other  hand,  a 
moderate  degree  of  calcaneus  from  the  contracture  of  the  antagonists.     In  the  arms 


670  DISEASES  OF  THE  NERVOUS  SYSTEM. 

and  in  the  vertebral  column,  in  paralyses  of  the  spinal  muscles,  the  most  manifold 
and  sometimes  very  considerable  contractures  and  deformities  may  also  arise,  the 
chief  cause  of  which  is  always  to  be  referred  to  the  contracture  of  unparalyzed 
antagonists  and  to  external  mechanical  conditions,  such  as  weight  and  pressure. 

In  conclusion,  if  we  simply  compare  tbe  type  of  disease  sketched  with  its  ana- 
tomical cause,  the  general  agreement  of  the  two  may  at  once  be  seen.  The  affec- 
tion of  the  anterior  gray  cornu  must  have  as  a  result  a  paralysis  with  a  subsequent 
atrophy  and  reaction  of  degeneration,  in  which  the  reflexes  must  be  lost  by  the 
destruction  of  the  reflex  arc,  but  the  sensibility  must  remain  perfectly  normal  from 
the  persistence  of  the  sensory  conduction  (tbe  posterior  columns  and  the  posterior 
gray  cornua),  and  the  vesical  functions  must  also  remain  normal.  The  subsequent 
paralysis  is  the  result  of  the  destruction  which  the  morbid  process,  in  itself  com- 
pletely ended,  has  caused  in  the  spinal  cord. 

Diagnosis. — The  diagnosis  of  the  spinal  paralysis  of  children  is  almost  always 
easy  to  make  and  certain  if  we  hold  strictly  to  the  definition  and  peculiarities  of 
the  disease,  and  do  not  reckon  as  spinal  paralysis  every  paralysis  appearing  in  a 
child.  We  should  consider  chiefly  the  acute  beginning,  the  subsequent  flaccid 
paralysis  with  atrophy  and  reaction  of  degeneration,  with  the  loss  of  the  reflexes, 
but  with  retained  sensibility.  If  we  observe  these  features,  we  are  sufficiently 
protected  against  confusion  with  cerebral  diseases  and  other  diseases  such  as  spon- 
dylitis, hereditary  muscular  atrophy,  or  spastic  spinal  paralysis. 

Prognosis. — It  is  not  impossible,  but  it  is  not  yet  proven,  that  many  of  the  cases 
where  children  die  speedily  with  convulsions  are  to  be  regarded  as  the  initial 
stage  of  acute  poliomyelitis.  If,  however,  the  first  stage  of  the  disease  be  past,  the 
prognosis  as  regards  life  is  entirely  favorable,  since  the  rest  of  the  child's  physical 
development  is  no  further  affected  in  any  way.  The  prognosis  as  regards  the 
complete  restoration  of  the  disturbance  of  function  is,  however,  much  more 
unfavorable.  What  has  not  recovered  in  the  first  weeks  or  months  usually 
remains  paralyzed  for  the  whole  life.  Nevertheless,  this  experience  should  not 
restrain  us  from  persevering  in  treatment,  at  least  in  the  first  years,  since  some- 
times a  very  noticeable  improvement  in  the  functions  of  the  paralyzed  parts  can 
thus  be  procured. 

Treatment. — If  we  have  an  opportunity,  even  during  the  initial  stage  of  the 
disease  (when,  of  course,  the  diagnosis  can  not  usually  be  made  with  certainty),  to 
attack  the  disease  by  our  treatment,  we  may  prescribe  cold  compresses  or  an  ice- 
bag  to  the  head,  and  eventually,  where  there  is  high  fever  or  great  stupor,  a  tepid 
bath  with  cool  affusions.  We  are  but  rarely  led  to  try  local  bloodletting  by 
leeches  behind  the  ears  or  on  the  temples,  where  there  are  signs  of  marked  cerebral 
hyperemia.  Internally  we  usually  prescribe  a  mild  "  intestinal  derivative,"  such 
as  half  a  grain  or  a  grain  (grm.  0-03-0"05)  of  powdered  calomel  every  two  or  three 
hours,  infusion  of  senna,  etc. 

After  paralysis  appears,  we  can  expect  the  most  success  from  electrical  treat- 
ment, kept  up  consecutively  for  months,  and,  with  interruptions,  for  years.  We 
put  a  large,  broad  electrode  on  the  vertebral  column  at  the  spot  which  corresponds 
to  the  place  of  the  lesion  in  the  spinal  cord — on  the  cervical  vertebras  in  paralysis 
of  the  arm,  and  the  lower  dorsal  in  paralysis  of  the  leg — while  the  other  electrode 
serves  for  peripheral  application  to  the  paralyzed  nerves  and  muscles.  In  this 
way  we  apply  a  moderately  strong  constant  current,  reversing  it  occasionally,  for 
two  or  three  minutes,  partly  stabile  and  partly  by  passing  the  cathode,  or  eventu- 
ally the  anode,  slowly  over  the  paralyzed  muscles  and  nerves.  We  may  also 
employ  occasional  interruptions  and  changes  of  the  current.  Duchenne  has  also 
found  persistent  treatment  by  the  faradic  current  of  advantage.  The  sittings 
should  take  place  three  or  four  times  a  week,  and  later  even  offener,  if  possible. 


ACUTE  AND   CHRONIC  POLIOMYELITIS.  671 

Besides  electrical  treatment,  methodical  gymnastic  exercises  of  the  muscles,  that 
can  still  be  moved  somewhat  actively,  may  be  of  distinct  advantage.  Regular  and 
persistent  massage  of  the  muscles  is  also  to  be  recommended  in  the  later  stages.  In 
pi^actice  we  can  not  avoid  prescribing  certain  embrocations,  such  as  spirits  of  cam- 
phor, spirits  of  mustard,  or  spirits  of  formic  acid.  Passive  motion  is  very  impor- 
tant to  guard  against  contractures,  and  to  improve  the  already  existing  deformities. 
In  regard  to  the  further  details  of  orthopaedic  treatment,  which  is  of  great  impor- 
tance, we  must  refer  to  the  appropriate  special  works  on  surgery  and  orthopaedics. 

The  use  of  baths,  of  brine  or  fei'ruginous  waters,  is  to  be  recommended, 
although,  of  course,  they  must  not  be  overvalued.  They  may  be  given  at  home. 
If  circumstances  permit  sending  the  child  to  a  bath  during  the  summer  months, 
we  should  chiefly  consider  the  brine  baths  at  Reichenhall,  Kreuznach,  Kosen,  and 
Colberg;  the  acid  salines  at  Rehme,  Nauheim,  and  Soden;  and  eventually,  with 
weak  and  anaemic  children,  the  use  of  the  iron  baths  at  Driburg,  Pyrmont,  or 
Schwalbach.  Good  results  are  sometimes  obtained  at  the  indifferent  thermal 
baths  at  Teplitz,  Wildbad,  Ragatz,  or  Gastein,  but  these  must  be  used  only  with 
caution.  We  also  obtain  good  results,  especially  with  older  children,  at  the  cold- 
water  cures. 

Very  little  is  to  be  expected  from  the  use  of  internal  remedies.  Iodide  of  potas- 
sium and  strychnine  are  recommended,  the  latter  in  the  form  of  subcutaneous 
injections,  ^  to  gV  grain  (grm.  0 '001-0  "003)  daily. 

In  old  cases,  where  there  is  no  longer  any  hope  of  further  improvement  of  the 
paralysis  worth  mentioning,  the  treatment  may  be  limited  to  keeping  up  and 
strengthening  the  patient's  general  condition  as  much  as  possible  by  proper  food 

and  good  air. 

» 
2.   Acute  Poliomyelitis  of  Adults. 

(Acute  Atrophic  Spinal  Paralysis  of  Adults.) 

Although  it  had  been  believed  for  a  long  time  that  the  form  of  acute  atrophic 
spinal  paralysis,  just  described,  occurred  only  in  children,  later  observations  by 
Moritz  Meyer,  Duchenne,  Erb,  F.  Schultze,  F.  Müller,  and  others,  have  established 
the  fact  that  precisely  analogous  cases  of  disease  may  also  develop,  although 
decidedly  less  frequently,  in  adults,  especially  in  young  persons  under  thirty. 
There  is  no  longer  any  doubt  of  this  fact,  especially  if  we  consider  an  undoubted 
anatomical  lesion  found  by  F.  Schultze.  We  have,  however,  already  stated 
that  for  a  long  time  we  have  regarded  the  diagnosis  of  acute,  and,  as  we 
shall  soon  see,  of  chronic  poliomyelitis  also,  as  too  readily  made,  and  that  cer- 
tainly very  many  of  the  cases  diagnosticated  and  published  as  poliomyelitis  are  to 
be  classed  as  primary  neuritis  (see  page  582):  Since  we  know  that  primary  degen- 
erative processes  may  develop  acutely  and  subacutely  in  the  motor  nerves,  and 
that  these  also  lead  to  an  atrophic  paralysis,  a  greater  part  of  the  teaching  on 
poliomyelitis  needs  new  and  careful  revision  in  order  to  exclude  what  does  not 
belong  to  it. 

The  type  of  acute  poliomyelitis  of  adults,  so  far  as  it  has  been  established  by 
definite  observations,  which  at  present  are  not  numerous,  is,  of  course,  not  mate- 
rially different  from  the  type  of  the  spinal  paralysis  of  children. 

We  often  can  not  make  out  any  ^etiological  conditions ;  sometimes  exposure 
to  cold,  overexertion,  etc.,  seem  to  favor  the  development  of  the  disease.  Cases 
are  seen  more  frequently  in  the  male  sex  than  in  the  female. 

The  disease  likewise  begins  with  quite  severe  initial  symptoms,  fever,  headache, 
somnolence,  delirium,  and  vomiting,  which  may  last  from  a  few  days  to  a  week  or 
two.  The  violent  spontaneous  pains  which  are  very  often  reported  as  occurring 
in  the  loins,  the  back,  and  the  extremities,  usually  belong  probably  to  those 


672  DISEASES  OF  THE  NERVOUS  SYSTEM. 

cases  in  which  a  primary  neuritis,  but  not  a  poliomyelitis,  is  the  chief  anatom- 
ical lesion.  After  the  end  of  this  stage  the  paralysis  appears.  This  develops 
with  varying  distribution,  usually  in  single  spurts,  but  always  rather  rapidly. 
The  paralyzed  muscles  are  perfectly  flaccid,  the  cutaneous  and  tendon  reflexes  are 
wholly  absent,  and  very  soon  a  pronounced  atrophy  and  reaction  of  degeneration 
appear,  while  the  sensibility  and  the  vesical  and  sexual  functions  remain  normal. 

The  distribution  of  the  paralysis  shows  certain  peculiarities,  which  must  be 
briefly  described  here,  since  they  can  be  studied  much  better  in  adults  than  in 
children.  The  paralysis  may  be  very  extensive,  it  may  affect  all  four  extremities, 
or  it  may  occur  in  the  form  of  paraplegia,  or  even  of  monoplegia.  In  the 
extremities  we  very  often  find  certain  groups  of  muscles  paralyzed,  to  which  E. 
Remak  first  called  attention.  Since  the  muscles  that  are  paralyzed  at  the  same 
time  are  not  supplied  by  the  same  peripheral  nerves,  but  usually  are  connected 
in  their  functions,  we  may  suppose  that  the  corresponding  ganglion-cells  in  the 
anterior  cornua  of  the  spinal  cord  also  lie  together,  without  regard  to  the  dis- 
tribution of  their  peripheral  processes  in  the  different  motor  nerves.  Thus,  for 
example,  it  is  worthy  of  note  that,  in  paralysis  of  the  crural  region,  the  sartorius 
often  remains  entirely  free;  that  in  the  leg  the  tibialis  anticus,  on  the  one  hand, 
and  the  peronei  and  the  extensor  digitorum  on  the  other,  may  be  separately  dis- 
eased; that  in  the  forearm  the  supinator  longus,  supplied  by  the  radial  nerve, 
remains  free,  while  all  the  other  muscles  on  the  extensor  side  of  the  forearm  are 
paralyzed  ("  forearm  type  "  of  E.  Remak) ;  and  that,  on  the  other  hand,  the  supi- 
nator may  be  paralyzed  alone  or  together  with  the  biceps,  brachialis  anticus,  and 
deltoid  ("upper-arm  type"  of  E.  Remak).  This  latter  form  of  paralysis  is  said  to 
correspond  to  a  lesion  in  the  cord  at  the  level  of  the  fourth  and  fifth  cervical  roots, 
the  forearm  type  to  a  lesion  at  the  level  of  the  eighth  cervical  and  first  dorsal 
roots.  According  to  Kahler  and  Pick,  the  center  for  the  muscles  of  the  calf  lies 
at  the  level  of  the  fourth  and  fifth  dorsal  roots.  Ferrier  and  Yeo,  in  their  experi- 
ments on  monkeys,  by  irritation  of  the  anterior  motor  spinal  roots  have  obtained 
results  which,  for  the  most  part,  agree  very  well  with  the  observations  on  men 
(vide  supra,  page  624). 

In  regard  to  diagnosis  in  the  future,  especial  attention  must  be  paid  to  the  dis- 
tinction between  poliomyelitis  and  neuritis.  The  greatest  stress  is  to  be  laid  on 
the  initial  pains  and  any  other  slight  disturbances  of  sensibility.  In  other  respects, 
the  course  of  the  two  diseases  is  so  similar  that  we  can  indeed  imagine  that  they 
are  closely  allied  in  their  aetiological  relations,  and  exhibit  merely  different  forms 
of  localization  of  the  same  (probably  infectious)  morbid  agency.  Some  observa- 
tions also  seem  to  favor  the  theory  that  transitional  forms  may  occur  with  a  co- 
existing primary  lesion  of  the  cord  and  of  the  peripheral  nerves. 

The  prognosis  is  not  wholly  unfavorable,  as  sometimes  a  complete  recovery 
has  been  observed,  although  only  after  months.  Of  course,  it  is  not  certain 
whether  these  cases  were  not  multiple  neuritis.  On  the  other  hand,  however,  the 
same  permanent  paralyses  as  in  spinal  paralysis  of  children  may  be  left,  with 
atrophy  and  contractures. 

The  treatment  follows  precisely  the  same  rules  that  we  have  mentioned  in  the 
spinal  paralysis  of  children.  The  internal  or  subcutaneous  use  of  ergotine  may 
be  added  on  the  recommendation  of  some  physicians.  F.  Müller  recommends  a 
solution  of  two  and  a  half  drachms  of  ergotine  (grm.  10)  with  a  third  of  a  grain 
of  sulphate  of  atropine  (grm.  0'02)  in  five  drachms  of  water  (grm.  20),  of  which 
he  injects  seven  to  fifteen  minims  twice  a  day. 


ACUTE  AND  CHRONIC  POLIOMYELITIS.  073 

3.   Subacute  and  Chronic  Poliomyelitis. 

(Subacute  and  Chronic  Atrophie  Spinal  Parah/sis.     I'aralysie  generale  xpinale  anterieure 
subaigue  [Duchenne]). 

While  the  anatomical  basis  of  acute  poliomyelitis  in  adults  is  still  lacking  in 
proof,  our  anatomical  knowledge  of  the  occurrence  of  a  subacute  and  chronic 
poliomyelitis,  in  the  sense  of  the  term  given  it  by  various  authors,  is  still  com- 
pletely defective.  Confusions  with  multiple  neuritis  are  also  undoubtedly  very 
common  here,  and  the  diagnosis  is  not  incontestable  in  all  the  cases  published 
under  the  name  of  "  subacute  poliomyelitis."  Therefore  we  will  limit  ourselves  to 
reproducing  here  briefly  the  picture  of  the  disease  at  present  described  under  the 
above  name,  while  we  especially  repeat  that  a  certain  and  accurate  confirmation 
of  its  anatomical  basis  must  be  left  to  the  future. 

In  the  cases  classed  under  tbis  heading  a  paralysis,  first  of  tbe  two  legs  and 
somewhat  later  usually  of  the  two  arms,  develops  in  a  comparatively  sbort  time — 
in  the  course  of  some  days,  or  weeks  at  most.  It  usually  has  no  special  cause 
or  any  severe  initial  symptoms.  The  patient  complains  at  first  of  weakness 
in  the  legs;  he  can  no  longer  walk,  and  is  confined  to  the  bed.  A  short  time 
later  the  same  disturbances  appear  in  the  arms,  and  lead  to  a  more  or  less  com- 
plete paralysis.  The  patient  often  feels  some  slight  paresthesia  in  the  affected 
parts,  but  in  general  tbe  sensibility  remains  perfectly  normal.  Tbe  paralyzed 
muscles  are  often  quite  sensitive  to  pressure  (neuritic  symptoms  ?).  Soon  after  the 
paralysis  an  equally  extensive  atrophy  develops,  and  a  distinct  loss  of  electrical 
excitability,  running  parallel  to  it;  which  passes  over  into  a  partial  or,  in  all 
severe  cases,  a  complete  reaction  of  degeneration.  The  cutaneous  and  ten- 
don reflexes  are  very  much  diminished  and  often  entirely  lost.  Tbe  bladder  and 
rectum,  however,  remain  intact,  and  bedsores  never  develop.  We  sometimes 
notice  a  striking  diminution  of  the  sweat  secretion.  In  rare  cases  the  mus- 
cles of  the  neck,  the  lips,  the  tongue,  and  the  pharynx  are  attacked  by  the 
disease. 

After  the  paralysis  has  reached  its  greatest  extent  there  is  usually  a  cessation. 
The  condition  remains  stationary  for  months  sometimes,  and  then  a  gradual 
improvement  begins,  which  may  go  on  to  complete  recovery ;  but  often,  of  course, 
the  recovery  remains  incomplete,  so  that  the  patient  has  a  more  or  less  marked 
disturbance  of  function  for  life.  The  "  middle  form  of  chronic  poliomyelitis  " 
described  by  Erb,  in  which  there  is  only  a  partial  reaction  of  degeneration  in  the 
paralyzed  muscles,  almost  always  gives  a  good  prognosis.  Those  rare  cases,  how- 
ever, in  which  the  muscles  of  deglutition  and  respiration  are  involved,  may  have 
an  unfavorable  termination,  although  even  then  the  possibility  of  an  improve- 
ment is  not  to  be  entirely  excluded. 

Anatomical  lesions,  which  confirm  the  hypothesis  of  a  subacute  (inflamma- 
tory ?)  affection  in  the  anterior  cornua  of  the  cord  ascending  from  below  upward, 
are  to  be  found,  as  we  have  said,  only  in  an  extremely  small  number  of  cases,  and  in 
part  of  them  even  they  are  not  entirely  trustworthy.  A  short  time  ago  Oppenheim 
published  an  undoubted  case  of  chronic  poliomyelitis,  which  ran  its  course  to  a  fa- 
tal termination  in  three  years.  There  was  finally  paralysis  and  atrophy  of  the 
muscles  of  all  four  extremities  without  a  trace  of  sensory  disturbance.  Tbe  ante- 
rior cornua  of"  the  cord  were  throughout  markedly  diseased,  while  only  very  slight 
changes  were  found  in  the  peripheral  nerves.  Clinically,  the  forms  of  disease 
belonging  in  this  category  are  well  characterized,  and  are  easy  to  diagnosticate 
with  proper  attention  and  knowledge.  Further  investigations  must  be  made  as 
to  its  anatomical  basis  and  its  relations  to  acute  poliomyelitis  and  the  primary 
neuritides. 

43  , 


674  DISEASES  OF  THE  NERVOUS  SYSTEM. 

As  follows  from  the  above  description,  the  treatment  is  by  no  means  fruitless, 
and  electrical  treatment  especially  may  produce  the  most  complete  and  rapid 
regeneration  of  the  affected  parts. 


CHAPTER  XI. 

ACUTE   ASCENDING   SPINAL  PARALYSIS. 

(Paralysis  ascendens  acuta.     Landnfs  Paralysis.) 

In  the  year  1859  Landry  described  a  disease  under  the  name  of  " paralysie 
ascendante  aigue"  which  is  chiefly  characterized  clinically  by  the  fact  that  first 
the  lower  and  soon  after  the  upper  extremities,  and  finally  a  number  of  the 
muscular  regions  supplied  by  the  medulla,  are  attacked  by  a  rapidly  advancing 
paralysis,  while  tbe  sensibility  and  the  functions  of  the  bladder  and  rectum 
remain  normal.  In  many  cases  the  disease  terminates  fatally.  Examination  of 
the  nervous  system  has  so  far,  however,  shown  no  lesion  which  can  be  regarded 
with  certainty  as  the  anatomical  cause  of  the  disease.  Considering  the  continued 
and  quite  numerous  observations  of  the  disease,  it  seems  questionable,  at  any  rate, 
whether  we  can  establish  a  uniform  anatomical  basis  for  it.  The  diversity  of 
many  symptoms  (vide  infra,  the  condition  of  the  reflexes,  the  condition  of  the 
electrical  excitability)  points  rather  to  the  fact  that  the  seat  of  the  disturbance  is 
not  always  the  same.  Nevertheless,  we  can  not  doubt  the  clinical  resemblance  of 
most  cases,  and  we  must  regard  it  as  possible  that  the  same  cause  of  disease  does 
not  always  need  exactly  the  same  localization  to  provoke  the  disease.  We  may 
very  well  recognize  the  aetiological  unity  of  "  acute  ascending  paralysis,"  without 
claiming  that  all  cases  also  agree  completely  in  the  clinical  anatomical 
details. 

General  Symptomatology.— Acute  ascending  paralysis  attacks  chiefly  persons 
previously  strong  and  healthy  in  youth  or  middle  life,  somewhere  between  twenty 
and  thirty-five  years  of  age.  Some  cases  have  also  been  seen  in  children  and  older 
people.     The  disease  seems  to  be  more  frequent  in  men  than  in  women. 

The  affection  almost  always  begins  with  certain  prodrornata.  These  consist  of 
general  malaise,  moderate  febrile  symptoms,  headache,  loss  of  appetite,  and  quite 
frequently  of  dragging  and  tearing  pains  in  the  back  and  the  extremities.  After 
these  symptoms  have  lasted  some  days,  or  more  rarely  some  weeks,  during  which 
they  are  comparatively  slight,  or  so  severe  that  many  patients  are  already  con- 
fined to  the  bed,  there  usually  comes  on  quite  suddenly,  or  sometimes  more 
gradually,  a  paresis,  first  of  one  but  very  soon  of  the  other  leg,  which  rapidly  in- 
creases, and  usually  in  a  few  days  leads  to  an  almost  complete  motor  paraplegia. 

The  paralysis  is  flaccid  in  almost  all  cases.  The  legs  may  be  moved  passively 
without  any  muscular  resistance,  and  the  muscles  show  neither  active  nor  reflex 
tension.  Their  electrical  excitability  remains  perfectly  normal  in  many  cases, 
but  there  is  sometimes  a  rapid  loss  of  faradic  muscular  excitability.  It  is  not  yet 
proven  whether  complete  reaction  of  degeneration  occurs.  The  reflexes,  both 
cutaneous  and  tendon  reflexes,  seem  to  be  diminished  or  wholly  lost  in  the 
majority  of  cases,  but  some  exceptions  to  this  rule  have  been  known. 

Sensibility  is  sometimes  perfectly  intact,  but  slight  alterations  do  occur,  and 
quite  rarely  there  may  be  even  marked  anaesthesia.  At  times  a  noticeable  delay 
of  sensation  is  observed.  We  find  no  changes  in  the  nerves  of  special  sense. 
There  is  occasionally  a  slight  oedema  in  the  legs,  which  is  perhaps  to  be  regarded 
as  a  vaso-motor  disturbance.     The  marked  sweating,  from  which  many  patients 


ACUTE  ASCENDING  SPINAL  PARALYSIS.  07.5 

suffer,  is  also  worthy  of  mention.     The  bladder  and  rectum  in  most  cases  are  not 
at  all  affected,  or  they  present  merely  slight  and  temporary  disturbances. 

A  short  time  after  the  legs  are  attacked  the  arms  also  begin  to  be  paretic. 
A  marked  motor  weakness  appears  first  in  one,  then  in  the  other  arm,  and  this 
may  also  increase  to  almost  complete  paralysis.  The  sensibility,  the  reflexes,  and 
the  electrical  excitability  show  conditions  like  those  in  the  lower  extremities.  The 
muscles  of  the  trunk  are  also  affected  at  the  same  time  as,  or  still  earlier  than,  the 
arms.  The  patient  can  no  longer  sit  up  in  bed,  turn  on  his  side,  or  make  similar 
movements.  In  some  cases  a  paralysis  of  the  muscles  of  the  neck  has  also  been 
observed. 

The  third  and  last  stage  of  the  disease  is  characterized  by  the  appearance  of 
respiratory  disturbances  and  bulbar  symptoms.  Manifest  signs  of  a  beginning 
respiratory  paralysis  appear;  the  respiration  is  labored  and  difficult,  the  move- 
ments of  the  diaphragm  grow  less,  and  the  paroxysms  of  coughing  are  weaker. 
Disturbances  in  swallowing,  difficulty  in  articulation,  and  paresis  of  the  soft  palate 
and  the  lips  may  set  in.  In  a  few  cases  a  facial  paralysis  and  disturbances  of  the 
ocular  muscles  have  been  observed.  The  condition  grows  worse  acutely,  and,  as 
we  have  said,  in  many  cases  death  ensues. 

Besides  the  symptoms  thus  far  mentioned,  referable  to  the  nervous  system,  we 
find  certain  other  symptoms  in  almost  every  case,  which  are  less  striking,  but  yet 
of  greater  significance  in  judging  of  the  disease.  The  first  of  these  is  fever.  The 
temperature  is  usually  elevated  from  the  beginning ;  it  may  temporarily  show  quite 
a  considerable  increase,  up  to  104°  (40°  C),  and  later  it  varies  somewhere  between 
100°  and  102°  (38°-39°  C),  but  between  times  it  may  even  sink  to  normal.  Of  the 
internal  organs  the  spleen  shows  the  most  frequent  changes.  It  is  usually  swollen 
moderately,  but  still  it  is  manifestly  swollen.  There  is  also  sometimes  a  slight 
albuminuria. 

In  the  cases  with  a  fatal  termination  the  whole  duration  of  the  disease  is  some- 
times only  a  few  days,  and  as  a  rule  a  week  or  two,  or  rarely  more.  Fortunately, 
however,  all  cases  do  not  terminate  fatally.  The  disease  may  come  to  a  stand- 
still at  any  time,  even  if  the  most  threatening  symptoms  be  present.  Then  the 
paralysis  shows  no  further  advance,  the  disturbances  present  disappear,  and 
recovery  ensues  after  a  course  of  several  weeks.  It  is,  of  course,  usually  quite  a 
long  time  before  the  patient  again  feels  himself  in  possession  of  his  full  powers. 

Pathological  Anatomy  and  Pathogenesis.— If  we  consider  the  whole  picture  of 
acute  ascending  paralysis,  the  idea  is  necessarily  forced  upon  us  that  we  have  to 
do  here  with  an  acute  infection  of  the  body,  with  a  predominating  localization  in 
the  motor  nervous  system,  an  opinion  which  was  first  expressed  by  Westphal. 
The  beginning  of  the  disease  with  general  malaise  corresponds  perfectly  to  the 
prodromal  stage  of  many  other  acute  infectious  diseases.  The  fever,  the  acute 
splenic  tumor,  and  the  occasional  albuminuria  can  also  scarcely  be  explained  in 
any  other  way,  according  to  our  present  views,  except  by  the  above  hypothesis. 

The  anatomical  examination  has,  of  course,  as  yet  brought  no  absolute  proof  of 
this  theory.  A  notable  case,  published  by  Baumgarten,  in  which  many  rods,  like 
the  bacilli  of  splenic  fever,  were  found  in  the  spinal  cord,  is  at  present  wholly 
unique ;  but  the  completely  negative  anatomical  lesions  in  many  cases  seem  to 
point  to  the  fact  that  we  must  look  for  the  cause  of  the  severe  nervous  symptoms 
chiefly  in  the  disturbance  of  function  excited  by  a  toxic  (infectious)  influence. 
We  have  already  signified  that  the  point  of  attack  of  the  infectious  agent  need 
not  always  be  precisely  the  same.  The  condition  of  the  reflexes  and  the  rapid 
loss  of  electrical  excitability,  in  connection  with  the  pains  at  the  beginning,  seem 
to  justify  the  hypothesis  that  the  disturbance  sometimes  has  its  chief  seat  in  the 
peripheral  motor  nerves,  that  the  disease  then  exhibits  the  most  acute  form  of 


(376  DISEASES  OF  THE  NERVOUS  SYSTEM. 

infectious  " multiple  neuritis"  (vide  supra).  More  accurate  anatomical  investi- 
gations directed  to  this  point  will  perhaps  procure  some  positive  support  for  this 
theory.  In  other  cases,  however,  the  motor  portions  of  the  spinal  cord,  the  lat- 
eral columns,  and  the  anterior  gray  cornua,  are  perhaps  chiefly  affected.  This 
idea  is  supported  by  the  occasional  discovery  (R.  Schulz  and  F.  Schultze,  Von  den 
Delden)  of  an  acute  myelitic  affection  in  the  paints  named. 

Diagnosis  and  Prognosis. — In  every  paralysis  of  the  lower  extremities  begin- 
ning acutely  and  accompanied  by  general  symptoms  and  fever  we  must  consider 
the  possibility  of  an  acute  ascending  paralysis,  but  only  the  further  course  of  the 
disease  can  decide  the  question.  Inasmuch  as  only  a  well-characterized  clinical 
group  of  symptoms  is  meant  by  the  above  term,  the  diagnosis  is  always  easy  to 
make,  with  attention  to  the  peculiarities  given  above.  It  is  more  difficult,  how- 
ever, to  decide  accurately  whether  the  case  corresponds  rather  to  the  type  of  an 
acute  multiple  neuritis  or  to  the  type  of  an  acute  ascending  spinal  paralysis.  We 
can  judge  as  to  this  point  only  by  careful  attention  to  the  single  symptoms,  espe- 
cially the  condition  of  the  sensibility  (pains,  anaesthesia),  of  the  reflexes,  and  of 
the  electrical  excitability. 

The  prognosis  must  at  first  be  made  with  great  reserve,  and  we  must  especially 
bear  in  mind  the  possibility  of  a  rapidly  fatal  termination.  If  the  first  acute  stage 
pass  off  fortunately  and  there  be  a  decided  cessation  in  the  extension  of  the  symp- 
toms of  paralysis,  the  prognosis  is  quite  favorable,  for  we  may  then  expect  that  the 
patient  will  be  completely  restored. 

Treatment. — We  can  not  be  certain  whether  an  energetic  "  derivative  treat- 
ment ''  is  of  advantage  in  the  beginning  of  the  disease.  Dry  cups  along  the  verte- 
bral column  are  recommended,  and  even  the  use  of  the  hot  iron  to  the  back.  We 
would  hardly  advise  the  latter.  It  may  be  recommended,  however,  to  prescribe 
an  inunction  with  mercurial  ointment,  thirty  to  forty-five  grains  a  day,  as  in  anti- 
syphilitic  treatment.  Of  internal  medicines  we  may  give  iodide  of  potassium  or 
ergotine.  It  also  seems  to  be  a  good  plan  to  begin  galvanic  treatment  early,  gal- 
vanism to  the  spine  and  peripherally.  If  threatening  attacks  of  respiratory  insuf- 
ficiency come  on,  electrical  excitement  of  the  phrenic  nerve  and  of  the  respiratory 
muscles  sometimes  affords  relief  to  the  patient. 

If  the  symptoms  be  arrested,  electrical  treatment  and  the  use  of  baths  may  do 
most  to  hasten  convalescence. 


CHAPTER  XII. 
NEW   GROWTHS   OF    THE    SPINAL   CORD  AND    OP    ITS  MEMBRANES. 

Pathological  Anatomy. — Tumors  of  the  spinal  cord  are  rare.  The  commonest 
primary  new  growth  is  the  glioma,  which  probably  arises  from  the  neuroglia,  and 
is  a  cellular  and  vascular  tumor.  We  often  find  in  gliomata  secondary  softening 
(the  formation  of  cavities,  see  the  following  chapter)  and  haemorrhages.  The 
tumor  is  situated  most  frequently  in  the  cervical  or  upper  dorsal  cord,  and  may 
have  a  considerable  longitudinal  extent,  and  a  transverse  diameter  of  several 
centimetres. 

Of  other  new  growths  in  the  spinal  cord  we  may  mention  solitary  tubercles, 
syphilomata,  and  myxomata  (myxo-sarcomata) . 

In  the  spinal  meninges  have  been  found  sarcomata,  fibromata,  lipomata,  myxo- 
mata, and  syphilomata.  A  carcinoma  arising  from  the  vertebrae  may  also  reach 
the  spinal  meninges  by  direct  invasion.     Marked  signs  of  compression,  and  the  con  - 


CAVITIES  AND  FISSURES  IN  THE  SPINAL  CORD.  <;77 

sequent  secondary  degenerations,  often  show  themselves  in  the  spinal  cord  at  tin 
point  where  a  new  growth  is  situated  in  the  meninges. 

We  know  practically  nothing  of  the  aetiology  of  new  growths  in  the  spinal 
cord.  It  is  merely  worthy  of  note  that  in  the  cases  of  glioma  of  the  spinal  cord 
observed,  an  injury,  such  as  a  fall  on  the  back,  etc.,  very  often  preceded  the  appear- 
ance of  the  first  symptoms. 

Symptomatology. — A  general  description  of  the  tumors  of  the  spinal  cord  can 
not  be  given,  since,  of  course,  the  individual  symptoms  must  differ  in  almost  every 
case,  according  to  the  seat  and  the  extent  of  the  new  growth. 

In  tumors  of  the  meninges  the  symptoms  of  compression  of  the  cord  are  often 
quite  prominent.  In  the  beginning  we  notice  pronounced  "  root  symptoms  " — 
that  is,  shooting  pains,  stiffness,  paresthesia,  anaesthesia,  etc.  Later  on  the  results 
of  the  compression  of  the  cord  show  themselves:  motor  weakness,  which  may 
increase  to  a  complete  motor  and  sensory  paraplegia.  We  can  net  here  go  more 
fully  into  the  details.  They  follow  of  themselves  from  attention  to  the  general 
laws  to  be  considered  for  localization  of  lesions  in  the  spinal  cord. 

In  tumors  of  the  spinal  cord  marked  symptoms  of  sensory  irritation  are  usually 
absent  at  first.  A  complicated  type  of  spinal  disease  gradually  develops,  in  which 
all  those  symptoms  may  be  present  in  a  single  case  which  we  have  learned  to  recog- 
nize more  exactly  in  the  description  of  diffuse  chronic  myelitis.  In  fact,  the  dif- 
ferential diagnosis  between  tumor  and  transverse  myelitis  is  often  impossible,  but 
certain  peculiarities  in  the  type  of  disease  are  sometimes  present,  which  at  least 
turn  our  suspicions  to  the  possibility  of  a  tumor.  Among  them  especially  is  the 
early  asymmetry  of  the  symptoms  on  the  two  sides.  Since  a  tumor  may  at  first 
be  confined  to  one  half  of  the  spinal  cord  (which  scarcely  ever  happens  in  mye- 
litis), the  signs  of  a  unilateral  lesion  of  the  spinal  cord  {vide  infra,  Chapter  XV; 
are  often  observed  in  tumors  in  a  more  or  less  pronounced  fashion.  A  certain 
change  in  the  symptoms,  improvements,  and  new  and  quite  sudden  changes  for 
the  worse,  are  sometimes  noticed,  a  circumstance  which  is  probably  to  be  referred 
to  a  change  in  the  fullness  of  the  vessels,  or  to  haemorrhages  in  the  substance  of 
the  tumor.  The  diagnosis  of  a  tumor  of  the  spinal  cord,  however,  can  be  made  best 
only  with  a  certain  probability.  The  decision  as  to  the  seat  and  the  extent  of  the 
tumor  is  based  upon  precisely  the  same  rules  as  in  the  diagnosis  of  the  different 
forms  of  myelitis.  We  can  hardly  ever  predict  anything  definite  as  to  the  kind 
of  tumor. 

The  prognosis  of  tumors  of  the  spinal  cord  is  utterly  unfavorable.  The  course 
of  the  disease  is  often  protracted  for  several  years,  but  the  final  termination  is 
always  fatal,  from  general  weakness,  cysto-pyelitis,  and  bedsores.  The  treatment 
is  purely  symptomatic,  and  is  the  same  as  in  chronic  myelitis.  If  there  be  a  sus- 
picion of  a  previous  syphilis,  we  must  try  inunction  and  the  internal  exhibition  of 
iodide  of  potassium.  [In  a  few  cases,  where  the  growth  has  not  involved  the  sub- 
stance of  the  cord,  it  has  been  successfully  removed  by  surgical  interference. — K.J 


CHAPTER  XIII. 

THE   FORMATION   OF    CAVITIES  AND   FISSURES   IN  THE   SPINAL 

CORD. 

Pathological  Anatomy  and  Pathogenesis.— The  abnormal  formation  of  cavi- 
ties in  the  spinal  cord  either  arises  from  a  dilatation  of  the  central  canal  (hydro- 
myelus),  or  it  develops  outside  of  the  central  canal,  and  near  it  (syringomyelia). 


678  DISEASES  OF  THE  NERVOUS  SYSTEM. 

The  cases  of  pure  hydromyelus  are  recognized  by  the  fact  that  the  cavity  is 
found  in  the  middle  of  the  cord,  corresponding  to  the  position  of  the  central 
canal,  and  that  its  walls  ai'e  covered  by  cylindrical  epithelium.  Slight  degrees  of 
hydromyelus,  in  which  the  dilated  central  canal  has  a  diameter  of  a  millimetre, 
or  a  millimetre  and  a  half,  are  quite  frequently  found.  The  dilatation  usually 
extends  over  only  a  portion  of  the  spinal  cord.  Higher  degrees  of  hydromyelus, 
where  the  central  canal  is  dilated  to  a  diameter  of  half  a  centimetre,  or  a  centi- 
metre, are  much  rarer.  In  such  cases  the  substance  of  the  cord  suffers  from  the 
internal  pressure  on  it. 

In  regard  to  the  origin  of  hydromyelus,  following  Leyden's  example,  we  may 
consider  anomalies  of  development  in  the  formation  of  the  central  canal  to  be  a 
cause  in  at  least  a  part  of  the  cases.  Certainly  only  exceptionally  do  we  have  a 
process  of  stasis,  as  Langhans  has  found  in  some  cases,  which  may  have  its  origin 
in  an  increased  pressure  in  the  posterior  fossa  of  the  skull,  from  tumors,  etc. 

As  to  most  cases  of  syringomyelia,  however,  the  discoveries  of  Westphal,  Sirnon, 
and  F.  Schultze  leave  scarcely  a  doubt  but  that  they  arise  from  a  destruction  of 
proliferated  masses  of  neuroglia.  We  have  the  formation  of  a  central  glioma, 
probably  ainsing  usually  from  the  ependyma  of  the  central  canal  itself,  or  from 
its  vicinity,  with  a  secondary  disintegration  and  the  formation  of  a  cavity.  In 
these  cases  we  can  make  out  the  newly  formed  masses  of  neuroglia  about  the  cavi- 
ties, either  proliferating  or  disintegrating.  The  cavity  is  usually  situated  quite 
close  to  the  centei',  and  extends  most  frequently  into  the  substance  of  the  posterior 
columns.     In  its  longitudinal  extent  it  may  involve  a  great  part  of  the  cord. 

Clinical  Symptoms.— We  can  not  give  a  uniform  picture  for  the  formation  of 
cavities  in  the  spinal  cord,  since  the  symptoms,  of  course,  must  vary  very  much, 
according  to  the  seat  and  the  extent  of  the  change.  Slight  dilatations  of  the  cen- 
tral canal  may  run  their  course  entirely  without  symptoms.  In  the  cases  of  exten- 
sive cavity  formation,  with  much  damage  to  the  surrounding  substance  of  the 
cord,  there  usually  arise  a  severe  and  complex  array  of  spinal  symptoms,  whose 
correct  interpretation  can  hardly  ever  be  made  with  certainty  during  the  patient's 
life.  If  the  posterior  columns  and  posterior  cornua  be  chiefly  involved  in  the 
cavity  formation,  the  results  of  the  disturbance  of  function  of  those  parts  are  espe- 
cially prominent.  In  the  celebrated  case  of  general  anaesthesia  which  Späth  and 
Schtippel  have  described,  a  very  extensive  syringomyelia  was  found  in  the  spinal 
cord  on  autopsy.  In  other  cases  there  exists  a  form  of  disease  which  resembles 
spastic  spinal  paralysis,  or  there  develops  a  composite  spinal  affection  in  which 
the  symptoms  of  unilateral  lesion  are  to  a  degree  prominent.  In  all  such  cases 
the  diagnosis  can  be  made  with  a  certain  probability  by  excluding  other  chronic 
morbid  processes  in  the  cord.  A  very  slow  course,  extending  over  years  and  years, 
is  especially  worthy  of  consideration. 

In  one  class  of  cases  the  symptoms  of  syringomyelia  are  more  characteristic, 
and  here,  with  due  attention  and  knowledge,  we  can,  in  fact,  often  succeed  in 
making  a  correct  diagnosis.  By  many  observations  by  F.  Schultze,  Kahler,  and 
others,  it  has  been  proven  that  central  gliosis  with  secondary  cavity  formation 
very  often  begins  in  the  cervical  cord,  and  gives  rise  to  so  characteristic  a  type  of 
disease  that  the  process  may  often  be  diagnosticated  with  great  certainty  during  the 
patient's  life.  The  morbid  symptoms  appear  in  the  upper  extremities.  A  gradually 
increasing  muscular  atrophy  sets  in,  with  a  corresponding  loss  of  strength  and 
power  to  work ;  this  is  often  precisely  like  true  spinal  progressive  muscular  atrophy 
in  the  small  muscles  of  the  hand,  the  forearm,  the  deltoid,  etc.  With  this  are 
next  associated  peculiar  disturbances  of  sensibility,  chiefly  in  the  domain  of  the 
temperature  sense  (anaesthesia  to  heat  and  cold)  and  of  the  pain  sense  (analgesia), 
while  the  tactile  sensibility  for  a  long  time  remains  normal.     Trophic  disturbances 


SPINA  BIFIDA.  67g 

are  often  observed  and  are  very  interesting;  among  them  are  atrophy  of  the  finger- 
tips, thickening  of  the  joints,  changes  in  the  nails  and  skin,  etc.  Felons  and 
similar  inflammations,  from  which  the  patients  often  suffer,  are  either  connected 
with  these  trophic  disturbances  or  are  due  to  external  injuries,  such  as  burns  as  u 
result  of  analgesia,  etc.  Anomalies  of  the  sweat  secretion  have  been  repeatedly 
observed.  The  lower  extremities  remain  for  a  long  time  normal ;  later  spastic  and 
paretic  symptoms  may  come  on  iu  the  legs. 

With  this  type  of  disease,  which  we  can  usually  distinguish  sufficiently  well 
from  the  very  similar  amyotrophic  lateral  sclerosis,  progressive  muscular  atrophy, 
multiple  neuritis,  etc.,  and  which  has  something  very  characteristic,  as  we  can 
confirm  from  our  own  experience,  we  can  make  the  diagnosis  of  syringomyelia  of 
the  cervical  cord.  The  onset  of  other  clinical  symptoms  corresponds,  of  course, 
to  the  further  slow  progress  of  the  anatomical  process. 

The  prognosis  is,  of  course,  always  unfavorable,  but  the  course  is  very  slow, 
and  there  are  long-continued  apparent  cessations  of  the  disease. 

The  treatment  is  purely  symptomatic,  and  follows  the  same  rules  as  in  chronic 
myelitis. 

[Morvan's  Disease. — Analgesic  Paresis  ivith  Panaritium. — Morvan,  a  Breton 
physician,  has  described  an  affection  which  seems  quite  common  in  a  small  dis- 
trict in  Brittany,  some  twenty  cases  having  occurred  in  a  population  of  50,000. 
One  or  two  cases  have  been  reported  in  America.  It  is  characterized  by  severe 
pains  at  the  outset,  paresis  with  analgesia,  and  the  formation  of  panaritia  (felons), 
which  are  usually  painless.  There  is  also  tactile  and  thermal  anaesthesia.  The 
presence  of  tactile  anaesthesia  is  considered  the  distinction  between  it  and  syrin- 
gomyelia, but  mere  recent  observations  indicate  that  the  trouble  is  merely  syrin- 
gomyelia associated  perhaps  with  neuritis. — K.] 


APPENDIX. 

SPINA  BIFIDA. 

{Hydrorrhachis.    Myelocele.    Meningocele.) 

We  give  the  name  of  spina  bifida  to  a  congenital  fissure-formation  on  the  pos- 
terior side  of  the  vertebral  arches,  due  to  anomalies  of  development,  and  associated 
with  a  hernia-like  protrusion  of  the  sac  of  the  dura.  The  most  frequent  seat  of  the 
malformation  is  in  the  sacral  and  lumbar  regions.  Only  rarely  is  the  tumor  so  great 
as  to  hinder  the  birth  of  the  child.  Children  afflicted  with  spina  bifida  are  usually 
born  normally,  and  only  after  delivery  do  we  find  the  tumor  in  the  sacral  region ; 
its  size  may  be  from  that  of  a  small  nut  to  that  of  the  fist  or  lai'ger.  The  skin 
above  the  tumor  is  sometimes  entirely  normal,  but  in  other  cases  very  tense  and 
reddened.  If  we  have  an  opportunity  to  examine  the  tumor  carefully  anatomi- 
cally, we  usually  find  beneath  the  skin  the  protruded  sac  of  the  dura,  and  beneath 
it  the  arachnoid.  Only  rarely  is  the  dura  also  fissured,  so  that  the  sac  is  formed 
exclusively  of  the  arachnoid.  It  is  filled  with  a  clear  fluid  which  is  precisely 
identical  with  the  cerebro-spinal  fluid.  In  rare  cases  there  is  also  a  dilatation  of 
the  central  canal,  hydromyelus ;  then  the  substance  of  the  cord  is  atrophied  to  a 
greater  or  less  extent,  and  the  central  canal  communicates  directly  with  the  cavity 
of  the  spina  bifida.  In  other  cases  the  condition  of  the  cord  is  normal ;  sometimes 
its  lower  end  is  adherent  to  one  spot  of  the  sac.  We  must  refer  to  the  text-books 
of  pathological  anatomy  in  regard  to  the  many  further  details  of  the  anatomy 
and  the  history  of  development. 

In  regard  to  the  clinical  symptoms  of  spina  bifida,  the  condition  of  most  chil- 
dren at  first  is  perfectly  normal,  apart  from  the  malformation.     The  tumor  itself 


680  DISEASES  OF  THE  NERVOUS  SYSTEM. 

usually  feels  tense.  If  we  exert  pressure  on  it  with  the  hand,  we  can  often  force 
part  of  its  contents  back  into  the  vertebral  canal.  This  causes  an  increase  of  the 
cerebral  pressure,  and  we  notice,  besides  the  lessening  of  the  spina  bifida,  a  marked 
expansion  of  the  fontanelles,  and  also  the  appearance  of  somnolence,  contractions, 
and  changes  in  the  pulse  and  respiration,  which  demand  a  speedy  interruption  of 
this  rather  dangerous  experiment.  If  such  symptoms  do  not  appear  at  all,  we  can 
conclude  that  the  sac  is  completely  constricted  and  closed. 

Only  rarely,  however,  does  the  child's  condition  remain  normal  later  on.  The 
tumor  usually  shows  a  slow  growth,  and  the  results  of  pressure  on  the  spinal 
cord  or  on  the  cauda  equina  gradually  appear.  Paralysis,  anaesthesia,  vesical  dis- 
turbances, bedsores,  etc.,  develop,  and  these  symptoms  finally  lead  to  death.  Still 
more  frequently  the  sac  bursts,  or  its  walls  inflame,  and  this  becomes  fatal  from 
the  onset  of  a  purulent  meningitis. 

The  prognosis  of  most  cases  of  spina  bifida  is  accordingly  to  be  regarded  as 
unfavorable  unless  we  succeed  in  curing  the  disease  by  surgical  treatment. 
Recovery  has  been  brought  about  in  many  cases  by  methodical  compression  of 
the  sac,  and  by  puncture,  with  evacuation  of  the  fluid  and  a  subsequent  injection 
of  a  solution  of  iodine  to  obtain  an  obliteration  of  the  sac ;  but,  on  the  other  hand, 
the  operative  treatment  of  spina  bifida  is  attended  with  many  dangers,  such  as 
meningitis,  so  that  we  can  note  frequent  bad  results  as  well  as  favorable  ones. 
We  can  not  here  go  into  the  details  of  the  surgical  methods  for  the  cure  of  spina 
bifida ;  they  can  be  found  in  full  in  the  text-books  of  surgery. 


CHAPTER  XIV. 
SECONDARY  DEGENERATIONS  IN  THE    SPINAL   CORD. 

Although  the  secondary  degenerations  in  the  spinal  cord  are  chiefly  interest- 
ing merely  from  an  anatomical  point  of  view,  we  must  briefly  describe  them, 
because,  in  the  first  place,  a  clinical  significance  has  been  ascribed  to  them  in  cer- 
tain quarters,  and  also  because  the  study  of  secondary  degenerations  has  been  the 
starting-point  of  all  our  present  knowledge  as  to  the  systemic  diseases  of  the 
spinal  cord. 

1.  Secondary  Degeneration  in  the  Spinal  Cord  after  Cerebral  Lesions. — We 
already  know  (compare  page  538)  that  every  lesion  of  the  great  motor  ganglion- 
cells  in  the  anterior  cornua  of  the  spinal  cord,  and  every  permanent  break  in  con- 
duction in  the  motor  nerves  themselves,  is  followed  by  a  secondary  degeneration 
of  the  peripheral  portion  of  the  motor  fibers.  We  assume  as  the  reason  for  this, 
as  we  have  seen,  a  "  trophic  influence  "  of  the  said  ganglion-cells  on  the  motor 
fibers  arising  from  them,  so  that  the  latter  degenerate  when  the  conduction  of 
that  trophic  influence  is  interrupted,  or  when  the  trophic  ganglion-cells  them- 
selves are  destroyed.  Precisely  analogous  conditions  exist  for  the  first  great  por- 
tion of  the  motor  conducting  tract,  the  lateral  pyramidal  tract,  from  the  cortex 
cerebri  to  the  anterior  cornua  of  the  spinal  cord.  The  great  ganglion-cells  of  the 
motor  portion  of  the  cortex  cerebri  also  exert  a  trophic  influence  on  the  motor 
fibers  arising  from  them,  which  extends  to  the  motor  ganglion-cells  of  the  spinal 
cord.  If  there  be  disease  situated  in  the  motor  portion  of  the  cortex  cerebri  itself, 
or  in  any  part  of  the  motor  tract  in  the  brain  (the  motor  fibers  of  the  corona  radi- 
ata,  the  internal  capsule,  the  crus,  or  the  pons),  by  which  disease  the  conduction  is 
interrupted — if  there  be  disease  there,  we  repeat,  a  secondary  descending  degenera- 
tion of  the  motor  fibers  ensues  in  the  whole  portion  below,  down  to,  but  exclusive  of, 


SECONDARY  DEGENERATIONS  IN   THE  SPINAL  CORD.        081 


the  anterior  cornua  of  the  gray  matter.  This  secondary  descending  degeneration 
of  the  pyramidal  tract  is  found  correspondingly  in  the  pyramid  of  the  same  side 
on  which  the  focus  of  disease  in  the  brain  is  situated. 
From  this  point  we  can  trace  the  main  part  of  the  degenera- 
tion farther  down  the  lateral  column  of  the  spinal  cord  on 
the  opposite  side  (secondary  degeneration  of  the  lateral 
crossed  pyramidal  tract)  (see  Fig.  96),  while  in  many  cases 
besides  we  find  a  slighter  secondary  degeneration  in  the  an- 
terior column  of  the  spinal  cord  on  the  same  side  (secondary 
degeneration  of  the  anterior  uncrossed  pyramidal  tract).  As 
we  know  from  Flechsig's  investigations,  the  relative  amounts 
of  the  crossed  lateral  fibers,  and  the  anterior  fibers  that  re- 
main uncrossed,  vary  in  individual  cases  within  certain  lim- 
its. In  the  cases  where  no  anterior  pyramidal  tract  exists — 
that  is,  where  all  the  motor  fibers  pass  over  to  the  lateral 
column  of  the  opposite  half  of  the  spinal  cord  in  the  decus- 
sation of  the  pyramids — of  course  a  descending  degeneration 
in  the  anterior  column  is  wholly  wanting.  We  must  add, 
however,  that  in  some  cases  a  small  number  of  fibers  seem 
to  proceed  uncrossed  in  the  lateral  column,  so  that  accord- 
ingly we  may  also  have  a  slight  secondary  descending  de- 
generation in  the  lateral  pyramidal  tract  of  the  same 
(affected)  side  (Pitres). 

2.  Secondary  Degenerations  in  the  Spinal  Cord  in 
Transverse  Affections  of  the  Spinal  Cord  itself. — If  a  lesion 
be  situated  in  any  part  of  the  spinal  cord,  by  which  more  or 
less  of  its  transverse  section  is  affected,  the  interruption  of 
conduction  in  these  fibers  is  also  followed  by  the  appearance 
of  secondary  degenerations  which  may  be  made  out  both  in 
a  descending  and  in  an  ascending  direction  (see  Fig.  97). 
It  is  most  frequently  transverse  myelitis,  compression  of  the 
spinal  cord,  and  tumors  of  the  cord,  which  give  rise  to  second- 
ary degenerations.  The  latter,  however,  of  course,  are 
never  due  to  the  sort  of  lesion,  but  only  to  its  seat,  and  to  the 
interruption  of  conduction  caused  by  it. 

The  secondary  descending  degeneration  affects  the  pyra- 
midal tract  in  a  fashion  precisely  analogous  to  that  which 
we  have  also  learned  to  recognize  in  secondary  degenera- 
tions after  cerebral  lesions;  but  since  the  primary  affection 
usually  affects  the  pyramidal  tract  on  the  two  sides,  the  de- 
scending secondary  degeneration  of  course  develops  in  both 
lateral  pyramidal  tracts,  and  also  in  the  anterior  pyramidal 
tracts,  if  they  exist  below  the  point  of  lesion. 

The  secondary  ascending  degeneration,  developing  up- 
ward from  the  primary  point  of  disease,  affects  two  systems 
of  fibers,  the  so-called  columns  of  Goll  (the  internal  portion 
of  the  posterior  columns),  and  also  at  the  same  time  the 
lateral  cerebellar  tracts  *  on  the  periphery  of  the  lateral  col- 
umns and  external  to  the  lateral  pyramidal  tracts.     Both 


*  The  area  of  the  ascending  degeneration  of  the  "  lateral  cerebellar  tract," 
as  may  be  seen  in  the  picture,  shows  at  its  anterior  end  a  marked  expansion. 
Possibly  this  anterior  portion  of  the  degenerated  fibers  corresponds  to  an- 
other system  (Bechterew). 


Fig.  96.  —  Secondary  de- 
scending degeneration 
of  the  pyramidal  tracts 
in  a  primary  lesion  of 
the  left  half  of  the  cer- 
ebrum. The  lateral 
pyramidal  tract  of  the 
right  half  of  the  cord  is 
degenerated  down  to 
the  lowest  part  of  the 
lumbar  region  (1-8)  ; 
the  anterior  pyramidal 
tract  of  the  left  half  of 
the  cord  is  degener- 
ated to  the  beginning 
of  the  lumbar  enlarge- 
ment (1-6). 


682 


DISEASES  OF  THE  NEEVOUS  SYSTEM. 


systems  of  fibers  mentioned,  whose  conduction  is  in  a  centripetal  direction,  must 
accordingly  receive  trophic  influences  from  more  peripheral  ganglion-cells.  The 
connection  of  the  columns  of  Goll  with  the  gray  matter  (spi- 
nal ganglia?  posterior  cornua?)  is  not  yet  accurately  known. 
The  fibers  of  tbe  lateral  cerebellar  tracts,  however,  are  cer- 
tainly connected  with  the  cells  of  the  columns  of  Clarke.  If 
tbese  also  be  destroyed  by  any  process  in  the  lower  dorsal 
and  upper  lumbar  cord,  an  ascending  degeneration  of  the 
lateral  cerebellar  tracts  develops,  which  may  be  traced  up- 
ward into  the  restiform  body.  The  further  course  of  the 
fibers  to  the  cerebellum  is  not  yet  certainly  known. 

Although  no  clinical  significance  at  all  can  be  attributed 
to  secondary  ascending  degeneration,  the  theory  first  ad- 
vanced by  the  French  observers  (Charcot  and  others)  pre- 
vails almost  universally,  that  secondary  descending  degener- 
ation causes  definite  clinical  symptoms.  The  secondary  con- 
tractures and  the  increase  of  the  tendon  reflexes  in  the  par- 
alyzed limbs,  occurring  in  hemiplegia,  are  especially  referred 
to  this.  We  shall  see  in  a  later  section  that  this  theory  is  by 
no  means  proven,  and  is  even  improbable,  so  that,  in  our 
opinion,  the  secondary  descending  degeneration  also  has  no 
material  clinical  significance. 

3.  Secoyidary  Degeneration  in  the  Spinal  Cord  after  In- 
juries of  the  Cauda  Equina. — After  injuries  of  the  cauda 
equina — for  example,  after  fractures  or  caries  of  the  lower 
lumbar  vertebras  and  of  the  sacrum,  in  new  growths  in  this 
region,  etc. — a  secondary  ascending  degeneration  occurs  in 
the  spinal  cord,  if  an  actual  solution  of  continuity  of  the 
fibers  have  existed  for  a  long  time,  which  depends  exclusive- 
ly upon  the  lesion  of  the  affected  posterior  root-fibers.  This 
is  accordingly  limited  to  the  posterior  columns  of  the  spinal 
cord,  and  in  its  distribution  it  shows  a  great  resemblance  to 
the  condition  of  the  degeneration  in  tabes  dorsalis.  In  the  lumbar  cord  the 
greater  portion  of  the  posterior  columns  is  degenerated,  with  the  exception  of  a 
little  median  zone  and  the  most  anterior  portion  (compare  Fig.  87).  The  de- 
generation grows  smaller  upward,  and  finally  limits  itself  in  the  cervical  cord  to 
the  region  of  the  columns  of  Goll.  Thus  this  condition  again  affords  a  proof  of 
the  correctness  of  the  statements  advanced  by  Singer,  Kahler,  and  others,  that  the 
columns  of  Goll  form,  at  least  in  part,  the  prolongation  of  the  fibers  from  the 
root-zones  of  the  lumbar  cord  (compare  page  510). 


Fig.  97.— Secondary  as- 
cending and  descend- 
ing degeneration  in  a 
transverse  affection 
of  the  upper  dorsal 
region.  The  columns 
of  Goll  and  the  direct 
cerebellar  tracts  are 
degenerated  upward. 
The  lateral  pyramid- 
al tracts  are  degener- 
ated downward. 


CHAPTER  XV. 

UNILATERAL   LESION   OF   THE    SPINAL   CORD. 

(Brown-SequarcPs  Spinal  Paralysis.) 

Unilateral  lesion  is  not  a  definite  disease  of  the  spinal  cord,  but  a  peculiar 
group  of  symptoms,  which  occurs  whenever  an  interruption  of  conduction  is 
produced  by  any  affection  in  one  lateral  half  of  the  spinal  cord.  Since  the  symp- 
toms in  these  cases  were  first  carefully  studied  clinically  and  experimentally  by 
Brown-Sequard  in  particular,  we  often  call  the  type  of  disease  in  question  "  Brown- 


UNILATERAL  LESION   OF  THE  SPINAL  CORD. 


683 


Sequard's  paralysis."  We  see  this  paralysis  most  frequently  and  jii  its  purest 
form  iu  injuries  of  the  spinal  cord.  Almost  perfectly  exact  sections  of  one  lateral 
half  of  the  spinal  cord  are  often  produced  hy  stabs  from  a  knife,  a  sword,  etc.  In- 
flammatory processes,  compression,  and  especially  tumors  of  the  cord,  may  also, 
during  a  certain  period  of  their  course,  cause  the  symptoms  of  a  more  or  less 
sharply  defined  unilateral  lesion. 

The  peculiar  condition  of  the  symptoms  in  unilateral  lesion  is  easily  explained 
by  a  consideration  of  the  course  of  the  fibers  in  the  spinal  cord.  In  the  accom- 
panying diagram  (see  Fig.  98)  the  motor  fibers  from  the  anterior  roots  are  marked 
v,  the  sensory  fibers  from  the  posterior 
roots,  h .  As  we  have  already  said,  the  sen- 
sory fibers,  h,  pass  at  once  into  the  opposite 
half  of  the  spinal  cord,  and  accordingly  de- 
cussate with  the  corresponding  sensory 
fibers  of  the  other  side.  The  motor  fibers, 
v,  however,  pass  upward  uncrossed  on  the 
side  they  enter  the  spinal  cord,  especially 
in  the  lateral  column.  If  now,  for  exam- 
ple, there  be  situated  on  the  right  side  of 
the  spinal  cord  at  a  a  lesion,  causing  a  sec- 
tion of  one  half  the  cord,  the  conduction  of 
those  motor  fibers  "which  come  from  the 
right  side  is  interrupted,  as  well  as  the  con- 
duction of  those  sensory  fibers  "which  come 
from  the  left  side.  From  this  it  follows 
that  there  must  be  a  motor  paralysis  on  the 
same  side  of  the  body  as  the  lesion  in  the 
spinal  cord,  and  a  sensory  paralysis  (anaes- 
thesia) on  the  other  side  of  the  body.  If 
the  affection  be  situated  in  the  dorsal  or 
lumbar  cord,  the  leg  on  the  corresponding 
side  is  paralyzed,  and  the  leg  on  the  other 
side  is  anaesthetic.  If  the  lesion  be  situated 
in  the  cervical  cord,  above  the  entrance  of  Fig. 
the  nerves  for  the  upper  extremities,  the 
arm  and  the  leg  on  the  side  of  the  lesion 
are  both  paralysed  (spinal  hemiplegia), 
while  the  arm  and  the  leg  on  the  other  side 
are  anaesthetic,  but  their  motility  is  nor- 
mal.* 

On  more  careful  examination,  further  conditions  of  physiological  interest 
appear.  The  sensibility  on  the  side  of  the  motor  paralysis  is  usually  not  only 
normal,  but  there  is  even  a  pronounced  hyperaesthesia  for  all,  or  at  least  for  some, 
of  the  forms  of  irritation.  Slight  pricks  are  very  painful,  and  tickling  the  soles  of 
the  feet  is  felt  with  abnormal  strength.  The  muscular  sense  alone  (the  feeling 
for  passive  motion)  is  a  noteworthy  exception,  since  it  is  usually  markedly  dimin- 
ished on  the  paralyzed  side.  We  can  explain  this  fact  only  by  Brown-Sequard's 
theory  that  the  fibers  for  the  muscular  sensibility  (see  2  and  2'  in  Fig.  98),  in  dis- 
tinction from  all  the  other  sensory  fibers,  run  their  course  in  the  spinal  cord 
uncrossed,  just  like  the  motor  fibers. 


(From  Erb.)  Schematic  representation 
of  the  course  of  the  main  tracts  in  the  cord, 
represented  for  a  single  pair  of  roots,  v. 
Anterior  roots,  h.  Posterior  roots.  1.  Paths 
for  motor  and  vasomotor  conduction.  2. 
Paths  for  muscular  sense.  3.  Paths  for  cu- 
taneous sensibility  on  the  right.  1',  2',  3'. 
The  same  paths  on  the  left.  The  arrows  in- 
dicate the  direction  of  physiological  conduc- 
tion. 


*  [More  recent  investigations  by  Mott  render  this  theory  of  immediate  decussation  somewhat  doubt- 
ful, and  unilateral  lesion  may  not  always  present  this  group  of  symptoms. — K.] 


684 


DISEASES  OF  THE  NERVOUS  SYSTEM. 


Above  the  hyperaesthetic  territory  in  the  skin  we  usually  find  a  small  anses- 
thetic  zone  (Fig.  99,  6),  and  above  this  at  times  again  a  small  hyperaesthetic  strip 
(see  Fig.  99,  c).  The  anaesthetic  zone  is  easily  explained.  It  corresponds  pre- 
cisely to  the  level  of  tbe  lesion  in  the  spinal  cord 
— that  is,  to  those  sensory  fibers  coming  from 
the  same  side,  which  are  immediately  involved 
as  soon  as  they  enter  the  cord ;  but  a  satisfactory 
explanation  is  entirely  lacking  for  the  appear- 
ance of  the  hyperesthesia  on  the  paralyzed  side, 
and  for  the  origin  of  the  uppermost  small  hyper- 
assthetic  zone. 

The  reflexes,  especially  the  tendon  reflexes, 
are  usually  increased  on  the  paralyzed  side. 
There  is  often  a  vigorous  ankle  clonus,  a  symp- 
tom which  must  be  explained  by  the  loss  of  the 
reflex  inhibitory  influences  coming  from  above. 
Finally,  Ave  often  find  on  the  side  of  the  lesion 
the  signs  of  a  vasomotor  paralysis,  especially  a 
marked  rise  in  the  cutaneous  temperature  of 
even  2°  (1°  C),  or  more. 

On  the  anaesthetic  side,  however,  in  pure 
cases,  the  motility  and  also  the  muscular  sense 
are  perfectly  normal,  in  distinction  from  the 
other  forms  of  sensation.  Anaesthesia  is  not  al- 
ways complete,  but  it  sometimes  affects  only  sin- 
gle qualities  of  sensation  to  a  greater  or  less  de- 
gree. Thus  we  have  often  seen  partial  paralyses 
of  the  temperature  sense,  especially  partial  an- 
aesthesia to  cold.  Above  the  anaesthetic  region 
we  also  find  frequently  a  small  hyperaesthetic 
zone  (see  Fig.  99,  c).  The  reflexes  are  usually 
normal,  or  only  a  little  increased. 

Of  the  other  spinal  symptoms  we  have  still 
to  mention  the  almost  invariable  disturbance  of 
micturition  and  defecation,  neuralgic  pains  now 
more  on  one  side  and  now  more  on  the  other, 
muscular  atrophy,  changes  in  the  electrical  ex- 

Fio.  99.-Schematic  representation  of  the  citability,  etc.  All  these  Symptoms  are  not  Char- 
chief  symptoms  in  unilateral  lesion  of  acteristic  of  the  unilateral  lesion  as  such,  and 
the   left   dorsal   cord.     (After  Erb.)  .  ' 

The  oblique  shading  signifies  motor   are  always  easily  explained  in  any  given   case 
cafshadJng°sfei^  from  the  localization  of  the  disease.     We  must 

hypergesttesia0*3  Signify  cutaneous   also  mention  that  the  symptoms  of  unilateral 

lesion  may  not  be  perfectly  pure,   but  we  can 

often  recognize  only  a  few  prominent  features  of  them. 

We  need  add  nothing  as  to  the  prognosis  and  treatment  of  unilateral  lesion, 

because,  of  course,  they  are  governed  entirely  by  the  form  of  the  primary  disease. 


PROGRESSIVE  BULBAR  PARALYSIS.  685 


IV.— The  Diseases  of  the  Medulla  Oblongata. 


CHAPTER   I. 


PROGRESSIVE    BULBAR    PARALYSIS. 

(  G-losso-labio-laryngcal   Paralysis. ) 

DUCHENNE  in  1860  described  for  the  first  time  with  completeness  the  symptoms 
of  a  disease  to  which  Wachsmuth  has  since  given  the  name  of  progressive  bulbar 
paralysis.  Ducbenne  did  not,  however,  recognize  the  true  seat  of  the  disease,  and 
it  was  not  till  1870  that  Charcot  in  France,  and  E.  Leyden  in  Germany,  were 
enabled  to  confirm  the  suggestion  of  Wachsmuth  that  the  lesion  is  a  progressive 
degeneration  and  atrophy  of  the  nuclei  in  the  medulla  oblongata.  Since  then 
our  knowledge  of  the  disease  has  grown  rapidly,  both  from  the  clinical  and  the 
anatomical  standpoints ;  and  Kussmaul  and  others  have  thoroughly  investigated 
its  relations  to  two  other  closely  allied  forms  of  disease — amyotrophic  latex*al 
sclerosis,  and  progressive  muscular  atrophy. 

.ZEtiology. — We  have  scai'cely  any  certain  information  about  the  cause  of  the 
disease.  Heredity  seems  of  slight  importance.  In  some  cases  its  origin  is  ascribed 
to  catching  cold,  emotional  excitement,  traumatic  influences,  and  excessive  bodily 
exertion.  Perhaps  it  is  sometimes  occasioned  by  excessive  use  of  the  muscles  to 
which  the  disease  is  chiefly  confined,  as  in  playing  on  wind-instruments ;  but  in 
many  instances  no  possible  cause  can  be  found.  Men  seem  somewhat  more  liable 
to  be  attacked  than  women.  The  disease  hardly  ever  appears  till  middle  or  old 
age — that  is,  after  thirty-five. 

Clinical  History. — The  symptoms  are  almost  always  very  slow  in  their  develop- 
ment. There  may  be  mild  premonitory  symptoms — such  as  painful  sensations  in 
the  back  of  the  neck.  Then  there  is  a  very  gradual  appearance  of  difficulty  in 
articulation.  Many  words'are  pronounced  indistinctly.  The  first  trouble  is  noticed 
especially  with  letters  in  the  utterance  of  which  the  tongue  plays  an  essential  part : 
E,  R,  L,  S,  G  (hard),  K,  D,  T,  and  N.*  It  is  easily  seen  that  the  derangement  is  not 
aphasic.  There  is  no  forgetting  or  confounding  of  the  words  or  letters ;  but  the 
innervation  of  the  tongue  has  become  impaired.  Long  before  the  ordinary  move- 
ments of  this  member  are  visibly  embarrassed,  the  patient  has  lost  the  ability  to 
make  those  more  delicate  manipulations  of  it  which  are  essential  to  normal 
speech.     This  disturbance  of  articulation  is  termed  alalia  or  anarthria. 

By  the  time  this  has  become  somewhat  marked,  it  is  usually  possible  to  detect, 
on  close  examination,  that  the  tongue  is  beginning  to  atrophy.  It  seems  flabby, 
thin,  and  less  rounded.  Here  and  there  its  surface  presents  furrows  and  depres- 
sions; and  often  the  individual  fasciculi  exhibit  active  fibrillary  contractions. 
Just  as  in  progressive  muscular  atrophy,  the  impairment  of  motion  usually 
keeps  equal  pace  t  with  the  atrophy.     The  greater  the  atrophy,  the  less  is  the 

*  [Except  as  otherwise  specified,  the  letters  and  words  used  as  examples  here  and  later  on  are  to 
be  given  the  ordinary  English  pronunciations. — Trans.] 

t  At  the  commencement  of  the  disease  the  paralysis  may  possibly  seem  greater  than  the  atrophy, 
so  far  as  the  latter  can  be  detected.  Nor  would  it  be  impossible  for  a  primary  lesion  of  the  nuclei  of 
nerves  to  result  in  a  paralysis  before  the  secondary  descending  degeneration  had  become  completely 
developed.  On  the  other  hand,  it  must  be  borne  in  mind  that  numerous  individual  fibers  in  the  lip  or 
tongue  might  be  already  atrophied  before  the  eye  or  the  touch  could  appreciate  any  change  in  bulk. 


686  DISEASES  OF  THE  NERVOUS  SYSTEM. 

mobility.  Finally  it  becomes  quite  impossible  to  project  the  tongue  from  the 
mouth  or  move  it  from  side  to  side.  The  tongue  lies  flat  and  limp  on  the  floor  of 
the  mouth.  Its  surface  is  often  diversified  with  furrows  and  depressions,  contain- 
ing much  desquamated  epithelium  or  the  like.  Evidently  any  great  impairment 
of  motility  in  the  tongue  hinders  not  only  speaking,  but  also  chewing  and  swal- 
lowing. The  organ  can  no  longer  bring  out  such  portions  of  the  food  as  get 
between  the  cheeks  and  the  teeth,  nor  can  it  push  the  bolus  backward  within  the 
grasp  of  the  pharyngeal  constrictors. 

Even  before  the  atrophy  of  the  tongue  becomes  extreme,  analogous  disturb- 
ances usually  appear  in  neighboring  groups  of  muscles.  As  a  rule,  the  muscles  of 
the  lips  are  next  affected  after  the  tongue.  The  first  thing  the  patient  notices  is 
a  peculiar  feeling  of  stiffness  or  tension  in  the  lips.  Movement  becomes  gradually 
more  and  more  difficult ;  and  the  patient  becomes  unable  to  pucker  up  his  lips  so  as 
to  whistle.  Speech  is  also  noticeably  interfered  with,  for  now  all  those  letters  the 
pronunciation  of  which  demands  labial  movements  are  very  imperfectly  articu- 
lated, and  at  last  can  not  be  uttered  at  all.  These  are  O,  A  (long),  P,  F,  B,  M, 
and  V ;  and  also  the  sound  of  double  O,  as  in  tool.  It  also  becomes  gradually 
evident  that  the  lips  atrophy.  They  grow  thin,  with  sharp  edges  and  wrinkled 
skin.     Fibrillary  contractions  are  not  infrequently  visible. 

This  atrophy  of  the  orbicularis  oris  is  followed  by  atrophy  and  paresis  of  some 
of  the  other  muscles  of  expression  supplied  by  the  lower  division  of  the  facial 
nerve.  The  general  facial  expression  of  a  patient  with  bulbar  paralysis  thus 
comes  to  bear  a  very  characteristic  stamp  :  the  mouth  remains  half  open,  and 
seems  to  be  broadened  out,  the  lower  lip  hangs  down,  the  naso-labial  folds  are 
deepened,  and  indeed  the  whole  aspect  is  persistently  lachrymose.  Even  in 
laughing,  the  lower  half  of  the  face  relaxes  comparatively  little;  while  the  region 
supplied  by  the  upper  division  of  the  facial  nerve,  and  the  movements  of  the  eye- 
ball, remain  as  a  rule  perfectly  normal. 

The  third  group  of  muscles  affected  are  those  of  the  pharynx  and  larynx. 
The  soft  palate  becomes  paretic,  and  produces  further  trouble  in  swallowing. 
Quite  often  the  liquid  ingesta  are  regurgitated  through  the  nose.  The  voice 
becomes  nasal.  The  production  of  many  sounds,  and  in  particular  of  B  and  P, 
is  now  impossible,  since,  in  addition  to  the  labial  paresis,  a  portion  of  the  essential 
current  of  ah  escapes  through  the  nostrils.  This  explains  why  the  letters  men- 
tioned can  sometimes  be  pronounced  better  if  the  nose  be  compressed.  The 
paralysis  of  the  constrictors  of  the  pharynx  impedes  deglutition  more  and  more, 
till  the  impairment  of  nutrition  becomes  extreme. 

The  enfeebled  action  of  the  laryngeal  muscles  is  betrayed,  in  the  earlier 
stages  of  the  disease,  by  a  certain  weakness  and  monotony  in  speaking.  Modula- 
tions of  the  voice,  and  the  production  of  the  higher  notes,  as  in  singing,  are  no 
longer  possible.  If  the  innervation  of  the  larynx  becomes  still  more  impaired,  it 
becomes  a  very  serious  matter.  If  the  arytaenoid  cartilages  do  not  press  together 
firmly  on  swallowing,  the  entrance  to  the  larynx  is  inadequately  closed,  and  food 
is  often  swallowed  the  wrong  way.  Liquid  and  even  solid  ingesta  get  into  the 
larynx,  and  excite  a  violent  cough  ;  or,  being  inhaled  into  the  air-passages,  they 
cause  bronchitis  or  lobular  pneumonia.  The  paralysis  may  reach  such  a  degree 
that  the  voice  is  at  best  a  hoarse  whisper.  With  the  laryngoscope  we  can  see  that 
the  vocal  cords  are  paralyzed.  The  inability  to  close  the  glottis  tightly  is 
extremely  unfavorable,  for  it  renders  the  patient  unable  to  cough  vigorously. 
Mucous  accumulations  may  therefore  come  to  be  the  source  of  extreme  dyspnoea. 

The  catalogue  of  symptoms  is  not  yet  ended.  As  we  have  seen,  the  muscular 
atrophy  of  the  tongue  and  lips  can  invariably  be  detected.  That  of  the  pharyn- 
geal and  laryngeal  muscles  can  not  be  demonstrated  during  life,  although  it  is  to 


PROGRESSIVE  BULBAR  PARALYSIS.  687 

be  found  post  mortem.  Inasmuch  as  the  process  is  one  of  genuine  degeneration 
with  consequent  atrophy,  the  affected  fibers  ought  to  give  the  reaction  of  degenera- 
tion to  electricity;  but  this  is  difficult  of  actual  proof,  just  as  it  is  in  progressive 
muscular  atrophy,  because  numerous  healthy  fibers  lie  side  by  side  with  the 
degenerated  ones.  Still,  in  an  advanced  case,  careful  examination  will  usually 
bring  out  an  evident  degenerative  reaction  here  and  there  in  the  tongue  and 
lips. 

The  disturbance  of  reflex  action  is  often  striking.  Usually  the  reflexes  are 
greatly  diminished  or  even  absent,  so  that  one  can  tickle  the  root  of  the  tongue  and 
the  epiglottis  without  causing  the  patient  to  gag.  In  a  few  instances  the  facial 
muscles  exhibit  an  increase  of  tendon  reflex,  as  can  be  shown  by  tapping  upon 
the  tendons,  the  periosteum  of  the  jaws,  or  the  bridge  of  the  nose.  This  behavior 
reminds  one  of  the  condition  of  the  muscles  in  amyotrophic  lateral  sclerosis  (q.  v.). 

Exceptionally,  still  other  muscular  groups  are  involved.  Of  such  disturbances, 
the  most  frequent  is  in  the  region  supplied  by  the  motor  branch  of  the  trigeminus, 
impairing  mastication.  The  impairment  of  these  muscles  now  combines  with  the 
labial  and  lingual  atrophy  to  render  chewing  almost  impossible.  In  very  rare 
cases  the  ocular  muscles  are  also  involved,  with  resulting  ptosis  and  strabismus. 

All  the  symptoms  thus  far  enumerated  are  exclusively  motor.  Sensation  is 
perfect  to  the  end.  The  sensibility  of  the  skin  of  the  face  and  of  the  mucous 
membrane  of  the  tongue  and  mouth,  as  well  as  the  sense  of  taste,  are  unimpaired. 
Disturbances  of  sensation  in  the  distribution  of  the  trigeminus,  and  more  or  less 
deafness,  have  been  reported  in  one  or  two  cases  ;  but  there  is  some  doubt  about 
the  observations.  It  does,  however,  seem  certain  that  secretory  and  vaso-motor 
derangements  are  frequent.  Salivation  deserves  especial  mention.  In  many 
cases  of  bulbar  paralysis  it  is  a  constant  symptom,  so  that  the  patient  is  obliged 
to  keep  a  pocket-handkerchief  to  his  mouth,  to  catch  the  fluid  as  it  dribbles  away. 
This  is  due,  to  a  certain  extent,  to  the  fact  that  the  secreted  saliva  can  not  be 
swallowed,  and,  as  the  lips  do  not  shut  tightly,  it  naturally  escapes  from  the 
mouth  ;  but  volumetric  examinations  have  rendered  it  pretty  certain  that  the 
amount  of  saliva  is  abnormally  large.  The  explanation  of  this  has  not  been 
determined.  Nor  as  yet  do  we  know  much  about  the  vaso-motor  disturbances. 
Many  patients  complain  of  a  feeling  of  heat  and  "  boiling "  in  the  head.  "We 
may  also  mention  in  this  connection  that  occasionally,  toward  the  close  of  the 
disease,  the  pulse  becomes  very  rapid  (140-160).  This  is  probably  due  to  paralysis 
of  the  vagus. 

The  course  of  the  disease  is  invariably  protracted.  The  order  in  which  the 
symptoms  appear  is,  as  a  rule,  that  in  which  they  have  just  been  described.  The 
atrophy  and  paresis  appear  first  in  the  tongue,  then  in  the  lips  and  the  neighbor- 
ing muscles  of  the  face,  and  lastly  in  the  muscles  of  the  soft  palate,  pharynx,  and 
larynx.  Still,  there  may  be  some  deviation  from  this.  Usually  the  progress  of 
the  disease  is  very  gradual.  There  may  be  an  apparent  arrest  of  the  trouble ;  or 
less  often  there  are  quite  sudden  exacerbations.  When  all  the  different  symptoms 
are  well  developed,  the  clinical  picture  is  unusually  characteristic.  The  peculiar 
immobility  of  expression;  the  broad,  slightly  gaping  mouth,  with  the  atrophied 
lips;  the  almost  unintelligible  speech,  low,  monotonous,  and  labored;  and  the 
inability  to  swallow — these  often  betray  the  disease  at  once.  The  last  stage  of 
the  illness  is  the  more  distressing,  in  that  the  intelligence  remains  to  the  end 
entirely  unclouded. 

The  entire  duration  of  the  disease  is  usually  several  years — say  two  to  five.  If 
death  is  not  caused  by  some  intercurrent  trouble,  it  is  brought  about  in  one  of 
three  ways  :  either  through  inanition,  due  to  the  increasing  difficulty  of  degluti- 
tion ;  or  through  pulmonary  complications — namely,  bronchitis,  lobular  pneumo- 


688  DISEASES  OF  THE  NERVOUS  SYSTEM. 

nia,  or  gangrene,  as  a  result  of  food  passing  down  the  trachea  ;  or  through  sudden 
asphyxia  or  cardiac  failure. 

Pathology.  Nature  of  the  Disease,  and  its  Appearance  as  a  Symptom  of  Pro- 
gressive Muscular  Atrophy  or  of  Amyotrophic  Lateral  Sclerosis. — If  we  seek  the 
anatomical  lesion  corresponding  to  the  group  of  symptoms  above  depicted,  we 
shall  find,  on  microscopic  examination  of  the  nervous  system,  in  all  cases  of  this 
description,  a  typical  disease  of  the  medulla  oblongata.  The  ganglionic  nuclei 
and  the  nerves,  corresponding  to  those  muscles  which  we  have  found  to  undergo 
atrophy  in  bulbar  paralysis,  present  distinct  evidences  of  degeneration.  This  is 
most  readily  demonstrated  in  the  nucleus  of  the  hypoglossus.  The  ganglionic 
cells  have  some  of  them  entirely  disappeared,  while  others  are  greatly  atrophied. 
The  connective  tissue  is  increased  in  amount,  and  the  walls  of  the  blood-vessels 
traversing  the  nucleus  are  thickened.  In  the  earlier  stages  there  are  often  many 
cells  which  contain  granules  of  fat.  The  same  changes,  though  perhaps  less  pro- 
nounced, are  exhibited  by  the  common  nucleus  of  the  vagus  and  accessorius,  that 
of  the  facial,  and  sometimes  also  that  of  the  glosso-pharyngeal  nerve.  The  other 
nuclei  are  perfectly  normal.  We  never  find  a  diffuse  "inflammation,"  but  in 
every  case  a  primary  degeneration  of  the  nuclei,  which  spreads  no  farther. 

Starting  from  these  nuclei,  the  degeneration  and  atrophy  may  be  seen  to 
extend  into  the  nerve-fibers  which  issue  from  them.  The  roots  of  the  hypo- 
glossus, vagus,  accessory,  and  facial  nerves  can  often  be  seen  by  the  naked  eye  to 
be  diminished  in  size  and  of  a  gray  color.  The  microscope  always  shows  a  partial 
atrophy  of  their  fibers.  Finally,  there  is  a  corresponding  atrophy  of  muscles  of 
the  tongue,  lips,  and  other  parts.  We  need  not  enter  into  detail,  for  the  histolo- 
gical conditions  are  precisely  those  seen  in  the  muscles  of  the  trunk  and  extremi- 
ties in  the  spinal  form  of  progressive  muscular  atrophy. 

Thus  we  find  progressive  bulbar  paralysis  perfectly  analogous  with  progressive 
muscular  atrophy.  The  nuclei  in  the  medulla  oblongata  are  the  motor  and  trophic 
centers  of  the  bulbar  nerves  and  of  the  muscles  which  these  nerves  supply.  The 
relation  is  precisely  that  which  exists  between  the  anterior  cornua  of  the  spinal 
cord  on  the  one  hand,  and  the  spinal  nerves  and  the  muscles  which  they  inner- 
vate on  the  other.  In  both  diseases  there  is  a  degeneration  and  atrophy  of  the 
trophic  and  motor  center  and  the  corresponding  nerves  and  muscles.  In  both 
diseases  the  atrophy  and  the  functional  disability  of  the  muscles  keep  pace  with 
each  other,  and  in  both  the  affection  is  strictly  limited  to  the  motor  tract,  sensibility 
suffering  no  impairment  whatever.  Certain  questions  about  bulbar  paralysis  are 
as  unsettled  as  similar  ones  about  progressive  muscular  atrophy.  It  is  uncertain 
whether  the  primary  degenerative  process  is  limited  to  the  bulbar  nuclei,  and  the 
degeneration  of  the  nerves  and  muscles  is  to  be  regarded  as  secondary  ■  or  whether 
the  entire  motor  apparatus,  from  the  ganglionic  cell  to  the  muscular  fiber,  is  simul- 
taneously attacked  ;  or,  finally,  whether,  as  Friedreich  maintains,  the  atrophy 
begins  in  the  muscles,  and  thence  ascends  along  the  nerve-fibers  to  the  medulla. 
We  think  it  improbable  that  these  points  will  be  cleared  up  very  speedily.  Their 
solution  would  seem  to  be  only  of  theoretical  interest. 

We  certainly  must  recognize,  however,  the  essential  identity  of  progressive 
bulbar  paralysis  and  progressive  muscular  atrophy.  The  resemblance  becomes 
even  more  striking  if  we  consider  that  very  frequently  both  diseases  are  present 
simultaneously.  Often,  after  a  case  of  progressive  muscular  atrophy  has  lasted 
for  some  time,  the  symptoms  of  bulbar  paralysis  also  appear.  And,  on  the  other 
hand,  an  illness  may  begin  with  bulbar  symptoms,  and  later  on  be  complicated  by 
atrophy  of  the  muscles  of  the  extremities — almost  always  first  seen  in  the  arms. 
If  cases  of  this  sort  come  to  autopsy,  we  find  a  combination  of  the  anatomical 
lesions  of  both  diseases;  in  addition  to  the  degeneration  of  the  nuclei  in  the 


PROGRESSIVE  BULBAR  PARALYSIS.  089 

medulla  oblongata,  there  is  marked  atrophy  of  the  ganglionic  cells  in  correspond- 
ing places  in  the  anterior  gray  cornua  of  the  spinal  cord. 

We  must  here  refer  again  to  the  occurrence  of  the  symptoms  of  bulbar  paraly- 
sis in  amyotrophic  lateral  sclerosis  (see  page  650).  In  this  disease,  too,  there 
is  the  same  combination  of  a  degeneration  of  the  nuclei  in  the  medulla,  oblongata 
and  of  the  anterior  cornua  of  the  gray  matter  of  the  cord ;  but  in  addition  there  is  a 
derangement  of  the  motor  tract  in  the  lateral  columns.  This  addition  modifies  the 
picture,  but  otherwise  the  symptoms  are  almost  precisely  the  same  as  in  progressive 
muscular  atrophy.  Even  the  derangement  of  the  crossed  pyramidal  tract  is  in  per- 
fect harmony  with  the  other  lesions,  for  it  represents  merely  a  further  invasion  of 
the  tract  by  which  motor  impulses  are  conducted.  It  seems  justifiable,  therefore,  to 
say  that  these  three  diseases — progressive  bulbar  paralysis,  progressive  muscular 
atrophy,  and  amyotrophic  lateral  sclerosis — differing  as  they  do  in  the  localization 
of  their  lesions,  are  yet  closely  allied.  They  are  essentially — that  is,  pathogenetic- 
ally,  and  perhaps  also  setiologically — different  results  of  one  disease  ;  or,  at  least, 
the  pathological  process  in  each  case  must  be  nearly  the  same.  In  each  there  is 
a  primary  chronic  degeneration  of  portions  of  the  chief  motor  tract,  varying  only 
in  region  or  in  extent.  If  we  accustom  ourselves  to  regard  these  three  groups 
of  symptoms  as  really  identical,  we  shall  be  less  puzzled  by  the  slight  variations 
which  different  cases  may  present  than  if  we  attempt  to  differentiate  the  disoi*" 
ders  too  nicely  on  account  of  unessential  variations. 

Diagnosis. — The  diagnosis  of  a  typical  case  of  progressive  bulbar  paralysis  has 
no  difficulties,  if  we  only  hold  firmly  to  the  definition  of  the  disease  and  its  symp- 
toms as  above  depicted.  Upon  careful  examination  of  the  other  muscles,  and  con- 
sideration of  the  course  of  the  disease  as  a  whole,  we  shall  be  able  in  each  case  to 
determine  whether  the  bulbar  trouble  is  the  sole  disease,  or  merely  a  part  of  a 
more  extended  degeneration  of  the  motor  tract.  If  there  are  no  symptoms  but 
those  referable  to  the  medulla  oblongata,  we  must  bear  in  mind  that  the  phe- 
nomena of  genuine  progressive  bulbar  paralysis  may  be  closely  simulated  by  other 
bulbar  diseases.  The  acute  troubles,  like  thrombosis  or  haemorrhage,  although 
they  produce  similar  symptoms,  can  easily  be  differentiated  by  the  manner  of  their 
appearance,  contrasting  with  the  invariably  slow  development  of  genuine  bulbar 
paralysis.  It  is,  however,  much  more  difficult  to  eliminate  gradually  forming 
tumors  situated  in  the  medulla  oblongata  or  its  vicinity.  Here  prolonged  observa- 
tion is  frequently  needed,  until  finally  such  phenomena  appear  as  are  foreign  to  typ- 
ical bulbar  paralysis.  Such  symptoms  are  disturbances  of  sensation  and  invasion  of 
the  upper  division  of  the  facial,  the  nerves  of  special  sense,  and  the  ocular  muscles. 
The  same  is  true  of  that  rare  trouble,  diffuse  sclerosis  of  the  medulla  oblongata. 

It  should  also  be  mentioned  that  bilateral  cerebral  trouble  may  occasion  so 
complete  a  paralysis  of  the  tongue  and  lips,  according  to  Lepine  and  others,  as  to 
simulate  bulbar  paralysis.  Such  cases  have  been  termed  "  glosso-labio-pharyngeal 
paralysis  of  cerebral  origin,"  or  pseudo-bulbar  paralysis.  Indeed,  in  rare  instances,  a 
similar  group  of  symptoms  seems  to  be  referable  to  unilateral  cerebral  disturbances. 
This  is  explained  by  assuming  that  the  muscles  involved  upon  both  sides  receive 
at  least  a  portion  of  their  motor  nervous  fibers  from  the  same  hemisphere.  And 
yet  in  most  of  these  cases  of  pseudo-bulbar  paralysis  the  exclusion  of  the  genuine 
disease  is  possible,  because  certain  variations  from  the  typical  course  of  the  disease 
are  pronounced  enough  to  set  us  right.  Thus  there  is  an  abrupt  onset,  the  paralysis 
is  not  perfectly  symmetrical,  or  the  lips  and  tongue  react  normally  to  electricity. 

Prognosis  and  Treatment.— Despite  the  unfavorable  prognosis  of  progressive 
bulbar  paralysis,  we  must  at  least  try  to  check  the  progress  of  the  disease.  Elec- 
tricity might  perhaps  be  regarded  as  the  most  promising  means  to  employ.  To  in- 
fluence the  seat  of  the  trouble,  galvanization  is  chiefly  used.    The  poles  are  applied 

44 


690  DISEASES  OF  THE  NERVOUS  SYSTEM. 

to  the  two  mastoid  processes,  if  possible,  every  day  for  two  or  three  minutes,  and 
the  current  is  repeatedly  reversed.  We  may  also  galvanize  the  sympathetic 
nerve  and  the  affected  muscles  of  the  lips  and  tongue.  Upon  the  muscles  the 
faradic  current  might  also  be  tried.  When  deglutition  begins  to  be  impaired,  it  is 
an  excellent  thing  to  excite  the  action  of  swallowing,  by  galvanism.  For  this  the 
anode  is  placed  upon  the  nape  of  the  neck,  and  the  kathode  upon  one  side  of  the 
larynx.  At  every  kathodic  closure  (KaS),  or  every  time  that  the  kathode  is  passed 
across  the  side  of  the  larynx,  there  is  a  reflex  act  of  deglutition.  The  current 
should  be  of  medium  strength. 

It  might  be  well  to  prescribe  further  a  resort  to  treatment  by  baths,  as  at 
Rehme,  or  the  "  cold-water  cure  "  might  be  cautiously  tried.  The  same  internal 
remedies  are  recommended  as  in  the  chronic  diseases  of  the  cord,  especially  argen- 
tic nitrate,  ergotine,  and  potassic  iodide.  For  salivation,  atropine  may  prove  bene- 
ficial, in  pills  of  T|-jy  of  a  grain  (grin.  0"0005),  three  or  four  to  be  taken  daily. 

The  way  of  giving  nourishment  is  important  if  deglutition  is  impaired.  We 
should  try  carefully  to  avoid  having  the  food  go  down  the  wrong  way,  lest  pul- 
monary complications  ensue.  It  is  therefore  wise  not  to  defer  the  use  of  the  stom- 
ach-tube too  long,  through  which  we  may  introduce  milk,  eggs,  wine,  and  the 
various  infant  foods. 
•  In  the  distressing  close  of  the  disease,  narcotics  must  be  exhibited  to  lessen  the 
patient's  suffering,  at  least  as  far  as  we  can. 

APPENDIX. 

THE  RARER  FORMS  OF  CHRONIC  BULBAR  PARALYSIS,  AND  PROGRESSIVE  OPHTHAL- 
MOPLEGIA. 

As  we  have  seen,  the  typical  form  of  chronic  bulbar  paralysis  is  practically 
limited  in  its  effects  to  the  distribution  of  the  hypoglossus,  the  labial  division  of 
the  facial,  and  the  pharyngeal  muscles.  Possibly  the  reason  it  extends  no  farther 
is  merely  that  death  is  so  speedy.  But  there  are  a  few  rare  cases  where  the  chronic 
degenerative  process  comes  to  involve  other  motor  nuclei,  together  with  the  corre- 
sponding nerve-fibers  and  muscles.  Of  course  the  clinical  phenomena  of  these 
cases  vary  from  the  ordinary ;  and  yet  there  is  no  real  reason  to  distinguish  these 
from  common  bulbar  paralysis,  particularly  as  all  sorts  of  transitional  forms  are 
to  be  observed.  Thus,  we  have  ourselves  noticed  that  there  is  sometimes  a  sym- 
metrical and  slowly  progressive  paresis  of  the  upper  division  of  the  facial,  and  in 
particular  of  that  portion  which  supplies  the  cheek,  complicating  the  glosso-pha- 
ryngeal  paralysis.  In  other  cases  we  have  seen  the  degeneration  attack  from  the 
start  the  entire  distribution  of  the  facial,  gradually  producing  a  complete  "  diple- 
gia facialis.'1'1  Sometimes,  also,  the  ordinary  symptoms  of  bulbar  pai'alysis  are 
accompanied  by  disturbances  in  the  area  of  distribution  of  the  ocular  nerves, 
the  result  of  degeneration  of  the  corresponding  nerve-nuclei.  Erb  relates  a  few 
cases  where  there  were  not  only  ptosis  and  impairment  in  the  movements  of  the 
tongue  and  in  deglutition,  but  also  paresis  of  the  muscles  supplied  by  the  accesso- 
rius  and  the  motor  branch  of  the  trigeminus. 

What  seems  very  remarkable  is  that  the  process  may  be  confined  entirely  to 
the  ocular  muscles.  A.  von  Graefe  named  this  condition  progressive  ophthalmo- 
plegia. Another  name  is  "anterior  bulbar  paralysis."  The  disease  progresses 
with  extreme  slowness  and  is  perfectly  symmetrical.  The  movements  of  the  eye 
are  impaired  in  all  directions.  Diplopia  is  never  present.  The  pupil  reacts  to 
light,  and  usually  the  power  of  accommodation  is  preserved.  Finally  both  eye- 
balls become  absolutely  motionless,  and  there  is  a  well-marked  though  incomplete 
ptosis.     There  is,  beyond  a  doubt,  a  progressive  degeneration  of  the  nuclei  and 


ACUTE  AND  APOPLECTIFORM  BULBAR  PARALYSIS.  691 

fibers  of  the  corresponding  nerves — i.  e.,  the  abducens  and  motor  oculi ;  hut  with 
these  the  process  may  stop,  spreading  no  farther.  We  have  ourselves  lately  met 
with  a  patient  who  presented  total  bilateral  ophtbalmoplegia,  and  in  whom  this 
condition  had  existed  without  the  slightest  change  for  fifteen  years.* 

We  must  add,  in  conclusion,  that  our  anatomical  knowledge  concerning  these 
rarer  forms  of  chronic  bulbar  paralysis  is  very  incomplete.  The  results  of  a  few 
autopsies,  however,  join  with  the  clinical  phenomena  in  strongly  confirming  the 
surmise  above  expressed  as  to  the  pathological  lesions. 


CHAPTER  II. 
ACUTE   AND   APOPLECTIFORM   BULBAR    PARALYSIS, 

1.    HEMORRHAGE  INTO  THE  MEDULLA  OBLONGATA  AND  THE  PONS. 

Hemorrhage  into  the  medulla  oblongata  and  the  pons  is  much  more  frequent 
than  into  the  spinal  cord,  but  it  is  much  rarer  than  cerebral  haemorrhage.  As  to 
its  production,  the  same  views  are  held  as  will  be  considered  in  detail  under  cere- 
bral haemorrhage,  in  the  next  section.  In  the  first  place,  there  is  probably  always 
some  disease  of  the  blood-vessels — that  is,  atheroma  or  miliary  aneurism — and 
then  some  factor  productive  of  increased  arterial  tension.  There  may  be  cardiac 
hypertrophy,  nephritis,  excessive  bodily  exertion,  or  alcoholism.  Now  and  then 
injuries  of  the  occiput  are  followed  by  an  effusion  into  the  medulla.  It  is  not  rare 
to  have  secondary  and  usually  small  ecchymoses  in  acute  inflammation  of  the 
spinal  cord  (vide  infra),  and  in  purulent  meningitis  or  in  connection  with  new 
growths  which  are  richly  vascular. 

The  anatomical  conditions  produced  by  bulbar  haemorrhage  are  so  completely 
analogous  with  those  of  cerebral  haemorrhage  that  the  reader  may  safely  be 
referred  to  the  succeeding  section  about  these  also.  The  size  of  the  lesion  varies 
greatly.  Bleeding  extensive  enough  to  affect  the  greater  part  of  a  transverse  sec- 
tion is  more  frequent  in  the  pons  than  in  the  medulla  oblongata.  If  the  blood 
is  poured  out  close  under  the  floor  of  the  fourth  ventricle,  as  has  been  repeatedly 
observed,  it  may  break  into  the  ventricle.  If  death  be  not  speedy,  the  blood  is 
mostly  absorbed,  and  in  its  place  develops  either  an  "  apoplectic  scar  "  or  an  apo- 
plectic cyst. 

There  may  be  slight  prodromata,  but  the  real  symptoms  of  bulbar  haemorrhage 
are  very  sudden.  There  is  almost  always  a  pronounced  apoplectic  seizure.  The 
patient  has  a  shock,  falls  down,  and  becomes  dizzy  or  even  unconscious.  In  other 
cases  there  may  be  headache,  vomiting,  tinnitus  aurium,  and  clonic  spasms,  or 
even  a  typical  epileptiform  attack. 

In  most  cases  death  is  speedy,  if  not  immediate.  This  is  probably  due  in  every 
instance  to  grave  lesions  of  the  respiratory  and  circulatory  centers,  rendering 
continued  existence  impossible.  Sometimes  the  initial  symptoms  abate,  where- 
upon the  local  results  of  the  lesion  become  appreciable. 

One  of  the  characteristics  of  bulbar  paralysis  now  seen  is,  that  disturbances  are 
particularly  great  in  the  distribution  of  the  bulbar  nerves.  In  cerebral  apoplexy 
they  never  appear  in  the  same  way.  Another  point  is,  that  these  paralytic  symp- 
toms are  combined  with  paralysis  of  the  extremities  in  a  peculiar  way,  as  a  result 

*  It  seems  that  total  ophthalmoplegia  may  also  appeal-  as  one  of  the  symptoms  of  locomotor  ataxia 
or  of  general  paralysis.  It  has  been  observed  by  Mendel  as  a  sequel  to  diphtheria.  In  these  cases» 
however,  the  symptom  is  probably  in  part  due  to  a  degeneration  of  the  fibers  of  the  peripheral  nerves. 


692 


DISEASES  OF  THE  NERVOUS  SYSTEM. 


of  the  anatomical  relations.  For  the  same  reason,  the  order  of  the  paralysis  in 
the  extremities  may  also  he  peculiar.  Of  the  hulbar  paralyses  we  may  mention 
more  or  less  complete  paralysis  of  the  tongue,  and  a  consequent  difficulty  in  articu- 
lation (anarthria) ;  frequent  inability  to  swallow;  and  paralysis  in  the  distribu- 
tion of  the  accessorius,  facial,  and  trigeminus.  If  there  is  a  lesion  of  the  pyram- 
idal tracts  in  the  pons  or  medulla,  we  have  paralysis  of  the  extremities  in  addition 
to  the  specific  bulbar  symptoms.  If  the  haemorrhage  be  extensive,  all  four 
extremities  may  be  more  or  less  completely  paralyzed  ;  but  in  most  instances  the 
paralysis  is  unilateral.  In  the  larger  number  of  haemorrhages  into  the  pons  there 
is  crossed  paralysis.  The  paralysis  of  the  extremities  is 
upon  one  side,  and  that  of  the  facial  is  on  the  other  side. 
This  is  a  great  aid  to  diagnosis.  It  is  easy  to  see  how  this 
happens  if  we  bear  in  mind  that  the  cerebral  fibers  of  the 
facial  cross  at  a  point  certainly  much  higher  than  the 
decussation  of  the  pyramids,  in  which  latter  place  the 
motor  fibers  of  the  extremities  cross.  Now  a  haemorrhage 
may  be  situated  in  one  side  of  the  pons,  above  the  decussa- 
tion of  the  pyramids  but  below  that  of  the  facial.  This 
would  occasion  (vide  Fig.  100,  y)  a  paralysis  of  the  facial  on 
the  same  side  with  the  lesion,  and  of  the  extremities  upon 
the  opposite  side ;  but  if  the  lesion  be  higher,  above  the  place 
where  the  facial  crosses  over,  all  the  paralytic  symptoms 
would  be  on  the  opposite  side  of  the  body  (videFig.  100, x). 

In  other,  rarer  instances  we  observe  similar  combina- 
tions; only  some  other  bulbar  nerve  replaces  the  facial, 
such  as  the  hypoglossus  or  abducens.  In  a  few  cases  the 
lesion  is  at  the  very  decussation  of  the  pyramids.  This 
is  extremely  rare  in  haemorrhage,  though  somewhat  more 
frequent  in  troubles  of  a  different  nature.  The  result 
may  be  that  the  motor  fibers  for  one  extremity  are  cut 
off  before  they  cross,  and  those  of  the  other  extremity 

after  they  have  crossed.      Thus  is  produced  the  rare  phenomenon  of  a  crossed 
hemiplegia — i.  e.,  paralysis  of  the  arm  on  one  side  and  of  the  leg  on  the  other. 

Disturbances  of  sensation  in  the  skin  of  the  paralyzed  extremities  sometimes 
result  from  trouble  in  the  pons,  but  they  are  very  seldom  extreme,  and  can  not 
be  made  available  for  making  out  the  exact  locality  of  the  haemorrhage,  since  the 
course  of  the  sensory  fibers  through  the  upper  extremity  of  the  spinal  cord  is  still 
almost  unknown.  The  anaesthesia  sometimes  observed  in  the  distribution  of  the 
trigeminus  is  of  more  value,  as  this  may  be  due  to  a  lesion  of  the  nucleus  or  root 
of  the  nerve. 

There  are  other  symptoms,  which  are  indeed  rare,  but  which  bear  an  impor- 
tant relation  to  certain  nervous  centers  of  the  medulla.  Thus,  there  may  be 
marked  respiratory  disturbance ;  the  pulse  may  become  rapid  or  irregular ;  there 
may  be  vaso-motor  derangement,  as  shown  by  a  rise  of  the  cutaneous  temperature 
and  by  a  subjective  sensation  of  Avarmth ;  and  occasionally  there  are  temporary 
albuminuria  and  glycosuria.  The  temperature  of  the  body  is  generally  normal  at 
first,  or  nearly  so ;  but  in  case  of  a  fatal  termination  it  often  rises  greatly,  even 
to  107-5°  (42°  C.)  and  higher. 

As  to  the  prognosis  of  bulbar  haemorrhage,  speedy  death  has  been  repeatedly 
observed,  as  we  have  said.  If  the  immediate  effects  be  successfully  withstood,  the 
prospect  becomes  more  favorable.  The  effusion  is  gradually  absorbed,  the  symp- 
toms of  compression  abate,  and  there  is  a  steady  progress  toward  comparatively 
good  or  even  perfect  health.     More  often,  however,  some  of  the  paralytic  symp- 


Fig.  100.— Diagram  of  focal 
diseases  in  the  pons. 
L.  Left.  B.  Right.  P. 
Pons.  Mo.  Medulla  ob- 
longata. DP.  Decussa- 
tion of  the  pyramids. 
E.  Fibers  to  the  ex- 
tremities. F.  Facial 
fibers,  x.  Lesion  in  the 
upper  half  of  the  pons. 
y.  Lesion  in  the  lower 
half  of  the  pons. 


ACUTE  AND  APOPLECTIFORM  BULBAR  PARALYSIS.  693 

toms  remain  stationary,  either  in  the  distribution  of  the  bulbar  nerves  dike  the 
lingual  or  pharyngeal),  or  in  the  extremities,  as  shown  by  persistent  hemiplegia. 
If  this  latter  be  the  case,  the  subsequent  contractions  and  other  symptoms  are  the 
same  as  in  ordinary  cerebral  hemiplegia. 

The  diagnosis  of  bulbar  haemorrhage  is  based  upon  the  apoplectic  onset,  and 
upon  the  presence  of  specific  bulbar  symptoms,  such  as  disturbance  of  speech  and 
of  deglutition,  and,  most  characteristic  of  all,  if  it  occur,  a  crossed  hemiplegia. 
The  differential  diagnosis  between  embolism  and  haemorrhage  can  hardly  ever  be 
made  with  certainty  (vide  infra). 

The  treatment,  not  only  of  the  seizure  but  of  the  persistent  paralysis,  should 
conform  to  the  principles  which  will  hereafter  be  set  forth  in  describing  the 
treatment  of  cerebral  haemorrhage.  If  the  bulbar  nerves  present  obstinate  symp- 
toms, we  must  employ  the  same  means  as  in  chronic  bulbar  paralysis,  the  most 
»effective  being  electricity. 

2.   Embolism  and  Thrombosis  of  the  Basilar  Artery. 

The  medulla  and  pons  receive  their  blood  chiefly  from  branches  of  the  anterior 
spinal,  vertebral,  and  basilar  arteries.  These  branches  penetrate  the  anterior 
median  fissure  and  then  proceed  to  the  nerve-nuclei.  A  far  smaller  portion  of 
the  circulation  flows  through  the  "arteries  of  the  roots."  These  are  minute  off- 
shoots of  the  lateral  branches  of  the  basilar  and  vertebral  arteries,  which  enter 
the  cord  at  the  roots  of  the  nerves  and  penetrate  to  the  corresponding  nuclei. 
According  to  Duret,  the  nuclei  of  the  hypoglossal  and  accessory  nerves  are  sup- 
plied from  the  anterior  spinal  and  vertebral  arteries  ;  those  of  the  vagus,  glosso- 
pharyngeal, and  auditory  nerves  by  branches  of  the  upper  end  of  the  vertebral 
arteries  ;  and  the  nuclei  of  the  facial,  trigeminus,  and  the  three  nerves  to  the  ocular 
muscles  by  branches  of  the  basilar.  There  may  be  individual  exceptions  to  these 
rules.  Occlusion  by  embolism  or  thrombosis  of  the  arteries  just  named  must  , 
occasion  a  secondary  softening  in  corresponding  portions  of  the  medulla,  and  is, 
therefore,  a  not  very  infrequent  cause  of  apoplectic,  or  at  least  very  rapidly 
developed,  bulbar  paralysis. 

The  causes  of  thrombosis  or  embolism  in  the  arteries  just  mentioned  are  the 
same  as  we  shall  consider  minutely  when  treating  of  cerebral  softening.  Emboli 
are  most  frequent  in  cardiac  disease.  They  occur  only  in  the  vertebi'al  arteries, 
oftenest  in  the  left  one,  and  are  never  primary  in  the  basilar  artery  ;  but  an 
embolus  may  be  enlarged  by  thrombosis  after  lodging  in  one  of  the  vertebral  arte- 
ries, and  then  block  up  the  basilar.  Thrombosis  is  of  more  frequent  occurrence, 
and  results  from  chronic  changes  in  the  arteries,  mainly  atheroma  or  syphilitic 
endarteritis.  The  latter  disease,  one  favorite  locality  for  which  is  the  basilar 
artery,  is  the  commonest  cause  of  acute  softening  of  the  pons. 

The  anatomical  condition  is  likewise  similar  to  that  in  cerebral  softening 
(q.  v.).  In  the  region  which  is  deprived  of  arterial  blood  by  the  occlusion  of  the 
affluent  vessel,  the  acute  anaemia  entails  necrosis  and  disintegration  of  tissue.  A 
spot  of  "softening"  results,  made  up  mainly  of  vestiges  of  nervous  tissue  and 
numerous  cells  filled  with  granules  of  fat. 

When  the  basilar  artery  is  blocked  up,  the  symptoms  appear  very  suddenly. 
There  is  either  an  apoplectic  seizure,  or  at  least  a  very  rapid  development  of  paralysis 
(occupying  only  a  few  days).  The  symptoms  of  the  first  onset  are,  in  all  essential 
points,  those  of  bulbar  or  even  of  cerebral  apoplexy.  Although  there  is  usually 
no  marked  loss  of  consciousness  in  apoplectic  bulbar  paralysis,  yet  no  great  diag- 
nostic significance  can  be  assigned  to  its  absence.  The  sudden  obstruction  of  the 
basilar  artery  produces  such  a  disturbance  of  the  circulation  even  in  anterior  por- 
tions of  the  brain  as  may  suspend  consciousness.     In  some  few  instances  this  cir- 


094  DISEASES  OF  THE  NERVOUS  SYSTEM. 

dilatory  derangement  may  even  give  rise  to  choked  disk,  as  seen  by  the  ophthal- 
moscope. Often  there  are  noticeable  respiratory  and  cardiac  symptoms,  such  as 
Cheyne-Stokes'  respiration,  and  rapid  pulse. 

If  death  be  not  immediate,  and  we  are  therefore  enabled  to  make  out  the  symp- 
toms due  to  the  local  disturbance,  we  usually  observe  the  same  phenomena  as  have 
just  been  described  under  bulbar  haemorrhage.  There  is  sometimes  paralysis  of 
all  the  extremities,  but  usually  there  is  trouble  only  upon  one  side.  Then  we 
have  the  characteristic  crossed  hemiplegia.  The  facial  nerve  or  the  nerves  of  the 
ocular  muscles  may  be  paralyzed.  It  has  repeatedly  happened  that  the  paralysis 
seemed  at  first  much  greater  upon  one  side,  but  after  a  few  days  changed  over  to 
the  opposite  one.  This  must  be  due  to  changes  in  the  circulation ;  the  thrombus 
grows  larger,  or  a  collateral  circulation  is  developed.  The  specific  bulbar  symp- 
toms are  the  familiar  ones  of  all  bulbar  derangements — namely,  lingual  paralysis 
with  resulting  difficulty  in  articulation,  pharyngeal  paralysis,  and  rarely  deafness, 
as  a  result  of  lesion  of  the  acoustic  center.  Of  course,  the  severity  and  extent 
of  all  these  symptoms  must  vary  according  to  the  location  and  size  of  the  spot  of 
softening. 

The  prognosis  of  cases  of  this  sort  is  almost  always  unfavorable.  Death 
results  at  latest  after  a  few  days.  It  is  often  ushered  in  by  a  high  temperature, 
Exceptionally,  there  is  a  transition  into  a  chronic  form. 

We  need  say  nothing  about  treatment,  except  that  the  same  remedies  are 
employed  as  in  other  acute  bulbar  diseases. 

3.  Acute,  or  Inflammatory,  Bulbar  Paralysis. 

(Acute  Bulbar  Myelitis.) 

"  Acute  bulbar  paralysis,"  in  the  stricter  sense  of  the  term,  means  a  form  of 
disease  where  marked  symptoms  of  bulbar  derangement  appear  acutely — that  is, 
within  a  few  days  or  weeks.  The  anatomical  lesion  is  probably  an  acute  inflam- 
mation of  the  medulla  oblongata.  It  is  a  rare  disorder,  and  its  aetiology  is  doubt- 
ful. There  are  usually  mild  prodromata :  vertigo,  headache,  and,  in  one  case  of 
our  own,  painful  sensations  in  the  back  of  the  neck.  Evident  bulbar  symptoms 
very  quickly  follow.  Usually  the  first  of  these  is  dysphagia.  Not  only  is  deglu- 
tition unpaired,  but  the  paresis  of  the  soft  palate  and  of  the  laryngeal  muscles 
allows  liquids  to  enter  the  nostrils  or  the  larynx.  The  tongue  also  becomes  grad- 
ually paralyzed,  speech  becomes  indistinct,  and,  if  the  soft  palate  be  involved,  nasal. 

Sometimes  the  extremities  also  become  paretic,  as  a  result  of  the  extension  of 
the  disease  to  the  region  of  the  pyramids ;  but  in  many  instances  the  extremities 
remain  unimpaired  to  the  end.  Paralyses  of  the  facial  nerve  and  of  the  ocular 
muscles  are  somewhat  more  frequent.  The  temperature  is  sometimes  a  little  ele- 
vated (100°-102°,  38°-39°  C),  but  not  always.  The  pulse  is  almost  invariably 
rapid  ;  in  our  patient  it  was  148. 

The  prognosis  is  apparently  always  bad.  Often  death  takes  place  in  four  to 
eight  days,  or  it  may  be  not  till  the  end  of  two  or  three  weeks.  It  is  invariably 
preceded  by  all  the  tokens  of  paralysis  of  respiration.  In  our  case  there  was 
well-marked  paralysis  of  the  diaphragm  at  the  end. 

As  yet,  few  autopsies  have  been  reported.  Generally  the  medulla  presents  no 
macroscopic  changes.  Exceptionally,  it  can  be  seen  to  be  softened  and  mottled 
with  minute  haemorrhages.  The  microscope  detects  abundant  evidence  of  inflam- 
mation :  granule-cells,  infiltration  with  nuclei  around  the  blood-vessels,  thicken- 
ing of  the  walls  of  some  of  the  blood-vessels,  small  extravasations,  swollen  axis- 
cylinders,  etc.  It  should  also  be  borne  in  mind  that  precisely  similar  clinical 
phenomena  seem  often  to  be  referable  to  peripheral  changes,  such  as  multiple 
neuritis  affecting:  the  bulbar  nerves. 


COMPRESSION  OF  THE  MEDULLA.  695 

The  treatment  of  acute  bulbar  paralysis  is,  of  course,  almost  hopeless.  In 
early  stages  we  should  apply  counter-irritation  to  the  nape  of  the  neck;  and  we 
might  prescribe  mercurial  inunction.  It  might  also  be  well  to  employ  the  <:<»> 
stant  current,  applied  at  the  back  of  the  neck,  and  also  used  to  excite  the  move- 
ments of  deglutition.  We  found  injections  of  strychnine  useless.  Toward  the 
end,  narcotics  are  indispensable. 


CHAPTER  III. 
COMPRESSION    OF    THE    MEDULLA. 

Acute  compression  and  other  injuries  of  the  medulla  are  most  frequently  due 
to  fracture  or  dislocation  of  the  atlas  and  axis.  As  is  well  known,  dislocation  of 
the  axis,  or  backward  dislocation  of  the  atlas,  usually  causes  instant  death. 

Gradual  compression  is  seen  in  chronic  disease  of  the  bones  around  the  medulla, 
in  caries  and  tumors  of  the  occiput  and  of  the  first  two  vertebrae.  Enchon- 
droma  of  the  base  of  the  skull  ;  new  growths  of  the  sphenoid,  at  its  junction 
with  the  occipital  ;  tumors  of  the  dura ;  and  sometimes  even  tumors  of  the  cere- 
bellum— may  all  excite  by  their  pressure  the  gravest  bulbar  symptoms.  We 
should  also  mention  aneurism  of  the  vertebral  artery  at  its  upper  end,  and  of  the 
basilar,  as  capable  of  doing  similar  harm.  In  all  these  cases  the  main  cause  of 
disturbance  is  undoubtedly  the  mechanical  pressure,  either  directly  destroying 
the  nervous  tracts  or  interrupting  the  transmission  of  nervous  influences  ;  but 
the  circumstances  may  be  further  complicated  by  haemorrhages,  and  sometimes 
perhaps  by  inflammation  of  the  medulla  itself. 

The  clinical  phenomena  of  gradual  bulbar  compression  resemble  those  of  spinal 
compression,  in  that  they  usually  begin  with  symptoms  of  irritation  in  the  distri- 
bution of  those  nerves  the  roots  of  which  are  first  affected.  There  are  neuralgia 
of  the  trigeminus,  twitching  of  the  facial  muscles,  tinnitus  aurium,  etc.  If  the 
compression  becomes  greater,  there  are  more  serious  bulbar  symptoms :  disturb- 
ances of  speech  and  deglutition,  paralysis  of  the  tongue,  soft  palate,  face,  and  very 
likely  motor  and  sensory  symptoms  in  the  extremities.  Usually  we  also  see  gen- 
eral cerebral  symptoms,  such  as  vertigo,  headache,  vomiting,  and  sometimes  epi- 
leptiform convulsions. 

We  can  not,  of  course,  draw  up  a  definite  and  rigid  list  of  symptoms,  since 
both  the  individual  symptoms  and  the  general  course  of  the  disease  exhibit  great 
variations  according  to  the  way  in  which  the  compression  is  brought  about.  The 
diagnosis  can  be  made  in  those  cases  only  where  some  aetiological  factor  like 
trauma  or  caries  of  the  vertebrae  is  known  to  exist.  Aneurism  of  the  vertebral 
artery  is  said  by  Moser  sometimes  to  give  rise  to  a  loud  systolic  murmur  heard 
between  the  mastoid  process  and  the  spine.  In  all  other  cases  we  can  seldom  do 
more  than  surmise  the  truth.  Slow  compression  is  distinguished  from  genuine 
progressive  bulbar  paralysis  chiefly  by  the  course  it  pursues — that  is,  there  are 
initial  symptoms  of  irritation — by  the  greater  complexity  of  the  clinical  phenom- 
ena, like  sensory  lesions  and  hemiplegia,  and  sometimes  by  the  asymmetry  of  cer- 
tain symptoms.  If  the  anterior  part  of  the  medulla  is  compressed,  in  the  region 
of  the  pyramids,  there  may  for  a  time  be  no  bulbar  symptoms,  but  merely  motor 
symptoms  in  the  extremities.     These  are  chiefly  paretic  or  spastic. 

The  prognosis  is  almost  always  bad,  as  can  be  inferred  from  the  nature  of  the 
causative  disease.  Death  is  brought  on  either  by  inhalation-pneumonia,  or  by 
paralysis  of  respiration.  Treatment  must  be  purely  symptomatic,  and  should  fol- 
low the  same  rules  as  in  progressive  bulbar  paralysis. 


696  DISEASES  OF  THE  NERVOUS  SYSTEM. 


V. — The  Diseases  of  the  Brain. 


SECTION  I. 
Diseases  of  the  Cerebral  Meninges. 

CHAPTER  I. 

H2EMATOMA  OF   THE   DURA  MATER. 

{Internal  Hemorrhagic  Pachymeningitis.) 

JEtiology  and  Pathology. — Hematoma  of  the  dura  mater  is  the  name  given  to 
effusions  of  blood  found  on  the  inner  surface  of  the  dura  mater.  They  are  of  con- 
siderable area,  but  of  moderate  thickness,  and  are  usually  encapsulated.  There 
has  been  much  discussion  as  to  their  mode  of  origin,  and  views  still  differ.  One 
is  that  the  haemorrhage  is  the  primary  lesion,  and  that  the  connective-tissue  mem- 
branes are  developed  only  by  the  organization  of  the  clot.  This  conception  was 
originally  the  prevailing  one,  but  was  opposed  by  Virchow,  who  was  led  by  the 
results  of  his  own  investigations  to  maintain  that  the  haemorrhage  was  always 
secondary.  The  primary  process  he  believed  to  be  a  peculiar  sort  of  inflammation 
— " hemorrhagic  pachymeningitis."  This  gave  rise  to  a  new  growth  of  richly 
vascular  connective  tissue,  into  which  the  haemori'hage  took  place.  Of  late,  how- 
ever, the  tendency  is  again  to  regard  the  hemorrhage  as  the  initial  change,  at  least 
in  certain  cases,  and  to  refer  it  to  an  affection  of  the  walls  of  the  blood-vessels 
which  diminishes  their  power  of  resistance. 

The  mildest  forms  of  internal  pachymeningitis  present  a  delicate  membrane 
upon  the  inner  surface  of  the  dura  mater,  quite  easily  separable,  of  a  reddish 
color,  and  dotted  with  numerous  red  and  brownish  spots.  These  spots  are  due  to 
minute  haemorrhages  and  collections  of  haematoidin.  The  membrane  itself  is  a 
delicate  interstitial  tissue,  traversed  by  numerous  wide  capillaries. 

In  more  advanced  cases  the  thickening  is  much  greater.  There  are  usually  sev- 
eral layers,  the  newest  and  most  superficial  being  nearest  the  brain.  The  oldest, 
which  is  in  apposition  with  the  dura  mater,  is  composed  of  connective  tissue  that 
has  already  become  rather  firm  and  fibrous.  It  is  evident  from  this  lamellar 
structure  that  the  whole  process  goes  on  by  fits  and  starts.  The  clinical  course  of 
the  disease  will  be  seen  below  to  agree  well  with  such  a  view.  The  effusions  are 
sometimes  very  extensive,  even  larger  than  a  hen's  egg,  and  exercise  no  slight 
pressure  upon  the  underlying  cerebral  parenchyma.  The  haemorrhage  always 
takes  place  inside  the  mass,  or  between  its  layers.  The  effusion  may,  however, 
break  through  the  innermost  layer,  so  that  the  blood  flows  into  the  arachnoid 
spaces  ;  this  is  known  as  "  intermeningeal  apoplexy." 

The  favorite  location  of  the  haematoma  is  the  parietal  region.  It  is  sometimes 
found  at  the  base  of  the  brain,  in  the  posterior  or  middle  fossa.  Occasionally  the 
haematoma  is  bilateral. 

Haemorrhagic  pachymeningitis  is  not  a  rare  disease.  It  is  sometimes  found  to 
exist  in  a  moderate  degree  in  chronic  cardiac,  renal,  or  pulmonary  cases,  which 
come  to  autopsy.  Usually  there  have  been  no  special  symptoms,  the  lesion  being 
discovered  incidentally.     It  has  been  found  in  like  manner  in  connection  with 


HEMATOMA  OF  THE  DURA  MATER.  697 

a  great  many  acute  infectious  diseases,  like  typhoid  fever  and  small-pox.  It  is  a 
more  important  and  more  frequent  complication  in  other  chronic  cerebral  diseases, 
in  particular  such  as  induce  marked  atroj)hy  of  the  brain  as  a  whole.  It  is  espe- 
cially common  in  general  paralysis  of  the  insane  and  in  other  forms  of  demen- 
tia. Chronic  alcoholism  is  also  regarded  as  a  potent  etiological  factor.  In  topers 
it  is  not  very  unusual  for  the  hematoma  to  be  so  extensive,  if  it  occurs  at  all, 
as  to  cause  grave  cerebral  derangement.  Very  likely  changes  in  the  vascular 
walls,  like  atheroma  and  fatty  degeneration,  contribute  an  important  part  to  the 
result  in  such  patients.  HEematoma  may  also  occur  in  all  diseases  where  there  is 
a  general  haemorrhagic  diathesis.  Thus  it  is  seen  in  pernicious  anemia,  leukae- 
mia, and  scurvy.  Here  certainly  the  hemorrhage  is  the  primary  event,  as  it  also 
is  in  the  traumatic  cases,  of  which  a  number  have  been  observed. 

As  might  be  inferred  from  the  etiological  factors  enumerated,  the  disease  is 
found  chiefly  in  advanced  life,  and  much  offener  in  men  than  in  women. 

Symptoms. — Not  infrequently  a  hematoma  of  the  dura  is  found  post  mortem, 
which  had  during  life  been  entirely  unsuspected.  Either  the  haemorrhage  was 
not  extensive  enough  to  cause  any  symptoms,  or  the  brain  exercised  that  remark- 
able tolerance  which  it  sometimes  shows  even  when  there  are  wide-reaching 
lesions ;  or  such  symptoms  as  there  may  have  been  escaped  particular  notice,  in  the 
severity  of  the  more  general  symptoms  (of  typhoid  fever  or  some  similar  disease). 
But  in  other  cases  haemorrhagic  pachymeningitis  excites  grave  symptoms,  although 
they  are  seldom  so  characteristic  as  to  reveal  the  diagnosis  ;  for  individual  cases 
vary  greatly,  according  to  the  size  of  the  haemorrhages,  their  location,  and  the  fre- 
quency of  their  recurrence. 

Almost  always  the  beginning  of  the  disease  is  rather  sudden.  It  may  even  be 
like  an  apoplectic  seizure.  The  symptoms  are  referable  partly  to  the  general 
effect  of  the  haemorrhage  upon  the  brain,  and  partly  to  the  exact  locality  of  the 
haemorrhage.  The  more  general  symptoms  comprise  headache;  impairment  of 
intelligence  (that  is,  stupor  or  even  complete  coma) ;  slow  or  irregular  pulse ;  vom- 
iting ;  and  contracted  pupils — all  being  symptoms  of  cerebral  compression.  Now 
and  then  we  even  find  choked  disk.  Other  phenomena  are  added  to  the  above 
when  the  haematoma  occupies  its  usual  position,  upon  one  side  and  in  the  neigh- 
borhood of  the  motor  cortical  region,  or  central  convolutions.  The  hemiplegic 
symptoms  are  not  infrequent,  such  as  hemiparesis,  and,  from  the  irritation  which 
the  effusion  produces  in  the  motor  centers,  twitchings  and  convulsions  in  one  half 
of  the  body.  Sometimes  these  symptoms  are  limited  to  a  single  extremity  or  to 
the  distribution  of  the  facial  nerve.  Aphasia  has  been  repeatedly  observed  when 
the  haemorrhage  was  near  the  island  of  Reil.  If  the  effusion  increases,  the  motor 
disturbance  becomes  correspondingly  aggravated,  and  may  become  bilateral.  Sen- 
sation is  usually  little  impaired. 

The  further  course  of  the  disease  varies  greatly  in  different  cases.  In  the 
worst  cases  there  is  speedy  death,  usually  ushei'ed  in  by  deep  coma.  In  others,  the 
first  symptoms  are  followed  by  improvement,  although  mild  indications  of  cerebral 
pressure  persist,  such  as  headache  or  vertigo,  or  else  local  symptoms,  like  hemi- 
paresis. It  is  possible  for  the  effused  blood  to  be  absorbed,  and  complete  recovery 
to  ensue ;  but  usually  new  haemorrhages  and  corresponding  symptoms  arise.  It 
is  precisely  this  appearance  of  the  symptoms  in  separate  attacks,  this  frequent 
recurrence  of  severe  cerebral  disturbances,  that  is  characteristic  of  haematoma  of 
the  dura  mater.  As  already  intimated,  the  way  in  which  the  anatomical  lesions 
develop  explains  this  perfectly.  Thus  the  disease  may  drag  on  for  months  and 
years,  sometimes  improving  and  sometimes  aggravated.  Then  some  attack  at  last 
proves  fatal.  Arrest  and  actual  improvement  are  still  possible  even  in  the  later 
stages,  although  often  the  features  of  the  case  have  meanwhile  undergone  essen- 


698  DISEASES  OF  THE  NERVOUS  SYSTEM. 

tial  alteration  because  of  the  progress  of  some  causative  disease.  In  general,  the 
clinical  phenomena  of  hematoma  of  the  dura  are  often  complicated  and  obscured 
by  the  co-existence  of  the  primary  disease. 

The  diagnosis  is  therefore  difficult.  The  main  points  may  be  recapitulated  as 
follows  :  First,  the  existence  of  etiological  factors,  like  alcoholism,  or  chronic 
cerebral  disease  ;  second,  the  sudden  onset,  and  also  the  abrupt  appearance  of 
further  symptoms,  the  alternation  of  rapid  aggravation  and  improvement;  and 
third,  the  existence  of  symptoms  which  experience  has  taught  us  to  refer  mainly 
to  the  cortex  of  the  brain,  namely,  unilateral  convulsions,  monoplegic  paresis 
and  contractures,  and  contracted  pupils.  Nevertheless,  frequent  errors  in  diagnosis 
can  not  be  avoided. 

Treatment. — The  possibility  of  therapeutic  interference  being  successful  is  very 
small.  In  apoplectic  shocks,  ice  to  the  head  is  useful ;  and  if  the  patient  be  robust, 
it  may  also  be  advisable  to  use  local  depletion,  by  leeches  on  the  temples  or  behind 
the  ears.  It  is  also  customary  to  prescribe  some  such  thing  as  senna  or  calomel 
for  "intestinal  depletion." 

If  the  first  onset  is  successfully  withstood,  the  main  things  as  to  further  treat- 
ment are  general  hygienic  and  dietetic  directions,  so  as  to  guard  as  far  as  possible 
against  fresh  haemorrhages.  Alcohol  and  excessive  bodily  or  mental  exertion 
should  be  forbidden.  Of  course,  paralysis  or  other  persistent  disturbances  may 
call  for  special  treatment. 


CHAPTER  II. 


PURULENT   MENINGITIS. 

{Purulent  Cerebral  Leptomeningitis.     Meningitis  of  the  Convexity.) 

.ffitiology. — Purulent  inflammation  of  the  dura  mater  has  no  clinical  impor- 
tance, for  it  is  very  rare,  and  occurs  only  as  the  result  of  the  extension  of  disease 
from  neighboring  parts.  We  shall  accordingly  consider  below  purulent  inflam- 
mation of  the  pia  mater  only.  One  important  variety  of  this  disease  has  already 
been  discussed  (see  page  103  et  seq.)  as  one  of  the  infectious  diseases,  under  the  name 
of  epidemic  cerebro-spinal  meningitis.  There  we  saw  also  that  the  occasional 
sporadic  cases  of  primary  or  "  idiopathic  "  meningitis  are  probably  identical  astiolo- 
gically  with  those  of  epidemic  meningitis.  In  all  other  instances,  purulent  menin- 
gitis is  a  secondary  disease — that  is,  the  specific  agent,  which  excites  the  purulent 
inflammation,  originates  in  some  other  organ  primarily,  and  affects  the  meninges 
only  secondarily.  We  should,  therefore,  seek  most  carefully  in  every  case  of  puru- 
lent meningitis,  at  the  bedside  and  more  particularly  at  the  autopsy,  to  discover 
the  way  by  which  the  pathogenetic  virus  reached  the  meninges.  We  have  no 
right  to  say  that  the  case  is  one  of  primary  meningitis,  strictly  so  called,  until  we 
have  made  a  most  careful  examination  with  a  negative  result.  From  a  clinical 
standpoint,  it  is  true  that  many  cases  of  secondary  meningitis  do  seem  as  if  they 
were  primary,  because  not  infrequently  the  really  primary  disease  excites  insig- 
nificant symptoms,  or  perhaps  no  symptoms  at  all. 

Secondary  purulent  meningitis  is  most  often  due  to  disease  of  the  cranial  bones, 
and  in  particular  to  disease  of  the  petrous  portion  of  the  temporal  bone,  with  the 
auditory  apparatus  therein  contained.  If  we  consider  the  anatomical  relations  of 
the  middle  and  internal  parts  of  the  ear,  we  can  easily  understand  why  inflamma- 
tion in  them  is  not  infrequently  followed  by  meningitis.  Usually  it  is  a  caries  of 
the  petrous  portion,  itself  due  to  an  otitis  media,  which  leads  to  an  irruption  into 
the  cranial  cavity.     This  is  especially  apt  to  take  place  through  the  thin  vault  of 


PURULENT  MENINGITIS.  699 

the  tympanic  cavity.  It  may  also  extend  from  the  mastoid  cells,  or  by  direct 
propagation  along-  the  sheaths  of  the  acoustic  or  facial  nerves,  or  along  the  vessels 
which  lie  in  the  petroso-squamous  suture.  The  dura  is  first  attacked,  and  then 
the  pia.  In  many  instances,  the  neighboring  venous  sinuses  (transverse,  caver- 
nous, and  superior  petrosal)  transmit  the  inflammation,  being  first  attacked  by  ;i 
suppurative  thrombo-phlebitis.  Again,  exceptionally,  a  purulent  inflammation  in 
the  upper  part  of  the  nasal  cavity  may  lead  to  meningitis. 

Another  and  frequent  source  of  meningitis  is  found  in  the  various  traumatic 
injuries  of  the  cranium.  In  the  great  majority  of  these  cases  there  is  an  open 
wound,  admitting  infectious  agents  which  are  suspended  in  the  air.  The  suppura- 
tion often  commences  in  the  spongy  texture  of  the  diploe,  thence  extending  to  the 
dura  and  pia,  either  directly  or  by  way  of  a  purulent  thrombosis  of  some  sinus 
into  which  the  veins  of  the  diploe  enter.  It  is,  indeed,  generally  affirmed  that  we 
may  have  a  traumatic  purulent  meningitis  without  any  open  wound  ;  but  this  is 
not  easily  explained,  according  to  our  present  views  as  to  the  origin  of  purulent 
inflammations.  It  is  equally  difficult  to  understand,  what  many  authors  affirm, 
that  the  heat  of  the  sun's  rays,  striking  upon  an  uncovered  head,  may  excite 
purulent  meningitis.  In  most  cases  of  sunstroke  we  find  marked  hyperemia  of 
the  meninges,  but  no  inflammation. 

Meningitis  may  have  an  intra-cranial  origin  ;  it  is  sometimes  the  sequel  of 
cerebral  abscess.  No  matter  what  starts  the  abscess,  if  it  extends  to  the  surface  of 
the  brain,  it  causes  a  more  or  less  extensive  purulent  meningitis  at  that  point. 
An  abscess  may  burst  into  one  of  the  lateral  ventricles,  and  the  infection  be 
carried  from  that  point  to  the  pia  at  the  base  of  the  brain. 

All  the  cases  thus  far  contemplated  allow  of  the  explanation  that  the  inflam- 
mation reaches  the  meninges  by  direct  extension  ;  but  there  is  another  group  of 
cases  where  the  agent  that  infects  the  pia  mater  originates  at  some  distant  part  of 
the  body,  and  is  probably  conveyed  by  the  blood  or  lymph  currents.  These  cases 
are  often  termed  metastatic  meningitis. 

Of  this  sort  is  the  secondary  meningitis  seen  in  connection  with  genuine  lobar 
pneumonia,  a  combination  already  discussed  (see  page  198).  The  meningitis  is 
also  sometimes  a  complication  of  empyema,  rarely  of  pyaemia  and  septicaemia, 
ulcerative  endocarditis,  and  very  rarely  of  typhoid  and  the  acute  exanthemata 
(small-pox,  scarlet  fever),  and  of  acute  articular  rheumatism.  In  each  case  we 
must,  of  course,  determine  whether  the  meningitis  may  not  have  a  connecting 
link  between  itself  and  the  primary  disease,  such  as  otitis  in  scarlatina,  or  second- 
ary empyema  in  typhoid  fever. 

Pathology. — For  the  pathological  anatomy  of  purulent  meningitis,  we  may  refer 
mainly  to  the  statements  made  on  page  94,  under  epidemic  meningitis,  for  the 
lesions  are  similar.  The  only  way  to  determine  whether  a  meningitis  is  secondary 
or  primary  is  by  finding  or  failing  to  find  disease  in  neighboring  or  remote  parts, 
for  example  pneumonia.  The  seat  of  the  meningitis  will  vary  according  to  that  of 
the  primary  inflammation,  if  there  be  any.  If  the  meningitis  is  due  to  caries  of  the 
petrous  bone  or  to  an  injury  of  the  skull,  the  purulent  exudation  is  usually  most 
abundant  in  the  immediate  neighborhood  of  the  primary  lesion,  between  the  pia  and 
arachnoid.  Thence  it  gradually  extends  along  the  surface  of  the  brain,  sometimes 
chiefly  on  the  convexity  and  sometimes  at  the  base.  But  in  general  it  may  be  said 
that  both  the  secondary  and  the  metastatic  varieties  of  meningitis  as  a  rule  affect 
the  convexity,  although  this  is  by  no  means  invariably  the  case.  This  rule  explains 
why  these  cases  are  sometimes  termed  meningitis  of  the  convexity,  in  contrast  to 
tubercular  meningitis,  which  latter,  as  we  shall  find,  has  a  preference  for  the  base 
of  the  brain,  and  hence  is  called  basilar  meningitis.  The  spinal  pia  mater  is 
sometimes  simultaneously  attacked,  but  not  so  constantly  as  in  primary,  or  epi- 


TOO  DISEASES  OF  THE  NERVOUS  SYSTEM. 

demic  meningitis.  The  brain  is  almost  always  involved — the  inflammation  extends 
along  the  vessels  which  dip  from  the  pia  mater  into  the  cerebral  parenchyma.  It 
is  not  a  rare  thing  to  find  minute  abscesses  or  ecchymoses  in  the  interior  of  the 
brain.  The  whole  parenchyma  is  usually  moist,  cedematous,  and  of  a  doughy 
consistence.  The  meningeal  exudation  exerts  upon  the  brain  a  pressure  which 
gives  rise  to  important  symptoms ;  by  it  the  superficial  cerebral  convolutions  are 
often  considerably  flattened.  The  lateral  ventricles  almost  always  contain  more 
or  less  sero-pus. 

Clinical  History. — So  varied  are  the  primary  diseases  which  may  entail  a  men- 
ingitis, that  it  is  hardly  possible  to  make  a  sketch  of  the  disease  which  would  suit 
all  cases.  If  the  meningitis  comes  on  during  the  course  of  pyaemia,  pneumonia, 
or  some  other  severe  illness,  its  proper  symptoms  are  often  inextricably  confused 
with  those  of  the  primary  trouble;  and  when  the  skull  or  the  brain  has  been 
mechanically  injured,  it  is  very  hard  to  determine  whether  a  meningitis  has  been 
excited,  because  the  trauma  may  of  itself  produce  such  serious  effects.  The  fol- 
lowing description,  therefore,  applies  chiefly  to  cases  of  apparently  primary  men- 
ingitis, or  to  cases  where  the  meningitis,  although  secondary,  is  well  marked. 

The  beginning  in  such  cases  may  be  sudden,  or  it  may  be  somewhat  insidious. 
Sometimes  the  grave  symptoms  appear  almost  at  once,  accompanied  by  a  chill  and 
high  fever.  Sometimes  there  are  for  a  while  indefinite  and  more  or  less  ambigu- 
ous prodromata,  but  almost  always  it  is  the  headache  which  first  attracts  attention. 
This  grows  worse  with  more  or  less  rapidity,  and  almost  always  becomes  very 
violent.  Exceptionally  it  may  be  insignificant.  Not  infrequently  it  varies  con- 
siderably, being  much  worse  at  some  hours  or  on  some  days  than  on  others.  The 
location  of  the  pain  is  sometimes  frontal,  sometimes  occipital,  and  sometimes  over 
the  whole  head.  Next  in  prominence  to  the  headache,  particularly  in  the  later 
stages  of  the  disease,  is  the  mental  disturbance.  The  patient  complains  of  vertigo, 
becomes  dull  and  stupid,  or  begins  to  wander.  The  delirium  may  be  extremely 
violent,  but  usually  there  is  depression  rather  than  exaltation,  and  the  stupor 
merges  into  coma.  That  the  headache  still  continues  may  be  inferred  from  the 
frequent  raising  of  the  hand  to  the  head  and  the  grimace  of  pain  whenever  the 
head  is  moved,  till  finally  the  coma  becomes  so  profound  that  even  these  reflex 
actions  cease. 

Usually  these  general  cerebral  symptoms  are  attended  by  others  referable  to 
the  particular  locality  affected.  The  neck  is  rigid.  This  is  most  marked  when 
the  posterior  fossa  and  the  medulla  are  affected.  Then  there  are  all  sorts  of 
paralytic  or  irritative  symptoms  in  the  distribution  of  the  cranial  nerves,  mainly 
due  to  lesions  of  the  nerves  where  they  emerge  from  the  base  of  the  brain  ;  there 
is  derangement  of  the  motores  oculi,  as  shown  by  paralysis  or  nystagmus  ;  the 
pupils  are  unequal,  or  are  contracted  or  dilated,  and  do  not  react  to  light  ;  there 
is  paresis  of  the  facial,  or  trismus,  or  grinding  of  the  teeth.  All  these  symptoms 
may  appear  equally  plainly  in  other  forms  of  meningitis.  Sometimes  we  can 
detect  optic  neuritis  with  the  ophthalmoscope.  Other  symptoms  are  due  to  cere- 
bral disturbance,  often  apparently  located  chiefly  in  the  cortex.  Thus  there  may  be 
twitchings  of  individual  muscles,  or  even  pronounced  convulsions  in  one  or  more 
limbs,  or  paralysis  of  one  extremity  or  of  half  the  body.  Sometimes  the  autopsy 
explains  these  phenomena,  but  often  we  fail  to  find  any  marked  anatomical  lesion 
to  correspond  to  them,  and  are  obliged  to  ascribe  them  to  circulatory  or  functional 
derangement. 

Of  the  remaining  symptoms,  the  fever  is  most  important.  Almost  always  the 
temperature  is  decidedly  elevated,  not  infrequently  reaching  104°  or  105°  (40°-40"5° 
C).  The  fever  is,  however,  very  irregular.  There  may  be  repeated  chills  with 
great  elevations  of  temperature.     The  pulse  is  generally  rapid,  and  often  some- 


PURULENT  MENINGITIS.  701 

what  irregular.  Exceptionally  it  is  less  frequent  than  normal,  because  of  cerebral 
compression.  Vomiting  is  not  a  rare  symptom,  particularly  at  first.  There  i 
almost  invariably  constipation,  and  the  abdomen  is  often  tense  and  concave.  The 
urine  is  scanty,  and  often  contains  a  trace  of  albumen.  Secondary  diseases  are 
sometimes  found  iiost  mortem,  such  as  lobular  pneumonia,  due  to  inhalation  of 
food  during  the  comatose  state. 

The  entire  course  of  the  disease  occupies  only  a  few  days  in  very  acute  cases, 
and  scarcely  ever  exceeds  a  week  or  ten  days.  The  termination  is  almost  sure 
to  be  fatal.  In  the  few  cases  of  recovery  which  have  been  reported  the  diagnosis 
is  doubtful.  In  most  instances  deep  coma  precedes  death,  though  sometimes  it  is 
ushered  in  by  convulsions.  There  is  often  a  great  rise  of  temperature  (107'5°,  42° 
C,  or  higher)  before  the  close  of  life. 

Diagnosis. — The  diagnosis  of  purulent  meningitis  is  sometimes  pretty  evident; 
but  it  may  be  very  obscure,  so  that  we  can  not  always  avoid  confounding  it  with 
other  severe  acute  diseases,  such  as  typhoid,  pyaemia,  and  general  tuberculosis.  In 
general  the  most  characteristic  symptoms  of  any  variety  of  meningitis  are  intense 
headache,  rapid  onset  of  grave  cerebral  disturbances,  delirium  and  insensibility, 
stiffness  of  the  neck,  and  disturbances  in  the  distribution  of  the  cranial  nerves 
(especially  impaired  motion  of  the  eyeball  and  optic  neuritis).  These  last,  although 
often  slight,  are  generally  present  ;  and  in  connection  with  these  separate  symp- 
toms we  must  also  always  consider  the  whole  course  of  the  disease  and  any  aetio- 
logical  factors  which  may  exist.  Typhoid  fever  is  excluded  by  its  usually  slower 
onset,  the  greater  delay  in  the  appearance  of  grave  cerebral  symptoms,  the  rose- 
spots,  the  greater  size  of  the  spleen,  the  characteristic  stools,  and  the  peculiar  fever- 
curve.  Severe  septic  and  pyaemic  diseases,  including  ulcerative  endocarditis,  like- 
wise excite  cerebral  disturbances  which  might  be  misleading,  but  these  diseases 
are  to  be  recognized  by  their  aetiology  (external  wounds,  abortion,  etc.),  cutaneous 
ecchymoses,  septic  retinitis,  swelling  of  the  joints,  and  repeated  rigors.  Uraemia 
may  also  simulate  meningitis.  Sometimes  the  character  of  the  urine,  and  the 
predominance  of  convulsions,  will  set  us  right,  but  not  always.  We  may  state 
in  conclusion  that  every  one  who  sees  many  cases  (including  ourselves),  must 
repeatedly  have  met  with  patients  presenting  the  symptoms  of  a  severe  and  acute 
cerebral  affection  apparently  primary,  without  demonstrable  cause,  and  seeming  to 
justify  a  diagnosis  of  meningitis,  but  yet  yielding  post  mortem  no  signs  of  disease 
beyond  "  hyperaemia,"  "  cedematous  swelling,"  and  similar  changes  of  only  second- 
ary importance.     We  are  as  yet  wholly  unable  to  explain  such  cases. 

Granting  that  meningitis  exists,  what  variety  is  present  ?  The  aetiology  is  a 
great  help  in  answering  this  question.  We  should  endeavor  to  learn  whether 
there  has  been  traumatism  or  some  old  ear  trouble.  It  is  well  to  employ  the  aural 
speculum.  We  can  not  say  that  a  patient  has  epidemic  meningitis  unless  several 
cases  occur  simultaneously,  although  herpes  is  very  characteristic,  as  it  appeals 
only  exceptionally  in  other  varieties.  Usually  tubercular  meningitis  also  can 
be  diagnosticated  only  by  means  of  the  aetiology.  Its  symptoms,  of  course,  are  in 
almost  all  particulars  identical  with  those  of  purulent  meningitis.  Sometimes, 
however,  tubercles  can  be  detected  in  the  choroid  by  means  of  the  ophthalmoscope. 
For  further  particulars  see  the  next  chapter. 

Treatment. — The  treatment  of  the  different  forms  of  meningitis  varies  but  little. 
Locally,  the  favorite  remedies  are  ice  applied  to  the  head,  which  should  be  shaved 
if  practicable,  and  local  depletion  by  means  of  leeches  behind  the  ears  or  on  the 
temples.  Many  physicians  recommend  cutting  off  the  hair  and  rubbing  in  anti- 
monial  ointment,  or  applying  ethereal  tincture  of  iodine.  We  have  never  tried 
this.  Gool  baths  with  douching  can  not  be  employed  unless  the  patient  can  be 
moved  without  too  much  pain.     For  violent  pain  or  great  restlessness  we  must 


702  DISEASES  OF  THE  NERVOUS  SYSTEM. 

use  narcotics.     The  best  is  morphine  subcutaneously.    We  can  not  hope  for  much 
benefit  from  other  internal  remedies,  such  as  iodide  of  potassium  or  calomel. 

Prophylaxis  demands,  above  all,  prompt  recourse  to  the  otologist  for  aural 
trouble  of  any  kind,  and  strictly  antiseptic  treatment  of  all  injuries  of  the  skull. 


CHAPTER  III. 

TUBERCULAR  MENINGITIS. 

(Basilar  Meningitis.) 

etiology.— Tuberculosis  of  the  leptomeninges  is  always  a  secondary  affection — 
a  sequel  to  previously  existing  tubercular  disease  of  some  other  organ.  Why  the 
pia  mater  should  be  so  often  singled  out  for  secondary  infection  with  the  tuber- 
cular virus,  or  what  path  that  virus  traverses  to  reach  the  pia — about  these  ques- 
tions we  know  very  little.  We  can  merely  state  what  the  other  tubercular  diseases 
are,  which,  as  experience  shows,  entail  tubercular  meningitis  most  frequently. 
These  primary  affections  may  be  of  themselves  productive  of  grave  clinical  phe- 
nomena, the  meningitis  merely  adding  to  the  complexity  of  the  picture.  Again, 
the  primary  trouble  may  not  have  betrayed  itself  at  all,  or  its  symptoms  may  have 
been  long  ago  arrested,  so  that  the  meningitis  seems  to  be  a  primary  disease.  In 
some  cases  even  the  most  careful  examination  will  fail  to  detect  the  origin  of  the 
trouble. 

Tubercular  meningitis  is  of  tenest  a  sequel  to  pulmonary  tuberculosis.  It  may 
appear  as  a  terminal  complication  in  cases  of  advanced  phthisis,  or  it  may  come  on 
while  the  signs  of  pulmonary  disease  are  as  yet  very  slight.  Next  in  order  as  a 
causative  affection  comes  tubercular  pleurisy.  This  origin  is  not  infrequent.  As 
we  have  already  seen,  most  cases  of  apparently  primary  pleurisy  are  due  to  tuber- 
cle. This  statement  is  supported  by  the  fact  that  it  is  not  very  exceptional  for  the 
symptoms  of  tubercular  meningitis  to  supervene  suddenly  upon  what  had  seemed 
to  be  genuine  convalescence  from  pleurisy.  In  children,  and  sometimes  in  adults, 
the  virus  may  be  carried  to  the  meninges  from  cheesy,  tubercular,  bronchial  or 
mesenteric  glands,  or  from  tubercular  or  "  fungous  "  disease  of  the  bones  or  joints. 
Another  danger  to  adults  is  tubercular  disease  of  the  genito-urinary  apparatus. 
It  should  also  be  noticed  that  a  single  large  tubercle  in  the  brain  may  lead  to  mili- 
ary tuberculosis  of  the  meninges.  In  short,  we  see  that  it  is  not  impossible  for  any 
tubercular  infiltration,  wherever  situated,  to  communicate  infection  either  to  the 
meninges  alone  (in  some  remarkable  way),  or  simultaneously  to  them  and  many 
other  organs.  In  this  last  case,  where  in  all  probability  the  blood  carries  the 
virus  through  the  system,  the  meningitis  is  merely  a  part  of  a  general  miliary 
tuberculosis  (see  page  236).  When  the  meninges  are  alone  or  predominantly 
affected,  there  must  be  some  peculiar  manner  of  infection,  about  which,  how- 
ever, as  we  have  already  confessed,  we  have  no  information. 

We  sometimes  hear  the  attack  ascribed  to  such  causes  as  over-exertion,  mental 
excitement,  or  traumatism;  but  we  need  hardly  say  that  these  can  not  be  properly 
regarded  as  aetiological  factors,  and  that  usually  they  are  merely  coincidences. 
Age,  howevei\  does  have  an  influence ;  children  are  much  offener  attacked  than 
adults,  although  the  latter  also  are  liable  to  it. 

Pathology. — As  in  tuberculosis  of  serous  membranes,  so  in  tuberculosis  of  the 
pia,  there  are  two  effects  of  infection  to  be  distinguished  from  each  other :  (1)  the 
development  of  the  specific  new  growth — that  is,  of  miliary  tubercles  ;  and  (2) 
the    inflammation.     The  relative  degree  of    these  two  varies.      Sometimes  the 


TUBERCULAR  MENINGITIS.  703 

tubercles  are  very  abundant  and  the  inflammatory  exudation  comparatively 
scanty;  and  in  other  cases  the  inflammation  is  considerable,  although  relatively 
few  tubercles  are  discoverable.  The  tubercles  are  usually  found  in  greatest 
number  along  the  course  of  the  larger  blood-vessels,  and  therefore  chiefly  in  the 
furrows  and  clefts  of  the  surface  of  the  brain,  in  the  fissure  of  Sylvius,  at  the 
chiasma,  the  pons,  the  medulla,  and  the  cerebellum.  And,  in  general,  the  base  of 
the  brain  is  usually  more  affected  than  the  convexity — hence,  as  we  have  said,  the 
name  of  "basilar  meningitis."  There  are,  however,  exceptions  to  this  rule.  We 
very  often  find  that  the  region  supplied  by  one  or  more  arteries  suffers  above 
other  parts;  this  must  be  due  to  the  manner  of  infection.  The  inflammatory 
lesions  consist  of  hypersemia,  usually  well  marked,  and  a  sero-gelatinous  exuda- 
tion of  variable  amount..  That  this  exudation  is  partly  cellular  can  always  be 
proved  by  the  microscope,  and  often  even  macroscopically  from  the  great  cloudi- 
ness of  the  pia;  but  still  we  seldom  find  enough  to  justify  us  in  calling  the  pro- 
cess one  of  genuine  purulent  inflammation.  Small  haemorrhages  into  the  pia  are 
quite  often  found.  The  brain  itself  is  usually  flattened  from  the  pressure  of  the 
meningeal  exudation.  Often  the  inflammation  involves  the  brain-substance  itself, 
as  shown  microscopically  by  tubercles,  inflammatory  changes,  and  capillary 
haemorrhages.  The  ventricles  usually  contain,  although  not  invariably,  a  hydro- 
cephalic effusion.  This  led  earlier  observers  to  term  the  disease  ''  acute  hydro- 
cephalus."- The  effusion  is  serous,  but  generally  turbid  from  cellular  constituents, 
and  not  infrequently  tinged  with  blood.  The  choroid  plexus  is  engorged,  and  may 
present  tubercles.  The  spinal  cord,  in  the  majority  of  cases,  shares  in  the  tuber- 
cular disease.  Here,  too,  we  find  inflammation  of  the  pia  and  miliary  tubercles. 
This  fact  has  a  clinical  bearing,  being  explanatory  of  many  of  the  symptoms. 

Clinical  History. — Tubercular  meningitis  almost  always  begins  with  a  pro- 
dromal stage,  which  is  often  brief,  but  may  last  one  or  two  weeks,  or  even  longer. 
The  patient  may  be  apparently  well  (vide  supra)  until  this  comes  on,  or  he  may 
have  already  shown  signs  of  some  other  tubercular  affection.  He  now  feels  badly, 
at  any  rate,  and  begins  to  complain  of  headache,  worse  at  some  times  than  at 
others.  There  is  anorexia  and  very  often  constipation.  Another  frequent  pro- 
drome is  an  attack  of  vomiting,  which  may  or  may  not  recur.  Sleep  is  disturbed, 
either  by  the  headache  or  by  a  certain  general  restlessness.  We  have  occasionally 
met  with  cases  where  the  illness  began  with  pronounced  mental  disturbance.  The 
patient  became  irrational  and  said  and  did  queer  things,  and  then  a  few  days  later 
there  appeared  distinctive  meningeal  symptoms.  In  two  patients,  who  were 
topers,  the  disease  began  just  like  delirium  tremens. 

After  an  initial  period  of  variable  duration,  the  general  health  becomes  more 
and  more  impaired.  The  headache  increases.  The  patient  takes  to  his  bed,  begins 
to  be  delirious,  and  soon  presents  well-marked  symptoms  of  grave  brain  trouble. 
Intelligence  becomes  more  and  more  impaired.  The  patient  is  sleepy,  and  can  be 
roused  imperfectly  by  the  voice,  if  at  all.  At  the  same  time  he  is  usually  quite 
restless  at  first,  grasping  at  invisible  objects  in  the  air,  picking  the  bed-clothes, 
and  continually  moving  his  legs.  The  delirium  may  be  low  or  noisy ;  the  patient 
may  keep  up  a  constant  singing  or  screaming  or  whistling.  The  persistence  of 
the  headache  even  in  this  stage  is  shown  by  the  facial  contortions  and  complaints 
of  the  sufferer,  whenever  there  is  a  temporary  approach  to  consciousness.  There 
is  also,  as  a  rule,  decided  tenderness  in  the  nape  of  the  neck  on  pressure,  frequently 
accompanied  by  great  stiffness  of  the  neck.  Sometimes  there  is  stiffness  of  the 
entire  spinal  column,  and  pain  in  the  same.  This  is  certainly  due  to  the  coinci- 
dent spinal  meningitis. 

Another  group  of  symptoms  in  the  distribution  of  the  cranial  nerves  are  iden- 
tical with  those  seen  in  the  other  forms  of  meningitis.     Ptosis  is  not  infrequent, 


704  DISEASES  OF  THE  NERVOUS  SYSTEM. 

on  one  or  both  sides,  due  to  paresis  of  the  motor  oculi.  There  is  strabismus,  either 
internal  or  external.  Symptoms  of  irritation  of  the  nerves  governing  the  move- 
ments of  the  eye  are  very  frequent,  especially  in  the  early  stages  of  the  disease. 
Thus  we  see  slow  involuntary  lateral  movements  of  the  eyeballs,  and  sometimes 
nystagmus.  The  pupils  are  often  unequal  ;  they  may  be  enlarged  or  contracted, 
and  often  they  undergo  marked  and  repeated  variations  in  size.  The  reaction  of 
the  pupils  to  light  is  usually  sluggish,  and  may  be  absent.  With  the  ophthal- 
moscope we  find  not  infrequently  neuritis,  or  choked  disk.  In  some  instances, 
but  not  in  all,  we  find  also  tubercles  in  the  choroid,  which,  of  course,  greatly 
assists  diagnosis.  Sometimes  there  is  occasional  twitching  in  the  distribution  of 
the  facial  nerve,  or  a  slight  tonic  contraction,  or  again  paresis  on  one  side.  The 
natural  explanation  of  all  these  phenomena  is  that  the  nerve-trunks  are  inter- 
fered with  at  the  base  of  the  brain,  whether  by  the  pressure  of  the  exudation  or  by 
participation  in  the  inflammatory  process,  or  by  the  minute  haemorrhages  which 
sometimes  take  place  into  the  sheath  of  the  nerves. 

Disturbances  in  the  extremities  may  be  caused  by  various  lesions.  Motor 
symptoms  of  irritation  are  apparently  referable  for  the  most  part  to  changes  in 
the  cortex  of  the  brain.  We  see  occasional  twitching  of  larger  or  smaller  groups 
of  muscles,  or  rarely  convulsions.  These  latter  may  be  unilateral,  or  in  a  single 
extremity.  Sometimes  there  is  well-marked  paresis  of  one  half  the  body  or 
paralysis  of  one  limb,  or  there  may  be  aphasia,  although  it  is  only  in  a  part  of  the 
cases  that  we  find  post  mortem  any  lesion  which  explains  these  symptoms.  In 
most  cases  there  is  a  particularly  large  collection  of  tubercles  in  certain  places 
upon  the  cortex  cerebri,  occasioning  a  local  compression  or  an  inflammatory  oede- 
ma, which  in  its  turn  excites  the  phenomena  mentioned.  Sometimes  the  brain- 
substance  itself  is  found  in  a  state  of  red  softening  underneath  these  spots.  An- 
other and  not  very  rare  symptom  is  a  peculiar  stiffness  of  the  limbs,  due  either  to 
direct  irritation  or  to  reflex  action.  The  reflexes  in  the  lower  extremities  are  gen- 
erally exaggerated  at  first,  but  later  on  become  diminished,  and  finally  abolished. 
The  reflexes  upon  one  side  may  be  more  vigorous  than  upon  the  other.  As  to 
sensation,  it  is  hard  to  reach  definite  conclusions,  because  of  the  patient's  stupor. 
Sometimes  there  is  well-marked  cutaneous  hyperesthesia,  probably  referable  to  an 
implication  of  the  spinal  cord  in  the  process. 

The  behavior  of  the  pulse  and  temperature  is  interesting.  The  temperature 
is  usually  elevated,  but  often  only  to  a  slight  extent — that  is,  varying  between 
100"5°  and  102°  (38°  and  39°  C).  Often  the  temperature  falls  quite  low,  only  to 
rise  again,  the  alternations  being  at  irregular  intervals.  Exceptionally  the  tem- 
perature may  remain  high  (104°  F.,  40°  C)  most  of  the  time.  Toward  the  end 
there  is  usually  a  decided  change  in  temperature,  either  upward  or  downward. 
In  many  instances  there  is  a  very  low  temperature  before  death ;  in  two  cases  we 
have  seen  a  temperature  of  87'8°  (31°  C).  Or  the  temperature  may  rise  to  106° 
(41°  C)  or  higher  just  before  death.  The  pulse  is  often  abnormally  slow  in  the 
early  stages  of  the  disease,  even  numbering  only  40  to  50  beats  per  minute.  This 
is  referable  without  doubt  to  the  increased  intra-cranial  pressure.  Later  on  the 
pulse  becomes  small  and  rapid.  The  transition  may  be  very  sudden.  The  vagus 
is  at  first  irritated,  and  then  paralyzed.     The  pulse  is  often  irregular. 

Respiration  is  generally  moderately  accelerated.  If  the  breathing  is  very  deep 
and  rapid,  we  should  always  think  of  simultaneous  miliary  tuberculosis  of  the 
lungs.  Toward  the  close  of  the  disease  the  respiration  often  assumes  the  Cheyne- 
Stokes  type :  there  is  a  long  pause,  followed  by  very  superficial  and  gentle  respi- 
ration, which  gradually  grows  deeper  and  deeper,  then  diminishes  again,  and  is 
succeeded  by  another  complete  pause.  This  symptom  is  always  most  ominous,  for 
it  indicates  that  the  excitability  of  the  respiratory  center  is  already  greatly  impaired. 


TUBERCULAR   MENINGITIS.  705 

Symptoms  referable  to  still  other  organs  are  few.  Vomiting  is  rare  in  the 
later  stages  of  the  disease.  The  abdomen  often  presents  a  :'  boat-shaped  "  concav- 
ity, as  the  result  of  tonic  muscular  contraction,  and  is  hard  and  tense.  There  is 
almost  always  constipation.  The  spleen  maybe  somewhat  enlarged.  The  urine 
sometimes  contains  a  trace  of  albumen.  On  account  of  the  drowsiness,  it  is  usu- 
ally voided  in  the  bed  or  retained  in  the  bladder.  Almost  invariably  there  is  rapid 
marasmus. 

The  entire  duration  of  tubercular  meningitis  varies  somewhat,  chiefly  because 
of  the  varied  length  of  the  first  stage.  When  the  disease  is  once  fully  developed, 
the  illness  seldom  lasts  more  than  three  to  ten  days  longer.  Frequently  the 
illness  is  divided  into  three  stages  :  1.  The  stage  of  cerebral  irritation,  with  head- 
ache, stiff  neck,  vomiting,  and  delirium  ;  2.  The  stage  of  cerebral  compression, 
chiefly  due  to  the  hydrocephalus,  and  causing  drowsiness,  slowness  of  the  pulse, 
paralysis  of  the  mo  to  res  oculi,  hemiplegia,  etc. ;  and  3.  The  paralytic  stage,  pre- 
senting deep  coma,  relaxation  of  the  previously  contracted  muscles,  accelerated 
pulse,  and  marked  variations  of  temperature.  Such  a  division  is  too  diagrammatic 
to  correspond  accurately  to  the  real  phenomena,  but  will,  nevertheless,  often  aid 
us  in  getting  a  general  idea  of  the  course  of  the  disease. 

The  termination  of  tubercular  meningitis  seems  to  be  inevitably  fatal.  Sooner 
or  later  the  patient  loses  consciousness  completely,  his  pulse  grows  very  small  and 
rapid,  his  respirations  irregular  and  intermittent  (Cheyne-Stokes),  his  temperature, 
as  we  have  said,  either  rises  high  or  falls  far  below  normal,  and,  finally,  death  is 
ushered  in  by  a  paralysis  of  all  the  vital  functions.  A  few  physicians  have 
reported  cases  of  recovery ;  but  was  the  diagnosis  correct  ?  While  we  would  by 
no  means  absolutely  deny  that  recovery  from  tubercular  meningitis  might  occur, 
it  would  certainly  be  very  difficult  to  prove,  in  any  particular  instance,  that  such 
a  thing  had  happened. 

Tubercular  Meningitis  in  Children. — The  disease  is  so  prone  to  attack  children 
that  it  seems  desirable  to  subjoin  a  few  remarks  about  the  peculiarities  of  the  affec- 
tion as  observed  in  them. 

Often  the  little  patient  is  pale  and  weakly,  with  tubercular  antecedents ;  but 
sometimes  apparently  healthy  and  vigorous  children  are  attacked.  Tubercular 
meningitis  may  be  the  sequel  of  measles,  whooping-cough,  or  some  other  disease, 
which  has  occasioned  the  development  of  the  tubercular  process.  Usually  the 
severer  symptoms  are  preceded  by  a  rather  long  prodromal  stage,  during  which 
the  child  is  fretful,  eats  little,  and  grows  thin  and  pale.  In  children  as  well  as 
adults,  the  second  stage  is  generally  ushered  in  by  headache  and  vomiting.  The 
headache  is  not  very  often  violent  ;  but  children  complain  with  remarkable 
frequency  of  pain  in  the  abdomen  and  chest.  The  cause  of  this  symptom  is 
unknown.  The  pulse  is  almost  invariably  slow,  often  somewhat  irregular,  and 
it  frequently  undergoes  surprisingly  rapid  changes  in  rate — for  example,  varying 
twenty  or  more  beats  inside  of  a  few  hours.  Very  early  the  child  becomes  dull 
and  drowsy.  Frequently  it  emits  a  peculiar  deep  sigh,  or  that  sudden  loud  scream 
or  "  cephalic  cry  "  which  physicians  long  ago  learned  to  recognize  and  fear.  The 
symptoms  referable  to  the  cranial  nerves  and  the  nervous  disturbances  in  the 
limbs  are  similar  to  those  seen  in  adults.  Strabismus  is  almost  constant.  Very 
often  there  is  trismus,  and  a  distinctly  audible  grinding  of  the  teeth,  most  dis- 
tressing to  the  by-standers.  Trousseau  laid  weight  upon  the  appearance  of  red 
spots  (taches  cerebrales)  upon  the  skin  after  it  has  been  mechanically  irritated ; 
but  these  have  no  diagnostic  value.  They  are  due  to  increased  reflex  action,  and 
are  seen  in  all  sorts  of  acute  diseases.  The  fever  is  generally,  as  in  adults,  not 
very  high,  100°  to  102°  (38°-39°  C).  Respiration  is  usually  rapid,  and  often  is 
irregular. 

45 


706  DISEASES  OF  THE  NEEVOÜS  SYSTEM. 

The  change  from  bad  to  worse  is  almost  always  announced  by  a  rapid  increase 
in  the  pulse-rate,  to  160  or  200.  The  child  becomes  completely  comatose.  Very 
often  there  are  repeated  epileptiform  convulsions,  either  universal  or  affecting 
single  extremities.     Death  is  usually  preceded  by  a  decided  rise  in  temperature. 

Diagnosis. — When  the  symptoms  are  pronounced,  the  diagnosis  of  meningitis 
is  easy,  and  we  have  merely  to  determine  just  what  variety  is  before  us.  That 
the  disease  is  due  to  tuberculosis  is  never  to  be  ascertained  by  means  of  the 
meningeal  symptoms  themselves,  but  is  rendered  possible  only  by  the  aetiology,  if 
that  be  discoverable.  Here,  as  in  all  tubercular  diseases,  we  have  chiefly  to  con- 
sider (1)  heredity  and  (2)  the  evidence  of  previous  or  existing  tubercular  affections 
in  other  parts  of  the  body.  Under  this  second  head  are  to  be  considered  scrofula, 
diseases  of  the  bones  and  joints,  pulmonary  tuberculosis,  pleurisy,  and  tuberculosis 
of  the  genitals  or  of  the  choroid.  If  our  search  be  unsuccessful,  we  may  some- 
times get  a  hint  of  the  truth  from  the  general  appearance  of  the  patient  :  for 
example,  he  may  be  pale,  or  narrow-chested.  And,  again,  the  absence  of  trauma, 
aural  disease,  or  epidemic  meningitis  will  make  tuberculosis  more  probable. 

In  its  early  stages,  or  when  it  varies  from  the  usual  course,  tubercular  menin- 
gitis may  be  very  difficult  to  diagnosticate.  This  is  particularly  true  when  the 
patient  is  a  child.  The  early  malaise  and  vomiting  are  treated  as  "ordinary 
gastric  catarrh  "  until  the  grave  cerebral  symptoms  disclose  the  mistake  in  diag- 
nosis. In  such  cases  we  should  be  careful  not  to  disregard  the  initial  slowness 
and  irregularity  of  the  pulse.  This  alone  should  make  our  prognosis  guarded. 
The  fever  may  be  prominent  at  the  commencement,  and  tempt  us  to  call  the  case 
one  of  incipient  typhoid  fever ;  and,  indeed,  the  correct  diagnosis  is  often  impos- 
sible until  the  disease  develops  further.  In  regard  to  this,  see  the  preceding 
chapter  on  purulent  meningitis,  where  the  exclusion  of  severe  septic  diseases  and 
of  uraemia  is  also  considered. 

Before  the  autopsy  we  must  remain  in  great  uncertainty  as  to  the  number  and 
distribution  of  the  tubercles,  the  existence  of  a  large  effusion  into  the  lateral 
ventricles,  etc.  We  are  often  amazed  at  the  post-mortem  examination  by  the 
apparent  insignificance  of  the  lesions.  Paralysis  of  the  cranial  nerves  (eyes,  face) 
implies  that  the  base  of  the  brain  is  gravely  affected.  If  such  symptoms  are 
absent,  and  there  are  mental  disturbances,  and  motor  symptoms  of  irritation  dis- 
played in  the  extremities,  we  are  led  to  infer  meningitis  of  the  convexity.  If  the 
nervous  disorder  be  mainly  unilateral,  we  may  assume  that  one  hemisphere  is 
more  affected  than  the  other. 

Treatment. — However  hopeless  the  prospect,  we  are  nevertheless  bound  to 
employ  all  the  remedies  at  our  command,  as  in  other  forms  of  meningitis. 
Above  all,  we  should  be  thorough  in  applying  ice  to  the  head,  and  may  also  try 
local  depletion  and  lukewarm  baths,  with  douching.  The  inunction  of  mercurial 
ointment  has  also  been  recommended.  The  most  common  internal  remedies  are 
calomel — half  a  grain  to  a  grain  (grm.  0 "03-0 '05)  for  a  child  every  two  hours — and 
infusion  of  senna.  Iodide  of  potassium  may  also  be  freely  given,  fifteen  grains 
daily  to  a  child,  and  two  or  three  times  as  much  to  an  adult.  Whether  it  does 
any  good  is  extremely  doubtful.  If  the  patient  is  very  restless,  narcotics  are 
indispensable.  Stimulants  are  often  given  in  the  last  stage  of  the  disease,  but 
generally  without  effect. 

About  prophylaxis,  we  need  merely  refer  to  the  general  statements  on  page 
231,  in  regard  to  prophylaxis  from  the  various  tubercular  diseases. 


THROMBOSIS  OF  THE  CEREBRAL  SINUSES.  707 

CHAPTER  IV. 
THROMBOSIS   OF   THE    CEREBRAL   SINUSES. 

JEtiology  and  Pathology. —The  sinuses  of  the  dura  mater  sometimes  present  a 
thrombosis,  under  circumstances  similar  to  those  which  induce  the  same  process 
in  other  veins.  The  most  frequent  occasion  for  such  thrombosis  is  marasmus, 
however  brought  about,  with  the  accompanying  feebleness  of  circulation.  This 
is  the  explanation  of  those  not  very  rare  cases  found  among  wretched  and  ill- 
nourished  children  in  the  first  year  of  life,  and  also  among  adults  in  a  similar 
physical  condition,  as  in  phthisis.  In  many  of  these  instances  passive  congestion 
also  seems  to  contribute  to  the  formation  of  the  thrombus. 

Half  way  between  marantic  thrombosis  and  the  inflammatory  variety  imme- 
diately to  be  described,  come  those  cases  which  are  seen  in  typhoid  fever  and 
other  severe  acute  infectious  diseases.  Here  the  specific  virus  apparently  plays 
an  important  part  (just  as  in  thrombosis  of  the  femoral  vein),  although  very 
likely  the  cardiac  weakness  also  promotes  the  thrombosis. 

Genuine  inflammatory  thrombosis — that  is,  thrombosis  in  connection  with  real 
phlebitis  of  the  sinus — is  almost  always  due  to  the  extension  of  inflammation  from 
some  neighboring  part.  The  most  fruitful  cause  is  suppuration  in  the  petrous 
bone,  the  result  of  otitis  or  caries.  This  spreads  to  the  walls  of  the  transverse  or 
petrosal  sinuses,  which  are  close  by.  Also  wounds,  necrosis,  or  other  affections  of 
other  cranial  bones  may  excite  thrombosis  ;  likewise,  although  seldom,  deep- 
seated  inflammation  of  the  soft  parts  of  the  head  and  face,  like  large  furuncles  or 
erysipelatous  abscesses,  may  produce  the  same  result. 

Thrombosis  due  to  marasmus  is  most  frequently  found  in  the  superior  longi- 
tudinal sinus,  while  the  inflammatory  variety  usually  occupies  either  the  trans- 
verse, petrosal,  or  cavernous  sinuses.  Of  course  the  thrombus  may  grow  out  from 
its  original  sinus  into  neighboring  ones.  Important  clinical  symptoms  are  caused 
by  secondary  venous  stasis  in  the  veins  which  empty  into  the  occluded  sinus. 
These  symptoms  are  most  pronounced  when  the  longitudinal  sinus  is  affected  ; 
objectively,  we  find  the  meningeal  veins  which  lie  on  the  surface  of  the  brain  dis- 
tended and  tortuous ;  and  often  there  are  extensive  meningeal  ecchymoses.  Even 
the  cerebral  parenchyma  beneath  shows  distinct  evidence  of  passive  congestion, 
and  minute  capillary  haemorrhages  have  been  repeatedly  found  in  it. 

Symptoms. — In  some  instances  moderate  thrombosis  of  the  cerebral  sinuses 
has  been  found  post  mortem,  although  there  had  been  no  symptom  suggesting  it 
before  death.  In  other  cases  the  thrombosis  does  excite  undeniable  cerebral  dis- 
order, but  the  symptoms  are  so  general  and  ambiguous  that  the  most  we  can  do 
is  to  suspect  the  existence  of  the  clot  without  being  at  all  certain  about  it. 

Sinus  thrombosis  in  marantic  children  usually  causes  coma,  stiffness  of  the 
neck  and  back,  strabismus,  nystagmus,  and  sometimes  clonic  spasms  in  the  face 
and  limbs.  The  symptoms  in  adults  are  similar,  comprising  headache,  drowsi- 
ness, occasionally  delirium,  sometimes  coma,  and  varying  symptoms  of  irritation 
or  of  paralysis  in  the  distribution  of  the  cranial  nerves  (nystagmus,  strabismus, 
trismus)  and  in  the  extremities.  But  even  all  these  symptoms  are  insufficient  to 
make  the  diagnosis  certain.  They  must  be  re-enforced  by  certain  other  phenom- 
ena more  distinctly  referable  to  the  peculiar  circulatory  disturbances  occasioned 
by  the  thrombosis.  Occlusion  of  the  cavernous  sinus  sometimes  excites  well- 
marked  symptoms  of  stasis  in  the  ophthalmic  veins.  Thus  the  retina  may  be 
seen  through  the  ophthalmoscope  to  be  passively  congested,  there  is  oedema  of 
eyelids  and  the  conjunctiva,  the  eyeball  is  unusually  prominent,  and  the  frontal 


708  DISEASES  OF  THE  NERVOUS  SYSTEM. 

rein  is  distended.  In  case  of  an  inflammatory  thrombosis,  the  periphlehitic  swell- 
ing may  cause  symptoms  in  the  distribution  of  the  neighboring  nerves,  especially 
paresis  of  the  oculo-motor  or  abducens,  or  trigeminal  neuralgia.  In  thrombosis  of 
the  transverse  sinus  an  cedematous  swelling  is  occasionally  seen  behind  the  ear, 
near  the  mastoid  process.  If  the  clot  projects  into  the  petrosal  sinus  or  even  actu- 
ally into  the  internal  jugular,  the  lower  part  of  this  vein  collapses.  And  inas- 
much as  the  external  jugular  can  empty  itself  with  unusual  ease  into  the  unfilled 
internal  jugular  vein,  the  external  jugular  is  also  affected  and  becomes  less  promi- 
nent upon  the  affected  than  lipon  the  normal  side.  Sometimes  it  is  even  possible 
to  feel  the  thrombus  in  the  internal  jugular.  Such  thrombosis  causes  pain  and 
swelling  in  the  neck  on  the  abnormal  side.  When  the  superior  longitudinal 
sinus  is  blocked  up,  there  are  symptoms  of  nasal  engorgement  (epistaxis),  and 
distention  of  the  veins  about  the  temples,  which  veins  are  connected  with  the  lon- 
gitudinal sinus  by  emissary  veins.  We  must  confess,  however,  that  all  these 
special  symptoms  are  comparatively  rare,  and  often  difficult  of  demonstration 
even  when  present. 

The  symptoms  become  more  complex  where  there  is  a  suppurative  phlebitis, 
because  there  are  usually  pyaemic  symptoms  as  the  disease  progresses.  Thus, 
there  may  be  rigors  and  high  fever,  pulmonary  abscess,  suppurative  arthritis,  etc. 
We  have  already  mentioned  the  combination  of  thrombosis  of  a  sinus  with  puru- 
lent meningitis. 

The  prognosis  is  almost  always  bad,  both  because  of  the  nature  of  the  causa- 
tive disease  and  because  of  the  grave  cerebral  derangement  or  the  secondary 
pysemia.     Treatment  can  be  only  symptomatic. 


SECTION  II. 
Diseases  of  the  Brain-Substance. 

CHAPTER  I. 

DISTURBANCES    OF    CIRCULATION    IN    THE    BRAIN. 

{Cerebral  Hypercemia.     Cerebral  Ancemia.) 

It  is  presumable  that  so  sensitive  an  organ  as  the  brain  is  much  influenced  even 
by  slight  disturbances  of  circulation  ;  but  as  yet  we  have  comparatively  little 
knowledge  of  the  production  and  character  of  such  disturbances,  their  very  exist- 
ence being  very  difficult  to  demonstrate.  There  are  many  instances  where  marked 
cerebral  symptoms  justify  the  assumption  that  the  brain  is  in  some  abnormal  con- 
dition, and  yet  where  there  are  many  arguments  against  any  marked  anatomical 
lesion.  Here  we  surmise  that  there  is  some  circulatory  derangement,  although 
we  have  no  actual  and  direct  arguments  to  rely  upon.  For  example,  we  refer  to 
this  cause  certain  cases  of  headache,  sensations  of  pressure  in  the  head,  vertigo, 
general  hyperesthesia,  and  of  that  protean  and  nevertheless  easily  distinguishable 
disease  known  as  cerebral  neurasthenia  (q.  v.).  At  present,  however,  we  can  not 
determine  how  far  circulatory  disturbances  are  actually  concerned  in  these  cases, 
or  of  what  kind  they  are,  or  whether  there  may  not  be  purely  functional  dis- 
ease of  the  brain  entirely  independent  of  changes  in  the  blood-vessels. 

Certain  groups  of  cerebral  symptoms,  which  come  on  in  paroxysms,  seem  the 
most  clearly  referable  of  all  to  circulatory  disturbance.     There  can  hardly  be  a 


DISTURBANCES  OF  CIRCULATION  IN  THE  BRAIN.  709 

doubt  that  the  phenomenon  known  as  fainting  or  syncope  is  due  to  sudden  cerebral 
anaemia.  As  is  well  known,  fainting  is  usually  the  result  of  a  clearly  demon- 
strable cause.  Frequent  and  familiar  causes  arc  emotional  excitement,  terror, 
unusual  psychical  impressions  (like  the  sight  of  blood),  the  influence  of  great  heat, 
or  great  physical  strain,  as  by  long  standing.  The  condition  of  the  stomach  has 
certainly  a  great  influence  in  many  cases.  There  are  many  persons  who,  if  they 
go  long  beyond  the  usual  time  without  eating  (particularly  without  breakfast),  are 
very  liable  to  syncope.  Some  individuals  are  especially  subject  to  fainting  fits. 
Such  persons  are  often  slight  and  anaemic  (for  example,  convalescents),  but  some 
are  in  appearance  robust  and  vigorous.     Many  children  are  subject  to  fainting. 

Just  what  causes  the  cerebi'al  anaemia  in  all  these  cases  is  doubtful.  Mental 
excitement  is  usually  supposed  to  lead,  in  fainting,  to  a  contraction  of  the  minute 
cerebral  arteries.  It  is  not,  however,  impossible  that  in  these  cases  also,  as  in 
others,  sudden  cardiac  weakness  is  one  factor,  although,  if  so,  it  is  strange  that  we 
never  see  a  trace  of  cyanosis.  Where  the  attack  is  apparently  connected  with 
unusual  conditions  of  the  abdominal  organs  we  are  reminded  of  the  relations  of 
the  splanchnic  nerve  to  the  heart  (Goltz's  experiment  of  beating  the  belly  of  a 
frog),  and  of  the  possibility  that  the  brain  might  be  left  anaemic  if  the  abdominal 
vessels  suddenly  dilated  and  absorbed  a  large  proportion  of  the  whole  blood- 
supply. 

The  symptoms  of  an  ordinary  fainting  fit  are  known  to  every  one.  There  are 
usually  certain  prodromata.  The  person  begins  to  "  feel  badly."  Dizziness  comes 
on,  the  senses  are  confused,  the  ears  ring,  there  are  spots  before  the  eyes  or  total 
darkness,  the  floor  seems  to  move,  and  surrounding  objects  begin  to  spin  around. 
All  this  is  almost  always  accompanied  by  nausea,  and  sometimes  there  is  actual 
vomiting.  If  the  person  can  lie  down  promptly  the  attack  is  sometimes  averted 
without  complete  loss  of  consciousness.  Otherwise  there  is  unconsciousness  for  a 
time  varying  from  some  minutes  to  even  a  half -hour  or  longer.  What  the  by- 
stander notices  most,  even  at  the  first,  is  the  pallor  which  overspreads  the  face  and 
often  becomes  extreme,  and  which  is  the  visible  expression  of  the  coincident  cere- 
bral anaemia.  Very  often  the  face  and  body  are  bathed  in  cold  perspiration.  The 
pulse  is  usually  small  and  rapid. 

There  is  no  real  danger  in  an  ordinary  attack.  The  most  important  therapeu- 
tic measure  is  to  lay  the  patient  horizontally  as  soon  as  possible,  to  favor  the 
return  of  blood  to  the  brain.  Mild  stimulants  should  also  be  employed ;  the  face 
should  be  sprinkled  with  cold  water,  the  temples  rubbed  with  vinegar  or  cologne- 
water  ;  brandy  or  wine  should  be  administered.  We  can  overcome  a  tendency  to 
fainting  fits  only  by  strengthening  the  constitution. 

The  results  of  chronic  cerebral  anaemia  are  observable  when  the  cerebral  con- 
dition is  part  of  excessive  general  anaemia.  Almost  all  cases  of  chlorosis,  per- 
nicious anaemia,  and  acute  anaemia  from  loss  of  blood  (as  in  ulcer  of  the  stomach) 
display  most  plainly  the  symptoms  of  cerebral  anaemia.  The  phenomena  are 
essentially  the  same  as  in  syncope,  only  less  in  degree.  Consciousness  is  main- 
tained, except  in  the  worst  cases.  A  sort  of  persistent  drowsiness,  however,  often 
attended  by  frequent  gaping,  is  one  of  the  most  constant  symptoms.  The  patient 
is  most  distressed,  as  a  rule,  by  loud  tinnitus  aurium,  persistent  nausea,  and  some- 
times by  obstinate  headache.  All  these  symptoms  are  aggravated  if  the  patient 
sits  up  in  bed,  and  are  least  marked  when  he  lies  as  quietly  as  possible  in  a  hori- 
zontal position.  The  treatment  of  this  condition  is  of  course  identical  with  that 
of  the  causative  disease  and  the  general  anaemia. 

Cerebral  hyperaemia,  like  cerebral  anaemia,  may  be  either  chronic  or  paroxys- 
mal. Of  the  chronic  variety  we  know  almost  nothing.  It  seems  doubtful,  to  say 
the  least,  whether  there  is  really  a  "  general  plethora,"  or  whether  the  headaches 


710  DISEASES  OF  THE  NERVOUS  SYSTEM. 

and  vertigo  that  "  full-blooded  "  persons  complain  of  are  due  to  hyperemia  of  the 
brain.  Nor  have  we  any  direct  proof  that  the  cerebral  symptoms  resulting  from 
chronic  poisoning  (alcohol,  tobacco),  or  from  persistent  mental  over-exertion,  are 
brought  about  by  hyperaarnia,  as  some  assume,  and  not  rather  by  functional  dis- 
order of  the  nervous  elements  themselves. 

We  have  the  best  reason  to  claim  cerebral  hyperaemia  as  the  cause  of  cerebral 
symptoms  in  instances  of  "cerebral  congestion"  or  "rush  of  blood  to  the  head." 
There  is  a  more  or  less  sudden  appearance  of  general  excitement,  with  a  sensation 
of  warmth  in  the  head  and  neck,  strong  pulsation  of  the  carotids,  a  red  face,  gen- 
eral hyperesthesia  and  irritability,  headache,  vertigo,  tinnitus,  spots  before  the 
eyes,  and  nausea.  An  attack  lasts  half  an  hour  to  an  hour.  Apparently  there  is 
vaso-motor  disturbance,  causing  a  sudden  enlargement  of  the  cerebral  blood-ves- 
sels, and  due  either  to  a  paralysis  of  the  vaso-constrictors  or  to  a  stimulation  of  the 
dilators.  In  severe  cases  there  may  be  maniacal  excitement,  or  there  may  be 
stupor  and  drowsiness  and  other  symptoms  of  lowered  intellectual  activity,  resem- 
bling a  slight  apoplectic  attack  (see  a  later  chapter).  In  such  a  case  we  can  not 
determine  whether  there  is  hyperaemia  alone,  or  whether  there  is  not  some  further 
lesion,  like  a  small  haemorrhage. 

In  treating  congestion  we  should  keep  the  patient  as  quiet  as  possible,  with 
head  and  shoulders  raised ;  and,  secondly,  we  should  endeavor  to  draw  the  blood 
away  from  the  brain.  This  purpose  will  be  served  by  hot  foot-baths,  sinapisms 
applied  to  the  chest  and  the  calves,  and  purgatives,  like  senna  or  colocynth.  It  is 
also  beneficial  to  apply  cold  to  the  head.  In  a  severe  case  it  is  proper  to  put 
leeches  to  the  temples  or  the  mastoid  processes. 

To  prevent,  as  far  as  possible,  the  recurrence  of  the  attacks,  we  must  have 
regard  to  the  general  constitution  of  the  patient.  We  may  mention,  as  of  chief 
importance,  diet  (no  alcohol)  and  a  course  at  some  watering-place,  or  "  cold-water 
treatment." 


CHAPTER  II. 


GENERAL    PRELIMINARY  REMARKS    UPON  THE    LOCALIZATION   OP 

CEREBRAL   DISEASES. 

{Topical  Diagnosis  of  Cerebral  Lesions) 

The  physiological  relations  of  the  brain  are  such  that  the  symptoms  of  cere- 
bral disease  are  determined  to  a  greater  extent  by  the  locality  than  by  the  nature 
of  the  lesion.  If,  for  example,  there  arises  at  any  place  a  break  in  the  con- 
tinuity of  the  cerebral  motor  tract,  the  result,  as  we  already  know  (see  page  536), 
is  hemiplegia  upon  the  opposite  side  of  the  body.  The  result  is  precisely  the 
same,  whether  the  interruption  is  due  to  a  haemorrhage,  an  abscess,  a  new  growth, 
or  an  embolic  softening.  If  in  any  way  the  function  of  the  motor  fibers  is  sus- 
pended, then  the  necessary  sequence  in  every  case  is  a  paralysis  of  definite  extent 
and  definite  characteristics.  Much  the  same  may  be  said  of  many  other  symptoms 
which  appear  when  there  is  a  lesion  of  one  or  more  definite  places,  but  which  are 
never  referable  to  a  special  abnormal  process,  regardless  of  the  portion  of  brain 
thereby  affected. 

However  self-evident  these  simple  statements  may  appear,  it  required  a  long 
time  for  them  to  gain  universal  acceptance  among  physicians.  The  chief  cause  of 
this  was  the  conception  entertained  by  the  older  physiologists  in  regard  to  the 
functions  of  the  brain.  Flourens,  in  1842,  taught  that  functionally  all  parts  of  the 
cerebrum  were  alike,  and  therefore  any  one  part  could  act  vicaiiously  for  any 


THE  LOCALIZATION  OF  CEREBRAL  DISEASES.  71 1 

other;  and  this  view  had  numerous  adherents  among  physicians,  as  well  as  physi- 
ologists. It  was  nevertheless  experience  at  the  hedside  and  the  autopsy-table 
which  first  led  to  observations  and  discoveries  irreconcilable  with  this  view. 
Above  all,  it  was  the  lesions  found  in  aphasia  which  forced  men  to  localize  one 
cerebral  symptom  as  due  to  an  affection  of  one  particular  spot  in  the  brain.  In  1 861 
Broca  announced  that  the  appearance  of  aphasia  is  always  due  to  a  lesion  of  the 
third  left  frontal  convolution;  and  this  was  the  starting-point  of  the  doctrine  of 
localizations  in  general.  Nine  years  later  (1870)  appeared  the  famous  treatise  of 
Fritsch  and  Hitzig  detailing  successful  attempts  at  irritation  of  the  surface  of  the 
brain  in  animals,  and  thus  overthrowing  the  old  idea  that  the  gray  cortical  sub- 
stance could  not  be  irritated.  It  was  shown  that  irritation  of  certain  places  in  the 
cortex  is  followed  by  muscular  contractions  in  well-defined  portions  of  the  oppo- 
site side  of  the  body,  so  that  we  are  justified  in  assuming  the  existence  of  a  num- 
ber of  cortical  centers,  the  boundaries  of  which  are  comparatively  narrow.  These 
results  were  soon  confirmed  by  numerous  observations  in  cerebral  pathology  in 
man ;  and  to-day  our  information  about  the  motor  functions  of  the  cerebral  cortex 
forms  the  best-known  portion  of  the  doctrine  of  cerebral  localization.  Of  late 
years  successful  work  has  been  done  in  this  exceedingly  difficult  field  by  Mey- 
nert  and  Flechsig  among  anatomists;  Ferrier,  Munk,  Goltz,  and  other  physiolo- 
gists ;  and  such  pathologists  as  Charcot  and  his  pupils,  Nothnagel  and  Hughlings 
Jackson.  It  is  true  that  we  are  only  just  beginning  to  know  something  about 
the  subject.  There  are  numerous  contradictory  views  asserted,  and  numerous 
questions  unanswered.  The  following  summary,  therefore,  is  to  be  regarded 
merely  as  expressing  the  prevailing  opinions  now  existing.  Much  in  it  will  surely 
be  altered  in  the  course  of  time  ;  but  still  this  doctrine  of  special  localization  of  the 
various  cerebral  functions  marks  out  in  general  outlines  the  only  foundation 
upon  which  we  can  hope  to  erect  a  system  of  cerebral  pathology  and  diagnosis. 
In  the  following  sketch  we  shall,  for  practical  reasons,  put  the  results  of  clinical 
observations  in  the  foreground,  and  merely  speak  incidentally  of  the  correspond- 
ing experimental  achievements.  This  will  be  the  quickest  way  to  gain  acquaint- 
ance with  the  practical  points  in  the  diagnosis  of  what  Griesinger  called  the  "  focal 
diseases  " ;  and  then,  when  we  take  up  the  separate  varieties  of  cerebral  disease, 
we  shall  have  these  general  remarks  to  refer  to. 

1.  The  Motor  Region  op  the  Cortex  Cerebri. 

Clinical  observation  and  the  results  of  experiment  both  teach  that  a  part  of 
the  cerebral  cortex  is  distinct  from  the  rest,  inasmuch  as  it  is  the  exclusive  seat 
of  motor  functions.  This  "  motor  region "  {vide  Figs.  102  and  103,  page  713)  is 
made  up  of  the  two  central  convolutions  (gyri  centrales  anterior  et  posterior,  in 
Fig.  101),  and  the  paracentral  lobule  (vide  Fig.  103),  which  lies  on  the  median  sur- 
face of  the  cerebrum.  It  is  also  anatomically  different  from  the  other  regions  of 
the  cortex,  as  Betz  was  the  first  to  point  out,  for  it  alone  possesses  certain  large 
pyramidal  ganglion-cells,  which  are  in  all  likelihood  motor.  However  extensive 
the  destructive  processes  which  attack  other  parts  of  the  surface  of  the  brain,  pro- 
vided they  do  not  involve  these  particular  convolutions,  they  cause  no  paralytic 
symptoms  ;  while  all  diseases  which  destroy  any  considerable  portion  of  the 
"  motor  "  region  inevitably  result  in  a  paralysis  on  the  opposite  side  of  the  body. 

We  can  differentiate  still  further.  There  are  separate  regions  which  act  as 
special  centers  for  the  various  groups  of  muscles.  The  center  for  the  movements 
of  the  facial  muscles  (lower  division  of  the  facial  nerve)  lies,  as  it  would  seem,  at 
the  lower  end  of  the  central  convolutions,  and  particularly  of  the  anterior  central 
convolution.  Near  by,  apparently  still  lower,  is  found  the  center  for  the  move- 
ments of  the  tongue.      The  center  for  the  movements  of  the  arm  lies  somewhat, 


712 


DISEASES  OF  THE  NERVOUS  SYSTEM. 


higher  than  the  center  for  the  facial,  occupying  roughly  the  middle  portion  of  the 
anterior  central  convolution.  The  center  for  the  lower  extremity  is  found  partly 
in  the  uppermost  portions  of  the  central  convolutions,  hut  apparently  lies  for  the 
most  part  in  the  paracentral  lobule.     Any  minuter  division  is  not  yet  possible. 

There  are  already  quite  a  large  number  of  cases  of  hemiplegia  known  which 
were  caused  by  some  disease  in  the  motor  region,  like  a  tumor  or  spot  of  soften- 
ing. "We  should  add,  in  regard  to  the  pathological  anatomy  of  these  cases,  that 
they  all,  without  exception,  presented  a  secondary  descending  degeneration  of  tbe 
pyramidal  tract  (compare  page  680),  extending  through  the  internal  capsule,  crus 
cerebri,  and  medulla  into  the  corresponding  lateral  and  anterior  columns  [that  is, 
on  the  same  side  in  the  anterior  columns  and  on  the  opposite  side  in  the  lateral]. 
The  hemiplegia  due  to  cortical  lesion  does  not  differ  from  that  due  to  focal  disease 
lower  down  in  the  motor  tract  (compare  page  536)  in  its  clinical  aspects.  We  shall 
consider  the  symptoms  more  particularly  in  the  chapter  on  cerebral  haemorrhage. 


Fig.  101.— Lateral  aspect  of  the  brain  (from  Ecker).    The  gyri  and  lobules  are  in  Roman  type,  the  sulci 

and  fissures  in  italics. 


It  is  nevertheless  possible  in  many  instances  to  decide  that  the  disease  involves 
the  motor  portion  of  the  cortex  of  the  brain.  This  is  due  to  the  following  pecu- 
liarities : 

In  the  first  place,  we  have  already  remarked  (page  536)  that  the  relative  posi- 
tions of  the  motor  centers  for  the  face,  arm,  and  leg  are  such  as  to  allow  readily 
of  isolated  paralysis  of  any  one  of  these  portions  of  the  body — that  is,  "  mono- 
plegia." In  fact,  we  already  possess  a  long  series  of  observations  where  circum- 
scribed lesions  in  the  motor  area  of  the  cortex  produced  paralysis  of  one  side  of  the 
face,  or  of  one  arm  or  leg,  and  of  no  other  part.  Such  paralysis  is  termed  mono- 
plegia of  the  face,  or  the  arm,  or  the  lower  extremity.  And  it  follows,  from  what 
has  been  said,  that  even  during  life  we  can  state,  with  considerable  accuracy,  the 
spot  on  the  surface  of  the  brain  where  the  disease  must  be  situated.  Still  more 
frequently,  a  combined  paralysis  of  two  portions  of  the  body  is  to  be  observed  as  a 
result  of  cortical  lesion ;  the  commonest  is  a  simultaneous  paralysis  of  the  arm 


THE  LOCALIZATION   OF  CEREBRAL  DISEASES. 


713 


and  face;  more  rarely  we  see  the  arm  and  leg-  paralyzed  together.  On  the  other 
hand,  we  may  feel  certain,  from  the  position  of  the  motor  centers,  that  no  sing]'; 
center  of  disease  could  paralyze  simultaneously  the  leg  and  the  face,  while  the 
arm  escaped  injury.  As  a  matter  of  fact,  no  such  combination  has  ever  been 
observed. 


Fig.  102.— Lateral  aspect  of  the  brain  (after  Ecker).  The  motor  region  of  the  cortex,  consisting  of  the 
anterior  and  posterior  central  convolutions,  as  well  as  of  the  paracentral  lobule  shown  in  Fig.  103,  is 
shaded. 


Fig.  103.— Aspect  of  the  median  surface  of  the  cerebrum,  which  is  shown  when  the  two  hemispheres  are 
separated  from  each  other  by  a  sagittal  section.  B.  Corpus  callosum.  The  differences  in  the  type 
have  the  same  meaning  as  in  Fig.  101.  The  paracentral  lobule,  as  a  part  of  the  motor  region  of  'the 
cortex,  is  shaded.  (Copied  from  Ecker,  only  the  paracentral  lobule  is  made  more  sharply  prominent 
than  in  the  original). 

Beside  this  limitation  of  the  paralysis  just  discussed,  localized  disease  of  the 
cortex  has  another  characteristic.     In  it  the  symptoms  of  irritation  of  the  motor 


714 


DISEASES  OF  THE  NERVOUS  SYSTEM. 


centers  are  noticeably  frequent.  There  are  tonic  and  clonic  spasms,  which,  like 
the  paralysis,  not  infrequently  affect  a  single  arm,  or  an  arm  combined  with 
half  the  face.  Sometimes,  however,  they  involve  the  entire  half  of  the  body. 
These  paroxysmal  spasms  are  termed  "  cortical  epilepsy,"  or  partial  epilepsy,  or 
Jacksonian  epilepsy ;  for  the  movements  are  just  the  same  as  in  genuine  epilepsy. 
Numerous  cases  of  disease  have  taught  us  that  these  circumscribed  epileptiform 
attacks  occur  almost  exclusively  in  affections  of  the  motor  cortex.  They  furnish 
information  as  to  the  precise  locality  of  the  lesion ;  for  spasms  in  the  distribution 
of  the  facial  nerve  imply  that  mainly  the  lower  third  of  the  central  convolutions 
is  affected ;  of  the  arm,  the  middle  third ;  and  of  the  lower  extremity,  the  upper 
portions  of  the  same.  At  the  same  time,  the  spasms  and  the  paralysis  vary 
greatly  in  their  relations  to  each  other.  Often,  for  example,  when  there  is 
haemorrhage  into  the  central  convolutions,  violent  unilateral  convulsions  come 


Fig.  104.— (Drawn  according  to  Ecker.)  Explanation  of  the  topographical  relations  between  the  surface  of 
the  brain  and  the  skull,  c.  Fissure  of  Rolando.  HC.  and  VC.  Posterior  and  anterior  central  convolu- 
tions. S.  Si.  and  Su.  Fissure  of  Sylvius.  P1.  P2.  Upper  and  lower  parietal  lobes.  O.  Occipital  lobe. 
Cb.  Cerebellum.    T.  Temporal  lobe.    F.  Frontal  lobe. 

on  simultaneously  with  the  paralysis.  In  the  case  of  tumors  and  other  lesions 
which  develop  slowly,  partial  epileptiform  spasms  will  often  appear  quite  a  long 
while  before  there  are  symptoms  of  paralysis.  Finally,  it  is  not  rare  for  epilepti- 
form attacks  to  occur  repeatedly  in  regions  that  are  already  paralytic.  Either 
of  the  occurrences  described  in  the  two  preceding  sentences  are  particularly  strong 
evidence  that  the  cortex  cerebri  is  diseased.  Beside  the  pronounced  epileptic 
attacks,  disease  of  the  motor  region  of  the  cortex  may  give  rise  to  less  violent 
symptoms  of  motor  irritation,  like  occasional  twitching,  rhythmical  twitching, 
and  tonic  contraction. 

About  the  condition  of  sensation  when  there  is  cortical  paralysis  we  know  as 
yet  too  little.  The  late  experimental  researches  of  Munk  have  led  to  the  conclu- 
sion that,  in  animals,  the  so-called  "  sphere  of  sensation  "  lies  in  the  same  region 
as  the  motor  centers  of  the  cortex.  We  might,  therefore,  be  somewhat  inclined 
to  presuppose  that  a  disturbance  of  sensation  would  invariably  accompany  cortical 
paralysis  in  man  also,  but  about  this  point  clinical  observations  do  not  yet  give 
perfectly  harmonious  results.     In  many  cases  sensation  is  undoubtedly  normal, 


THE  LOCALIZATION  OF  CEREBRAL  DISEASES.  715 

while  in  others  simultaneous  disturbances  of  sensation  have  been  clearly  demon- 
strated. Of  especial  interest  is  the  well-attested  fact  tbat  the  muscular  sense  may- 
be diminished  in  the  extremities  involved — that  is,  the  patient  can  not  tell,  with 
eyes  closed,  the  position  of  the  affected  limbs. 

2.   The  other  Parts  of  the  Cortex  Cerebri,  except  the  Center  for 

Speech. 

1.  Frontal  Convolutions. — Unilateral  disease  of  the  anterior  portion  of  tbe 
brain  may  be  quite  extensive  without  causing  notable  disturbance  of  any  kind. 
Certainly  the  upper  two  frontal  convolutions  have  no  motor  functions.  It  is, 
however,  maintained  that  the  portion  contiguous  to  the  anterior  central  convolu- 
tion, called  the  foot  of  the  frontal  convolutions,  does  contain  motor  centers;  but 
even  about  this  doubt  has  lately  arisen.  The  third  (lowest)  frontal  convolution 
on  the  left  side  has,  as  we  shall  soon  see,  an  undoubted  connection  with  the  motor 
processes  of  speech. 

There  is  a  quite  generally  accepted  view  that  the  cortex  of  the  frontal  portion 
of  the  brain  is  to  be  regarded  as  the  "seat  of  the  higher  psychical  functions." 
Some  few  cases  are  on  record  where  extensive  bilateral  lesions  of  these  parts  had 
for  their  only  symptoms  mental  disturbances.  In  general  paralysis  also,  and  in 
other  forms  of  dementia,  it  is  veiy  probable  that  the  atrophy  is  greatest  in  the 
anterior  part  of  the  cerebrum.  Nevertheless,  we  can  not  emphasize  too  much  the 
fact  that,  at  present,  we  have  no  certain  knowledge  about  the  minute  relations  of 
the  psychical  functions  to  the  different  sections  of  the  brain. 

2.  Parietal  Convolutions. — We  know  practically  nothing  about  the  functions 
of  the  cortex  of  the  parietal  lobe,  and  the  symptoms  which  might  imply  disease  of 
that  portion  of  the  cerebrum.  The  results  of  clinical  observations  thus  far  made 
with  these  points  in  view  are  quite  contradictory.  In  regard  to  the  motor  func- 
tions of  the  parietal  region,  apart  from  the  posterior  central  gyrus,  we  know  only 
that  in  the  supra-marginal  and  angular  gyri  seem  to  lie  the  centers  for  associated 
conjugate  movements  of  the  eyes.  In  the  angular  gyrus  is  perhaps  also  a  center 
for  the  ocular  portion  of  the  facial  nerve,  orbicularis  oculi,  and  levator  palpebral 
superioris.  The  parietal  lobe  seems  to  have  important  relations  to  sensibility. 
According  to  Flechsig,  most  of  the  sensory  fibers  of  the  tegmentum  seem  to  have 
their  central  termination  here.  Disturbances  of  the  muscular  sense  seem  to  be 
especially  common  with  lesions  in  the  parietal  region. 

3.  Occipital  Convolutions. — The  clinical  and  experimental  investigations  of 
the  last  few  years  have  all  shown  that  the  occipital  portion  of  the  cerebrum  con- 
tains the  cortical  center  for  visual  sensations.  It  is  here,  in  all  probability,  that 
the  fibers  of  the  optic  nerve  terminate  in  the  cortex  cerebri.  A  glance  at  the  fol- 
lowing diagram  (Fig.  105)  will  make  it  easy  to  understand  the  disturbances  of 
vision  which  result  from  lesions  of  the  occipital  lobe.  L  represents  the  left  eye 
and  R  the  right,  Ch  the  optic  chiasma,  where,  as  is  now  certain,  some  of  the  fibers 
of  the  optic  nerves  cross  to  the  opposite  side.  The  fibers  (distinguished  by  a 
broken  line)  from  the  outer  or  temporal  half  of  each  retina  extend,  without  cross- 
ing, into  the  corresponding  optic  tract  (Tract,  opt.),  while  those  from  the  inner  or 
nasal  half  of  the  retina  cross  over  in  the  chiasma.  The  right  occipital  lobe,  for 
example,  comes  in  this  way  to  receive  the  fibers  from  the  outer  half  of  the  right 
retina  and  from  the  inner  half  of  the  left.  If  the  right  occipital  lobe  becomes 
disorganized,  then  the  images  formed  upon  the  parts  of  the  retinae  just  named,  be- 
longing to  the  left  half  of  the  field  of  vision,  are  unperceived.  With  each  eye 
the  patient  sees  only  such  objects  as  lie  in  the  right  half  of  his  field  of  vision,  and 
is  blind  to  all  that  lies  upon  his  left.     This  sort  of  visual  disturbance,  where  each 


IG 


DISEASES  OF  THE  NERVOUS  SYSTEM. 


eye  becomes  blind  to  the  same  "  homonymous  "  portions  of  the  field  of  vision,  is 
termed  hemianopsia,  or  hemiopia.     A  lesion  of  the  right  occipital  lobe  causes, 

therefore,  left-sided  hemiopia,  and,  vice  ver~ 
sa,  destruction  of  the  left  occipital  lobe  en- 
tails right-sided  hemiopia. 

It  may  also  be  well  to  mention  briefly 
another  peculiar  disturbance  of  vision  which 
is  perhaps  due  to  a  lesion  of  the  occipital 
cortex.  Fürstner  noticed  certain  phenom- 
ena in  the  insane,  which  implied  that  the 
patient,  although  he  could  see,  and  could 
not  therefore  properly  be  called  blind,  yet 
did  not  recognize  the  objects — that  is,  was 
no  longer  able  to  interpret  the  meaning  of 
the  visual  image.  Munk  has  given  to  this 
condition  the  name  of  "soul  blindness," 
conceiving  it  to  be  a  "  loss  of  visual  memo- 
ry." Soul  blindness  seems  to  occur  chiefly 
in  superficial  lesions  in  the  occipital  region, 
while  the  special  visual  center  itself  seems 
to  lie  chiefly  in  the  cuneus  and  the  first  occipital  convolution. 

4.  Temporal  Convolutions. — The  relation  of  the  temporal  lobe  to  hearing  is 
apparently  analogous  with  that  of  the  occipital  to  vision.  Whether  extensive 
disorganization  of  the  temporal  lobe,  or  of  the  fibers  that  enter  it,  can  produce 
actual  deafness  of  the  opposite  ear,  has  not  yet  been  proven,  inasmuch  as  very 
few  cases  have  yet  been  studied.  It  may,  however,  be  regarded  as  extremely 
probable  that  a  lesion  of  the  first,  or  uppermost,  temporal  convolution  occasions 
that  peculiar  phenomenon  known  as  "word  deafness  "or  "soul  deafness,"  with 
which  we  are  at  once  to  become  more  intimately  acquainted. 


105. — Diagram  of  the  course  of  the  optic 
fibers  in  the  chiasma. 


3.  The  Centers  of  Speech  and  the  Disturbances  op  Speech. 

(Aphasia  and  Allied  Conditions.) 

The  Various  Forms  of  Aphasia,  and  their  Anatomical  Localization.— As  -we 

remarked  at  the  very  beginning  of  this  chapter,  the  peculiar  derangements  of 
speech  observed  in  many  cerebral  diseases  were  the  first  symptoms  which  were 
found  to  be  caused  by  a  distinctly  localized  cerebral  lesion.  For  the  better  under- 
standing of  this  extremely  interesting  subject,  it  is  necessary  that  we  should  enter 
somewhat  minutely  into  the  processes  connected  with  normal  speech. 

Incitement  to  speech — that  is,  to  the  oral  expression  of  our  thoughts  to  others 
— comes  either  from  an  internal  impulse  or  from  external  causes  which  excite 
this  impulse.  Speech  always  requires  internal  mental  activities — the  presence  of 
ideas  and  their  transformation  into  that  which  we  wish  to  communicate  by 
speech.  Where  there  are  no  conceptions  there  can  be  no  words.  The  idiot  is 
silent,  because,  like  the  newborn  infant  or  the  brute,  he  has  nothing  to  say ;  but? 
on  the  other  hand,  the  impulse  to  speak  must  also  be  present.  In  melancholic 
insanity  we  sometimes  observe  persistent  loss  of  speech,  not  from  any  lack  of 
something  to  say,  but  because  there  is  no  incitement  to  the  act,  or  because  inhibi- 
tory influences  immediately  repress  any  tendency  to  utter  words.  If  we  take  for 
granted  that  the  mental  material  for  speech  exists,  then  the  transformation  of  this 
material  into  actual  speech  is  a  result  of  the  following  complicated  processes,  the 
disturbance  of  which,  individually,  produces  the  various  forms  of  aphasia. 

In  the  first  place,  the  speaker  must  be  acquainted  with  the  word  which  ex- 


THE  LOCALIZATION  OF  CEREBRAL  DISEASES.  717 

presses  the  mental  conception.  If,  for  instance,  he  wishes  to  tell  another  tlu: 
name  of  some  animal,  he  must  know  the  appropriate  word — "dog,"  "sparrow," 
"frog."  This  knowledge,  which,  as  far  as  our  mother  tongue  is  concerned,  we  all 
acquired  in  childhood,  may,  as  experience  shows,  he  lost  again  in  case  of  cerebral 
disease.  Just  as  we  may  ourselves  forget  a  word  momentarily,  or  as  any  healthy 
person  may,  at  the  sight  of  an  animal  that  is  perhaps  rather  rare,  he  "  unable  at 
the  minute  to  think  of  its  name,"  so  in  disease  one  may  forget  all  or  a  greater  or 
less  number  of  words.  Such  a  patient  sees  a  dog,  and  knows  well  enough  that  it 
is  an  animal  possessed  of  such  and  such  qualities,  but  he  has  forgotten  its  name. 
The  association  between  the  conception  "  dog,"  and  likewise  between  the  percep- 
tion of  a  clog  by  the  eye,  and  the  appropriate  vocal  representation  "  dog,"  is  lost. 
This  condition  is  termed  amnesic  aphasia,  because  it  is  due  to  complete  or  partial 
loss  of  the  memory  for  words.  The  patient  knows  perfectly  well  what  I.e  wishes 
to  say,  but  the  words  escape  him.  At  the  same  time,  in  cases  of  pure  amnesic 
aphasia,  the  power  of  repetition  is  unimpaired.  As  soon  as  we  say  "  dog  "  to  the 
patient,  he  repeats  the  word  perfectly  well  ;  and  sometimes  he  also  perceives 
that  this  is  really  the  correct  word;  but  in  other  instances,  although  the  word  is 
correctly  repeated,  the  patient  does  not  become  conscious  of  its  meaning  {vide 
infra  "  word  deafness  "). 

Of  great  interest  are  certain  cases  where  there  is  only  partial  amnesia.  These 
have  been  repeatedly  observed.  Thus  a  patient  forgot  nothing  but  his  own  name, 
remembering  all  other  words  perfectly ;  or  the  loss  of  words  may  be  confined  to 
but  one  language,  the  patient  being  still  able  to  express  himself  tolerably  well  in 
another  tongue.  In  a  case  observed  by  Graves,  the  patient  still  knew  the  initial 
letter  of  all  words ;  if,  for  example,  he  saw  a  cow,  he  would  know  that  the  corre- 
sponding word  began  with  C,  and  would  look  under  C  in  a  dictionary  till  he 
found  the  word. 

If  the  memory  for  words  be  retained,  the  next  requisite  for  speaking  is  the 
transfer  of  the  word  image  into  such  action  of  the  muscles  of  our  organs  of  speech 
as  is  calculated  to  produce  the  word  in  question  as  an  actual  sound.  This  motor 
process  is  so  complicated  that  an  extremely  accurate  co-ordination  of  movements 
is  demanded  for  the  correct  pronunciation  of  the  word.  Man  therefore  possesses 
a  separate  center,  in  which  this  transfer  of  the  word  image  into  the  motor  pro- 
cesses of  speech  takes  place.  If  this  center  be  diseased,  there  again  results  a  loss, 
or  at  least  a  greater  or  less  impairment,  of  speech.  The  patient  is  in  this  case  well 
aware  of  the  word  he  wishes  to  say,  but  he  can  not  pronounce  it.  He  has,  if  we 
may  use  the  expression,  forgotten  the  movements  that  are  essential  to  speaking. 
His  tongue  and  lips  are  not  really  paralyzed,  but  the  patient  no  longer  knows  how 
to  make  use  of  them  for  talking.  He  has  reverted  to  the  condition  of  childhood, 
before  he  had  learned  to  talk.  The  patient  often  makes  the  greatest  effort  to 
speak.  The  word  he  wishes  to  utter  "  keeps  hovering  before  him  " ;  he  moves  his 
mouth  in  the  most  striking  manner,  but  brings  out  only  an  occasional  sound,  and 
that  incorrect.  This  form  is  known  as  ataxic  aphasia.  Of  course  it  is  equally 
impossible  for  the  patient  to  repeat  a  word  after  some  one  else.  He  keeps  his  eyes 
fixed  on  the  mouth  of  the  speaker,  and  endeavors  to  imitate  the  motions  of  his 
mouth,  but  he  is  either  partially  or  totally  unable  to  reproduce  the  sound. 

Ataxic  aphasia  exhibits  many  degrees  of  intensity.  On  the  one  hand  there  are 
cases  of  complete  aphasia,  where  the  patient  can  utter  only  such  separate  sounds 
as  "  a."  "e,"  etc.  And,  on  the  other  hand,  there  are  also  very  mild  cases  where 
there  are  merely  slight  errors  in  pronunciation.  The  patient  pronounces  many 
words  correctly,  but  with  others  there  are  such  mistakes  as  the  transposition  of 
individual  letters,  the  misplacement  or  omission  of  letters,  or,  finally,  the  adding 
on  of  letters.     For  example,  he  will  say  thens  instead  of  then,  widow  instead  of 


718  DISEASES  OF  THE  NERVOUS  SYSTEM. 

window,  dipter  instead  of  dipper,  hefd  instead  of  held,  wrelster  instead  of  wrest- 
ler and  belnow  instead  of  below.  This  mildest  form  of  ataxic  disturbance  is 
termed  "  stumbling  over  syllables  "  (Silbernstolpern),  or  "  literal  ataxia."  In  most 
instances  the  patient  can  pronounce  some  words  tolerably  well,  others  only  imper- 
fectly and  with  difficulty,  and  still  others  not  at  all.  Usually  the  patient  gradu- 
ally learns  a  few  common  words  and  expressions  (e.  g.,  "  good  morning")  by 
means  of  persistence  in  repeating  them  as  they  are  uttered  by  another,  so  that  he 
pronounces  them  better  and  better.  What  is  very  remarkable,  and  not  so  very 
rare,  is  that  a  patient  will  be  able  when  in  a  passion  to  pronounce  a  word,  such  as 
an  oath  or  an  exclamation,  perfectly  well,  because  it  is  done  to  a  certain  extent 
involuntarily,  while  he  can  not  utter  the  same  words  if  he  wishes  to  say  them. 
Association  also  often  exerts  an  appreciable  influence ;  for  example,  a  patient  who 
finds  it  absolutely  impossible  to  pronounce  "  six,"  utters  it  with  perfect  distinct- 
ness if  he  begins  to  count  from  one,  in  the  ordinary  way,  up  to  six.  There  are 
many  facts  connected  with  this  subject  which  can  not  here  be  discussed.  Each 
case  demands  separate  and  earnest  study,  and  will  usually  be  found  to  present  an 
abundance  of  interesting  peculiarities. 

Allied  to  ataxic  aphasia  are  two  other  disturbances  of  speech,  known  as  mono- 
phasia  and  paraphasia.  Monophasia  is  very  rare ;  in  it  the  patient  has  command 
of  but  one  single  syllable,  or  a  single  short  phrase,  and  this  is  pronounced  when- 
ever he  attempts  to  talk.  A  patient  of  our  own  could  for  a  long  while  utter  noth- 
ing but  meaningless  words,  "  selber  sag  ich  nämlich  selber  "  (self  say  I  namely 
self).  The  entire  verbal  thesaurus  of  another  (female)  patient  whom  we  saw  con- 
sisted of  the  meaningless  sounds  "bibi"  and  "eibibi."  Still  a  third  could  say 
only  "tinne,  tinne."  The  patient  is  quite  well  aware  that  what  he  says  is  wrong, 
but,  despite  all  his  efforts,  every  attempt  to  speak  excites  these  same  sounds.  It 
produces  a  comical  impression  to  see  the  patient  use  the  same  invariable  word, 
with  all  sorts  of  facial  expression.  Thus  the  woman  mentioned  above  begged  for 
things,  with  "  bibi,"  in  a  coaxing  tone,  while  sometimes  she  would  give  vent  to 
violent  anger  with  a  loud  "  bibibibi." 

Paraphasia  is  a  confounding  together  of  words.  The  association  between  the 
idea  and  the  corresponding  word  is  broken  up,  and  instead  other  words  come  to 
the  tongue.  Some  of  these  are  proper  words  enough,  but  others  are  quite  mean- 
ingless. Such  a  patient  may  talk  a  long  while  without  conveying  any  idea  to  the 
listener,  inasmuch  as  he  says  "brush"  instead  of  "bed,"  or  "gove"  instead  of 
"  give,"  etc.  It  is  a  very  interesting  fact  that  in  paraphasia  the  influence  of  cer- 
tain associations  are  often  manifest.  The  patient,  for  instance,  utters  a  wrong 
word  which  has  a  certain  resemblance  in  sound  to  the  right  one,  begins  with  the 
same  syllable,  etc.  Purely  ideal  associations  sometimes  also  play  a  part ;  thus  one 
of  our  patients  called  a  white  handkerchief  "  snow,"  etc. 

As  has  been  already  shown,  in  amnesic  aphasia  the  connection  between  the 
word  and  the  conception  it  represents  is  so  imperfect  that  the  rising  up  to  con- 
sciousness of  the  idea  fails  to  call  up  the  corresponding  word.  Now,  on  the  other 
hand,  the  opposite  may  occur;  the  word,  when  it  is  heard,  may  fail  to  call  up  the 
appropriate  mental  image.  Kussmaul  has  given  this  condition  the  name  of  word 
deafness  (Wernicke's  sensoiy  aphasia).  The  patient  is  not  really  deaf,  for  he  hears 
everything,  but  he  no  longer  understands  what  he  hears,  and  he  has  forgotten 
what  the  words  signify.  The  vernacular  sounds  to  him  as  a  foreign  tongue  would 
to  a  healthy  but  unlearned  man.  A  moderate  amount  of  word  deafness  is  very 
frequent  in  aphasia,  particularly  in  the  amnesic  variety ;  but  this  last,  and  word 
dumbness,  are  not  identical.  A  person  may  forget  the  word  corresponding  to  some 
idea  and  yet  understand  the  meaning  of  that  wox*d  perfectly  when  he  hears  it. 
It  is  an  easy  matter  to  prove  whether  word  dumbness  exists  or  not  by  asking  the 


THE  LOCALIZATION  OF  CEREBRAL  DISEASES.  719 

patient  to  do.something — for  example,  to  touch  certain  parts  of  his  body,  or  to 
perform  certain  motions  (without,  however,  making  any  explanatory  gestures  our- 
selves), and  seeing  whether  he  understands  and  complies.  Of  course,  the  demon- 
stration of  word  deafness  can  usually  be  made  with  regard  to  the  names  of  con- 
crete things  only,  and  certain  verbs  and  adjectives,  but  is  hardly  practicable  in 
other  cases  (for  example,  with  abstract  words  and  adverbs),  particularly  if  there  be 
aphasia  at  the  same  time. 

These  various  forms  of  aphasia,  just  described,  seldom  occur  singly  and 
unmixed.  They  are  usually  found  in  combinations,  which  vary  greatly,  so  that 
a  complete  idea  of  the  derangement  existing  in  any  case  can  be  obtained  only  by 
careful  examination  and  continued  observation  of  the  patient.  Granting,  how- 
ever, that  the  variety  of  aphasia  has  been  determined,  what  light  will  this  throw 
upon  the  localization  of  the  cerebral  disease? 

As  early  as  1825  Bouillaud  affirmed  that  disease  of  the  anterior  lobes  of  the 
brain  is  alone  capable  of  producing  disturbances  of  speech.  In  1836  another 
French  physician,  Marc  Dax,  pointed  out  for  the  first  time  that  only  lesions  of  the 
left  half  of  the  brain  cause  aphasia ;  and  in  1861  Broca  was  able,  as  already  stated, 
at  last  to  declare  that  the  "  center  for  speech  "  lies  in  the  third  left  frontal  convo- 
lution. This  statement  has  since  been  confirmed  innumerable  times,  although  it 
must  be  added  that  disease  here  is  a  cause  of  ataxic  or  motor  aphasia  alone.  Still 
more  accurately,  it  is  the  posterior  portion  of  the  third  left  frontal  convolution,  the 
pars  opercularis,  so  called,  which  gives  rise  to  this  symptom.  It  is  in  this  region, 
therefore,  that  those  complicated  processes  of  motor  co-ordination  which  are  essen- 
tial to  the  utterance  of  a  word  take  place.  Word  deafness,  on  the  other  hand, 
according  to  all  the  newer  observations  of  Wernicke,  Kahler,  and  Pick,  seems 
invariably  to  be  referable  to  disease  of  the  first  or  uppermost  left  temporal  convo- 
lution. Probably  the  same  is  true  of  amnesic  aphasia.  It  is  apparently,  then,  this 
region  which  is  essential  to  the  normal  association  between  the  auditory  image  of 
the  words  we  hear  and  the  appropriate  mental  conceptions.  Any  minuter  local- 
ization of  these  and  the  remaining  forms  of  disturbance  of  speech  is  at  present 
impossible.  It  is  probable,  though  not  certain,  that  the  left  island  of  Reil  also 
has  some  connection  with  aphasic  disorders.  However  this  may  be,  the  corre- 
sponding portions  of  the  right  hemisphere  are  not  usually  connected  with  this 
sort  of  disturbance — a  fact  perhaps  analogous  with  the  predominant  use  of  the 
right  hand ;  that  is,  of  the  left  cerebral  hemisphere.  It  is  only  in  a  few  exceptional 
cases— for  example,  of  left-handed  persons,  or  of  such  as  present  congenital  defects 
in  the  left  half  of  the  brain— that  observers  have  noticed  aphasia  in  connection  with 
disease  of  the  corresponding  frontal  and  temporal  convolutions  of  the  right  side. 

The  diagnosis  of  aphasia  in  general  is  an  easy  matter  if  we  stick  closely  to  the 
true  conception  of  aphasia.  The  examination  would  have  to  be  a  superficial  one 
to  lead  to  confounding  it  with  bulbar  symptoms  such  as  dysarthria  (vide  supra, 
page  685),  or  with  the  disturbances  of  speech  which  result  from  other  lesions  which 
entail  paresis  or  paralysis  of  the  hypoglossus  or  certain  fibers  of  the  facial. 

No  general  rules  can  be  laid  down  as  to  the  prognosis  and  treatment  of  aphasia, 
inasmuch  as  everything  must  of  course  depend  upon  the  nature  of  the  disease 
which  excites  this  symptom.  We  will  merely  emphasize  here  the  therapeutic  fact 
that  methodical  exercises  in  speaking  and  in  language  may  be  decidedly  beneficial. 
In  ataxic  aphasia  such  instruction  may  be  imparted  in  about  the  same  way  as  to 
the  deaf  and  dumb,  sight  and  touch  being  invoked  to  aid  in  a  fresh  training  of  the 
appropriate  muscles.  In  amnesic  aphasia  the  memory  must  be  trained,  that  the 
forgotten  words  may  once  more  be  "  stamped  "  upon  it.  Of  course,  all  such  efforts 
demand  great  tact  and  patience,  and  accomplish  little  unless  they  are  methodical 
and  persistent. 


720  DISEASES  OF  THE  NERVOUS  SYSTEM. 

Disturbances  Allied  to  Aphasia :  Agraphia,  Alexia,  Amimia,  and  Apraxia. — 

Aphasia  is  very  often  accompanied  by  a  group  of  other  symptoms,  which  are  like- 
wise due  to  disturbance  of  the  processes  of  association.  Besides  the  language  of 
words  we  possess  two  other  means  of  expression — writing  and  gesticulation.  Our 
mental  concepts  are  associated  not  only  with  certain  sounds  but  also  with  certain 
visible  forms,  so  that,  on  the  one  hand,  we  use  them  to  impart  our  thoughts  to 
others,  and,  on  the  other,  by  their  aid  we  learn  the  thoughts  of  other  people.  In 
aphasia  this  capability  also  is  often  more  or  less  lost.  If  it  be  impossible  for  the 
patient  to  make  himself  understood  by  means  of  words,  and  we  give  him  a  pen, 
that  he  may  write  down  his  wishes,  it  is  often  found  that  this,  too,  is  out  of  the 
question.  The  patient  tries  to  write,  and  may  indeed  set  down  one  or  two  words, 
or  one  or  two  letters,  but  he  is  no  longer  capable  of  writing  a  single  sentence,  or 
perhaps  even  a  single  word,  correctly.  This  is  termed  "agraphia."  Probably,  in 
most  instances,  the  agraphia  is  amnesic.  The  patient  has  forgotten  the  written 
characters.  Usually,  although  not  in  every  case,  he  can  copy  correctly  what 
another  has  written.  When  the  patient  writes  a  wrong  word  in  place  of  the  right 
one,  we  call  it  paragraphia.  Here,  too,  processes  of  mental  association  become 
manifest  as  in  paraphasia  (vide  supra).  With  the  disturbance  in  writing  is  often 
associated  alexia;  the  patient  can  not  read  any  better  than  he  can  write — that 
is,  the  characters  which  he  sees  fail  now  to  call  up  the  associated  mental  con- 
ception. Alexia  is  not  inseparably  connected  with  word  deafness.  It  is  possible 
for  a  patient  not  to  understand  a  spoken  word,  and  yet  to  recognize  it  at  once  if 
written. 

The  aphasic  are  also  quite  often  unable  to  express  themselves  by  pantomime  or 
"dumb  show."  Frequently  the  patient  makes  no  effort  whatever  of  this  kind,  or 
what  signs  he  does  make  are  evidently  wrong  and  misleading.  We  have  repeat- 
edly seen  an  aphasic  patient  nod  his  head,  when  it  was  plain  that  he  meant  to  say 
No,  and  vice  versa. 

Finally,  there  is  apraxia,  a  disturbance  which,  to  be  sure,  is  often  associated 
with  aphasia,  but  implies  more  extensive  lesions.  The  essential  point  in  apraxia 
is  that  the  patient  has  more  or  less  completely  forgotten  what  the  different  objects 
about  him  really  are.  The  condition  must  be  closely  allied  to  that  in  so-called 
"soul  blindness."  The  patient  sees  the  objects,  but  fails  to  recognize  them  for 
what  they  are.  He  takes  a  knife  for  a  spoon,  the  washbowl  for  the  chamber-pot, 
the  soap  for  a  piece  of  bread,  and  acts  accordingly ! 

A  definite  anatomical  localization  of  all  these  disorders  which  have  just  been 
briefly  alluded  to  can  not  at  present  be  given.  Alexia,  and  still  more  apraxia, 
suggest  lesion  of  those  tracts  which  are  connected  with,  or  situated  in,  the  posterior 
part  of  the  cerebrum,  the  region  of  memory  for  visible  objects. 

•i.  The  Centrum  Ovale,  Internal  Capsule,  Central  Ganglia,  and  Region 
of  the  Corpora  Quadrigemina. 

Centrum  Ovale. — The  white  substance  of  the  hemispheres  is  made  up,  so  far 
as  we  know  at  present,  both  of  commissural  fibers,  which  connect  the  various 
cortical  centers  together,  and  of  fibers  which  proceed  downward  from  the  centers 
of  the  cortex  and  connect  these  centers  with  pei'ipheral  parts  of  the  body  (corona 
radiata).  As  to  the  symptoms  caused  by  diseases  which  destroy  the  commissural 
fibers,  there  is  hardly  anything  known.  We  can  only  surmise  that  in  case  of 
disturbances  of  association,  such  as  we  have  studied  under  aphasia  and  kindred 
disorders,  there  may  sometimes  be  a  lesion  of  commissural  fibers,  as  of  those  con- 
necting together  the  temporal  and  frontal  lobes.  A  break  in  the  continuity  of 
the  fibers  of  the  corona  radiata  must  of  course  result  in  the  same  symptoms  as  if 


THE  LOCALIZATION  OF  CEREBRAL  DISEASES.  721 

the  corresponding  center  were  itself  destroyed.  This  explains  why  circumscribed 
lesions  of  the  centrum  ovale,  if  they  involve  the  motor  fibers  of  the  corona  radi- 
ata,  which  proceed  from  the  central  convolutions  (and  only  if  they  do  this;,  cause 
hemiplegia,  or,  if  very  limited,  monoplegia.  In  an  analogous  manner,  disease  of 
the  white  substance  of  the  occipital  lobe  may  entail  hemiopia;  of  the  temporal 
lobe,  auditory  disturbances,  such  as  word  deafness.  More  than  once,  quite  exten- 
sive disease  of  the  white  substance  of  the  frontal  lobe  on  one  side  has  been  discov- 
ered post  mortem,  although  no  symptoms  whatever  had  been  caused  by  it.  Only 
when  the  coronal  fibers  which  proceed  from  the  third  left  frontal  convolution  are 
involved  in  disease  is  motor  or  ataxic  aphasia  inevitable. 

Internal  Capsule. — The  most  important  facts  relating  to  the  functions  of  the 
internal  capsule,  as  far  as  at  present  known,  have  been  already  stated.  In  par- 
ticular, it  was  pointed  out  that  through  the  posterior  limb  of  the  internal  capsule, 
in  a  comparatively  narrow  space,  passes  the  pyramidal  tract  on  its  way  from  the 
central  convolutions  to  the  crura  cerebri  (see  Fig.  64,  page  534).  Here,  then,  even 
a  very  limited  focal  disease  must  lead  to  complete  hemiplegia  on  the  opposite  side 
of  the  body.  Clinical  experience  also  shows  that  the  largest  number  of  cases  of 
persistent  hemiplegia  are  occasioned  by  disease  in  this  spot.  In  these  cases  the 
facial  nerve  is  usually  also  involved,  although  its  fibers  apparently  lie  somewhat 
further  forward  than  the  tracts  which  are  destined  for  the  extremities. 

The  sensory  tract  (compare  page  511,  and  Fig.  64,  page  534)  lies  at  the  posterior 
extremity  of  the  internal  capsule,  and  apparently  includes  not  only  the  fibers  for 
cutaneous  sensation,  but  also  for  the  organs  of  special  sense.  Complete  disorgan- 
ization of  this  spot  ought  therefore  to  cause,  in  the  opposite  half  of  the  body,  not 
only  anaesthesia  of  the  skin,  but  also  simultaneously  a  corresponding  impairment 
of  smell,  taste,  and  hearing,  and  hemiopia — in  short,  a  so-called  complete  cere- 
bral hemianEesthesia.  Still,  in  regard  to  this  very  point  we  are  much  in  need  of 
further  and  definite  observations.  Charcot's  statement  that  in  these  cases  the 
disturbance  of  vision  is  not  hemiopia,  but  total  amblyopia  of  the  eye  opposite  to 
the  focal  lesion,  has  caused  great  confusion,  for  such  a  fact  would  of  course  be 
hard  to  reconcile  with  the  appearance  of  hemiopia  in  diseases  of  the  occipital  lobe, 
although  this  latter  occurrence  is  well  established.  However,  this  statement  of 
Charcot's  is  by  no  means  absolutely  proven,  so  that  meanwhile  we  are  at  liberty 
to  maintain  the  view  that  the  visual  disturbance  in  cerebral  hemianEesthesia  may 
be  hemiopia. 

Certain  practical  conclusions  in  regard  to  diagnosis  can  be  deduced  from  the 
preceding  facts.  A  purely  motor  hemiplegia,  unattended  by  impairment  of  sensa- 
tion, implies  a  lesion  that  does  not  involve  the  posterior  portion  of  the  internal 
capsule ;  but  probably  this  portion  is  also  affected,  when  there  is  not  only  paraly- 
sis, but  considerable  sensory  disturbance.  The  sensory  disturbance  does  not  in- 
variably extend  to  all  the  senses  ;  quite  often  there  is  nothing  but  cutaneous 
anaesthesia. 

About  the  importance  of  the  other  parts  of  the  internal  capsule,  not  mentioned 
here,  nothing  is  known.  A  statement  made  by  Charcot  should  be  added  in  con- 
clusion— namely,  that  when  there  are  also  post-hemiplegic  symptoms  of  irritation, 
such  as  post-hemiplegic  chorea,  there  is  very  probably  a  lesion  of  the  posterior 
extremity  of  the  internal  capsule. 

Central  Ganglia;  Caudate  Nucleus  (Corpus  Striatum  proper),  Lenticular 
Nucleus,  and  Optic  Thalamus. — Before  the  course  of  the  pyramidal  tract  had  been 
accurately  determined,  ordinary  cases  of  cerebral  hemiplegia  were  almost  uni- 
versally ascribed  to  lesions  of  the  central  ganglia,  and  in  particiliar  of  the  caudate 
and  lenticular  nuclei.  At  present,  however,  observations  seem  to  force  one  to  the 
conclusion  that  a  complete  hemiplegia  can  be  produced  only  by  a  cutting  off  of 
46 


722  DISEASES  OF  THE  NERVOUS  SYSTEM. 

the  pyramidal  tract.  There  are,  indeed,  numerous  cases  of  hemiplegia  presenting 
circumscribed  disease  of  the  central  ganglia ;  but  they  can  probably  all  be  ex- 
plained by  supposing  either  that  the  pyramidal  tract,  as  it  lies  in  the  contiguous 
internal  capsule,  is  directly  involved  in  the  disease,  or  that  its  functions  are  sus- 
pended by  the  indirect  effects  of  the  neighboring  lesion — for  instance,  by  the 
pressure  it  exercises.  Accordingly,  we  find  that  circumscribed  lesions  of  the 
central  ganglia  in  the  neighborhood  of  the  internal  capsule  generally  produce  a 
temporary  hemiplegia — that  is,  the  paralysis  gradually  improves  as  the  indirect 
influence  of  the  focal  disease  upon  the  internal  capsule  ceases.  Chronic  and  in- 
curable hemiplegia,  however,  if  due  to  a  lesion  anywhere  in  this  region,  always 
implies  an  actual  lesion  of  the  pyramidal  tract  in  the  internal  capsule.  In  regard 
to  hemianaesthesia,  also,  the  facts  seem  to  be  quite  analogous.  It  was  formerly 
held  that  this  phenomenon  was  especially  connected  with  a  lesion  of  the  optic 
thalamus,  the  reason  being  that  the  sensitive  fibers  lie  so  close  to  the  thalamus 
in  the  posterior  extremity  of  the  internal  capsule  that  they  become  themselves 
involved. 

About  the  symptoms  which  lesions  of  the  central  ganglia  directly  produce 
little  is  definitely  known.  The  results  of  both  clinical  observation  and  experiment 
are  quite  contradictory,  and  in  repeated  instances  quite  extensive  disorganization 
of  these  parts  has  existed  without  producing  any  symptoms  to  speak  of  during  life. 
In  particular,  it  should  be  borne  in  mind  that  softening  may  occur  in  the  lenticu- 
lar and  caudate  nuclei,  and  yet  not  a  trace  of  hemiplegia  be  observable.  It  seems 
probable  also  that  the  optic  thalamus  has  nothing  to  do  with  voluntary  motion ; 
but  it  seems  to  have  some  importance  for  movements  of  mimetic  expression  (Bech- 
terew, Nothnagel).  In  hemiplegics  we  sometimes  see  that  one  half  of  the  face 
can  not  be  moved  voluntarily,  but  it  is  moved  very  actively  in  emotional  expres- 
sion, such  as  laughing  or  crying.  In  such  cases  we  can  decide  that  the  thalamus 
is  intact,  while  in  lesion  of  the  thalamus  the  contrary  is  observed — the  affected 
half  of  the  face  can  be  moved  voluntarily,  but  it  remains  completely  rigid  in 
emotional  expression.  As  to  perceptive  functions,  there  is  only  one  which  the 
optic  thalamus  is  certainly  known  to  possess:  the  central  termination  of  some 
fibers  of  the  optic  nerve  lies  in  its  posterior  portion  (known  as  the  posterior 
tubercle  or  pulvinar),  while  other  fibers  go  to  the  corpus  geniculatum  externum. 
Destruction  of  the  hinder  part  of  the  thalamus  accordingly  produces  complete 
hemiopia  (vide  page  716)  of  the  opposite  side.  It  has  been  affirmed  that  the  optic 
thalamus  has  connections  with  other  sensory  tracts,  but  definite  proof  is  lacking. 
Focal  disease  of  the  thalamus  has  repeatedly  occasioned  "  post-hemiplegic  chorea  " 
and  other  post-hemiplegic  symptoms  of  irritation.  According  to  recent  experi- 
ments, the  lenticular  nucleus  contains  centers  for  regulating  heat. 

Corpora  Quadrigemina  and  Crura  Cerebri. — Diseases  of  the  corpora  quadri- 
*  gemina  are  infrequent,  and  usually,  when  they  do  occur,  they  are  merely  a  part 
of  more  extensive  lesions  of  the  brain.  They  are  therefore  very  rarely  considered 
from  a  diagnostic  point  of  view. 

The  anterior  tubercles  are  certainly  connected  with  the  fibers  of  the  optic  nerve. 
If  both  of  the  anterior  tubercles  be  destroyed,  total  blindness  is  inevitable,  while 
if  only  one  be  disorganized,  hemiopia  is  to  be  anticipated.  Still,  these  symptoms 
are,  of  course,  too  ambiguous  ever  to  be  regarded  as  pathognomonic  of  localized 
disease  of  the  anterior  corpora  quadrigemina.  Another  point  to  be  considered, 
whenever  the  corpora  quadrigemina  are  diseased,  is  the  position  of  the  nuclei  of 
the  nerves  which  preside  over  the  motions  of  the  eyeball,  and  in  particular  of  the 
oculomotor  nerve.  This  explains  why  unilateral,  or  even  bilateral,  paralysis  of 
the  oculomotorius  has  been  repeatedly  observed  in  connection  with  lesions  of  the 
corpora  quadrigemina,  as  have  also  nystagmus  and  immobility  of   the  pupil. 


THE  LOCALIZATION  OF  CEREBRAL  DISEASES.  723 

[Nothnagel  considers  that  a  staggering1  gait,  resemhling  that  of  a  drunken  man, 
associated  with  oculomotor  paralysis,  if  associated  with  general  symptoms  of 
tumor,  is  strongly  indicative  of  tumor  of  the  corpora  quadrigemina.  The  eye 
paralysis  must,  however,  be  an  early  symptom  in  order  to  be  of  value.  The 
paralysis  in  such  cases  is  apt  to  be  of  irregular  distribution,  often  involving  up- 
ward and  downward  movements  of  the  eye. — K.] 

Should  the  crura  cerebri  become  involved  in  the  disease,  the  resulting  symptoms 
are  often  very  characteristic  of  the  locality  affected;  there  is  paralysis  of  one  side 
of  the  body  (arm,  leg,  facial  nerve),  and  at  the  same  time  a  crossed  paralysis  (that 
is,  one  situated  upon  the  opposite  side)  of  the  motor  oculi.  A  glance  at  Fig.  65 
(page  535)  will  explain  this  phenomenon.  Thus,  a  circumscribed  lesion  on  the 
right  side  would  destroy  the  fibers  of  the  third  nerve  on  that  side,  and  therefore 
produce  a  right-sided  paralysis  of  the  oculomotor  nerves,  and  at  the  same  time,  if 
extensive  enough,  the  lesion  would  involve  the  pyramidal  fibers  of  the  right  crus, 
and  thus  occasion  left  hemiplegia.  That  disease  of  the  tegmentum  would  neces- 
sarily entail  sensory  disturbances  may  be  taken  for  granted,  although  there  is  as 
yet  very  little  clinical  proof  of  it. 

5.    The  Cerebellum. 

Quite  extensive  destruction  of  the  cerebellum  may  take  place  without  any 
symptoms  to  indicate  it.  In  such  cases,  however,  the  disease  is  almost  invariably 
confined  to  the  hemispheres ;  but,  if  the  central  portion  or  vermiform  appendix  be 
attacked  to  any  great  extent,  peculiar  symptoms  almost  always  result,  pointing  in 
many  instances  with  considerable  certainty  to  disease  of  the  cerebellum. 

There  are  two  especially  characteristic  symptoms — a  peculiar  uncertainty  of 
gait  (cerebellar  ataxia),  and  troublesome  vertigo. 

Cerebellar  ataxia  affects  only  the  trunk  and  lower  extremities.  Both  standing 
and  locomotion  are  interfered  with.  When  the  patient  is  lying  in  bed  he  can 
move  his  legs  almost  as  well  as  ever,  and  with  normal  vigor;  but  as  soon  as  he 
gets  up,  the  characteristic  motor  disturbances  become  very  evident.  Even  while 
standing  still  the  whole  body  can  usually  be  plainly  seen  to  sway  back  and  forth. 
This  becomes  more  marked  if  the  patient  bring  his  heels  together.  If  he  stand 
with  his  legs  widely  apart,  the  trouble  is  less  noticeable.  Closing  the  eyes,  as  a 
rule,  does  not  aggravate  the  swaying,  inasmuch  as  the  cutaneous  and  muscular 
sensibility  of  the  lower  limbs  remains  normal  in  uncomplicated  cerebellar  disease. 
When  the  patient  tries  to  walk,  he  sways  and  totters,  precisely  as  if  he  were  deeply 
intoxicated,  but  usually  in  a  very  different  way  from  that  seen  in  tabes  dorsalis. 
Instead  of  the  uniform  stamping  and  pitching  gait  of  the  latter,  cerebellar  ataxia 
causes  a  real  staggering  of  the  whole  body,  so  that  in  severe  cases  the  patient  loses 
entirely  the  ability  to  walk  straight,  but  seems  to  fall  forward,  as  it  were,  in  a  zig- 
zag line,  now  to  the  right  and  now  to  the  left.  Sometimes,  but  by  no  means  inva- 
riably, it  is  noticed  that,  in  walking,  the  body  sways  principally  in  one  particular 
direction,  either  forward  or  backward,  or  to  one  side.  Such  peculiarities,  however, 
do  not  enable  us,  with  our  present  knowledge,  to  determine  with  certainty  just 
what  position  in  the  cerebellum  the  lesion  occupies.  The  most  we  can  do  is  to 
surmise,  in  such  a  case,  that  the  middle  peduncles  of  the  cerebellum  (vide  infra) 
are  involved.  It  is  worthy  of  note  that,  with  few  exceptions,  the  ataxia  does  not 
involve  the  upper  extremities.  Many  a  patient  who  can  scarcely  walk  unaided  is 
still  able  to  perform  the  most  delicate  manipulations  with  his  hands.  This  shows 
that  it  is  only  in  maintaining  the  bodily  equilibrium — essential  to  standing  and 
locomotion — that  the  function  of  the  cerebellum  is  important. 

As  already  stated,  this  cerebellar  ataxia  is  in  most  cases  attended  with  pro- 


724  DISEASES  OF  THE  NERVOUS  SYSTEM. 

nounced  vertigo.  Therj  is  not,  however,  a  complete  correspondence  between  the 
locomotor  disturbance  and  the  dizziness.  Exceptionally  one  symptom  may  be 
present  without  the  other.  The  vertigo  is  usually  felt  only  when  the  patient 
stands  or  moves  about,  being  almost  always  absent  when  he  lies  quietly  in  bed. 
We  are  as  yet  ignorant  just  how  it  is  produced.  Vertigo  is  quite  frequently  pro- 
duced by  other  cerebral  diseases.  It  can  not,  therefore,  be  regarded  as  indicating 
disease  of  the  cerebellum  unless  it  is  very  persistent  and  decided,  and  is  associated 
with  the  characteristic  cerebellar  gait. 

Little  is  known  about  other  symptoms  of  disease  in  the  cerebellum.  There 
may  be  some  diagnostic  value  in  persistent  occipital  headache,  particularly  if 
other  cerebellar  symptoms  be  present.  If  they  do  not  exist,  the  headache  is  too 
ambiguous  to  be  of  much  value ;  and,  besides,  an  affection  of  the  cerebellum  may 
exceptionally  be  attended  by  pain  in  the  side  of  the  head  or  in  the  forehead.  Vom- 
iting is  of  still  less  value.  It  is,  to  be  sure,  frequently  occasioned  by  chronic 
disorders  of  the  cerebellum,  and  by  tumors  in  particular,  but  may  be  equally  well 
the  result  of  disease  elsewhere.  Tumors  of  the  cerebellum  are  very  apt  to  cause 
disturbances  of  vision;  but  it  is  certain  that  these  are  not  a  direct  result  of  the 
cerebellar  lesion,  but  are  occasioned  by  the  development  of  a  choked  disk  (vide 
chapter  on  cerebral  tumors). 

We  must  add  in  conclusion  a  few  words  about  diseases  of  the  middle  pedun- 
cles (crura  ad  pontem).  Usually  it  is  an  irritation  of  these  which  causes  those 
peculiar  symptoms  known  as  forced  movements  and  forced  positions.  Thus,  in 
such  a  case,  the  patient  always  lies  upon  one  particular  side  in  bed.  He  may  be 
quite  conscious,  or  in  a  state  of  complete  unconsciousness.  If  he  is  put  in  any 
other  posture,  he  at  once  involuntarily  reassumes  his  former  position.  Not  infre- 
quently this  forced  position  of  the  trunk  is  accompanied  by  a  corresponding  forced 
position  of  the  head  and  eyeballs,  while  the  extremities  are  seldom  affected. 
Genuine  forced  movements  are  seen  far  less  often.  They  produce  either  often- 
repeated  rotations  of  the  body  on  its  longitudinal  axis,  or,  if  the  patient  be  able 
to  walk  at  all,  involuntary  circular  movements  ("  circus  movements  "),  etc.  It  is 
not  possible,  even  by  minute  analysis  of  these  symptoms,  to  determine  in  which  of 
the  two  peduncles  the  source  of  irritation  exists.  In  a  few  very  rare  cases  of  brain 
disease  these  same  symptoms  have  been  observed,  although  no  affection  of  the 
middle  peduncles  of  the  cerebellum  could  afterward  be  detected. 


For  convenient  reference  we  subjoin  a  summary  of  the  most  important  facts 
bearing  upon  the  localization  of  cerebral  diseases. 

1.  The  most  frequent  cause  of  ordinary  hemiplegia  is  a  lesion  of  the  pyramidal 
tract  in  the  posterior  limb  of  the  internal  capsule.  If  the  hemiplegia  be  persistent, 
then  this  tract  is  actually  destroyed ;  if  temporary,  the  tract  has  been  functionally 
deranged  for  a  time  by  focal  disease  in  neighboring  parts  of  the  brain. 

2.  Monoplegie  cerebral  paralysis  is  usually  due  to  affections  of  the  cortex  of 
the  brain,  that  is,  the  central  convolutions  and  the  paracentral  lobule.  Mono- 
plegia of  the  face  and  tongue  is  the  result  of  lesions  in  the  lower  extremity  of  the 
anterior  central  convolution.  Monoplegia  of  the  arm  is  referable  principally  to 
some  lesion  of  the  middle  third  of  the  anterior  central  convolution.  Monoplegia 
of  the  lower  extremity  implies  some  affection  of  the  paracentral  lobule. 

3.  Hemiplegia  or  monoplegia,  if  associated  with  epileptiform  convulsions  affect- 
ing either  one  half  or  one  particular  portion  of  the  body,  are  almost  always 
caused  by  cortical  lesions.  These  same  symptoms  of  motor  irritation  without 
accompanying  paralysis  are  likewise  ascribable  to  some  irritation  of  the  above- 
mentioned  regions  of  the  cortex. 


CEREBRAL  HEMORRHAGE.  725 

4.  Hemiplegia  with  crossed  paralysis  of  the  oculomotor  nerve  indicates  a  lesion 
of  the  crura  cerebri. 

5.  Hemiplegia  with  crossed  facial  paralysis  implies,  with  an  approach  to  cer- 
tainty, that  the  lesion  is  situated  in  the  pons. 

6.  Post-hemiplegic  chorea  (vide  infra)  seems  to  occur  especially  when  there 
is  focal  disease  in  the  neighborhood  of  the  optic  thalamus  or  of  the  posterior  part 
of  the  internal  capsule. 

7.  Hemianaesthesia  (of  the  skin  and  of  the  organs  of  special  sensej  seems  to 
result  principally  from  lesions  of  the  most  posterior  portion  of  the  internal  cap- 
sule. 

8.  Hemiopia  may  be  due  to  a  lesion  of  the  occipital  lobe.  Probably,  also,  a 
lesion  of  the  posterior  extremity  of  the  internal  capsule  may  cause  it,  in  which 
case  it  is  usually  associated  with  hemianaesthesia.  Finally,  it  may  be  produced 
by  affections  of  the  posterior  tubercle  of  the  optic  thalamus,  or  of  one  of  the 
anterior  corpora  quadrigemina,  or  of  one  of  the  optic  tracts. 

9.  Genuine  motor  aphasia  indicates  disease  of  the  third  left  frontal  convolution. 

10.  Word  deafness  seems  to  be  due  to  disease  of  the  first  left  temporal  convolu- 
tion. 

11.  Difficulty  in  articulation  implies  disease  of  the  medulla,  as  does  also  dys- 
phagia. 

12.  Staggering  gait  and  vertigo  are  the  most  constant  symptoms  of  cerebellar 
disease.  Forced  positions  and  forced  movements  are  seen  chiefly  in  connection 
with  lesions  of  the  crura  cerebelli  ad  pontem. 

[13.  Staggering  gait  and  ocular  paralyses  are  indicative  of  lesions  of  the  cor- 
pora quadrigemina. -K.] 


CHAPTER  III. 

CEREBRAL   HEMORRHAGE. 

iEtiology. — The  cause  of  cerebral  haemorrhage  should  always  be  sought  in 
some  disease  of  the  coats  of  the  minute  cerebral  arteries.  In  1868  it  was  first 
shown  by  Charcot  and  Bouchard  that  in  almost  every  case  of  cerebral  haemor- 
rhage there  are  miliary  aneurisms  of  the  small  arteries  of  the  brain  substance, 
some  one  of  which  has  burst  and  allowed  the  blood  to  escape.  All  later  investi- 
gators have  confirmed  their  statements  about  the  occurrence  and  importance  of 
these  miliary  aneurisms.  The  aneurisms  may  attain  a  diameter  of  a  millimetre 
or  more.  They  usually  appear  like  spindle-shaped  dilatations  of  the  entire  cir- 
cumference of  the  vessel,  although  sometimes  the  bulging  is  confined  to  one  side 
of  it.  So  far  as  has  yet  been  learned,  the  process  of  development  starts  with  dis- 
ease of  the  intima.  This  layer  presents  at  first  proliferations  and  also  a  fatty 
degeneration  of  the  endothelium.  Later  on,  however,  the  intima  atrophies,  just 
as  the  muscular  coat  does.  Inasmuch  as  the  intra-cerebral  arteries  possess  almost 
no  true  adventitia,  it  is  easy  to  see  that  these  vessels  are  especially  predisposed  to 
aneurismal  dilatation.  It  has  been  affirmed  that  the  disease  of  the  vascular  wall, 
which  leads  to  the  formation  of  these  aneurisms,  is  identical  with  ordinary  arterio- 
sclerosis (vide  page  331)  or  atheroma.  Charcot  denies  it,  but  the  later  investiga- 
tions of  Eichler  make  it  seem  very  probable.  Indeed,  we  very  often,  although  not 
invariably,  find  that  cerebral  haemorrhage  attacks  persons  who  present  either  a 
general  arterio-sclerosis  or  a  more  limited  atheromatous  disease  of  the  cerebral 
arteries ;  and  most  of  the  factoivs  which  are  said  to  promote  cerebral  haemorrhage 
are  the  same  as  favor  the  development  of  arterio-sclerosis. 


726  DISEASES  OF  THE  NERVOUS  SYSTEM. 

It  has  long  been  recognized  that  age  has  an  important  bearing  on  these  cases. 
Although  exceptionally  a  younger  individual  may  be  attacked,  the  majority  of 
sufferers  are  over  fifty  years  old — that  is,  at  the  time  of  life  when  arterio-sclerosis 
usually  becomes  most  fully  developed.  Again,  cerebral  haemorrhage  is  decidedly 
more  frequent  in  men  than  in  women,  which  is  also  true  of  atheroma.  Alco- 
holism, syphilis,  and  gout  are  also  reckoned  among  the  aetiological  factors  of  both 
disorders,  and  in  both  a  hereditary  predisposition  is  not  veiy  rarely  demonstra- 
ble. What  is  called  the  "  apoplectic  habit "  also  deserves  brief  mention.  Although 
there  is  no  variety  of  constitution  which  exempts  its  possessor  from  the  possibility 
of  cerebral  haemorrhage,  yet  it  can  not  be  denied  that  often  the  victims  of  apo- 
plexy do  exhibit  a  certain  >l  habit."  Such  persons  are  not  very  tall,  but  are  corpu- 
lent, broad-chested,  with  a  short,  thick  neck  and  round  face.  They  have  not  been 
disinclined  to  the  pleasures  of  the  table  and  the  bottle,  and  sometimes  they  suffer 
from  emphysema,  moderate  hypertrophy  of  the  heart,  and  general  arterio-sclero- 
sis, as  the  condition  of  the  radial  and  temporal  arteries  may  disclose  even  during 
life. 

Granting,  therefore,  that  disease  of  the  arteries,  and  more  particularly  miliary 
aneurisms  resulting  from  chronic  endarteritis  of  the  smaller  cerebral  arteries, 
must  be  regarded  as  the  chief  cause  of  cerebral  haemorrhage,  then,  on  the  other 
hand,  the  question  suggests  itself  whether  an  abnormal  elevation  of  the  blood- 
pressure  may  not  have  some  part  in  determining  the  haemorrhage.  If  the  coats 
of  the  arteries  be  normal,  surely  they  would  not  be  torn,  no  matter  how  great  the 
arterial  tension  became;  but  if  aneurisms  have  already  been  developed,  then 
there  can  be  no  doubt  that  a  persistent  or  even  a  temporary  elevation  of  the  blood- 
pressure  must  favor  the  bursting  of  the  vessels.*  In  this  sense  a  cerebral  haemor- 
rhage, occurring  in  patients  with  certain  forms  of  cardiac  hypertrophy  (contracted 
kidney,  idiopathic  hypertrophy,  etc.),  combined  with  disease  of  the  vessels,  may  be 
referred  in  part  to  the  increased  arterial  tension ;  but  it  is  most  of  all  with  regard 
to  many  exciting  causes,  which  are  immediately  followed  by  a  cerebral  haemor- 
rhage, that  increased  blood-pressure  assumes  great  importance.  Here  it  is  tem- 
porary. Cerebral  haemorrhage  may,  for  example,  follow  excessive  muscular 
exertion,  the  ingestion  of  a  large  amount  of  food,  indulgence  in  alcohol,  taking  a 
cold  bath,  or  violent  mental  excitement.  In  all  such  cases,  however,  the  change 
in  the  arteries  is  a  necessary  prerequisite. 

It  should  be  mentioned,  in  conclusion,  that  quite  considerable  haemorrhage 
may  also  take  place  in  the  course  of  such  general  diseases  as  are  associated  with 
impaired  nutrition  and  a  consequent  diminution  in  the  resisting  power  of  the 
vascular  walls.  Cerebral  haemorrhage  under  these  circumstances  is  merely 
symptomatic  of  a  general  haemorrhagic  diathesis,  as  we  find  it  in  leukaemia, 
pernicious  anaemia,  and  those  affections  which  are  called,  in  a  stricter  sense, 
haemorrhagic  diseases,  such  as  scurvy  and  purpura  haemorrhagica.  The  grave 
infectious  diseases,  including  septicaemia,  typhus  or  typhoid  fever,  and  variola, 
may  occasion  haemorrhage  into  the  brain  as  well  as  into  other  organs.  The 
haemorrhages  are  generally,  however,  from  capillary  vessels,  and  are  very  rarely 
extensive. 

Pathology. — The  miliary  aneurisms  do  not  develop  in  all  the  cerebral  arteries 
with  equal  frequency,  and  accordingly  we  find  certain  regions  particularly  liable 
to  cerebral  haemorrhage,  being  very  much  offener  affected  by  it  than  others.  It 
is  the  large  central  ganglia  in  the  neighborhood  of  the  lateral  ventricles  that 

*  [Mendel  has  found  that  the  normal  blood-pressure  in  the  lentieulo-striatc  arteries,  which  arc 
most  prone  to  rupture,  is  much  higher  than  it  is  in  the  cortical  and  many  other  small  arteries  of  the 
brain. — K.] 


CEREBRAL  HEMORRHAGE.  727 

suffer  most  frequently  —  namely,  the  optic  thalamus;  caudate  and  lenticular 
nuclei,  and  also  the  adjacent  white  matter  of  the  internal  capsule  and  centrum 
ovale.  Haemorrhages  in  other  portions  of  the  brain  are  much  less  frequent — 
such  as  haemorrhages  into  the  convolutions,  the  pons,  the  cerebellum,  the  crura 
cerebri,  or  the  medulla.  If  the  blood  escapes  into  the  neighborhood  of  a  ven- 
tricle, it  may  burst  into  the  latter.  Likewise,  in  rare  instances,  an  effusion  of 
blood  near  the  cortex  may  make  its  way  out  upon  the  surface  of  the  brain. 

An  extensive  collection  of  blood  in  one  of  the  hemispheres  may  exercise  so 
decided  a  pressure  upon  surrounding  parts  that  the  results  of  increased  tension 
upon  the  affected  side  are  at  once  recognized  when  the  skull  is  opened.  The  dura 
on  that  side  is  more  tightly  stretched,  the  falx  is  crowded  over  to  the  opposite  side, 
the  convolutions  on  the  convexity  seem  flattened,  and  the  furrows  are  shallow. 
Exceptionally,  when  there  is  a  very  large  effusion  reaching  nearly  to  the  surface, 
we  may  even  detect  fluctuation. 

On  cutting  through  the  brain-substance  we  find  the  seat  of  haemorrhage,  and 
are  enabled  to  determine  its  position  and  extent.  Its  size,  of  course,  varies  con- 
siderably in  different  cases ;  it  may  be  small,  or  it  may  occupy  a  large  part  of  an 
entire  hemisphere.  The  wall  of  the  effused  mass  is  made  up  of  ragged  and  torn 
cerebral  tissue,  and  the  mass  itself  contains  debris  of  the  nervous  elements  entangled 
in  the  coagulated  blood.  The  blood-clots  are  almost  always  very  dark-colored 
when  fresh.  Later  on,  the  mass  changes  to  a  chocolate-colored  or  more  brownish- 
yellow  pulp,  composed  of  the  disintegrated  remnants  of  the  nervous  substance 
and  the  clotted  blood.  The  microscope  reveals,  particularly  in  the  immediately 
surrounding  tissues,  numerous  fatty  granular  cells.  These  are  white  blood- 
corpuscles  which  have  absorbed  the  fat  resulting  from  the  decomposition  of  the 
myeline  substance.  There  is  also  always  an  abundance  of  haetnatoidine  crystals, 
due  to  the  disintegration  of  the  red  blood-globules.  At  a  greater  distance  from 
the  effusion  the  tissues  present  a  yellowish  tinge,  from  the  imbibition  of  such 
blood-pigment  as  has  reached  them  in  a  state  of  solution ;  and  there  is  also  usually 
an  cedematous  softening  of  the  parts  not  too  far  removed  from  the  haemorrhagic 
focus. 

If  the  patient  survive,  the  mass  is  gradually  absorbed.  It  slowly  diminishes 
in  size,  and  the  surrounding  parts  tend  to  reassume  their  normal  relations.  The 
final  result  in  many  cases  is  a  cavity  filled  with  serous  fluid  and  bounded  by 
smooth  walls.  This  "apoplectic  cyst"  remains  stationary.  In  some  instances, 
however,  and  particularly  if  the  effusion  be  rather  small,  the  walls  approach  each 
other  as  more  and  more  of  the  fluid  is  absorbed ;  there  is  a  great  hyperplasia  of 
connective  tissue ;  and  so,  finally,  there  is  nothing  left  but  a  so-called  apoplectic 
scar,  usually  of  a  yellow  color,  due  to  vestiges  of  the  blood-pigment.  The  position 
and  dimensions  of  the  permanent  lesion  determine,  of  course,  the  question  of  sec- 
ondary descending  degeneration  {vide  page  680),  as  well  as  the  nature  and  extent 
of  the  persistent  clinical  symptoms. 

Clinical  History. — The  symptoms  of  cerebral  haemorrhage  agree  closely  with 
the  anatomical  lesions  just  described.  The  miliary  aneurisms  themselves,  even 
when  numerous,  seldom  excite  any  symptoms.  Sometimes,  however,  it  is  possible 
that  the  slight  circulatory  disturbances  they  occasion  produce  the  mild  headache 
and  similar  annoyances  which  often  precede,  for  a  longer  or  shorter  time,  the 
occurrence  of  cerebral  haemorrhage. 

As  soon  as  an  aneurism  bursts,  however,  and  blood  escapes  into  any  part  of 
the  brain -substance,  there  is  immediately  seen  a  group  of  grave  cerebral  symp- 
toms, collectively  termed  an  apoplectic  attack,  or  "  shock."  As  the  blood  escapes 
under  a  pressure  nearly  equal  to  the  general  arterial  pressure,  and  doubtless  much 
greater  than  that  to  which  the  soft  substance  of  the  brain  is  normally  exposed, 


72S  DISEASES  OF  THE  NERVOUS  SYSTEM. 

the  affected  portion  of  the  brain  is  at  once  subjected  to  a  considerable  increase  of 
tension,  which  is  transmitted  for  various  distances  in  all  directions.  It  need  not 
be  said  that  the  destructive  influence  of  the  haemorrhage  may  vary  exceedingly, 
and  that  therefore  the  symptoms  are  by  no  means  equally  severe  in  all  cases. 
The  larger  the  rent  in  the  blood-vessel,  and  the  more  rapid  and  abundant  the 
consequent  haemorrhage,  the  worse  is  the  apoplectic  attack.  Bleeding  from 
larger  vessels  is  therefore  usually  attended  by  graver  symptoms  than  from  the 
minute  arterial  twigs.  An  extensive  cerebral  haemorrhage  sometimes  causes 
the  patient  to  fall  down  suddenly  in  complete  unconsciousness,  while  smaller 
haemorrhages  may  occasion  only  a  temporary  attack  of  vertigo  and  slight  cloudi- 
ness of  intellect.  If  the  tear  in  the  wall  of  the  artery  be  very  small  and  narrow, 
permitting  the  blood  to  escape  but  slowly,  then  there  may  be  no  sudden  attack  at 
all,  the  phenomena  requiring  a  certain  length  of  time  for  then  development. 

There  is  also  an  important  relation  between  the  location  of  the  haemorrhage 
and  the  severity  of  the  apoplectic  attack.  The  chief  symptom  of  these  cases  is 
loss  of  consciousness  (about  which  we  shall  soon  speak  at  length) ;  and  as  this 
certainly  is  due  to  an  interruption  of  the  functional  activity  of  the  cerebral 
cortex,  it  is  plain  (1)  that  the  nearer  the  cortex  is  to  the  haemorrhagic  focus,  the 
more  apt  are  the  symptoms  to  be  serious.  It  is  confirmatory  of  this  that  haemor- 
rhage into  the  more  deeply  situated  portions  of  the  brain,  like  the  crura  cerebri 
or  the  pons,  quite  often  occasions  comparatively  slight  symptoms.  But  (2)  there 
is  a  fact  about  the  circulation  in  the  brain  that  often  causes  the  shock  from 
haemorrhage  into  the  brain-stem  to  be  greater  than  the  shock  following  haemor- 
rhage into  the  cortex  or  the  white  substance  of  the  hemispheres.  The  explana- 
tion is  that  the  brain-stem  has  comparatively  much  larger  ai'teries  than  the  other 
parts  just  mentioned,  which  contain  only  minute  blood-vessels.  Furthermore,  as 
Duret  and  Heubner  have  shown,  the  blood-vessels  are  so  distributed  that  the 
arterial  tension  in  the  brain-stem  is  not  a  little  higher  than  in  the  other  portions. 
This  renders  intelligible  the  clinical  phenomenon  that  haemorrhages  in  the  terri- 
tory of  the  main  arteries,  besides  being,  as  we  have  said,  the  most  frequent  of  any, 
produce  apoplectic  symptoms  even  when  the  effusion  is  comparatively  small; 
while  sometimes  haemorrhages  of  about  the  same  size  in  the  cortex  or  white  sub- 
stance may  not  be  noticed. 

The  clinical  phenomena  of  the  apoplectic  attack  will  now  be  considered  in 
detail.  The  onset  is  sometimes  absolutely  without  warning,  but  in  other  cases  it 
is  preceded  for  a  greater  or  less  length  of  time  by  certain  prodromata.  These  are 
either  the  result  of  the  disturbance  of  circulation  caused  by  the  disease  of  the 
blood-vessels  in  the  brain,  and  then,  as  already  stated,  they  comprise  occasional 
headache,  vertigo,  tinnitus  aurium,  spots  before  the  eyes,  languor,  and  muscular 
weakness;  or  they  are  caused  by  minute  haemorrhages,  which  seem  not  infre- 
quently to  precede  a  greater  one.  In  such  a  case,  the  friends  relate  that  of  late 
the  patient  has  had  one  or  more  slight  and  brief  attacks,  characterized  by  faint- 
ness,  temporary  trouble  in  speaking,  sudden  but  temporary  weakness  of  an  arm 
or  leg,  and  similar  symptoms.  The  prodromata  may  extend  over  several  days 
or  even  weeks  and  months  preceding  the  severe  attack. 

In  other  cases  there  are  no  such  premonitory  symptoms.  The  apoplexy  occurs 
unexpectedly  and  suddenly.  In  the  midst  of  apparently  vigorous  health  the 
patient  sinks  down  "as  if  he  had  been  struck."  In  still  other  cases  there  are 
indeed  no  prodromata,  but  the  symptoms  clo  not  at  first  appear  in  all  their  severity, 
and  occupy  some  hours  or  even  a  whole  day  in  their  gradual  development.  This 
is  due  to  a  slow  and  gradually  increasing  haemorrhage,  and  is  termed  a  slow  or 
delayed  apoplectic  attack.  The  patient  grows  confused,  anxious,  and  delirious  (a 
case  of  our  own  had  pronounced  hallucinations  of  sight) ;  the  arm  and  leg  on  one 


CEEEBRAL  HEMORRHAGE.  729 

side  become  paretic,  and  gradually  more  and  more  completely  paralyzed;   and 
after  a  few  hours  complete  unconsciousness  comes  on. 

The  attack  may  be  rapidly  fatal.  In  such  cases  the  abnormal  pressure  prob- 
ably involves  the  medulla  oblongata  and  paralyzes  the  cardiac  and  respiratory 
centers  there  situated.  Usually,  however,  there  is  merely  a  complete  loss  of  con- 
sciousness, more  or  less  rapidly  developed.  Sometimes  the  patient  has  time  to 
lie  down.  He  usually  sinks  back  in  his  chair  or  falls  to  the  floor,  and  becomes 
deeply  comatose.  The  face  is  often  noticeably  flushed,  and  the  pulse  full  and 
tense,  but  not  infrequently  somewhat  slow,  because  of  the  increased  cerebral 
pressure.  The  respirations  are  deep,  noisy,  stertorous,  and  likewise  often  slow. 
The  relaxed  cheeks  and  lips  are  often  drawn  deeply  in  at  every  inspiration,  and 
puffed  out  at  every  expiration.  The  temperature  is  usually  subnormal  at  first, 
later  regaining  the  normal,  or  even  a  higher  point.  In  a  rapidly  fatal  case,  how- 
ever, the  temperature  remains  depressed  till  death.  It  is  not  very  rare  in  severe 
cases  to  observe  a  peculiar  position  of  the  head  and  eyeballs,  they  being  all  turned 
in  one  direction.  This  phenomenon  is  termed  by  Prevost  conjugate  deviation 
(deviation  conjuguee)  of  the  eyes  and  head.  It  is  generally  temporary,  and  is 
said  by  Landouzy  to  be  connected  principally  with  a  lesion  of  the  lower  temporal 
lobe.  There  is  no  perfectly  constant  relation  between  the  lateral  deviation  and 
the  half  of  the  brain  affected.  Apparently  in  most  cases  the  eyes  are  directed 
toward  the  injured  side,  and  so  to  a  certain  extent  "  look  toward  the  lesion  "  and 
away  from  the  paralyzed  side  of  the  body  (vide  infra).  The  pupils  present  no 
constant  peculiarities.  Often  they  are  of  normal  size.  In  other  cases  they  are 
contracted,  dilated,  or  unequal.  No  definite  diagnostic  conclusions  can  be  drawn 
from  them.  In  the  worst  cases  the  pupils  will  not  react  to  light ;  in  other  cases 
they  react,  but  often  sluggishly. 

During  the  deep  apoplectic  coma  the  extremities  generally  lie  completely 
motionless  and  limp.  In  the  worst  cases  reflex  action  is  wholly  suspended ;  but 
sometimes  the  vigorous  thrust  of  a  pin  or  the  pinching  of  the  skin  will  excite  an 
occasional  slow  reflex  twitch,  or  a  motion  as  if  to  ward  off  the  tormentor. 
Whether  the  apoplexy  has  caused  hemiplegia  at  all,  and  if  so  on  what  side,  can 
not  always  be  easily  determined  during  the  initial  coma.  Still,  it  is  often  to  be 
observed,  even  now,  that  one  angle  of  the  mouth  hangs  down  lower  than  the 
other,  and  that  the  corresponding  cheek  is  more  puffed  out  during  expiration 
than  is  the  other;  that  the  extremities  of  one  side  are  even  more  completely 
relaxed  and  limp  than  those  on  the  opposite  side  of  the  body,  and  that  the  reflex 
action  and  defensive  movements  are  almost  absent  upon  one  side  (the  paralyzed 
side),  while  they  can  be  clearly  demonstrated  on  the  other. 

In  contrast  to  the  usual  laxness  of  the  arms  and  legs  during  the  apoplectic 
coma  is  the  tonic  rigidity  sometimes  seen  in  the  extremities,  particularly  on  the 
side  opposite  to  the  haemorrhage.  This  symptom  seems  to  be  especially,  although 
not  exclusively,  connected  with  a  bursting  of  the  escaping  blood  into  a  lateral 
ventricle.  It  is  rather  exceptional  for  cerebral  haemorrhage  to  be  attended  with 
general  or  unilateral  epileptiform  convulsions — a  symptom  which,  as  we  have 
seen,  is  referable  to  irritation  of  the  motor  regions  of  the  cortex. 

It  should  be  mentioned  that  in  many  cases  of  cerebral  haemorrhage  the  urine 
passed  after  the  attack  has  been  found  to  contain  small  amounts  of  albumen  or 
sugar.  This  symptom  is  usually  ascribed  to  compression  of  the  medulla  from  the 
effusion.  There  is  usually  retention  of  urine ;  in  other  cases  there  is  involuntary 
micturition. 

A  certain  number  of  patients  never  awake  from  the  initial  coma.  Death  may 
not  be  immediate,  but  they  remain  completely  unconscious;  the  respirations 
become  more  rapid  and  irregular  (sometimes  of  the  Cheyne-Stokes  character). 


730  DISEASES  OF  THE  NERVOUS  SYSTEM. 

and  there  is  a  rattling  in  the  throat,  because  mucus  and  saliva  run  down  into  it ; 
the  pulse,  which  was  at  first  retarded,  now  becomes  accelerated ;  the  face  grows 
paler  and  more  and  more  sunken;  the  eyes  are  deep  in  their  sockets;  the  cornea 
becomes  opaque;  and  at  last,  after  the  coma  has  lasted  some  hours,  or  even 
one  or  two  days,  death  occurs,  often  attended  by  a  considerable  rise  in  tempera- 
ture. 

This  termination  is,  however,  by  no  means  the  usual  one.  More  frequently 
the  patient  survives  the  attack.  The  bleeding  ceases,  the  clot  contracts,  and 
begins  to  be  disintegrated  and  absorbed.  At  the  same  time  the  pressure  exerted 
upon  surrounding  parts  grows  less  and  less,  the  more  distant  parts  of  the  brain 
gradually  recover  from  the  shock,  and  consciousness  slowly  returns.  The  patient 
begins  to  open  his  eyes  when  he  is  spoken  to  in  a  loud  tone ;  he  raises  his  hand  to 
his  head,  sighs,  and  yawns;  gradually  the  intellect  clears  up,  he  tries  to  talk,  or 
to  express  himself  by  signs;  memory  returns,  and  he  recognizes  those  about  him 
once  more.  Exceptionally,  recovery  is  interrupted  by  a  fresh  and  perhaps  a 
fatal  relapse.  This  may  result  from  a  renewal  of  the  haemorrhage.  Generally, 
however,  improvement  persists,  the  patient  fully  regains  his  consciousness  at  the 
end  of  a  few  days,  and  it  now  becomes  possible  for  the  first  time  to  "  estimate  the 
damages." 

The  symptoms  thus  far  described  belong  to  severe  apoplectic  attacks.  There 
are  also,  as  we  have  said,  cases  of  all  degrees  of  mildness,  as  regards  the  first  onset. 
In  these  there  is  no  deep  and  persistent  coma.  The  patient  loses  consciousness 
only  temporarily,  if  at  all.  He  is  seized  with  vertigo,  or  with  sudden  headache, 
and  is  for  a  time  stupefied.  Nausea  and  vomiting  are  of  quite  frequent  occurrence, 
just  as  in  ordinary  syncope.  Yet  cases  presenting  these  comparatively  slight 
early  symptoms,  and  with  few  even  of  these,  may  exhibit  the  genuine  focal 
symptoms  referable  to  the  haemorrhage,  such  as  hemiplegia,  in  all  their  severity. 
These  latter  phenomena  must  now  be  considered. 

Among  the  symptoms  of  impairment  of  function  resulting  from  cerebral 
haemorrhage,  only  those  are  to  be  regarded  as  direct  focal  symptoms  which  are 
caused  by  the  actual  destruction  of  a  region  of  the  brain.  "Where  the  haemorrhage 
takes  place  we  have  seen  that  a  larger  or  smaller  extent  of  the  brain-substance  is 
completely  destroyed  by  the  sudden  and  forcible  escape  of  the  blood.  The  dimen- 
sions of  this  lesion  are  represented  later  by  the  apoplectic  scar  or  cyst,  and  its 
position  by  the  nature  and  extent  of  the  persistent,  and  for  the  most  part  irrepa- 
rable, loss  of  function  (Ausfallserscheinungen).  But  there  are,  in  addition  to  these 
direct  symptoms,  other  indirect  focal  symptoms,  which  outlast  the  apoplectic 
shock,  and  vary  with  the  locality  of  the  haemorrhage.  These  do  not,  however, 
correspond  to  the  territory  actually  destroyed.  They  are  due  to  the  influence 
exerted  for  a  certain  length  of  time  by  the  haemorrhagic  focus  upon  the  immedi- 
ately surrounding  structures.  The  pressure  of  the  effusion,  the  disturbance  of  cir- 
culation resulting  from  it,  the  collateral  oedema,  and  perhaps  also  the  imbibition 
of  the  soluble  products  of  disintegration,  are  the  chief  factors  in  exciting  these  in- 
direct symptoms.  They  do,  indeed,  outlast  the  initial  shock,  but  are  nevertheless 
temporary,  vanishing  sooner  or  later,  at  the  end  of  several  days  or  weeks,  or  even 
months. 

Even  if  the  character  of  the  initial  attack  and  the  symptoms  still  exhibited 
have  been  minutely  determined,  yet  we  are  unable  to  say,  at  first,  whether  the 
existing  focal  symptoms  are  direct  or  indnect.  We  can  decide  about  this  only 
after  further  observation.  If  the  early  symptoms  disappear  within  the  next  few 
clays  or  weeks,  or  after  the  first  two  or  three  months,  we  can  then  affirm,  retro- 
spectively, that  they  were  indirect,  Such  as  outlast  the  first  six  months  are  to 
be  regarded  as  direct,  and  as  not  destined  to  improve  much.     From  a  practical 


CEREBRAL  HEMORRHAGE.  Y31 

point  of  view  this  distinction  is  of  extreme  importance.  We  shall  revert  to  the 
subject  when  considering  the  course  of  cerebral  apoplexy. 

A  minute  description  of  all  the  focal  symptoms  which  might  occur  after  cere- 
bral haemorrhage,  and  of  the  light  thus  thrown  upon  the  location  of  the  haemor- 
rhage, need  not  be  attempted  here,  for  it  would  necessitate  a  repetition  of  all  the 
facts  enumerated  in  the  preceding  chapter.  It  is  only  requisite  to  describe,  in 
detail,  the  chief  and  by  far  the  most  frequent  result  of  a  cerebral  haemorrhage — 
ordinary  cerebral  hemiplegia. 

It  has  been  mentioned  that  most  of  these  haemorrhages  occur  near  the  lateral 
ventricles.  Hence,  in  a  majority  of  instances,  the  motor  pyramidal  tract,  as  it 
traverses  the  internal  capsule,  is  either  directly  destroyed  or  at  least  indirectly 
affected.  Consequently,  most  patients  who  survive  the  apoplectic  shock  present 
a  paralysis  of  that  half  of  the  body  which  is  opposite  the  seat  of  haemorrhage. 
On  minute  examination  we  usually  find,  in  the  first  place,  that  even  in  the  dis- 
tribution of  the  facial  nerves  there  is  a  distinct  difference  between  the  two  sides, 
the  lower  division  of  the  facial  (which  supplies  the  muscles  of  the  cheek,  nose,  and 
mouth)  being  evidently  paralyzed  on  one  side,  while  its  upper  division  (going  to 
the  eyes  and  forehead)  is  entirely,  or  almost  entirely,  intact.  The  forehead  can 
be  wrinkled  on  one  side  as  well  as  on  the  other;  but  if  the  patient  tries  to  turn 
up  his  nose,  or  alter  the  shape  of  his  mouth,  the  paralysis  becomes  evident.  Often 
indeed,  while  the  face  is  quiet,  it  can  be  noticed  that  one  naso-labial  fold  is  oblit- 
erated, or  that  one  corner  of  the  mouth  hangs  clown.  It  is  an  interesting  fact  that 
the  paresis  of  the  lower  division  of  the  facial  is  much  more  noticeable  during 
voluntary  efforts,  as  in  showing  the  teeth,  than  when  the  patient  smiles  involun- 
tarily. A  patient  will  sometimes  try  in  vain  to  draw  back  the  corner  of  his 
mouth,  then  begin  to  laugh  at  his  own  awkwardness,  and  thereupon  open  his 
mouth  in  an  almost  perfectly  normal  manner.  We  have  seen  above,  in  the  chapter 
on  cerebral  localization,  that  this  condition  can  probably  be  explained  by  the  rela- 
tion of  the  optic  thalamus  to  the  movements  of  mimetic  expression.  Why  there  is 
such  a  difference  between  the  upper  and  lower  divisions  of  the  facial  nerve  in 
cerebral  hemiplegia  is  not  certainly  known.  Possibly  it  has  some  connection 
with  the  fact  that  the  muscles  supplied  by  the  upper  division  (frontalis,  corrugator 
supercilii,  and  to  a  certain  extent  the  orbicularis)  are  very  seldom  exercised  upon 
one  side  alone,  but  always  bilaterally.  Perhaps  both  sides  receive  nervous  fibers 
from  each  cerebral  hemisphere,  so  that,  if  a  single  center  be  intact,  it  alone  answers 
for  the  muscles  on  both  sides.*  Sometimes,  however,  careful  examination  shows 
a  slight  paresis  of  the  frontalis  muscle  on  the  paralyzed  side.  In  the  distribution 
of  the  lower  division  of  the  facial,  also,  ordinary  cases  of  cerebral  hemiplegia  pre- 
sent almost  always  a  more  or  less  marked  paresis,  and  only  exceptionally  a  com- 
plete paralysis. 

There  is  quite  often  a  slight  impairment  of  the  hypoglossus  in  addition  to  the 
paresis  of  the  facial  nerve.  If  the  patient  puts  out  his  tongue,  its  tip  deviates 
toward  the  paralyzed  side.  This  is  a  result  of  paresis  of  one  of  the  genio-hyo- 
glossi.  When  both  these  muscles  contract,  they  may  be  said  to  push  the  tongue 
forward.  If  this  thrust  be  more  vigorous  on  one  (the  healthy)  side,  the  tongue  is 
deflected  toward  the  other  (paralyzed)  side.  In  ordinary  cerebral  hemiplegia  this 
is  almost  always  the  sole  way  in  which  the  movements  of  the  tongue  can  be  seen 


*  There  is  a  remarkable  general  rule  which  should  be  mentioned  here,  and  which  is  perhaps  to  be 
explained  in  the  same  way,  namely,  that  those  muscles  which  are  usually  called  into  play  in  pairs  are 
never  completely  paralyzed  in  cerebral  hemiplegia.  Furthermore,  it  is  impossible  for  us  to  contract 
most  of  these  singly,  on  one  side  alone,  or  at  least  not  without  special  practice ;  this  applies,  for 
instance,  to  the  corrugator  supercilii,  the  frontalis,  the  motores  oculi,  and  the  muscles  of  mastication 
and  respiration. 


732  DISEASES  OF  THE  NERVOUS  SYSTEM. 

to  be  impaired.  Sometimes,  however,  the  slight  paresis  of  half  of  the  tongue, 
combined  with  the  facial  paresis,  entails  a  noticeable  difficulty  in  articulation. 
This,  to  be  sure,  is  not  great,  and  is  often  appreciated  by  the  patient  alone,  who  is 
conscious  that  an  effort  is  required  in  order  to  speak. 

The  soft  palate  is  rarely  much  affected.  It  may,  however,  hang  rather  lower 
down  on  the. paralyzed  than  on  the  unaffected  side,  and  move  less.  The  uvula  is 
inclined  sometimes  toward  the  healthy  and  sometimes  toward  the  paralyzed  side. 
There  are  no  special  disturbances  of  function  as  a  result  of  these  changes. 

The  trapezius  is  the  only  muscle  of  the  trunk  which  is  ordinarily  much 
affected  in  cerebral  hemiplegia.  As  a  result  of  the  paresis  of  this  muscle,  the 
shoulder  sags  and  can  not  be  raised  as  high  as  on  the  normal  side.  If  the  patient 
tries  to  take  a  very  deep  breath,  it  is  in  some  cases  possible  to  see  that  the  para- 
lyzed side  lags  behind  a  little  in  respiration,  which  is  undoubtedly  due  to  a  pare- 
sis of  the  respiratory  muscles  on  that  side.  It  is  perhaps  due  to  this  that  the 
pulmonary  diseases  which  attack  hemiplegic  patients  frequently  develop  in  the 
lung  on  the  affected  side,  where  respiration  is  deficient. 

The  most  important  element  in  the  hemiplegia  is  the  paralysis  of  the  extremi- 
ties. Immediately  after  the  haemorrhage  it  is  often  so  complete  that  even  the 
slightest  voluntary  motion  in  the  affected  arm  and  leg  is  impossible.  Other  cases, 
however,  exhibit  only  a  more  or  less  severe  paresis  (hemiparesis)  from  the  first; 
or  the  complete  paralysis  at  any  rate  is  confined  to  certain  groups  of  muscles,  the 
others  still  retaining  vestiges  of  their  normal  contractility.  Even  when  there  is 
total  hemiplegia  at  first  some  of  the  muscles  usually  regain  a  certain  amount  of 
their  old  power  later  on  {vide  infra). 

The  behavior  of  the  reflexes  is  comparatively  constant  in  nearly  all  cases. 
Almost  invariably  there  is  increased  tendon  reflex  on  the  paralyzed  side.  If, 
however,  the  initial  shock  be  very  severe,  there  may  at  first  be  no  tendon  reflex 
whatever.  In  all  cases  of  any  duration  it  is  always  exaggerated,  and  often  very 
much  so.  A  tap  upon  the  tendons  and  bones  (periosteal  reflex)  of  the  arm,  as 
well  as  of  the  leg,  excites  the  most  vigorous  and  manifold  contractions.  Very 
often  a  persistent  ankle  clonus  can  be  obtained.  It  is  noteworthy  that  even  on 
the  normal  side,  particularly  in  the  lower  extremity,  it  is  almost  always  possible 
to  demonstrate  an  exaggeration  of  the  tendon  reflex,  although  less  pronounced 
than  on  the  paralyzed  side.  Many  have  expressed  the  opinion  that  the  increased 
tendon  reflex  upon  the  paralyzeu  side  is  a  result  of  the  secondary  degeneration  of 
the  pyramidal  tracts  in  the  spinal  cord.  In  our  judgment  this  view  is  entirely 
unfounded,  inasmuch  as  the  exaggeration  of  the  tendon  reflex  often  appears 
within  a  few  days,  or  even  hours,  after  the  apoplectic  attack— that  is,  before  a 
secondary  degeneration  in  the  spinal  cord  is  to  be  thought  of.  We  would  rather 
seek  to  explain  the  phenomenon  as  being  due  to  the  suspension  of  certain  reflex 
inhibitory  influences  because  of  the  cerebral  lesion. 

There' is  very  often  found,  particularly  in  cases  of  long  standing  affected  with 
well-marked  contractions,  an  increase  of  "  direct  mechanical  excitability  "  in  the 
paralyzed  muscles,  such  that  a  tap  upon  them  causes  them  to  contract  vigorously. 
We  are,  however,  of  opinion  that,  in  part  at  least,  this  is  also  a  reflex  symptom, 
to  be  referred  to  the  mechanical  irritation  of  the  fascia  of  the  muscles  (fascial 
reflex). 

The  skin  reflexes  in  hemiplegia  behave  in  precisely  the  opposite  way  from  the 
tendon  reflexes,  being  almost  invariably  decidedly  diminished  on  the  paralyzed 
side.  In  the  paralyzed  arm  it  is  usually  impossible  to  excite  any  skin  reflex  what- 
ever ;  and  in  the  corresponding  leg  there  is  either  no,  or  at  any  rate  a  greatly 
diminished  reflex.  The  difference  is  seen  especially  well  in  the  abdominal  and 
cremaster  reflexes  {vide  page  543) ;  on  the  paralyzed  side  they  are  almost  or  quite 


CEREBRAL  HEMORRHAGE.  733 

absent,  while  they  remain  normal  upon  the  opposite  side.  This  contrast  often  is 
of  service  in  determining1  the  location  of  the  hemiplegia  when  the  patient  is  in  a 
stupor  or  coma. 

Sensation  is  but  little  impaired  in  most  cases  of  cerebral  hemiplegia.  It  is 
usually  possible,  in  a  hemiplegia  occasioned  by  this  particular  lesion  (cerebral 
haemorrhage),  to  find  at  first,  by  careful  testing,  a  slight  blunting  of  cutaneous 
sensibility ;  but  this  is  seldom  very  gi'eat,  and  later  on  frequently  becomes  even 
slighter  than  at  first.  Slight  parsesthesia  is  not  infrequently  complained  of  on 
the  affected  side,  especially  at  first.  Any  marked  disturbance  of  sensation  indi- 
cates, as  has  been  seen  (compare  page  721),  that  the  posterior  extremity  of  the 
internal  capsule  is  involved.  Such  cases  are  rare.  In  them  we  may  observe  a 
complete  cerebral  hemiansesthesia  combined  with  the  hemiplegia.  According  to 
Gowers,  a  temporary  hemiopia  is  often  present  directly  after  the  occurrence  of  a 
cerebral  haemorrhage.  Nor  is  it  very  exceptional  to  find  a  persistent  hemiopia 
associated  with  hemiplegia;  but  as  yet  little  is  known  about  the  pathological 
auatomy  of  such  cases.  The  most  likely  thing  would  seem  to  be  some  lesion  of 
the  fibers  of  the  optic  nerve  in  the  internal  capsule  or  in  the  posterior  tubercle  of 
the  optic  thalamus.  The  muscular  sense  is  not  usually  affected  in  hemiplegia. 
Lately  it  has  been  affirmed  that  paralysis  of  cortical  origin  invariably  causes 
anomalies  in  the  muscular  sensibility  of  the  parts  which  are  paralyzed,  but  the 
statement  lacks  confirmation.  Our  own  observations  would  certainly  lead  us  to 
doubt  whether  it  is  universally  true. 

Turning  now  to  the  further  course  of  hemiplegia,  we  find  a  new  group  of  im- 
portant symptoms.  First  of  all  should  be  considered  the  changes  in  the  paralyzed 
muscles.  If  the  hemiplegia  be  incomplete,  even  from  the  start,  almost  the  normal 
degree  of  motility  may  in  a  comparatively  brief  period  be  regained  by  the  affected 
side.  At  most  there  will  persist  a  certain  slight  amount  of  weakness  and  stiffness ; 
and  even  these  will  gradually  diminish.  From  what  has  been  already  said,  it  is 
evident  that  in  these  cases  the  initial  paresis  is  an  indirect  focal  symptom,  and 
accordingly  vanishes  as  soon  as  the  effusion  ceases  to  affect  the  tissues  not  im- 
mediately involved. 

But  even  where  there  is  a  complete  hemiplegia  it  is  exceptional  for  this  con- 
dition to  remain  unabated  throughout  the  entire  region  affected.  After  a  few 
weeks,  or  even  a  few  clays,  one  part  and  another  of  the  paralyzed  half  of  the 
body  begin  to  recover  their  former  motility.  The  improvement  goes  on  slowly, 
and  in  the  most  favorable  cases  the  paralysis  may  for  the  most  part  have  vanished 
at  the  end  of  some  months.  Usually,  however,  the  improvement  never  becomes 
more  than  partial.  It  is  noteworthy  that  the  lower  extremity  almost  always  im- 
proves more  than  does  the  upper.  Many  patients  gradually  become  able  to  walk 
alone  once  more,  perhaps  with  the  aid  of  a  cane,  although  the  arm  remains  almost 
useless.  It  must  be  confessed  that  the  gait  is  seldom  perfectly  natural.  The 
patient  takes  short  steps,  drags  the  affected  limb  more  or  less,  and  in  many  cases 
does  not  move  it  straight  forward,  but  with  an  outward  sweep.  Very  often  the 
functions  of  the  ileo-psoas  and  quadriceps  return.  The  patient  can  then  walk 
alone  even  if  the  other  muscles  remain  paralyzed,  because  by  these  muscles  the 
leg  can  be  held  firm  like  a  wooden  leg.  In  the  arm,  the  chief  improvement  is 
usually  in  the  fingers  and  the  elbow-joint,  the  movements  of  the  shoulder- joint 
recovering  least. 

The  explanation  of  this  improvement  during  the  first  few  months  is  not  fully 
ascertained.  Probably  it  is  largely  true  that  only  the  persistent  paralytic  symp- 
toms are  direct  focal  symptoms,  while  the  temporary  motor  disturbances  are  only 
an  indirect  result  of  the  hemorrhagic  focus,  and  vanish  when  once  the  pressure, 
oedema,  etc.,  have  ceased.     It  is,  however,  not  absolutely  impossible  that  gradually 


734  DISEASES  OF  THE  NERVOUS  SYSTEM. 

new  tracts  (perhaps  originating  in  the  sound  hemisphere  *)  assume  vicariously 
some  of  the  functions  which  are  at  first  arrested.  That  fibers  which  have  been 
destroyed  are  ever  actually  regenerated  is  very  improbable;  and,  as  has  been 
mentioned  already,  there  is  not  much  improvement  after  tbe  first  six  months. 

The  permanently  paralyzed  muscles  become  very  often  contracted  later  on. 
The  appearances  produced  exhibit  considerable  uniformity.  Tbe  arm,  which 
suffers  more  from  paralysis  than  the  leg,  is  also  usually  more  contracted.  The 
fingers  are  almost  invariably  flexed;  the  forearm  contracted  in  a  position  of 
pronation,  and  usually  flexed  rather  than  extended ;  and  the  upper  arm  adducted 
(the  pectoralis  major  being  chiefly  affected).  These  contractures  correspond  to 
the  natural  positions  which  the  paralyzed  arm  almost  always  assumes  if  left  to 
itself.  This,  taken  alone,  is  a  reason  for  ascribing  the  contractures  chiefly  to  the 
fact  that  the  arm  moves  less  than  normal,  and  that,  as  a  necessary  sequel,  certain 
muscles  become  permanently  shortened.  This  view  would  make  the  changes 
"passive  contractures."  Another  argument  in  its  favor  is  that  the  deformity  can 
to  a  certain  extent  be  prevented  by  the  persistent  use  of  passive  motion,  which 
renders  any  permanent  shortening  of  the  muscle  impossible.  Nevertheless,  Char- 
cot and  his  pupils,  including  Bouchard,  hold  an  entirely  diffei^ent  opinion — 
namely,  that  the  contractures  are  due  to  the  secondary  degeneration  of  the 
pyramidal  tract.  In  defense  of  their  position  no  fact  can  be  adduced,  save  that 
fatal  cases  exhibiting  hemiplegic  contractures  do  invariably  present  the  secondary 
degeneration  mentioned ;  but  of  course  this  is  no  proof  that  the  two  things  have 
any  causative  relation  to  each  other.  A  contracture  occurs  only  in  connection 
with  persistent  paralysis ;  a  persistent  paralysis  never  is  seen  unless  the  pyramidal 
tract  be  destroyed ;  and  if  it  be  destroyed,  a  secondary  degeneration  must  result. 
The  contractures  and  the  secondary  degeneration  are  therefore  two  sequelae,  inde- 
pendent of  each  other.  And  that  the  degeneration  should  "  irritate  "  the  fibers, 
and  thus  excite  muscular  contractions,  is  extremely  improbable ;  for,  according  to 
all  analogy,  fibers  which  are  undergoing  degeneration  can  not  be  stimulated,  and 
can  not  therefore  transmit  any  sort  of  stimulus  to  the  paralyzed  muscles. 

If  the  contractures  become  marked  in  the  lower  limb,  they  may  involve  either 
the  extensors  or  flexors.  In  the  leg  a  moderate  contracture  of  the  calf  is  the  most 
frequent  condition.  Hitzig  has  called  attention  to  a  remarkable  fact,  which  is 
that  often  the  contractures  are  very  slight  in  the  morning,  when  the  patient  first 
wakes  up,  becoming  aggravated  after  he  has  moved  about  a  little.  Hitzig  refers 
this  phenomenon  (which  has  not  yet  been  at  all  satisfactorily  studied)  to  abnor- 
mal "  associated  movements  "  of  the  paralyzed  muscles.  Such  associated  move- 
ments do  occur :  movements  of  the  sound  side  excite  associated  movements  in  the 
opposite  members ;  and  efforts  to  move  the  paralyzed  parts  excite  in  their  turn 
associated  contractions  of  the  normal  muscles.  Sometimes,  also,  involuntary 
movements  of  the  lower  limb  on  the  paralyzed  side  are  observed  when  the  patient 
exerts  himself  to  move  his  corresponding  arm  all  he  possibly  can.  Very  often  on 
drawing  the  affected  leg  up  on  the  trunk  we  observe  a  marked  dorsal  extension  of 
the  foot  as  an  associated  movement. 

Another  peculiar  phenomenon  must  be  mentioned  here.  It  is  what  Weir 
Mitchell  has  termed  post-hemiplegic  choi'ea.    Some  time  after  the  paralysis  begins 

*  As  has  been  already  stated  (page  731),  it  seems  proper  to  assume  that  certain  muscles  enjoy  a 
double  innervation— that  is,  from  each  hemisphere.  This  applies  particularly  to  such  muscles  as 
usually  are  exercised  in  pairs.  We  might  perhaps  in  this  way  explain  why  the  lower  extremity  is 
capable  of  more  improvement  after  hemiplegia  than  is  the  arm.  The  legs  have  to  be  used  simultane- 
ously or  consentaneously,  as  in  walking,  much  more  than  the  two  arms.  Another  fact  deserves  brief 
mention :  on  careful  examination,  it  is  sometimes  possible  to  make  out  a  slight  paresis  in  the  sound 
pide,  which  may  perhaps  be  referable  to  lesion  of  the  direct  motor  fibers  (Pitres). 


CEREBRAL  HAEMORRHAGE.  7.-55 

the  parts  affected  by  it  exhibit  involuntary  movements,  reminding'  one  of  chorea 
or  athetosis  [vide  page  541).  Sometimes  these  movements  are  continuous,  some- 
times they  occur  only  as  associated  movements  in  connection  with  voluntary 
motions  of  the  paralyzed,  or  even  of  the  sound,  side.  Hemiplegia  due  to  cerebral 
haemorrhage  very  seldom  exhibits  this  phenomenon.  It  is  said  to  occur  chiefly 
in  focal  disease  of  the  posterior  extremity  of  the  internal  capsule,  and  of  the  optic 
thalamus.     It  is  much  commoner  in  cerebral  infantile  paralysis  (vide  infra). 

It  is  interesting  to  observe  the  trophic  and  vasomotor  changes  in  the  paralyzed 
parts.  At  first  the  skin  may  be  somewhat  redder  and  warmer  on  the  paralyzed 
than  on  the  sound  side.  Nothnagel  has  shown  that,  even  in  the  distribution  of 
the  cervical  sympathetic,  symptoms  of  vasomotor  paralysis  occur.  They  are  partly 
temporary  and  partly  persistent  and  comprise  increase  of  temperature  and  color 
in  the  paralyzed  side  of  the  face,  swelling  of  the  eyelids,  and  contraction  of  the 
pupil ;  but  they  are  usually  slight.  We  very  frequently  find,  especially  on  the 
back  of  the  hands,  more  or  less  puffiness,  which  is  likewise  usually  regarded  as  of 
vasomotor  origin.  It  should,  however,  be  considered  that  the  natural  movements 
of  any  part  of  the  body  greatly  promote  the  nervous  and  lymphatic  circulation, 
and  that  the  quietude  of  paralysis  may  therefore  have  much  to  do  with  the  oedema. 
In  hemiplegia  of  some  duration  the  extremities  upon  the  paralyzed  side  are  always 
cooler  than  normal,  and  the  hand  in  particular  is  very  often  deeply  cyanotic. 
The  skin  sometimes  becomes  harsh  and  fissured,  and  often  is  thickened.  The  in- 
ternal surface  of  the  hand,  in  case  of  contracture,  is  frequently  quite  damp  with 
perspiration. 

Among  the  specific  trophic  symptoms  of  hemiplegia  Charcot  includes  "  acute 
malignant  decubitus."  This  sometimes  develops  with  extreme  rapidity  within  a 
few  days  after  the  shock,  and  usually  occupies  the  buttock  on  the  affected  side. 
There  appears  a  circumscribed  redness  with  the  formation  of  vesicles,  which  is 
soon  succeeded  by  a  deep-reaching  necrosis  of  the  soft  parts.  We  have  ourselves 
never  met  with  this  in  a  case  which  has  been  properly  nursed,  and  we  can  not  there- 
fore help  thinking  that  its  development  is  not  wholly  due  to  trophic  disturbance, 
but  to  pressure  and  to  the  penetration  of  septic  matter  below  the  skin.  Of  course, 
patients  long  confined  to  bed  with  hemiplegia  are  as  liable  to  bedsores  as  are  any 
others  similarly  situated. 

The  permanently  paralyzed  muscles  gradually  atrophy  somewhat  in  the  course 
of  years :  yet,  in  uncomplicated  cases  of  cerebral  hemiplegia,  this  atrophy  is  never 
of  the  degenerative  sort,  nor  is  it  usually  very  great.  The  paralyzed  muscles 
therefore  continue  to  react  perfectly  to  faradisni  (see  page  547).  The  joints  of  the 
paralytic  extremities,  and  in  particular  the  knee  and  shoulder,  may  exception- 
ally become  inflamed.  The  arthritis  is  sometimes  acute,  and  sometimes  more  of 
a  chronic  variety.  Its  cause  is  not  evident.  Charcot  thinks  that  it  is  probably 
a  neurotrophic  symptom,  and  he  is  of  the  same  mind  with  regard  to  the  rarely 
seen  swellings  of  the  peripheral  nerve-trunks  of  the  paralyzed  side  ("  hypertrophic 
neuritis  "). 

Mental  symptoms  are  rare,  except  the  initial  loss  of  consciousness.  There  is 
sometimes,  however,  a  persistent  general  uneasiness  of  mind,  accompanied  by 
great  excitability  and  wakefulness.  In  a  large  number  of  cases  of  persistent  hemi- 
plegia there  finally  come  on,  in  the  course  of  veal's,  constantly  increasing  indica- 
tions of  mental  weakness.  The  patient  grows  dull  and  forgetful.  Very  often  he 
exhibits  a  peculiar  tendency  to  weeping,  bursting  into  tears  at  the  slightest  provo- 
cation. But  frequently  he  is  subject  to  quick  alternations  of  feeling,  weeping  and 
laughing  in  the  same  minute. 

The  general  nutrition  is  often  good  for  a  long  while.  Sometimes  there  is  even 
a  decided  tendency  to  corpulence.    In  other  cases,  and  especially  in  the  bedridden, 


73G  DISEASES  OF  THE  NERVOUS  SYSTEM. 

marasmus  gradually  comes  on  and  hastens  the  fatal  termination,  particularly  if 
there  be  some  intercurrent  trouble,  such  as  a  bedsore  or  bronchitis. 

We  have  detailed  the  peculiarities  of  hemiplegia  somewhat  minutely,  because 
the  statements  will  apply  to  all  cases  of  cerebral  hemiplegia,  no  matter  in  what 
place  the  pyramidal  tract  is  interrupted  or  by  what  sort  of  a  lesion.  It  is  need- 
less to  enter  into  the  diverse  symptoms  which  are  caused  by  diversity  in  the  exact 
location  of  the  haemorrhage.  The  hemiplegia  itself  is  the  same,  whether  the  effu- 
sion be  in  the  cortex,  internal  capsule,  crus  cerebri,  or  pons.  It  it  easy  to  infer 
from  the  preceding  chapter  what  the  accessory  symptoms  are  which  would  en- 
able us  to  localize  the  trouble.  We  need  here  mention  only  the  frequent  com- 
bination of  right  hemiplegia  and  aphasia.  This  occurs  when  there  is  a  large 
effusion  in  the  left  hemisphere,  extending  from  the  internal  capsule  to  the  neigh- 
borhood of  the  third  frontal,  or  possibly  the  uppermost  temporal  (compare  page 
716)  convolution. 

Diagnosis. — The  diagnosis  of  cerebral  haemorrhage  rests  on  the  sudden  onset  of 
the  apoplectic  symptoms,  and  on  the  later  symptoms  (if  there  be  any)  of  impair- 
ment of  the  cerebral  functions.  The  diagnosis  can  scarcely  ever  be  made  with 
absolute  certainty,  for  cerebral  embolism  may  exhibit  almost  identical  phenomena: 
the  differential  diagnosis  between  the  two  will  be  given  in  the  following  chapter. 
Occasionally  there  may  be  danger  of  mistaking  other  cerebral  affections  for  a 
haemorrhage,  such  as  meningitis  and  tumors.  The  same  may  be  said  of  a  suddenly 
developed  uraemia,  and  of  constitutional  sepsis.  In  these  cases  the  rapid  onset  of 
grave  cerebral  symptoms  of  a  general  nature,  such  as  unconsciousness,  simulates 
the  apoplectic  coma. 

Prognosis. — The  first  question  is,  whether  the  patient  will  survive  the  initial 
shock.  The  answer  depends  upon  the  severity  of  the  early  symptoms.  The 
deeper  and  more  persistent  the  unconsciousness,  the  more  deficient  the  respiration 
and  pulse,  the  less  the  prospect  of  recovery ;  but  we  can  never  decide  absolutely. 
If  the  patient  have  withstood  the  fii'st  onset  and  be  hemiplegic,  then  the  possibility 
of  improvement  hinges  on  the  question  whether  the  paralysis  is  a  direct  or  an 
indirect  focal  symptom.  Inasmuch  as  there  are  no  means  of  knowing  about  this 
at  first,  we  must  speak  very  guardedly.  It  should  never  be  forgotten  that  the 
haemorrhage  may  recur.  The  predisposing  disease  of  the  blood-vessels  renders 
individuals  who  have  had  one  stroke  liable  to  be  visited,  sooner  or  later,  by 
another. 

Treatment.— The  treatment  of  the  apoplectic  shock  demands,  first  of  all,  rest 
in  bed,  with  the  head  and  shoulders  elevated.  To  avoid  bedsores  it  is  very  impor- 
tant to  maintain  cleanliness,  and  to  watch  attentively  that  portion  of  the  skin 
which  is  pressed  against  the  bed  by  the  weight  of  the  body.  An  ice-bag  should 
be  put  upon  the  head,  and  particularly  over  that  side  on  which  the  haemorrhage 
is  supposed  to  be.  Bleeding  was  formerly  universally  practiced,  but  of  late  its 
usefulness  is  doubted.  It  is  not  indicated  unless  the  deep  congestion  of  the  face, 
the  violent  pulsation  of  the  carotids,  and  the  full,  slow  pulse  show  increased  arte- 
rial tension.  In  such  a  case,  if  the  patient  seem  otherwise  robust,  we  may  bleed 
at  the  commencement  of  an  attack,  in  the  hope  of  checking  the  flow  of  blood  by 
lowering  the  intra-arterial  pressure.  In  similar  conditions  experience  shows  that 
the  local  abstraction  of  blood  from  the  temples  is  sometimes  advantageous.  The 
bowels  should  be  well  emptied  by  enemata,  and  later  on  by  drastic  purgatives.  If 
the  respiration  and  pulse  fail,  we  may  try  stimulants  (ether,  camphor),  but  very 
likely  they  will  be  without  success. 

[Horsley  and  Spencer  have  found,  by  experiments  on  animals,  that  if  the  in- 
ternal carotid  be  tied  the  bleeding  from  the  divided  lenticulo-striate  artery  is 
checked.     Horsley  therefore  suggests  that  in  the  very  earliest  stage  of  cerebral 


CEREBRAL  EMBOLISM  AND  THROMBOSIS.  737 

haemorrhage  ligature  or  compression  of  the  internal  carotid  may  check  the  Weed- 
ing, and  prevent  the  formation  of  a  large  clot  and  extensive  destruction  of  the 
brain.     This  procedure  has  not  yet  been  tried  upon  the  human  subject. 

Where  there  is  much  difficulty  in  respiration  during  the  period  of  coma,  relief 
may  sometimes  be  obtained  by  turning  the  patient  upon  the  side. — K.j 

When  the  patient  is  safely  over  the  shock,  our  resources  for  aiding  him  in  the 
further  stages  of  his  trouble  are  very  limited.  As  long  as  headache  and  symptoms 
of  fever  persist,  the  application  of  ice  to  the  head  should  be  kept  up,  and  other 
disturbances  should  be  treated  symptomaticaily.  For  uneasiness  and  wakefulness, 
small  closes  of  morphine  or  chloral  are  given.  Treatment  of  the  hemiplegia  must 
be  deferred  for  the  first  three  or  four  weeks,  until  all  the  initiatory  symptoms  of 
irritation  are  over.  Then  electricity  plays  the  chief  role.  Local  galvanization 
should  be  tried,  the  current  being  made  to  pass  transversely  through  the  head, 
with  as  much  regard  as  possible  to  the  position  of  the  haemorrhagic  focus ;  the 
current  should  be  feeble,  and  the  application  should  occupy  two  or  three  minutes. 
With  this  may  be  combined  galvanization  of  the  sympathetic  nerve  on  the  side  of 
the  haemorrhage.  Nor  should  galvanization  (stroking  with  the  cathode)  and  fara- 
dization of  the  paralyzed  muscles  and  nerves  be  neglected.  If  favorable  changes 
take  place,  it  is,  however,  uncertain  how  much  should  be  ascribed  to  treatment; 
since,  as  has  already  been  stated,  there  is  often  improvement  without  treatment. 

Passive  movements  and  massage  of  the  paralyzed  limbs  are  very  important  as 
a  prophylaxis  against  contractures.  They  should  be  commenced  promptly,  and 
be  methodically  continued.  Massage,  and  later  on  systematic  and  appropriate 
gymnastic  exercises,  may  contribute  much  to  the  restoration  of  voluntary  motions. 
The  same  object  is  also  promoted  by  rubbing  with  spirits  of  camphor,  chloroform 
liniment,  etc. 

Internally,  potassic  iodide  is  frequently  given,  out  of  regard  for  its  "  absoi'bent " 
properties.  We  may  also  try  the  effect  of  strychnine ;  it  is  most  adapted  for  cases 
of  some  duration. 

As  to  baths,  they  should  not  be  too  warm — that  is,  not  over  90°-93°  (26°-27° 
R.).  Moderately  warm  baths,  medicated  with  common  salt  if  it  seems  desirable, 
and  employed  three  or  four  times  a  week,  seem  to  be  beneficial.  If  it  be  thought 
best  to  send  the  patient  to  a  regular  bathing-place,  Wildbad,  Ragatz,  Teplitz,  Wies- 
baden, or  Rehme  may  be  chosen.  At  the  first-mentioned  places  none  but  the 
cooler  springs  should  be  used. 

Hemiplegie  paralysis  often  lasts  so  long  that  the  physician  must  repeatedly 
change  the  details  of  treatment,  so  as  to  support  the  courage  and  patience  of  the 
sufferer.  Particular  care  should  be  given  to  regimen,  in  order  that  any  recur- 
rence of  the  haemorrhage  may,  if  possible,  be  avoided.  The  diet  should  be  simple; 
any  large  amount  of  alcohol  should  be  forbidden ;  and  there  should  be  no  severe 
bodily  exertion  or  mental  excitement. 


CHAPTER  IV. 

CEREBRAL    EMBOLISM    AND    THROMBOSIS. 

{Softening  of  the  Brain  from  Embolism  or  Thrombosis.') 

-Etiology  and  Pathology.— Occlusion  of  the  cerebral  arteries  is  one  of  the  most 
frequent  injuries  inflicted  by  embolism.  Usually  the  emboli  originate  in  the  left 
side  of  the  heart,  from  thrombi  in  the  left  auricle,  or  from  the  thrombotic  deposits 
which  form  in  chronic  endocarditis  (mitral  or  aortic  disease)  upon  the  valves  of 

47 


738  DISEASES  OF  THE  NERVOUS  SYSTEM. 

the  left  ventricle.  Chronic  arterio-sclerosis  may  also  lead  to  thrornhosis  in  the 
larger  arteries,  particularly  the  aorta ;  and  in  case  the  cerebral  arteries  themselves 
are  extensively  atheromatous,  the  larger  vessels  at  the  base  of  the  brain  may  fur- 
nish material  for  embolism  of  the  smaller  cerebral  arteries. 

Thrombosis  of  the  arteries  of  the  brain  is  always  due  to  primary  disease  of  the 
blood-vessels,  the  most  common  cause  being  the  chronic  arterio-sclerosis  just  men- 
tioned. Wherever  the  atheroma  has  altered  the  normal  structure  of  the  intima, 
deposits  of  fibrine  may  take  place.  Their  development  is  further  promoted  by 
the  subnormal  elasticity  of  the  arteries,  and  by  the  occasional  narrowing  of  their 
lumen  ;  for  thus  the  flow  of  blood  is  rendered  slow,  if  not  even  completely 
checked.  It  is  easy  to  understand  that  thrombosis  and  embolism  may  each  give 
rise  to  the  other.  From  every  thrombus  an  embolus  may  be  detached ;  and  every 
firmly  lodged  embolus  may  form  a  nucleus  for  thrombosis. 

Next  to  arterio-sclerosis,  the  most  frequent  cause  of  a  cerebral  thrombus  is 
syphilitic  endarteritis.  In  the  chapter  on  cerebral  syphilis  this  subject  will  be 
minutely  considered.  Whether  thrombi  ever  form  here  independently  of  disease 
of  the  vessels  is  doubtful.  An  apparently  spontaneous  thrombosis  is  now  and 
then  seen  in  patients  who  are  cachectic  or  severely  ill  (cancer,  grave  typhoid  or 
typhus  fever,  pneumonia) ;  in  such  instances  the  cardiac  weakness,  and  possibly 
also  an  abnormal  tendency  of  the  blood  to  coagulate,  are  regarded  as  either  the 
causes,  or  at  least  the  predisposing  factors,  of  the  thrombosis. 

In  whatever  part  of  the  arterial  system  complete  occlusion  has  been  produced 
by  an  embolus  or  thrombus,  the  results  depend  upon  the  possibility  or  impossi- 
bility of  blood  reaching  by  collateral  channels  the  region  thus  deprived  of  its 
ordinary  supply.  If  the  collateral  circulation  prove  efficient,  no  harm  is  done ;  if 
not,  the  tissues  must  perish  and  undergo  "softening."  It  is  thus  a  matter  of  the 
greatest  practical  import  that  the  perforating  arteries  of  the  brain-stem,  and  par- 
ticularly the  branches  of  the  middle  cerebral  artery  in  the  fissure  of  Sylvius, 
which  supply  the  great  central  ganglia  and  internal  capsule,  are  all  "  terminal," 
in  Cohnheim's  sense— that  is,  they  form  few  anastomoses  with  neighboring  ves- 
sels. Now,  the  middle  cerebral  artery  and  its  branches  are  known  from  experience 
to  be  peculiarly  liable  to  embolism,  above  other  cerebral  arteries.  Hence  we  see 
why  the  region  they  supply  suffers  so  severely  and  so  very  frequently  from  emboli.. 
It  is  noteworthy  that  the  left  middle  cerebral  artery  is  more  frequently  plugged 
by  emboli  than  is  the  right.  In  the  centrum  ovale  and  cortex  there  is  more  op- 
portunity for  collateral  compensation  than  in  the  central  ganglia;  but  even  here 
the  supply  of  blood  often  proves  insufficient,  as  is  shown  by  the  not  infrequent 
occurrence  of  spots  of  softening  in  the  cortex  and  the  white  substance  of  the  cere- 
brum. On  the  other  hand,  embolic  foci  are  much  rarer  in  the  crura  cerebri,  pons, 
and  cerebellum. 

The  various  steps  in  the  process  which  begins  with  embolic  or  thrombotic 
occlusion  and  ends  in  softening  of  the  brain-substance  are  essentially  the  same  as 
occur  in  other  organs  (compare  chapter  on  pulmonary  embolism,  page  247).  The 
tissues  which  are  deprived  of  their  arterial  blood  perish,  become  disintegrated,  and 
are  transformed  into  a  soft  homogeneous  mass.  Into  the  empty  portion  of  the 
artery,  beyond  the  embolus,  blood  flows  in  the  reversed  direction  from  the  veins, 
and,  if  the  anatomical  relations  permit,  from  the  minute  arteries  in  the  neighbor- 
hood ;  but  the  supply  is  not  sufficient  to  nourish  the  tissues.  The  walls  of  the 
blood-vessels  become  abnormally  permeable  and  delicate,  so  that  some  red  glob- 
ules invade  the  disintegrating  region  by  diapedesis,  and  others  in  the  way  of 
minute  but  genuine  ecchymoses.  Actual  infarctions  are,  however,  never  formed 
in  the  brain,  perhaps  because,  as  Weigert  suggests,  the  nervous  structures  swell  so 
much  as  to  exclude  any  large  amount  of  blood;  but  the  little  punctiform  ecchy- 


CEREBRAL  EMBOLISM  AND  THROMBOSIS.  739 

moses  are  in  many  instances  so  abundant  that  the  whole  softened  spot  seems  dis- 
tinctly reddish  or  yellowish.  This  red  or  yellow  softening  is  also  duo  in  part  to 
the  tissues  being  stained  by  the  dissolved  pigment  of  disintegrated  blood-glob- 
ules. If  the  discoloration  be  not  very  striking,  then  we  speak  of  a  white  soft- 
ening. 

Fresh  foci  of  softening  are  seen  through  the  microscope  to  be  composed  of  drops 
of  myeline,  bits  of  swollen  nerve-fibers,  numerous  fatty  granular  cells,  and  free 
fat  globules.  The  minimum  time  required  for  these  changes  is  one  or  two  days. 
If  within  that  period  a  compensatory  collateral  circulation  is  set  up,  the  nervous 
structures  may  be  restored  and  resume  their  functional  activity.  If  not,  the  tis- 
sues perish  and  become  disintegrated.  The  white  blood-corpuscles  and  leucocytes 
(and  possibly  also  the  endothelial  cells  of  the  blood-vessels,  and  the  neuroglia  and 
ganglion-cells)  absorb  the  fatty  detritus  thus  made,  and  come  to  form  the  fatty 
granular  cells  above  mentioned.  If  the  patient  live,  the  dead  and  disintegrated 
tissue  is  gradually  absorbed,  and  it  may  even  finally  be  replaced  by  a  cyst  not  differ- 
ent in  appearance  from  those  which  occur  after  cerebral  haemorrhage.  A  minute 
focus  of  softening  may  sometimes  also  be  replaced  by  indurated  cicatricial  tissue. 
If  portions  of  the  surface  of  the  brain  become  softened,  quite  a  deep  depression 
often  results.  This  is  filled  up  in  part  with  serous  fluid  and  in  part  by  hyperplasia 
of  the  pia  mater.  Sometimes  the  convolutions  are  still  recognizable  in  places ; 
but  they  are  atrophied,  of  a  yellowish  color,  and  of  a  greatly  increased  consist- 
ence, due  to  the  growth  of  cicatricial  tissue. 

Clinical  History. — The  occurrence  of  cerebral  embolism  is  atteuded  with  almost 
precisely  the  same  sort  of  shock  as  is  cerebral  haemorrhage.  We  do  not  need 
to  enter  into  the  particulars  again  here,  but  will  refer  to  the  preceding  chapter 
(vide  page  727).  In  embolism,  also,  the  intensity  of  the  shock  varies;  it  ranges 
between  extreme  mildness,  when  it  occasions  only  transitory  confusion  of  intel- 
lect or  slight  vertigo,  to  the  greatest  severity,  when  there  is  deep  and  persistent 
coma.  One  chief  factor  in  determining  the  nature  of  the  case  is  the  size  of  the 
occluded  artery;  another  is  its  position,  according  as  the  embolism  has  taken 
place  in  the  hemispheres  or  toward  the  base  of  the  brain.  In  general,  the  shock 
of  embolism  is  not  often  so  severe  and  long  continued  as  that  of  haemorrhage ; 
and  embolism  does  not  so  frequently  give  rise  to  symptoms  of  cerebral  compres- 
sion, including  slowing  of  the  pulse.  On  the  other  hand,  epileptiform  convul- 
sions are  seen  more  often  in  embolism  than  in  haemorrhage.  Embolism  again 
may  have  a  rather  slow  onset,  where  there  is  at  first  a  small  embolus  and  this 
becomes  the  nucleus  of  a  gradually  formed  thrombus. 

It  is  not  easy  to  explain  why  there  should  be  a  shock  at  all  in  case  of  embolism. 
Perhaps  the  main  reason  is  the  diminution  of  pressure  which  the  embolism 
occasions  in  the  region  directly  affected  and  in  its  neighborhood.  The  portion  of 
the  artery  beyond  the  plug  becoming  empty,  not  only  causes  a  draught  upon  the 
blood  and  lymph,  but  subjects  all  the  soft  surrounding  structures  to  a  diminution 
of  tension  and  to  a  certain  amount  of  strain  (Wernicke).  It  is  not  impossible, 
however,  that  the  disturbance  of  circulation  occasioned  in  the  surrounding  blood- 
vessels by  sudden  embolism  of  a  good-sized  artery  is  of  itself  enough  to  account 
for  the  symptoms  of  shock. 

With  regard,  also,  to  the  persistent  symptoms  of  embolism  we  may  be  equally 
brief,  inasmuch  as  they  very  closely  resemble  those  which  follow  a  cerebral 
haemorrhage.  As  has  been  said,  it  is  only  when  a  compensatory  collateral  circu- 
lation is  developed  within  the  first  forty-eight  hours  that  the  early  symptoms  of 
focal  disturbance  can  entirely  vanish.  After  this  period,  the  tissues  which  have 
been  deprived  of  their  normal  blood-supply  must  undergo  necrosis;  although 
there  is  still  room  for  hope  that  some  of  the  symptoms  will  prove  indirect,  and 


740  DISEASES  OF  THE  NERVOUS  SYSTEM. 

therefore  capable  of  improvement,  so  that  embolic  hemiplegia,  like  that  from 
hemorrhage,  may  improve  decidedly  in  the  course  of  the  first  few  weeks. 

Inasmuch  as  the  middle  cerebral  artery  is  by  far  the  most  frequent  seat  of 
cerebral  embolism,  and  inasmuch  as  this  artery  supplies  the  internal  capsule  as 
well  as  the  great  central  ganglia,  the  most  frequent  focal  symptom  of  embolism 
of  the  brain  is  ordinary  cerebral  hemiplegia,  all  the  features  of  which  have  been 
depicted  in  the  preceding  chapter.  Aphasia  is  associated  with  it  with  comparative 
frequency,  for,  as  already  mentioned,  the  left  middle  cerebral  artery  is  especially 
apt  to  suffer.  Less  frequent  is  paralysis  of  a  single  member,  due  to  cortical  embo- 
lism, or  an  occipital  lesion  with  hemiopia. 

Where  softening  is  the  result  of  thrombosis,  the  symptoms  are  but  seldom 
abrupt  in  their  onset.  Usually  the  focal  symptoms  and  the  more  general  ones 
(such  as  unconsciousness)  are  developed  rather  gradually.  This  is  most  often  seen 
in  so-called  senile  softening  of  the  brain,  a  disorder  almost  always  caused  by 
sclerosis  of  the  cerebral  arteries.  The  various  symptoms  generally  come  on  under 
cover  of  repeated  relapses  and  fresh  aggravations  of  the  disease.  A  sevei'e  initial 
shock  seldom  occurs;  but  almost  invariably  there  is  a  gradual  and  progressive 
dementia. 

The  further  course  and  the  final  termination  of  cerebral  softening  vary  as  do 
those  of  cerebral  haemorrhage.  Embolism  of  a  larger  artery  may  cause  speedy 
death.  If,  however,  the  first  shock  passes  away,  the  impairment  of  function 
which  may  be  left  behind  may  last  for  years  without  seriously  affecting  the 
general  health.  There  is  always  danger  of  a  recurrence  when  the  source  of  the 
embolism  continues  unchanged,  as  in  cardiac  disease  or  atheroma. 

Diagnosis. — Both  the  onset  and  the  persistent  focal  symptoms  are  so  much  alike 
in  haemorrhage  and  embolism  that  in  many  cases  it  is  utterly  impossible  to  decide 
which  caused  the  apoplexy  and  hemiplegia.  The  following  are  factors  in  making 
a  differential  diagnosis,  if  one  can  be  made:  1.  It  is  very  important  whether  there 
be  any  source  for  an  embolus.  Thus,  if  the  patient  have  valvular  cardiac  disease 
(particularly  mitral),  embolism  is  more  probable  than  haemorrhage.  2.  A  young 
person  is,  on  the  whole,  more  apt  to  have  embolism  than  haemorrhage.  At  a  later 
period  of  life  one  is  about  as  probable  as  the  other.  3.  When  the  shock  is  severe 
and  persistent,  with  red  face,  strong  pulsation  of  the  carotids,  and  signs  of  cerebral 
compression  (slow  pulse),  we  would  think  of  haemorrhage  rather  than  embolism, 
in  which  latter  the  initial  symptoms  are  sometimes  comparatively  slight  {vide 
supra).  4.  Finally,  it  is  sometimes  possible  to  obtain  support  for  a  diagnosis  of 
cerebral  embolism  by  demonstrating  embolism  elsewhere,  as  in  the  fundus  oculi, 
by  means  of  the  ophthalmoscope. 

In  rare  instances,  also,  tumors  of  the. brain,  into  the  substance  of  which  haem- 
orrhage takes  place,  may  induce  symptoms  closely  simulating  a  primary  apoplec- 
tic shock,  as  may  also  abscesses  which  have  been  previously  latent,  and  then  sud- 
denly burst  into  a  ventricle.     In  such  cases  a  correct  diagnosis  is  seldom  possible. 

Softening  due  to  a  thrombus  is  the  most  readily  diagnosticated  in  those  cases 
where  there  is  cerebral  syphilis  (q.  v.).  Senile  softening  is  inferred  from  the  age 
of  the  patient,  the  signs  of  general  arterio-sclerosis,  the  abrupt  advances  of  tbe  dis- 
ease from  mildness  toward  severity,  and  the  developing  dementia. 

For  the  prognosis  and  treatment  of  cerebral  embolism  we  may  refer  simply  to 
what  was  said  in  the  preceding  chapter. 


INFLAMMATION  OF  THE  BRAIN.  741 

CHAPTER  V. 

INFLAMMATION   OF   THE   BRAIN 

(Acute  and  Chronic  Encephalitis.) 

1.  Abscess  of  the  Brain  (Suppurative  Encephalitis;. 

iEtiology. — In  most  cases  of  cerebral  abscess  it  is  possible  to  demonstrate  witb 
certainty  tbat  infectious  material  capable  of  exciting  suppuration  has  penetrated 
to  the  encephalon.  This  is  particularly  true  of  those  not  very  rare  abscesses  which 
follow  injuries  of  the  scalp,  cranium,  or  brain  (traumatic  abscess  of  the  brain). 
Here  the  wound  is  almost  always  an  open  one,  affording  free  ingress  to  the  virus. 
It  is  not  essential  that  the  bones  should  be  injured,  for  experience  shows  that,  even 
where  the  soft  parts  alone  are  wounded,  suppuration  may  extend  to  the  brain. 
The  manner  in  which  this  extension  takes  place  determines  the  question  whether 
a  suppurative  meningitis  (q.  v.)  or  an  abscess  shall  be  developed.  Not  infrequently 
we  find  the  two  combined.  Another  source  of  traumatic  cerebral  abscess  is  foreign 
bodies  which  penetrate  into  the  brain  (for  instance,  through  the  orbit),  and  thus 
carry  septic  matter  into  the  very  substance  of  the  organ.  Some  exceptional  cases 
have  been  reported  of  traumatic  cerebral  abscess  without  any  open  wound ;  as  yet 
they  are  beyond  our  comprehension.  Possibly  there  is  even  in  these  some  minute 
wound  invariably  present  but  overlooked. 

Analogous  to  the  above  causes  is  suppuration  in  neighboring  parts,  which  may, 
by  direct  extension,  occasion  cerebral  abscess.  The  same  processes  are  prominent 
in  this  connection  which  we  have  already  found  to  excite  purulent  meningitis  (vide 
page  698) — particularly  suppuration  (caries)  in  the  middle  ear  and  in  the  petrous 
bone.  In  such  a  case  the  most  frequent  position  of  the  abscess  is  naturally  the 
temporal  lobe  or  the  cerebellum.  Abscesses  also  occur  in  the  anterior  part  of  the 
brain,  from  suppurative  processes  in  the  nasal  cavity  and  the  ethmoid  bone ;  but 
this  mode  of  origin  is  much  less  frequent. 

In  yet  a  third  class  of  cases  the  morbific  agents  are  conveyed  from  foci  of 
disease  situated  in  distant  parts  of  the  body.  These  are  metastatic  or  embolic 
abscesses.  They  occur,  for  instance,  in  pyaemia  and  ulcerative  endocarditis. 
Abscesses  of  this  sort,  however,  are  usually  small,  and  seldom  are  conspicuous  in 
modifying  the  grave  general  disease.  Of  more  importance  are  cerebral  abscesses 
connected  with  certain  suppurative  affections  of  the  lungs  and  pleura.  These  are 
not  so  very  rare.  They  are  of tenest  associated  with  fetid  bronchitis,  pulmonary 
gangrene,  and  empyema.  Purulent  meningitis  (q.  v.)  may  occur  in  the  same  way. 
There  can  be  no  doubt  that  virus  is  in  some  way  conveyed  to  the  brain,  but  just 
how  is  not  yet  known. 

In  some  few  cases  of  cerebral  abscess  no  certain  aetiology  can  be  made  out. 
To  these  the  term  idiopathic  is  applied.  We  met  with  several  of  them  just  at  the 
time  of  an  epidemic  of  cerebro-spinal  meningitis ;  and  it  therefore  seems  reason- 
able to  suspect  that  possibly  many  apparently  spontaneous  cerebral  abscesses  are 
referable  to  the  same  poison  as  is  epidemic  meningitis. 

Pathology. — The  pathological  anatomy  of  abscess  of  the  brain  is  precisely  the 
same  as  that  of  abscesses  in  other  organs.  The  size  varies  from  minute  foci 
hardly  as  large  as  a  lentil  to  great  cavities  occupying  nearly  the  whole  of  one 
lobe.  Not  infrequently  several  abscesses  appear  simultanously  in  different  parts 
of  the  brain.  The  pus  is  usually  greenish  yellow.  It  may  be  odorless  or  offen- 
sive. Sometimes  remnants  of  the  destroyed  ("melted")  nervous  tissue  and  red 
blood-globules  are  mixed  with  it.  The  walls  of  the  abscess  often  bulge  out  irregu- 
larly.    The  cerebral  parenchyma  around  the  abscess  for  a  greater  or  less  distance 


742  DISEASES  OF  THE  NERVOUS  SYSTEM. 

exhibits  white  softening.  This  is  due  partly  to  the  pressure  and  partly  to  the 
spread  of  the  inflammation.  An  abundance  of  granular  cells  is  generally  to  be 
found  in  the  tissues  near  the  abscess. 

If  the  abscess  be  very  large  and  reach  nearly  to  the  surface  of  the  brain,  it  may 
sometimes  be  recognized  during  life  by  a  distinct  bulging  and  fluctuation.  The 
convolutions  on  the  surface  of  the  affected  hemisphere  are  almost  always  flat- 
tened. If  the  abscess  extend  clear  to  the  surface  of  the  brain,  purulent  menin- 
gitis is  excited.  Abscesses  which  are  centrally  situated  not  infrequently  burst 
into  a  lateral  ventricle.  An  abscess  of  long  standing  may  finally  become  encap- 
sulated— that  is,  become  incased  in  a  smooth,  Arm  layer  of  connective  tissue 
which  prevents  further  extension  of  the  process.  The  pus  inside  gradually 
becomes  thick  and  cheesy.  Apparently,  however,  it  is  very  seldom  entirely 
absorbed. 

Clinical  History.— Small  abscesses,  and  even  large  ones,  may  for  a  long  while 
have  scarcely  any  symptoms.  This  is  particularly  true  of  idiopathic  abscesses, 
and  of  those  which  develop  very  slowly  and  insidiously  after  apparently  insig- 
nificant injuries  of  the  head  or  in  connection  with  chronic  inflammation  of  the 
middle  ear. 

In  cases  following  more  extensive  injuries,  the  symptoms  are  more  violent 
from  the  start ;  which  is  also  true  of  many  abscesses  which  develop  acutely  and 
enlarge  rapidly.  The  symptoms  can  hardly  be  distinguished  from  acute  menin- 
gitis. The  patient  is  dull,  or  grows  delirious ;  he  has  violent  headache  and  fever. 
Sometimes  the  temperature  repeatedly  rises  to  a  high  point.  The  loss  of  conscious- 
ness becomes  more  and  more  complete ;  and  in  a  comparatively  brief  time  (one  or 
two  weeks)  there  may  be  profound  coma  and  death.  Rarely  the  violent  symp- 
toms abate,  and  the  acute  passes  into  a  chronic  stage. 

The  symptoms  of  cerebral  abscess,  when  it  pursues  a  chronic  course,  may  be 
divided  into  (1)  the  general  symptoms  and  (2)  the  focal  symptoms,  resulting  from 
the  special  position  of  the  abscess.  There  is  no  other  localized  cerebral  disorder 
in  which  the  focal  symptoms  are  so  often  absent,  either  for  a  long  while  or  even 
throughout  the  illness.  This  is  partly  because  the  abscesses  are  often  situated  in 
parts  of  the  brain,  injury  to  which  does  not  occasion  any  demonstrable  focal 
symptoms.  Such  localities  are  the  white  matter  of  the  frontal  lobe,  and  the  hemi- 
spheres of  the  cerebellum.  A  second  reason  is  that  an  abscess  seldom  excites  indi- 
rect focal  symptoms  by  affecting  the  parts  around  it. 

Among  the  general  symptoms,  the  most  important  is  a  persistent,  deeply  situ- 
ated, dull  headache.  For  a  long  while  it  may  be  the  only  symptom,  especially 
when  the  abscess  is  gradually  developed  after  an  injury  to  the  head  or  after  aural 
disease  of  long  standing.  The  pain  is  referred  mainly  to  the  seat  of  the  abscess; 
but  the  exceptions  to  this  rule  are  not  infrequent.  Another  frequent  symptom  is 
vertigo;  and  in  many  cases  there  is  vomiting,  either  after  meals  or  entirely  inde- 
pendently of  food.  Another  valuable  symptom  in  diagnosis  is  the  irregular  fever, 
sometimes  slight,  and  sometimes  exhibiting  great  elevations  with  intervals 
between  them ;  but  in  many  cases  also,  particularly  where  the  abscess  is  encap- 
sulated, there  may  be  no  fever  whatever.  An  important  negative  point  is  that 
choked  disk  is  much  rarer  in  cerebral  abscess  than  in  case  of  tumors  (q.  v.). 

The  general  health  may  be  but  slightly  disturbed.  Usually,  however,  there  is 
decided  indisposition.     The  patient  is  pale,  has  no  appetite,  and  loses  flesh. 

As  to  the  focal  symptoms,  little  need  here  be  added  to  what  is  contained  in 
Chapter  II  of  this  section.  Abscesses  involving  the  motor  region  of  the  cortex 
have  been  repeatedly  found  to  cause  limited  epileptiform  attacks  and  paralysis  of 
some  one  limb.  It  is  particularly  characteristic  that,  as  the  abscess  grows,  one 
symptom  of  paralysis  is  added  to  another,  and  that  often  the  advance  of  the 


INFLAMMATION  OF  THE  BRAIN.  743 

paralysis  is  ushered  in  by  epileptiform  convulsions.  Abscesses  in  the  occipital 
lobe  have  repeatedly  been  observed  to  cause  heiniopia,  and  abscesses  in  the  tem- 
poral lobe  word  deafness;  and  these  facts  have  been  used  in  making  a  diagnosis 
of  the  location  of  abscesses.  Abscesses  in  the  cerebellum  may  remain  unsuspected 
for  a  long  while ;  or  the  above-mentioned  general  symptoms  may  occur  in  especial 
severity  in  such  cases. 

The  duration  of  chronic  cerebral  abscess  varies  greatly.  In  most  cases  it  lasts 
for  months ;  and  sometimes  it  has  certainly  lasted  for  years.  Particularly  where 
the  abscess  gives  rise  to  no  symptoms,  or  merely  to  slight  and  indefinite  ones  refer- 
able to  the  head,  it  may  last  a  very  long  while.  It  is  quite  often  the  case  that 
there  are  separate  attacks  of  the  severe  symptoms,  such  as  headache,  vomiting,  and 
fever,  and  that  in  the  intervals  of  variable  duration  between  these  paroxysms  the 
patient  feels  pretty  well. 

The  final  termination  of  cerebral  abscess  is  almost  always  fatal.  Recovery  is 
not  impossible,  but  it  has  been  seen  with  certainty  in  only  a  very  few  instances. 
Death  either  comes  on  gradually,  where,  as  the  abscess  grows  larger,  all  the 
symptoms  become  correspondingly  aggravated ;  or  it  may  happen  quite  suddenly. 
Sometimes  it  is  brought  about  by  the  abscess  bursting  into  a  lateral  ventricle, 
or  by  the  supervention  of  meningitis.  Often  a  cerebral  abscess  terminates  in  a 
sudden  and  unexpected  death,  where  no  immediate  cause  for  the  event  can  be 
found. 

Diagnosis. — Although  it  is  often  possible  to  make  a  correct  diagnosis  of  cere- 
bral abscess,  yet  there  is  usually  a  good  deal  of  difficulty  in  arriving  at  such  a 
conclusion,  and  entire  certainty  is  seldom  attainable.  The  most  important  points 
in  diagnosis  are :  (1)  The  demonstration  of  some  cause  such  as  trauma,  chronic  otitis, 
fetid  pulmonary  diseases,  or  empyema.  (2)  The  presence  of  general  cerebral 
symptoms,  such  as  headache,  vertigo,  and  vomiting ;  and  the  fact  that  these  are 
sometimes  better  and  sometimes  worse.  To  aid  in  excluding  tumor,  we  have  (3) 
the  febrile  symptoms  frequently  caused  by  abscess,  but  rare  in  case  of  tumor; 
and  (4)  the  extreme  rarity  of  choked  disk,  which  is  very  frequently  occasioned 
by  tumors.  The  focal  symptoms,  if  there  be  any,  are  not  characteristic.  They 
grow  worse  by  fits  and  starts  in  tumor  just  as  in  abscess.  One  fact,  however,  is 
of  value,  namely,  that  while  tumors  {vide  infra)  frequently  cause  disturbances  in 
the  area  of  distribution  of  the  nerves  at  the  base  of  the  brain  (such  as  paralysis  of 
the  motor  oculi),  an  abscess  does  this  only  exceptionally.  It  is  often  quite  impossi- 
ble to  make  a  differential  diagnosis  between  acute  abscess  and  purulent  meningitis, 
unless  focal  symptoms  are  developed.  These  can  be  caused  by  a  circumscribed 
lesion  alone,  and  therefore  point  to  abscess. 

Treatment.— The  only  possible  way  in  which  to  cure  an  abscess  is  by  opera- 
tion; the  skull  is  trephined  and  the  abscess  laid  open.  It  can  be  readily  seen  that 
such  a  procedure  is  feasible  in  but  few  instances.  We  need  to  be  certain  that 
there  is  an  abscess  and  where  it  is  located,  and,  finally,  that  it  is  so  located  as  to 
render  operation  permissible.  Under  the  present  antiseptic  modes  of  procedure, 
the  dangers  of  an  operation  need  not  be  over-estimated.  For  particulars  we  must 
refer  to  works  on  surgery. 

If  operation  be  not  justifiable,  nothing  but  purely  symptomatic  treatment  is 
left  us.  Ice  to  the  head,  narcotics,  potassic  bromide,  electricity,  and  sometimes 
also  the  local  abstraction  of  blood,  are  the  main  remedies  beyond  general  hygienic 
measures. 

2.  Acute  and  Chronic  Non-suppurative  Encephalitis. 

While  the  spinal  cord  is  quite  frequently  affected  by  idiopathic  circumscribed 
inflammation   (transverse  myelitis),  analogous  cerebral  disease  is  much  more 


744  DISEASES  OF  THE  NERVOUS  SYSTEM. 

exceptional.     The  scanty  information  which  we  possess  upon  the  subject  is  as 
follows : 

1.  Idiopathic  (Inflammatory)  Softening  of  the  Brain.— In  rare  instances  there 
are  found  in  the  brain  quite  extensive  foci  of  softening,  the  pathological  anatomy 
of  which  is  almost  identical  with  that  of  embolic  softening,  and  yet  the  afferent 
blood-vessels  do  not  furnish  any  explanation  of  the  condition.  They  have  ac- 
cordingly been  termed  "foci  of  inflammatory  softening."  The  mode  of  their 
production  is  unknown.  The  symptoms  resemble  closely  those  of  softening  from 
thrombus. 

2.  Curable  Form  of  Encephalitis. — In  certain  cases  pronounced  symptoms  of 
focal  disease  exist  for  a  time,  and  suggest  a  tumor  or  the  like;  but  after  some 
months,  or  even  a  still  longer  time,  the  symptoms  gradually  abate,  and  finally 
there  is  complete  recovery.  Such  cases  undoubtedly  occur.  They  are  usually 
explained  by  assuming  that  there  has  been  a  localized  inflammation,  followed  by 
a  restoration  to  the  normal  state.  The  nature  of  the  symptoms,  as  we  have 
observed  them,  would  seem  to  imply  that  the  lesion  is  generally  in  the  neighbor- 
hood of  the  cortex,  for  there  is  usually  paresis  of  some  one  part  of  the  body,  often 
associated  with  certain  symptoms  of  irritation  and  impairment  of  speech.  Possi- 
bly the  recoveiy  of  these  cases  may  be  assisted  by  electricity  and  potassic  iodide; 
but  we  should  never  venture  upon  an  absolutely  favorable  prognosis. 

3.  Diffuse  Cerebral  Sclerosis.— Diffuse  sclerosis  of  the  brain  is  a  peculiar  dis- 
ease, which  is  usually  classed  as  a  chronic  inflammation.  The  whole  brain  may 
be  involved,  or  the  disease  may  be  confined  chiefly  to  a  large  part  of  one  hemi- 
sphere. There  is  a  very  marked  increase  in  the  consistency  of  the  brain-substance, 
so  that  it  cuts  like  a  tough  piece  of  leather.  The  microscope  reveals  in  many 
cases,  but  not  in  all,  diffuse  hyperplasia  of  the  neuroglia.  In  a  case  which  we 
recently  examined  there  was  a  decided  atrophy  of  the  nervous  fibers  lying  in  the 
white  substance  of  the  brain.  The  disease  is  rare,  and  its  characteristic  symptoms 
can  not  yet  be  stated  absolutely.  They  are  developed  slowly.  The  most  constant 
among  them  seem  to  be  hemiplegia  without  much  change  in  sensation ;  symp- 
toms of  motor  irritation,  such  as  epileptiform  convulsions  (sometimes  general  and 
sometimes  tmilateral),  or  single  twitchings,  which  may  be  rhythmical  or  like 
those  of  chorea;  and,  lastly,  dementia.  Where  both  hemispheres  are  involved, 
there  are  usually  marked  spastic  symptoms  in  the  lower  limbs. 

The  disease  has  been  observed  in  children  and  in  elderly  people.  Possibly 
chronic  alcoholism  sometimes  acts  as  an  ^etiological  factor.  Treatment  can  be 
only  symptomatic. 

Multiple  sclerosis  of  the  brain  is  almost  always  associated  with  the  same  affec- 
tion of  the  spinal  cord.  We  have,  therefore,  already  described  the  disease  in  the 
preceding  section  (page  627). 

4.  The  Acute  Encephalitis  of  Children.  (Cerebral  Paralysis  of  Children. 
Spastic  Infantile  Hemiplegia  of  Benedikt.) — Children  not  infrequently  suffer 
from  a  definite  form  of  hemiplegia,  which  deserves  a  brief  special  description. 

The  patient  is  usually  between  one  and  four  years  old.  The  commencement 
of  the  symptoms  is  almost  always  acute.  Having  been  previously  healthy,  the 
child  is  suddenly  attacked  with  malaise  and  fever.  Very  often  there  is  nausea 
and  vomiting,  speedily  or  at  once  followed  by  grave  cerebral  symptoms.  There 
is  stupor,  and  convulsions  are  particularly  frequent.  This  condition  may  last  but 
one  or  two  days ;  or  it  may  continue,  perhaps  with  unabated  severity,  for  two  or 
three  weeks.  Then  the  acute  symptoms  abate,  and  the  child  recovers  compara- 
tively fast ;  but  it  is  noticed  by  the  parents  to  be  paralyzed ;  and  this  paralysis 
seldom  entirely  disappears,  although  it  may  diminish. 

If  such  children  come  under  observation  after  the  pai'alysis  has  lasted  some 


INFLAMMATION  OF  THE  BRAIN.  745 

time,  as  is  usually  the  case,  their  condition  is  generally  as  follows:  The  cranial 
nerves,  as  a  rule,  are  but  little  affected.  The  main  change  is  in  the  extretnities  of 
one  side ;  and  the  arm  is  almost  always  worse  than  the  leg.  The  affected  parts 
betray  an  arrest  of  development,  more  or  less  impairment  of  motion,  in  many 
cases  a  marked  exaggeration  of  the  tendon  reflexes,  and  almost  invariably  con- 
tractures of  more  or  less  severity.  The  muscles,  although  generally  somewhat 
atrophied,  never  exhibit  the  reaction  of  degeneration.  Sensation,  as  a  rule,  is 
unimpaired.  Motor  symptoms  of  irritation  are  found  upon  the  affected  side  with 
striking  frequency;  the  commonest  are  movements  like  athetosis  or  chorea  (hemi- 
athetosis,  hemichorea) ;  and  associated  movements  are  also  not  infrequent.  The 
constant  movements  of  the  fingers  resulting  from  the  athetosis  sometimes  render 
the  articulations  so  lax  that  it  is  possible  to  make  the  fingers  assume  an  angle  of 
ninety  degrees  or  even  less  with  the  back  of  the  hand,  at  the  metacarpo-phalangeal 
joint.  The  child  may  keep  making  motions  with  its  paretic  arm  while  walking. 
It  is  not  very  rare  for  epilepsy  to  be  developed  later.  There  are  convulsive 
attacks,  which  usually  begin  on  the  paralyzed  side,  but  which  may  later  affect 
the  whole  body.  The  intellectual  development  of  many  such  children  is  tolerably 
normal.  Others,  however,  are  more  or  less  demented,  or  betray  defective  moral 
sense. 

The  whole  course  of  the  disease  suggests  very  strongly  an  acute  encephalitis. 
The  process  is  probably  in  most  cases  more  or  less  completely  limited  to  the 
motor  region  of  the  cortex,  and  has  hence  been  called  "  periencephalitis."*  It 
reminds  one  forcibly  of  the  acute  poliomyelitis  of  children,  with  a  difference 
merely  in  the  localization  of  the  disturbance.  It  is  not  impossible  that  the  two 
diseases  have  a  very  similar,  if  not  identical,  aetiology.  They  can  hardly  be  differ- 
entiated in  their  initial  stage ;  but  when  further  developed  they  can  not  be  con- 
founded, because  the  cerebral  disease  causes  unilateral  paralysis,  leaves  the  elec- 
trical reaction  unimpaired,  and  frequently  causes  exaggeration  of  the  tendon  reflex. 
It  deserves  mention  that  precisely  similar  phenomena  may  be  presented  by 
children  during  recovery  from  measles,  scarlet  fever,  and  other  acute  infectious 
diseases. 

The  pathological  conditions  of  the  early  stage  have  not  yet  been  studied.  Long 
after  the  process  has  run  its  course,  the  affected  portion  of  the  cerebrum  presents 
marked  atrophy  with  cicatricial  contraction.  If  the  surface  of  the  brain  has  been 
affected,  a  corresponding  depression  is  to  be  noticed  ("  porencephalia  ").  At  these 
places  the  pia  is  thickened.  Sometimes  limited  cystic  formations  are  found.  The 
pyramidal  tract  exhibits  a  secondary  descending  degeneration.  It  is  thus  evident 
that  the  process  is,  from  an  anatomical  point  of  view,  precisely  like  the  atrophy  of 
the  anterior  cornua  occasioned  by  poliomyelitis. 

Of  course  not  all  the  hemiplegias  arising  in  childhood  are  due  to  an  encepha- 
litis, for  in  not  a  few  cases  infantile  hemiplegia  may  be  due  to  embolic  softening, 
and  perhaps  sometimes  to  haemorrhage ;  but  in  most  cases  acute  encephalitis  is 
distinguished  from  these  by  the  peculiarity  of  its  initial  stage.  [There  is  really  no 
pathological  evidence  of  acute  polioencephalitis  in  children.  Sachs  and  Osier, 
from  the  study  of  a  large  number  of  cases,  find  that  the  cause  of  the  paralysis  is 
almost  always  haemorrhage  or  embolic  softening. — K.] 

The  treatment  at  first  is  to  be  governed  by  the  same  rules  as  in  the  initial 
period  of  acute  poliomyelitis  (q.  v).  The  hemiplegic  symptoms  which  persist 
after  the  first  few  months  will  never  improve  much.  The  most  we  can  do  will  be 
by  means  of  electricity,  massage,  and  cold  baths  with  friction  ("  cold  rubbing"). 

[*  This  name,  however,  has  been  previously  applied  by  Wernicke  to  that  form  of  external  ophthal- 
moplegia due  to  changes  in  the  nerve  nuclei  in  the  pons  (vide  page  690). — Trans.] 


746  DISEASES  OF  THE  NEEVOUS  SYSTEM. 

For  the  epileptic  attacks  large  doses  of  bromide  of  potassium  are  decidedly  bene- 
ficial. 

Only  a  very  few  cases  of  primary  acute  non-purulent  encephalitis  of  adults  are 
recorded.  A  short  time  ago  we  saw  such  a  case  in  a  young  man.  Death  occurred 
after  a  few  days'  illness  marked  by  very  severe  cerebral  symptoms  and  at  the 
autopsy  one  cerebral  hemisphere  was  found  studded  with  many  little  hasmorrhagic- 
encephalitic  foci.  ' 


CHAPTER  VI. 
INSOLATION.     SUNSTROKE.     HEAT  PROSTRATION.     THERMIC  FEVER. 

[JEtiology  and  Pathology.— Under  exposure  to  undue  heat,  either  in  the  direct 
rays  of  the  sun,  or,  during  hot  weather,  in  engine-rooms,  laundries,  and  the  like, 
marked  effects  may  be  produced  on  the  human  organism,  manifesting  themselves 
in  a  widely  different  manner  in  different  cases.  The  liability  to  these  effects  is 
much  greater  with  us  than  in  most  portions  of  Europe  or  in  Great  Britain,  and  is 
enhanced  by  a  moist  atmosphere  which  tends  to  prevent  evaporation  from  the 
surface  of  the  body.  Attacks  may  come  on  at  night  and  under  cover  as  well  as 
by  day.  While  excessive  heat  is  the  sole  and  sufficient  exciting  cause  of  the 
changes  and  symptoms  to  be  described,  exhaustion  due  to  muscular  exertion  or 
other  cause  plays  a  very  important  secondary  role.  A  vigorous  person,  however, 
of  regular  and  temperate  habits,  can  stand  much  greater  heat  and  exertion  than 
an  individual  who  is  debilitated  or  addicted  to  the  use  of  stimulants.  The  fre- 
quency of  attacks  after  a  full  meal  has  been  noted.  Those  newly  arrived  in  the 
country  are,  other  things  being  equal,  more  likely  to  succumb  than  natives  or 
those  who  have  become  accustomed  to  the  climate.  That  high  temperature  due  to 
solar  or  artificial  heat,  or  a  combination  of  the  two,  is  the  prime  causative  condi- 
tion, has  been  clearly  shown  by  experiments  on  animals.  There  is  practically  noth- 
ing to  add  to  the  researches  of  H.  C.  Wood. 

Pathological  Anatomy. — In  cases  of  sudden  death  from  shock  there  are  no  con- 
stant and  peculiar  lesions.  The  blood  is  dai'k,  imperfectly  coagulated,  and  col- 
lected in  the  veins ;  ecchymoses  are  frequently  found. 

After  death,  due  chiefly  to  abnormally  high  temperature — that  is  to  say,  in  cases 
of  thermic  fever — the  heart,  and  especially  the  left  ventricle,  is  firmly  contracted 
from  post-mortem  coagulation  of  its  myosin;  the  lungs  are  apt  to  be  much  en- 
gorged with  dark  fluid  blood,  and  may  be  the  seat  of  haemorrhage;  extravasation 
of  blood  under  the  skin  is  more  or  less  marked,  and  haemorrhage  into  and  about 
the  cervical  sympathetic  ganglia  has  also  been  observed.  The  membranes  of  the 
brain  and  cord  are  often  greatly  congested,  and  there  may  be  evidences  of  com- 
mencing meningitis.  The  blood-corpuscles  are  crenated  and  show  a  diminished 
tendency  to  the  formation  of  rouleaux.  Rigor  mortis  is  marked  and  early  in  the 
voluntary  muscles  as  well  as  in  the  heart,  and  is  attributable  to  the  same  cause. 
Parenchymatous  degeneration  of  the  organs  is  sometimes  found. 

Symptoms  and  Coarse. — The  onset  of  the  attack  is  usually  sudden,  though  there 
may  be  slight  premonitions,  such  as  dizziness,  pain,  or  uncomfortable  sensations 
in  the  head. 

It  will,  perhaps,  add  to  clearness  to  distinguish  three  leading  forms  of  attack, 
it  being  understood  that  Nature  does  not  always  classify  cases  as  sharply  as  is 
done  here.  The  first  of  these  comprises  cases  of  heat  prostration,  denoted  by  faint- 
ness,  syncope,  nausea,  and  sometimes  vomiting,  with  marked  muscular  and  gen- 
eral weakness.     The  surface  of  the  body  is  cool,  the  pulse  rapid  and  feeble.     The 


INSOLATION.  747 

great  majority  of  these  cases  are  mild,  and  the  symptoms  pass  away  more  or  less 
quickly  on  placing  the  patient  in  the  recumbent  posture  in  a  relatively  cool  and 
quiet  place  with  free  ventilation.  After  a  few  hours  the  patient  can  be  removed 
to  his  home,  and  in  a  day  or  two  has  recovered  perfectly,  except  for  some  sensi- 
tiveness to  heat  or  the  sun's  rays.  There  may  be  transient  insensibility,  or,  on 
the  other  hand,  the  case  may  terminate  fatally  very  soon  from  general  exhaustion 
and  cardiac  failure. 

The  second  form  includes  cases  with  respiratory  as  well  as  circulatory  failure, 
due  especially  to  the  exhaustion  of  the  nerve  centers  presiding  over  these  func- 
tions. Under  this  head  come  cases  of  true  sunstroke — patients  suddenly  losing 
consciousness  while  exposed  to  the  sun.  The  skin  is  cold  and  the  pulse  is  feeble ; 
death  may  quickly  ensue  or  recovery  may  follow,  especially  if  prompt  and  suit- 
able treatment  be  instituted.  The  after-effects  of  the  attack  may  be  very  slow  to 
pass  away,  and  may  never  disappear  entirely. 

The  most  striking  characteristic  of  the  third  form  is  the  great  increase  in  the 
temperature — a  symptom  which  has  given  rise  to  the  term  thermic  fever.  In  this 
form  premonitions  are  more  common  than  in  the  others.  The  thermometer  may 
register  110°  or  even  more;  the  skin  is  burning  hot  and  generally  dry;  the  pulse 
is  slow  and  full,  or  quick  and  jerking ;  the  respiration  is  quickened,  sighing,  or 
even  stertorous ;  the  pupils  at  first  are  usually  contracted ;  there  may  be  great 
restlessness;  coma  and  convulsions  sometimes  occur;  vomiting  is  common  ;  and, 
toward  the  close  of  life,  the  sphincters  are  sometimes  relaxed.  A  fatal  result  is 
due  to  apncea  and  asthenia  combined.  What  was  said  with  regard  to  recovery 
from  the  second  form  holds  good  also  for  the  third. 

Diagnosis. — This  is  seldom  difficult.  The  circumstances  under  which  the 
attack  comes  on  are  generally  patent ;  and  the  hyperpyrexia,  if  present,  is  dis- 
tinctive. Acute  alcoholism  and  meningitis  are  the  chief  affections  which  might 
lead  to  error. 

Prognosis.— The  mortality  rate  of  the  severer  forms  of  the  disease  is  very  high, 
but  the  prognosis  depends  much  on  the  possibilities  of  securing  prompt  and  skill- 
ful treatment.  Under  this  many  a  case  recovers  from  a  seemingly  desperate  con- 
dition. The  tediousness  and  imperfection  of  recovery  have  been  already  alluded 
to.  For  long  periods  in  some  cases  the  mental  and  physical  powers  are  much 
impaired,  and  great  care  has  to  be  exercised  as  regards  exertion,  high  temperature, 
and  the  sun's  rays.     Insanity  is  sometimes  a  sequel. 

Treatment. — In  the  first  place,  much  may  be  done  by  preventive  measures  to 
obviate  the  necessity  for  any  treatment.  A  regular  and  temperate  life  will  do 
much;  and  special  precautions  of  an  obvious  nature  should  be  taken  during  hot 
weather  by  those  whose  occupations  involve  a  liability  to  exhaustion  and  exposiu-e 
to  unusual  heat.  It  would  be  well  if  it  were  generally  known  that  there  is  com- 
paratively little  danger  of  sunstroke  so  long  as  perspiration  is  free.  Many  an 
attack  might  be  averted  by  noting  the  activity  of  the  skin  and  seeking  rest  and 
shelter  as  sweating  diminishes.  A  considerable  responsibility  rests  upon  militia 
surgeons  and  others  in  similar  positions  during  hot  weather. 

Mild  cases  of  heat  prostration  seldom  require  other  measures  than  those 
already  indicated  in  describing  the  symptoms.  If  there  be  nausea,  and  it  seem  de- 
sirable to  give  stimulants,  they  are  better  given  under  the  skin  or  by  the  rectum. 
The  clothing  should  be  loosened ;  the  cold  douche  and  other  refrigerating  meas- 
ures are  not  indicated  unless  there  is  fever,  and  they  should  then  be  used  with 
caution. 

For  true  sunstroke,  treatment  should  be  active  and  energetic,  the  indications 
being  to  reduce  the  temperature  of  the  overheated  centers  and  to  stimulate  their 
activity.    If  a  cool  or  shady  spot  be  near  at  hand,  the  patient  should  be  removed  to 


748  DISEASES  OF  THE  NERVOUS  SYSTEM. 

it  and  largely  stripped  of  clothing ;  if  not,  no  time  should  he  lost  before  resorting 
to  the  cold  douche  on  the  head  and  body  while  stimulants  are  administered  by 
enema  or  subcutan eously.  External  stimulation  by  mustard  or  flagellation,  and 
purgative  enemata,  are  said  to  be  sometimes  useful.  The  use  of  cold  externally 
should  not  be  prolonged  in  these  cases  unless  there  is  fever.  Nervous  exhaustion 
is  the  prominent  symptom,  and  all  depressing  measures  are  out  of  place. 

The  case  is  widely  different  with  the  third  form  of  the  attack.  Here  the  imme- 
diatfedanger  is  from  the  hyperpyrexia,  which  must  be  combated  by  rubbing  the 
patient  with  ice,  placing  him  in  a  tub  of  water  with  lumps  of  ice,  or  similar  meas- 
ures, until  the  temperature  in  the  rectum  is  reduced  nearly  but  not  quite  to  the 
normal  point.  In  the  application  of  the  refrigerating  measures  the  head  must  not 
be  neglected.  The  sole  indication  at  first  is  the  reduction  of  the  temperature. 
Antipyrine  subcutaneously  has  been  given  in  a  few  cases  in  the  Boston  City  Hos- 
pital, and  also  in  Brooklyn,  with  good  results.  After  a  reduction  of  the  tempera- 
ture, any  symptoms  of  collapse  or  exhaustion  demand  stimulants. 

With  regard  to  the  employment  of  bloodletting  there  is  considerable  differ- 
ence of  opinion.  That  cases  occur  in  which  this  procedure  is  indicated  is 
undoubtedly  true,  but  they  are  exceptional;  they  are  characterized  by  the  evi- 
dences of  great  cerebral  congestion  without  hyperpyrexia. 

The  subsequent  management  of  convalescents  from  any  form  of  sunstroke  is 
often  very  important.  Prolonged  rest,  and  sometimes  change  of  climate,  may  be 
demanded.  A  symptomatic  and  common-sense  treatment  is  in  place.  It  has 
seemed  to  the  editor  that  quinine,  especially  in  solution  with  a  moderate  excess  of 
sulphuric  acid,  is  distinctly  useful  in  those  suffering  from  mild  or  moderate  after- 
effects of  undue  heat.] 


CHAPTER  VII. 
TUMORS    OP    THE    BRAIN. 

iEtiology.— The  precise  causes  which  lead  to  the  development  of  tumors  in  the 
brain  are  no  more  certainly  known  than  in  regard  to  other  organs.  In  most 
cases  the  new  growths  are  formed  insidiously  and  gradually  in  persons  previously 
healthy,  without  ascertainable  cause.  A  circumstance  which  deserves  mention  is 
that  sometimes  the  first  symptoms  come  on  immediately  or  a  short  time  after 
some  injury  to  the  head ;  but  whether  this  is  a  matter  of  cause  and  effect,  or  of 
coincidence,  can  very  seldom  be  determined. 

The  sufferer  from  cerebral  tumor  is  usually  in  middle  life.  Certain  forms  of 
tumor,  however,  particularly  solitary  tubercles,  are  comparatively  frequent  in 
children.  Sex  seems  to  exert  a  decided  influence:  men  are  much  offener  attacked 
than  women. 

Varieties  of  Cerebral  Tumor.* — The  most  important  forms  of  tumor  seen  in  the 
brain  are  as  follows : 

1.  Glioma. — Glioma  is  a  kind  of  tumor  peculiar  to  the  central  nervous  system, 
but  seen  much  offener  in  the  brain  than  in  the  spinal  cord  (vide  page  676). 
Apparently  the  new  growth  always  originates  in  the  neuroglia,  which  is  the  con- 
nective-tissue framework  of  the  true  nervous  matter.  As  seen  under  the  micro- 
scope, a  glioma  is  made  up  of  fibers  and  cells,  the  latter  being  precisely  like  the 

*  From  a  clinical  standpoint,  the  term  "  cerebral  tumor "  usually  is  meant  to  include  also  such 
tumors  as  originate  in  the  neighborhood  of  the  brain  (as  in  the  base  of  the  skull),  if  they  finally 
involve  the  brain  itself. 


TUMORS  OF  THE  BRAIN.  749 

normal  cells  of  the  neuroglia,  while  the  fibers  seem  to  consist  mainly  of  the 
numerous  cell-processes.  Klebs  maintained  that  ihe  ganglion-cells  also  take  an 
active  part  in  the  new  growth;  but  this  has  not  yet  been  proven.  It  is  character- 
istic of  gliomata  that  they  are  seldom  sharply  defined,  but  shade  off  gradually 
into  the  healthy  tissue.  The  affected  portion  of  the  brain  is  usually  enlarged,  but 
yet  maintains  pretty  nearly  its  original  shape.  On  cross-section,  the  glioma 
presents  a  gray  or  reddish-gray  surface.  It  is  usually  rather  soft,  and  almost 
always  is  very  vascular.  This  great  vascularity  is  not  without  clinical  impor- 
tance, for  variations  in  the  fullness  of  the  blood-vessels,  and,  above  all,  sudden 
hemorrhages  into  the  interior  of  the  new  growth,  which  not  infrequently  occur, 
may  produce  marked  symptoms. 

Gliomata  are  most  frequent  in  the  white  substance  of  the  cerebral  hemispheres, 
but  they  are  also  found  in  the  central  ganglia,  cerebellum,  and  elsewhere.  They 
are  usually  single,  seldom  multiple. 

2.  Sarcoma. — It  is  very  seldom  that  any  form  of  sarcoma  originates  in  the 
brain-substance.  It  usually  commences  in  the  connective  tissue  of  neighboring 
parts,  in  the  dura  mater,  the  periosteum  of  the  cranium,  or  the  cranium  itself 
(osteo-sarcoma) .  The  sarcoma  is  most  often  found  at  the  base  of  the  skull,  in  the 
form  of  a  circumscribed  tumor  of  varying  consistency,  and  by  pressing  upon 
neighboring  parts,  or  by  involving  them  in  the  diseased  process,  it  may  cause 
the  gravest  disturbances.  Histologically,  we  have  here  such  varieties  as  round- 
celled,  spindle-celled,  fibro-sarcoma,  etc. 

3.  Gumma  and  Solitary  Tubercle. — Both  gumma  and  solitary  tubercle  are 
very  prone  to  attack  the  brain.  We  shall  revert  to  gumma  in  the  chapter  on 
cerebral  syphilis.  Solitary  tubercles  may  grow  to  the  size  of  a  cherry  or  larger. 
They  may  be  single  or  multiple,  and  may  occupy  any  part  of  the  brain.  They 
are  most  often  found  in  the  cortex,  and  in  the  cerebellum  and  pons. 

Solitary  tubercles  and  gummata,  upon  cross- section,  have  a  yellowish,  cheesy 
appearance,  and  are  usually  distinctly  defined.  Histologically,  they  are  composed 
of  granulation  tissue.  It  was  formerly  no  easy  matter  to  distinguish  gumma  from 
tubercle  in  all  cases;  but  now  complete  certainty  is  attainable  by  determining 
the  presence  or  absence  of  tubercle  bacilli  (and  likewise  of  syphilis  bacilli). 

4.  Carcinoma. — Carcinoma  completes  the  list  of  such  cerebral  tumors  as  have 
much  clinical  importance.  They  are  here  almost  always  secondary.  It  has  been 
our  experience  that  secondary  cancer  of  the  brain  is  principally  associated  with 
primary  cancer  of  the  breast,  or  of  the  lungs  and  pleura;  which  fact  bears  a 
remarkable  analogy  to  the  occurrence  of  secondary  cerebral  abscess  after  primary 
empyema,  pulmonaiw  gangrene,  etc. 

5.  Among  the  rarer  varieties  of  tumor  are  psammoma,  wThich  usually  starts 
from  the  meninges,  is  hard,  generally  comparatively  small,  and  therefore  often 
harmless,  and  contains  calcareous  matter,  so  that  it  grates  under  the  knife; 
cholesteatoma,  a  rare  tumor  which  has  the  brilliancy  of  mother  of  pearl ;  lipoma; 
and  angioma. 

The  General  Symptoms  of  Cerebral  Tumors.— As  is  the  case  with  all  focal  dis- 
eases of  the  brain,  some  of  the  symptoms  of  cerebral  tumors  are  connected  with 
the  special  localization  of  the  new  growth.  There  are  definite  focal  symptoms, 
varying  with  the  part  destroyed,  or  at  any  rate  functionally  impaired,  and  it  is  from 
these  symptoms  alone  that  wTe  are  enabled  to  determine  the  position  of  the  tumor. 
But,  in  addition  to  these  focal  symptoms,  there  are  certain  general  symptoms  com- 
mon to  almost  all  cerebral  tumors  of  any  size.  They  are  in  large  part  referable  to 
the  general  compression  of  the  brain  due  to  the  enlargement  of  the  new  growth. 
In  the  first  place,  numerous  clinical  facts,  which  will  be  immediately  enumerated, 
indicate  that  whenever  there  is  a  tumor  of  any  great  size,  a  large  part  of  the 


750  DISEASES' OF  THE  NERVOUS  SYSTEM. 

entire  enoeplialon  is  subjected  to  pressure;  and,  secondly,  the  anatomical  appear- 
ances of  almost  every  brain  affected  by  a  large-sized  tumor  lead  to  the  same  con- 
clusion. The  convolutions  are  flattened  and  obliterated,  the  dura  mater  is 
crowded  against  the  cranium,  and  perhaps  thinned  or  even  perforated  because  of 
the  persistent  pressure,  or,  on  the  other  hand,  thickened  as  a  result  of  chronic  in- 
flammation. Now  and  then  the  effects  of  pressure  are  visible  even  in  the  bones  of 
the  skull:  they  are  worn  thin,  or  even  perforated,  or  their  sutures  are  loosened. 
Another  result  of  the  general  intracranial  tension,  through  its  effect  upon  the 
venous  trunks  of  the  brain,  is  serous  effusion  into  the  ventricles  (internal  hydro- 
cephalus), which  occurs  very  frequently.  The  largest  effusions  are  caused  by 
tumors  in  the  posterior  cerebral  fossa,  which  directly  compress  the  vena?  Galeni. 

The  symptoms  of  cerebral  tumors,  referable  to  the  effects  of  general  compres- 
sion, are  as  follows : 

1.  Headache  is  one  of  the  earliest  and  most  constant  symptoms.  It  is  usually 
persistent,  although  subject  to  temporary  exacerbations  and  intermissions.  The 
patient  describes  it  as  dull,  deeply  seated,  and  stupefying.  Although  it  affects  the 
whole  head,  it  is  sometimes  (not  invariably)  referred  mainly  to  the  neighborhood 
of  the  tumor.  It  is  particularly  true  of  persistent  occipital  headache  that  it  indi- 
cates a  new  growth  in  the  posterior  fossa.  Sometimes  also  it  is  possible,  by  tap- 
ping upon  the  skull,  to  find  a  hypersesthetic  region.  Considerable  caution,  how- 
ever, should  be  used  in  drawing  diagnostic  conclusions  from  such  observations. 
The  headache  usually  lasts  to  the  close  of  the  disease,  and,  even  after  the  patient 
has  become  completely  comatose,  the  persistence  of  the  pain  is  still  evident,  from 
his  low  groans  and  the  way  in  which  his  hand  seeks  his  head. 

2.  Next  in  frequency  to  headache  are  intellectual  and  mental  disturbances. 
Even  the  facial  expression  may  be  somewhat  characteristic,  being  peculiarly  lan- 
guid, apathetic,  and  dull.  The  patient  talks  slowly,  often  having  to  think  a  long 
while  before  knowing  what  to  say.  Memory  becomes  impaired,  especially  with 
regard  to  the  most  recent  events.  The  interest  of  the  patient  in  those  about  him, 
and  the  things  he  used  to  care  for,  grows  less  and  less.  He  has  a  sleepy,  dazed 
look,  and  grows  careless  and  untidy.  Of  course,  individual  cases  present  various 
deviations  from  this  outline ;  but  in  general,  cases  are  a  good  deal  alike,  although 
the  degree  of  mental  disturbance  may  vary  from  a  slight  dullness  to  complete 
dementia. 

If  unusual  fullness  of  the  blood-vessels,  a  haemorrhage  into  the  new  growth,  or 
some  similar  cause,  induce  a  sudden  temporary  increase  of  tension,  there  may  be 
such  marked  symptoms  as  syncope  or  an  apoplectiform  shock. 

3.  Other  general  cerebral  symptoms  are  vertigo,  slowing  of  the  pulse,  and 
vomiting.  If,  however,  vertigo  be  a  very  prominent  symptom,  it  implies  that  the 
cerebellum  is  especially  encroached  upon  by  the  tumor.  The  retardation  of  the 
pulse  is  a  frequent  symptom,  and  not  without  diagnostic  value.  It  has  already 
been  mentioned  as  one  result  of  general  compression  of  the  brain,  in  connection 
with  cerebral  haemorrhage.  The  rate  may  be  put  at  about  50  to  60,  or  even  lower. 
The  pulse  is  also  sometimes  slightly  irregular.  Cerebral  vomiting  may  be  one  of 
the  earliest  and  most  troublesome  symptoms.  It  frequently  occurs  independently 
of  the  ingestion  of  food,  especially  in  the  morning,  and  is  not  infrequently  asso- 
ciated with  dizziness. 

4.  Epileptiform  convulsions  are  sometimes  excited  by  cerebral  tumors,  al- 
though many  patients  are  free  from  them.  Such  attacks  in  all  probability  origi- 
nate invariably  in  the  cortex  of  the  cerebrum,  and  it  is  therefore  natural  that 
they  should  be  seen  most  frequently  (as  they  are)  in  connection  with  tumors  in 
the  cerebral  hemispheres.  This  rule,  however,  is  not  without  exceptions.  If  the 
convulsions  are  not  general,  but  are  unilateral  or  confined  to  distinct  portions  of 


TUMORS  OF  THE  BRAIN.  Y51 

the  body,  they  are  to  be  regarded  rather  as  focal  than  as  general  symptoms,  and 
may  be  utilized  for  the  approximate  localization  of  the  lesion  (vide  page  711).  A 
certain  amount  of  information  in  the  same  direction  may  also  be  got  from  those 
attacks  which  begin  unilaterally  or  in  one  particular  limb,  and  then  quickly 
involve  the  entire  body. 

5.  Choked  disk  is  one  of  the  most  important  general  objective  symptoms  of 
cerebral  tumor.  We  should  never  omit  to  make  an  ophthalmoscopic  examination 
of  the  fundus  oculi  in  a  case  of  chronic  cerebral  disease.  Some  differences  of 
opinion  yet  exist  in  regard  to  the  special  pathology  of  choked  disk ;  but  we  may 
regard  it  as  extremely  probable  that  the  main  factor  in  its  production  is  the  purely 
mechanical  one  of  general  compression  of  the  brain.  The  original  view  of  Von 
Graefe  was  that  the  increased  intracranial  pressure  obstructs  the  venous  return 
through  the  vena  centralis  retinae  into  the  cavernous  sinus.  The  opinion  which 
prevails  at  present  is  that  advanced  by  Schmidt  and  Manz — namely,  that  the 
increased  tension  forces  the  cerebro-spinal  fluid  into  the  lymph-sheaf  of  the  optic 
nerve  (Schwalbe),  and  that  the  "  hydrops  vaginae  nervi  optici "  thus  produced 
compresses  the  nerve  and  the  blood-vessels  which  traverse  it.  [Leber  and  Deutsch- 
mann have  shown  pretty  conclusively  that  the  increased  pressure  is  not  the  chief 
cause  of  optic  neuritis.  It  favors  its  production,  but  probably  there  must  be  the 
presence  of  some  irritant  as  well,  in  order  to  produce  the  inflammation. — K.]  At 
any  rate,  choked  disk  is  not  a  focal  symptom.  The  tumor  occasioning  it  may 
have  any  position,  if  only  it  gives  rise  to  general  compression  of  the  brain. 

Disturbances  of  vision  may  or  may  not  be  entailed  by  choked  disk  ;  the 
patient  may  have  amblyopia,  defects  in  the  field  of  vision,  or  even  total  blind- 
ness. In  some  few  instances,  amblyopia  has  been  one  of  the  earliest  symptoms 
of  cerebral  tumor,  insomuch  that  the  patient  has  applied  first  of  all  to  an  oculist. 
Usually  the  sight  is  preserved  for  quite  a  long  while,  in  spite  of  the  abundant 
objective  evidences  of  choked  disk.  The  latter  consist  of  swelling  of  the  disk, 
marked  distention  and  tortuosity  of  the  veins,  possibly  haemorrhages  (from  passive 
congestion),  and  cloudiness  of  the  disk,  although  the  retina  still  exhibits  its  nor- 
mal transparency.  It  is  not  until  the  long-continued  congestion  impairs  nutri- 
tion to  such  an  extent  as  to  cause  atrophy  of  the  optic  nerve  that  vision  is  much 
impaired. 

6.  The  last  general  symptom  to  be  mentioned  is  general  loss  of  flesh  and 
strength.  This  often  appears  comparatively  early.  It  is  in  large  part  due  to  the 
small  amount  of  food  taken,  vomiting,  and  wakefulness ;  but  it  is  not  impossible 
that  the  grave  cerebral  disorder  itself  exerts  a  direct  and  unfavorable  influence 
upon  all  the  processes  of  nutrition.  There  is  in  most  cases,  also,  a  tendency  to 
obstinate  constipation. 

Tumors  in  the  Different  Parts  of  the  Brain— their  Focal  Symptoms.— The 
symptoms  above  discussed  indicate  the  existence  of  a  tumor,  but  not  its  particular 
location.  Other  phenomena  are  necessary  to  enable  us  to  localize  the  disease, 
but  it  is  not  exceptional  to  have  none  but  the  general  symptoms.  Tumors  in  the 
white  matter  of  the  frontal  lobe,  or  such  as  affect  the  corpus  striatum,  as  well  as 
others,  may  run  their  course  without  any  focal  symptoms ;  but  most  cases  afford 
evidence  which  points  with  more  or  less  certainty  to  the  exact  position  of  the 
tumor.  Almost  all  of  these  focal  symptoms  have  already  been  fully  discussed  in 
Chapter  II  of  this  section,  and  their  interpretation  follows  the  rules  for  all  focal 
lesions  of  the  brain.  We  may  therefore  be  brief  here.  It  is  necessary  only  to 
emphasize  the  fact  that  with  regard  to  cerebral  tumors,  as  well  as  other  lesions, 
focal  symptoms  should  be  divided  into  the  direct  and  the  indirect.  Direct  focal 
symptoms  are  the  immediate  result  of  the  destruction  of  nervous  tissue  by  the 
new  growth,  while  the  indirect  are  excited  by  the  pressure  exerted  by  the  tumor 


752  DISEASES  OF  THE  NERVOUS  SYSTEM. 

upon  the  parts  closely  surrounding  it.  This  pressure  varies  with  the  amount  of 
blood  in  the  vessels  of  the  new  growth,  and  therefore  the  indirect  symptoms  may 
undergo  temporary  exacerbations  and  remissions.  An  intermediate  position  is 
occupied  by  those  focal  symptoms  which  occur  in  many  cases  as  the  result  of 
certain  anatomical  changes  secondary  to  the  new  growth.  Not  infrequently  there 
is  white  softening  of  the  substance  of  the  brain  around  the  tumor  proper.  Prob- 
ably this  condition  is  generally  the  result  of  a  compression  of  the  minute  blood- 
vessels surrounding  the  new  gi'owth,  but  sometimes  it  is  the  sequel  of  an  obliterative 
endarteritis  (Friedläuder).  The  latter  cause  is  especially  operative  whei'e  the 
tumor  is  a  gumma  or  a  solitary  tubercle. 

1.  Tumors  of  the  cerebral  hemispheres  generally  lead  to  the  gradual  develop- 
ment of  hemiplegia — a  focal  symptom  which  is  to  be  regarded  as  partly  direct  and 
partly  indirect.  Since  the  new  growth  is  often  situated  near  the  cortex,  symp- 
toms referable  to  that  region  are  especially  frequent  with  tumors  of  the  cerebrum. 
It  is  therefore  not  infrequently  the  case  that  the  hemiplegia  is  the  result  of  the 
successive  paralysis  of  single  portions  of  the  affected  side ;  for  instance,  first  there 
is  only  facial  paralysis,  then,  in  addition,  paralysis  of  an  arm,  then  of  the  lower 
limb.  Very  often  the  extension  of  the  paralysis  is  accompanied  by  convulsions, 
which  either  are  confined  to  one  limb  or  one  side  of  the  body,  or  are  universal. 
There  may  be  still  other  focal  symptoms,  varying  with  the  exact  location  of  the 
tumor.  Thus,  there  is  hemiangesthesia,  if  the  parietal  region  or  the  posterior  pai*t 
of  the  internal  capsule  be  affected ;  hemiopia,  if  an  occipital  lobe  suffer ;  aphasia, 
if  the  neighborhood  of  the  left  island  of  Beil  be  involved,  and  so  on. 

2.  Tumors  at  the  Base  of  the  Brain. — The  base  of  the  brain  is  a  very  favorite 
place  for  new  growths.  The  symptoms  are  in  a  majority  of  cases  quite  character- 
istic. Some  of  the  tumors  spring  from  the  base  of  the  skull ;  among  these  are 
many  sarcomata  and  syphilitic  growths  ("  gummatous  periostitis  ").  Other  tumors 
originate  in  the  meninges,  especially  the  dura;  and  still  others  from  the  brain 
itself.  Of  these  last,  it  is  remarkable  that  some  spring  from  the  pituitary  gland. 
The  exact  starting  point  is  very  seldom  of  much  clinical  importance,  for  all  the 
parts  mentioned  are  in  such  close  proximity  to  one  another  that  there  is  no  great 
difference  in  the  symptoms  produced.  We  can  only  decide  that  there  is  a  tumor 
in  this  or  that  place  at  the  base  of  the  brain. 

Tumors  at  the  base  of  the  brain  owe  their  characteristic  clinical  stamp  to  the 
frequency  with  which  the  cranial  nerves  at  the  base  are  involved.  The  anatom- 
ical relations  are  such  that  these  nervous  trunks  are  often  compressed  by  the  new 
growth  or  actually  incorporated  in  it.  Of  the  symptoms  thus  occasioned,  the 
most  frequent  is  paralysis  of  the  motores  oculi  (oculomotor  and  abducens).  This 
is  at  first  usually  unilateral,  but  it  may  later  affect  both  sides.  If  one  of  the  optic 
tracts  be  involved,  hemiopia  may  result,  and  pressure  upon  one  optic  nerve  may 
produce  unilateral  choked  disk  with  unilateral  disturbance  of  vision.  Tumors  of 
the  pituitary  gland  are  especially  prone  to  cause  symptoms  referable  to  the  optic 
nerve  at  an  early  period.  Lesions  of  the  trigeminus  not  infrequently  cause  dis- 
tui'bances  of  sensation  in  the  face,  and  occasionally  also  paralysis  of  the  muscles 
of  mastication.  The  trunk  of  the  facial  often  suffers.  The  facial  paralysis  thus 
occasioned  throws  considerable  light  upon  the  diagnosis,  for  there  is  usually  to 
be  found  in  the  paralyzed  muscles  the  reaction  of  degeneration,  showing  that  the 
paralysis  is  peripheral.  We  have  therefore  reason  to  assume  that  the  lesion  is 
situated  at  the  base  of  the  cranium,  rather  than  central.  Another  factor  is 
almost  always  present  to  support  the  idea  of  a  peripheral  lesion— -namely,  the 
frontal  muscles  are  involved  {vide  pages  561  and  731).  Peripheral  paralysis  of 
the  hypoglossal  nerve  may  also  be  produced  by  tumors  at  the  base  of  the  brain ; 
but  this  is  much  rarer  than  facial  paralysis.     Whether  other  nerves  of  special 


TUMORS  OF  THE  BRAIN.  753 

sense  besides  the  optic  are  disordered  is  a  question  about  which  wo  possess  little 
information  as  yet,  but  probably  careful  examination  will  not  infrequently  reveal 
changes  in  them. 

As  might  naturally  be  expected,  various  degrees  and  forms  of  paralysis  in  the 
extremities  are  often  found  in  combination  with  the  above  disturbances  of  the 
cranial  nerves.  Such  conditions  are  most  frequent  where  the  crus  cerebri,  with 
its  pyramidal  tract,  is  affected.  There  is  no  need  of  enumerating  all  the  possible 
varieties  of  symptoms.  We  must  consider  them  all  carefully  in  each  individual 
case,  and  then,  by  bearing  in  mind  the  anatomy  of  the  parts,  we  shall,  in  a 
majority  of  instances,  be  enabled  to  determine  with  some  approach  to  accuracy 
the  place  at  the  base  of  the  brain  where  the  new  growth  must  be.  Sometimes, 
but  not  often,  we  may  be  led  into  error  by  tumors  which,  though  situated  in  the 
brain-substance  and  at  a  comparative  distance,  yet  by  their  pressure  give  rise  to 
indirect  symptoms  referable  to  the  cranial  nerves  at  the  base. 

3.  Tumors  of  the  Cerebellum— We  shall  refrain  from  describing  the  symp- 
toms which  may  be  excited  by  tumors  in  other  parts  of  the  brain,  with  a  single 
exception.  Tumors  of  the  cerebellum  are  comparatively  rather  common,  and 
deserve  a  brief  notice.  The  direct  focal  symptoms  of  cerebellar  lesions,  such  as 
the  peculiar  pitching  gait  and  the  vertigo,  have  been  discussed  at  page  723.  But 
cerebellar  tumors  generally  occasion  also  very  strongly  pronounced  general  symp- 
toms— namely,  headache,  mainly  occipital ;  sometimes  a  spasmodic  and  persistent 
stiffness  of  the  neck ;  vomiting;  and  visual  disturbances,  mainly  due  to  the  fre- 
quent existence  of  choked  disk.  Analogous  to  this  last  symptom  would  seem  to 
be  disturbances  in  other  nerves  of  special  sense.  Thus,  where  the  genei^al  intra- 
cranial pressure  is  elevated,  the  acoustic  or  olfactory  nerves  seem  liable  to  passive 
congestion.  Tumors  in  the  posterior  fossa  have  several  times  been  found  to  occa- 
sion bilateral  anosmia  and  deafness ;  and  they  should  always  be  considered  where 
such  a  condition  is  found. 

[In  view  of  the  increasing  importance  of  the  focal  diagnosis  of  tumors  of  the 
brain,  it  has  seemed  advisable  to  insert  the  following  brief  summary  of  the  focal 
symptoms  of  tumors  in  different  parts  of  the  brain : 

Prefrontal  Region. — Marked  mental  impairment  ;  symptoms  of  invasion  of 
the  central  region  (Jacksonian  epilepsy,  aphasia) ;  disturbances  of  smell. 

Central  Region.— SsiCksorädin  epilepsy;  monoplegia;  partial  anaesthesia ;  motor 
aphasia. 

Posterior  Parietal  Region.—  Word-blindness ;  disturbance  of  muscular  sense  (?) ; 
homonymous  hemianopsia. 

Occipital  Region.—  Homonymous  hemianopsia;  soul-blindness. 

Temporo- Sphenoidal  Region.— Latent  region.  Word-deaf nesa ;  disturbances 
of  taste,  smell,  and  hearing  (?). 

Corpus  Callosum  —  Latent  region.  Progressive  hemiplegia,  often  bilateral 
from  invasion. 

Optico-striate  Region. — Hemiplegia  ;  contracture.  In  posterior  part,  henii- 
anaesthesia,  homonymous  hemianopsia,  post-paralytic  chorea,  athetosis. 

Crus  Cerebri. — Crossed  paralyses  of  oculomotor  nerve  and  limbs. 

Corpora  Quadrigemina. — Oculomotor  paralyses;  reeling  gait;  blindness  (?); 
deafness  (?). 

Pons  and  Medulla. — Crossed  paralyses  of  face  and  limbs,  or  tongue  and  limbs. 
Other  cranial  nerve  lesions. 

Cerebzllum. — Marked  cerebellar  ataxia  ;  marked  vomiting.  Often  a  latent 
region. 

Base,  Anterior  Fossa. — Mental  impairment;  disturbances  of  smell  and  vision ; 
exophthalmus. 
43 


754  DISEASES  OF  THE  NERVOUS  SYSTEM. 

Base,  Middle  Fossa.—  Disturbance  of  vision;  oculomotor  disturbances;  hemi- 
plegia. 

Base,  Posterior  Fossa.—  Trigeminal  neuralgia;  neuro-paralytic  ophthalmia; 
paralyses  of  face  and  tongue ;  disturbance  of  hearing ;  crossed  paralyses. 

Hypophysis.—  Disturbance  of  vision;  oculomotor  disturbances. 

It  also  is  of  importance,  in  cases  which  may  come  to  operation,  to  determine 
whether  the  growth  be  cortical  or  subcortical.  Seguin  has  given  certain  rules 
which,  however,  are  not  absolute.  "  In  favor  of  a  strictly  cortical  or  epicortical 
lesion  are  these  symptoms,  none  of  them  having  specific  or  independent  value : 
localized  clonic  spasm,  epileptic  attacks  beginning  by  local  spasm,  followed  by 
paralysis;  early  appearance  of  local  cranial  pain  and  tenderness;  increased  local 
cranial  temperature.  In  favor  of  subcortical  location  of  a  tumor:  local  or  hemi- 
paresis  followed  by  spasm ;  predominance  of  tonic  spasm;  absence,  small  degree, 
or  very  late  appearance  of  local  headache  and  of  tenderness  on  percussion;  nor- 
mal cranial  temperature. " — K.] 

General  Course  of  Cerebral  Tumors.— The  symptoms  of  these  growths  almost 
always  cover  a  long  period  of  time.  Exceptionally  a  tumor  remaius  latent  till  a 
haemorrhage  or  some  similar  event  takes  place  in  it,  giving  rise  to  sudden  and 
grave  symptoms,  and  possibly  to  an  equally  sudden  termination.  The  rule  is, 
however,  for  the  phenomena  to  develop  gradually.  According  to  the  location  of 
a  new  growth,  either  the  general  or  the  focal  symptoms  may  come  first  into 
prominence.  They  generally  occur  in  the  order  named.  First  of  all  is  an  ill- 
defined,  deeply  seated  headache,  and  by  degrees  all  the  other  general  and  focal 
symptoms  follow  after.  The  symptoms  may  vary  repeatedly  and  greatly  in 
severity,  a  fact  due  mainly  to  the  varying  pressure  of  the  tumor  on  neighboring 
parts.  Repeated  mention  has  already  been  made  of  the  sudden  exacerbations 
which  may  come  on,  especially  in  case  of  the  vascular  gliomata. 

The  entire  duration  of  the  disease  is  usually  at  least  some  months,  and  may  be 
one  or  two  years  or  more.  The  termination  is  almost  invariably  tmfavorable. 
Death  may  be  rather  sudden,  or  it  may  not  come  till  after  a  long  period  of  wretch- 
edness. Fortunately,  however,  the  lameness,  blindness,  and  marasmus  are  fre- 
quently made  less  terrible  to  the  patient  because  of  his  mental  debility.  Recovery 
is  possible  only  where  the  growth  is  syphilitic.  It  is  indeed  possible  that  solitary 
tubercles  may  also  end  favorably,  but  the  matter  is  still  in  doubt. 

Diagnosis, — The  main  points  in  support  of  a  diagnosis  of  cerebral  tumor  would 
be  the  gradual  onset  and  continuous  slow  increase  of  the  general  symptoms  above 
detailed — namely,  headache,  vertigo,  vomiting,  convulsions,  dementia,  etc.  The 
most  constant  of  these  symptoms  is  the  headache.  They  all  indicate  the  develop- 
ment of  some  chronic  brain  trouble,  a  tumor  being  the  most  pi'obable  if  there  be 
no  definite  aetiology  to  suggest  some  other  process,  such  as  traumatism  resulting 
in  abscess,  or  syphilis.  Much  stress  may  also  be  laid  on  the  choked  disk,  which 
is  much  less  often  seen  in  case  of  abscess  or  softening  than  of  tumor. 

The  general  symptoms  indicate  that  a  tumor  of  the  brain  exists;  but,  in  order 
to  learn  the  position  of  that  tumor,  we  have  to  rely  mainly  upon  the  focal  symp- 
toms. Their  gradual  development  and  the  way  in  which  one  new  symptom  is 
slowly  added  to  another,  also  give  further  ground  for  the  opinion  that  some 
continuously  progressive  disease  exists,  and  most  likely  a  cerebral  tumor.  Of 
diseases  with  a  similar  course,  abscess  is  recognized  by  the  absence  of  choked 
disk  (an  important  point),  frequently  by  febrile  symptoms,  and  by  its  aetiology 
(trauma).  Inflammatory  and  thrombotic  softening,  if  they  come  on  slowly, 
usually  produce  less  general  disturbance  than  do  tumors;  they  seldom  cause  a 
choked  disk,  and  (unless  of  syphilitic  origin)  are  much  rarer  before  middle  age 
than  tumors  of  the  brain.     Sclerosis  sometimes  simulates  cerebral   tumor;  but 


TUMORS  OF  THE  BRAIN.  755 

here  also  there  is  no  choked  disk;  the  disease  lasts  much  longer  (five  or  ten  years, 
or  more),  and,  inasmuch  as  the  sclerosis  is  usually  multiple,  there  is  frequently 
too  great  a  complexity  of  symptoms  to  warrant  the  assumption  of  one  solitary 
lesion. 

[We  must,  however,  bear  in  mind  that,  in  about  one  seventh  of  the  cases, 
tumors  are  multiple. — K.] 

Certain  rare  cases  of  chronic  circumscribed  meningitis  can  not  be  differen- 
tiated from  a  tumor.  They  generally  occur  at  the  base,  lead  to  a  considerable  thick- 
ening of  the  tissues,  and  they  may  simulate  all  the  symptoms  of  a  new  growth  in 
this  region.  Occasionally,  also,  chronic  hydrocephalus  is  confounded  with  tumor 
of  the  brain.  We  met  with  a  case  of  dropsy  of  the  fourth  ventricle  which  pre- 
sented during  life  a  perfect  picture  of  tumor  of  the  cerebellum. 

As  to  the  nature  of  a  new  growth,  we  can  not  go  beyond  surmises.  If  the 
focal  symptoms  indicate  that  the  tumor  is  in  the  substance  of  the  brain  itself,  our 
first  thought  would  be  of  a  glioma,  because  it  is  by  far  the  commonest  sort  of 
growth  in  that  situation;  and,  as  has  been  stated,  certain  peculiarities  in  the 
course  of  the  disease  (especially  if  new  symptoms  add  themselves  abruptly)  would 
make  glioma  probable.  If,  on  the  other  hand,  the  tumor  be  at  the  base,  it  is 
most  apt  to  be  sarcoma,  which  is  the  most  frequent  form  of  new  growths  here. 
When  symptoms  referable  to  the  optic  nerve  occur  noticeably  early,  a  tumor  of 
the  pituitary  gland  is  to  be  thought  of.  In  all  cases,  and  especially  in  tumors  at 
the  base  of  the  brain,  we  should  bear  in  mind  the  possibility  of  syphilis.  The 
previous  history  and  the  entire  body  of  the  patient  should  be  closely  searched 
with  this  point  in  mind;  its  therapeutic  importance  need  not  be  dwelt  on. 

One  special  form  of  tumor  deserves  a  brief  mention  here — namely,  large 
cerebral  tubercles.  The  growth  may  be  single  or  solitary,  or  it  may  be  multiple. 
It  is  seen  chiefly  in  childhood,  and  any  chronic  cerebral  disorder  in  a  child  should 
suggest  the  possibility  of  such  a  growth.  It  is  rendered  all  the  more  probable  by 
the  co-existence  of  the  signs  of  tuberculosis  elsewhere,  as  in  the  lymph-glands, 
lungs,  or  bones.  The  symptoms  are  analogous  to  those  produced  by  other  tumors. 
Among  the  most  frequent  phenomena  are  headache  and  convulsions.  The  latter 
are  often  unilateral.  There  may  also  be  all  sorts  of  focal  symptoms,  according  to 
the  locality  of  the  lesion. 

Prognosis.— Except  gummata,  all  tumors  of  the  brain  have  a  very  unfavor- 
able prognosis.  It  is  said  that  in  very  rare  instances  tubercular  growths  have 
been  arrested  or  cured ;  but  in  practice  we  can  never  rely  upon  any  such  result. 
In  all  other  cases  recovery  is  next  to  impossible.  The  time  intervening  between 
the  appearance  of  the  first  symptoms  and  death  varies  greatly,  as  has  been  said. 
We  should  therefore  be  very  cautious  in  predicting  the  duration  of  the  illness.  It 
seldom,  however,  exceeds  one  or  two  years,  and  sudden  death  without  any  warn- 
ing may  occur  at  any  time. 

[Tubercular  growths  are  occasionally  found  at  autopsies,  which  have  become 
encapsulated,  and  have  apparently  existed  for  years  without  causing  symptoms. 
In  some  cases,  especially  with  tubercular  growths  in  children,  the  symptoms 
diminish  and  the  patient  may  live  for  years,  suffering  only  from  the  blindness, 
etc.,  caused  by  the  growth.  Other  cases  may  present  only  mild  symptoms,  and 
the  patient  may  lead  a  fairly  comfortable  life  for  years.— E.] 

Treatment.— Inasmuch  as  the  nature  of  the  tumor  can  not  be  determined  with 
absolute  certainty  in  any  instance,  antisyphilitic  treatment  should  always  be  tried. 
Forty  to  seventy -five  grains  of  mercurial  ointment  (grin.  3-5)  should  be  used  by 
inunction,  and  thirty  to  seventy-five  grains  (grm.  2-5)  of  potassic  iodide  should  be 
given  internally  each  day.  If  the  new  growth  be  syphilitic,  much  benefit  may  be 
done  in  this  way.     It  must  be  confessed  that  the  treatment  is  generally  of  little 


756  DISEASES  OF  THE  NEEVOUS  SYSTEM. 

avail,  because  the  tumors  are  not  of  a  syphilitic  character;  although  it  may  he 
that  iodide  of  potassium  sometimes  has  a  temporary  good  effect  upon  other  forms. 
A  long-continued  course  of  arsenic  has  also  been  recommended,  in  order  to  check 
the  growth  of  the  tumor.  This  remedy  particularly  deserves  a  trial  where  there 
is  a  suspicion  of  solitary  tubercle. 

Beyond  what  has  just  been  indicated,  treatment  must  be  symptomatic.  The 
headache  is  combated  with  ice-bags  and  narcotics;  the  convulsions  require  bro- 
mide of  potassium  or  the  inhalation  of  chloroform;  the  vomiting  is  lessened  by 
rest  in  bed,  opium,  and  bits  of  ice.  The  general  care  and  nursing  of  the  patient 
are  very  important,  so  that  bedsores  and  the  like  may  be  avoided  if  possible. 

[Within  the  last  few  years  it  has  been  demonstrated  that  tumors  of  the  brain 
may  be  successfully  removed  by  surgical  interference.  Out  of  forty-six  such  opera- 
tions, thirty  recovered  from  the  operation,  although  in  some  cases  the  growth  re- 
curred. Hence  the  propriety  of  such  an  operation  should  be  considered  in  every 
case,  but  unfortunately  the  growth  must  be  in  an  accessible  region  and  the  focal 
diagnosis  must  be  tolerably  certain,  so  that  an  operation  is  indicated  in  less  than 
ten  per  cent,  of  the  cases.  In  cases  with  intense  headache,  where  removal  is 
impossible,  relief  may  be  obtained  by  removing  a  portion  of  the  skull  and  tapping 
the  lateral  ventricles,  and  thus  taking  off  pressure.  Such  an  operation  will  relieve 
the  pain,  but  it  causes  cerebral  hernia,  and  probably  hastens  death. — K.] 

APPENDIX. 

HYDATIDS  OF  THE  BRAIN. 

It  was  stated  on  page  441,  that  the  Cysticercus  cellulosae,  which  originates 
from  the  taenia  solium,  may  occur  in  great  numbers  in  the  brain.  The  cysticerci 
most  frequently  occupy  the  pia  mater,  but  generally  project  downward  into  the 
cortex  of  the  brain.  The  meninges  not  infrequently  exhibit  signs  of  chronic 
inflammation,  and  may  present  haemorrhages,  which  are  not  always  minute.  If 
there  are  numerous  cysticerci  in  the  neighborhood  of  the  ventricles,  a  varying 
degree  of  internal  hydrocephalus  usually  develops  The  individual  cysticerci  are 
usually  enveloped  in  a  capsule  of  connective  tissue,  but  may  be  entirely  devoid 
of  such  a  covering. 

No  characteristic  clinical  sketch  of  hydatids  in  the  brain  can  be  drawn,  because 
the  symptomatology  of  each  case  differs  according  to  the  number  and  position  of 
the  parasites.  Sometimes  cysticerci  produce  absolutely  no  symptoms,  and  are 
discovered  incidentally  at  the  autopsy.  In  other  instances  they  cause  a  long  and 
tedious  illness.  Epileptiform  convulsions  seem  to  be  the  most  frequent  symptom, 
and  must  be  due  to  the  position  of  the  cysticerci  in  the  cortex  of  the  brain.  These 
may,  like  true  epileptic  attacks,  come  on  only  at  certain  times  when  the  general 
condition  is  otherwise  good ;  or  permanent  general  cerebral  symptoms  may  also 
appear,  such  as  persistent  headache,  vertigo,  and  mental  disorder.  Focal  symp- 
toms are  likewise  possible,  but  on  the  whole  are  rare. 

The  diagnosis  can  never  be  made  with  absolute  certainty.  The  presence  of 
cysticerci  in  the  brain  may  be  suspected  when  the  above-mentioned  symptoms 
occur  in  a  butcher  or  other  person  who  is  from  his  calling  especially  exposed  to 
infection,  or  who  is  known  to  have  had  or  still  to  have  a  tapeworm,  or  in  whom 
cysticerci  have  been  demonstrated  in  some  other  part  of  the  body,  such  as  the 
skin . 

We  know  of  no  remedy  capable  of  destroying  the  cysticerci.  Treatment,  there- 
fore, can  be  only  symptomatic.  [In  a  few  cases,  chiefly  in  Australia,  the  cysticerci 
have  been  successfully  removed  by  sui'gical  operations. — K.] 


CEREBRAL  SYPHILIS.  %% 

CHAPTER  VIII. 
CEREBRAL   SYPHILIS. 

iEtiology. — The  importance  of  syphilis  as  an  setiological  factor  in  many  chronic 
diseases  of  the  nervous  centers  has  been  repeatedly  adverted  to  in  preceding  chap- 
ters. Although  with  regard  to  its  influence  upon  the  spinal  cord  in  exciting  tabes 
dorsalis  and  certain  forms  of  myelitis  there  is  still  some  obscurity,  the  brain  pre- 
sents with  comparative  frequency  disorders  unmistakably  referable  to  constitu- 
tional syphilis. 

Cerebral  syphilis  is  almost  always  a  tertiary  symptom.  It  is  only  in  excep- 
tional instances  that  cerebral  symptoms  are  produced  by  the  end  of  a  year  from 
the  date  of  the  initial  lesion.  Usually  the  interval  is  several  years,  and  it  may  be 
ten  or  even  twenty. 

Liability  to  the  disease  does  not  seem  tobe  essentially  influenced  by  age  or  sex. 
Even  hereditary  syphilis  has  been  proved  to  cause  diseases  of  the  nervous  system. 
But  it  can  not  be  denied  that  a  predisposition  to  cerebral  syphilitic  disease  is  often 
engendered  by  those  influences  which  are  apt  to  promote  cerebral  disease  in  gen- 
eral. Just  as  the  position  of  syphilitic  cutaneous  lesions  is  often  determined  by 
external  irritation  at  some  one  place  on  the  skin,  so  the  disease  seems  more  liable 
to  attack  a  brain  which  is  exposed  to  certain  unfavorable  conditions  than  one 
which  is  perfectly  normal  and  vigorous.  Such  conditions  are  inherited  tendency 
to  nervous  diseases,  various  injurious  mental  influences,  poisons,  in  a  broad  sense, 
and  traumatism.  It  need  hardly  be  said  that  even  a  previously  sound  brain  does 
not  enjoy  immunity  from  the  affection. 

Pathology. — As  far  as  has  yet  been  ascertained,  there  are  two  chief  forms  as- 
sumed by  syphilis  in  this  organ :  (1)  a  circumscribed  syphilitic  tumor,  the  gumma, 
and  (2)  a  disease  of  the  arteries  of  the  brain,  which  is  usually  quite  extensive. 
There  is  no  essential  difference  underlying  these  two  varieties.  They  may  also 
occur  in  combination  with  each  other.  The  disease  of  the  blood-vessels  is  really 
a  syphilitic  new  growth  affecting  the  walls  of  the  arteries. 

The  circumscribed  syphilitic  tumors  are  yellowish  or  grayish-red,  and  fre- 
quently cheesy  in  the  center.  Their  most  frequent  seat  is  the  dura  mater  or  the 
subarachnoid  spaces,  whence  they  spread  to  the  brain-substance;  but  exceptionally 
they  may  originate  in  the  substance  of  the  brain  itself.  Histologically  they  are 
made  up  of  granulation  tissue  of  varying  degrees  of  vascularity,  and  presenting 
yellow  spots  usually  visible  to  the  naked  eye.  These  spots  are  of  firmer  consist- 
ency than  the  rest  of  the  growth,  and  have  undergone  coagulation-necrosis  (have 
become  cheesy).  Circumscribed  gummata  in  the  brain  which  have  become  cheesy 
do  not  differ  essentially  in  microscopic  appearance  from  a  collection  of  tubercles 
(see  preceding  chapter).  The  new  growth  sometimes  takes  on  a  more  diffuse  form 
in  the  meninges,  particularly  at  the  base  (gummatous  meningitis).  Often  the 
originally  delicate  granulations  become  transformed  into  a  firm  connective  tissue, 
forming  extensive  cicatricial  induration. 

The  syphilitic  disease  of  the  arteries  was  first  fully  appreciated  by  Heubner, 
who  has  described  it  accurately.  It  is  usually  most  pronounced  in  the  arteries  of 
the  base  of  the  brain,  and  especially  in  the  middle  cerebral  artery  and  its  branches. 
Even  the  unaided  eye  detects  a  grayish  opacity  in  the  arteries.  They  feel  firm 
and  stiff,  and  on  cross-section  their  walls  are  found  to  be  thickened,  either  uni- 
formly or  in  some  places  more  than  in  others.  This  causes  no  inconsiderable  nar- 
rowing of  the  lumen,  or  even  its  obliteration,  particularly  if  the  last  gap  be  closed 
by  the  formation  of  a  thrombus.  The  microscope  shows  that  the  new  growth 
originates  chiefly  in  the  intima  of  the  vessel,  where  there  is  a  hyperplasia  of  the 


758  DISEASES  OF  THE  NEKVOUS   SYSTEM. 

endothelium,  and  a  gradual  transformation  of  it  into  a  firm  connective  tissue. 
But  the  adventitia  also  undergoes  a  gradual  thickening  of  considerable  extent. 
Syphilitic  endartei'itis  presents  no  distinctive  histological  characteristics.  Entire 
certainty  that  the  inflammation  is  due  to  syphilis  can  be  attained  only  by  discov- 
ering other  evidences  of  syphilis,  whether  in  the  brain  or  elsewhere,  or  from  the 
personal  history  and  the  previous  course  of  the  disease. 

The  great  clinical  importance  of  syphilitic  endarteritis  is  due  to  its  cutting  off 
the  normal  supply  of  blood  from  the  regions  supplied  by  the  diseased  arteries.  If 
the  occlusion  be  complete,  cerebral  softening  is  inevitable,  as  in  ordinary  embolism 
and  thrombosis  of  cerebral  arteries ;  and,  inasmuch  as  the  middle  cerebral  artery 
is  particularly  liable  to  the  disease,  syphilitic  softening  is  most  often  found  in  the 
region  supplied  by  this  vessel. 

Clinical  History. — The  variety  of  the  pathological  processes  and  of  their  loca- 
tion produces  a  corresponding  variety  in  the  symptoms  of  cerebral  syphilis.  We 
shall  therefore  be  obliged  to  limit  ourselves  to  a  brief  description  of  some  few 
types  of  the  disease  which  are  oftenest  met  with  (Heubner). 

1.  The  group  of  symptoms  may  be  mainly  those  of  a  cerebral  tumor.  Here 
there  is  a  circumscribed  new  growth,  situated  either  at  the  base,  or  upon  the  con- 
vexity of  the  brain  (and  in  the  meninges).  If  at  the  base,  the  symptoms  are  analo- 
gous to  those  discussed  on  page  752.  The  focal  symptoms  are  often  preceded  for 
a  certain  length  of  time  by  general  cerebral  symptoms,  such  as  persistent  head- 
ache, worse  at  night,  wakefulness,  mental  depression,  and  impairment  of  mem- 
ory. Then  paralysis  of  the  nerves  at  the  base  of  the  brain  comes  on :  the  nerves 
controlling  the  motions  of  the  eyeball  suffer  the  most  frequently,  but  the  facial 
and  other  nerves  may  also  be  affected. 

In  the  second  subdivision,  where  the  syphilitic  new  growth  is  mainly  upon 
the  convexity  of  the  brain,  the  picture  is  a  tolerably  characteristic  one.  Often  in 
this  case,  also,  prodromata  similar  to  those  just  enumerated  precede  the  severer 
symptoms.  Then  appear  violent  epileptiform  convulsions.  These  often  come  on 
very  suddenly,  and  may  recur  at  considerable  intervals  or  in  quick  succession. 
There  are  usually  still  other  symptoms  of  cortical  disturbance,  especially  paresis 
of  one  limb  or  even  of  one  half  the  body;  very  frequently  slight  disturbance  of 
speech  (stumbling  over  syllables),  referable  to  the  cortex,  and  indications  of  men- 
tal impairment.  Many  of  these  cases  reach  a  fatal  termination  comparatively 
early.  The  epileptiform  convulsions  become  more  and  more  frequent,  and  uncon- 
sciousness increases  into  a  deep  coma  ending  in  death.  But  it  is  in  cases  of 
just  this  sort  that  prompt  and  energetic  treatment  may  accomplish  a  great  deal. 

2.  Another  common  and  important  variety  of  cerebral  syphilis  is  characterized 
chiefly  by  syphilitic  arteritis.  Not  infrequently  there  is  a  prodromal  stage;  then, 
as  a  result  of  the  occlusion  of  some  vessel,  which  often  occurs  quite  suddenly, 
there  is  a  pronounced  apoplectic  attack,  followed  in  most  cases  by  hemiplegia. 
The  intensity  of  the  initial  shock  may  vary  greatly ;  sometimes  there  is  only  a 
slight  dizziness,  sometimes  there  is  a  coma  that  lasts  for  clays.  Sometimes  the 
shock  is  succeeded  by  a  peculiar  condition  of  mental  confusion  and  dullness, 
which  may  persist  for  weeks.  In  severe  cases,  death  is  speedy,  and  is  usually 
ushered  in  by  a  great  rise  of  temperature.  Other  patients  improve  more  or  less 
rapidly,  especially  under  proper  treatment. 

Apoplectic  attacks  of  this  sort  may  recur  after  temporary  improvement  has 
taken  place,  and  may  be  associated  with  all  sorts  of  nervous  symptoms. 

3.  In  a  third  class  of  cases, .  cerebral  syphilis  assumes  the  form  of  a  diffuse 
chronic  disease  of  the  brain,  closely  resembling  multiple  sclerosis  or  certain  types 
of  progressive  general  paralysis  of  the  insane.  Perhaps  it  would  be  more  correct 
to  say  that  certain  cases  of  cerebral  syphilis  are  identical  with  general  pai'alysis. 


CEREBRAL  SYPHILIS.  759 

There  are  gradual  impairment  of  memory  and  of  speech,  and  various  motor  symp- 
toms (tremor,  ataxia,  paralysis  of  single  members).  The  intellectual  powers  grow 
less  and  less,  and,  after  passing  years  as  a  physical  and  mental  wreck,  the  patient 
at  last  dies,  unless  indeed  he  has  the  good  fortune  to  be  carried  off  earlier,  in  some 
apoplectiform  or  epileptiform  attack.  In  such  cases  the  autopsy  sometimes  also 
shows  specific  syphilitic  changes,  especially  in  the  smaller  vessels ;  but  we  find 
chiefly  atrophic  and  degenerative  processes  in  the  nerve-fibers,  which,  in  our 
opinion,  should  be  separated  from  the  special  syphilitic  new  formations  under  the 
name  of  "post-syphilitic  changes." 

Diagnosis. — While  some  few  of  the  phenomena  produced  by  cerebral  syphilis 
are  rather  characteristic — we  refer,  for  instance,  to  the  intense  prodromal  head- 
ache, the  epileptiform  convulsions,  and  the  apoplexy — still  these  symptoms  alone 
are  never  sufficient  to  establish  the  diagnosis,  for  they  may  be  precisely  simu- 
lated in  cases  of  tumor,  softening,  haemorrhage,  multiple  sclerosis,  and  other  cere- 
bral diseases.  The  most  important  diagnostic  criterion  is  in  every  case  the  demon- 
stration of  the  astiology — that  is,  a  previous  infection  with  syphilis.  We  can  not 
here  describe  in  detail  the  methods  of  determining  this  fact.  The  history  of  the 
patient,  as  well  as  previous  specific  affections— such  as,  in  women,  miscarriages, 
abortions,  etc. — and  the  objective  signs  on  other  parts  of  the  body,  are  the  two 
sources  of  information.  There  may  be  scars  on  the  skin  or  mucous  membranes, 
enlarged  glands,  ulcers,  tibial  periostitis,  or  changes  in  the  testicles.  Age  is  also 
important :  thus  an  apoplectic  attack  in  a  young  person  would  suggest  syphilis, 
because  the  other  causes  of  such  an  attack  operate  chiefly  upon  the  aged.  The 
results  of  treatment  often  throw  considerable  light  upon  the  diagnosis.  As  there 
is  nothing  to  lose  and  much  perhaps  to  gain,  we  should  always  give  specific 
remedies  in  doubtful  cases.  If  they  prove  successful,  the  diagnosis  of  syphilis 
receives  strong  confirmation. 

Prognosis  and  Treatment. — There  are  few  severe  and  dangerous  diseases  where 
timely  and  appropriate  treatment  is  attended  with  so  much  success  as  that  achieved 
in  many  cases  of  cerebral  syphilis.  In  order,  however,  both  to  understand  the 
favorable  results  and  not  to  be  misled  by  the  failures,  we  need  to  gain  a  clear  idea  of 
the  way  in  which  antisyphilitic  remedies  can  be  of  benefit.  They  can  accomplish 
this  only  by  causing  the  dissipation  and  absorption  of  the  new  growth — that  is, 
the  gumma  or  the  swelling  of  the  intima.  If  this  be  effected,  the  surrounding 
parts  are  of  course  relieved  from  pressure,  and  the  circulation  becomes  unim- 
peded. If  the  tissues  still  retain  functional  power,  they  resume  their  duties  and 
all  symptoms  of  disease  vanish.  But  when  the  tissue  has  already  been  consider- 
ably impaired  by  the  compression,  or  by  the  scanty  blood-supply,  the  results  are 
quite  different.  Even  then  the  nervous  trunks  at  the  base  of  the  brain  may  gradu- 
ally become  regenerated ;  but  such  parts  of  the  true  cerebral  parenchyma  as  have 
undergone  softening  have  lost  their  functional  capacity  forever.  In  this  case, 
antisyphilitic  treatment  is  unavailing. 

It  is  therefore  obvious  that  the  first  essential  of  success  is  to  begin  treatment, 
as  early  as  possible.  The  sooner  a  correct  diagnosis  is  reached,  the  sooner  will 
existing  symptoms  be  relieved,  and  further  danger  be  averted.  The  method  of 
treatment  which  will  probably  accomplish  all  that  can  be  accomplished,  and  in 
the  shortest  possible  time,  is  energetic  mercurial  inunction.  At  least  a  drachm 
(grm.  3-5)  of  mercurial  ointment  must  be  rubbed  in  every  day  at  first,  according  to 
the  ordinary  method.  We  should  not  venture  to  restrict  the  diet  unless  the  patient 
be  wTell  nourished  and  "full  blooded."  If  he  be  ana?mic  and  feeble,  a  generous 
regimen  is  demanded.  Usually  the  internal  administration  of  iodide  of  potassium 
is  combined  with  the  inunctions;  we  should  give  thirty  to  forty -five  grains  (grm. 
2-3),  or,  in  severer  cases,  even  a  drachm  or  a  drachm  and  a  half  (grm.  -4-6),  daily. 


760  DISEASES  OF  THE  NERVOUS  SYSTEM. 

[In  this  country  iodide  of  potassium  is  given  much  more  freely.  In  cases  where 
syphilis  is  suspected,  we  may  safely  begin  with  doses  of  thirty  grains  (grm.  2) 
three  times  a  clay.  If  the  symptoms  be  urgent,  the  dose  should  be  rapidly  increased 
uutil  the  patient  takes  three  or  even  four  drachms  (grm.  10-15)  three  times  a  day. 
If  the  patient  have  syphilis,  the  danger  of  iodism  seems  less.  The  drug  must  be 
given  in  large  amounts  of  water,  and  it  is  better  borne  if  given  in  Vichy  or  Giess- 
hubler  water.  Sometimes  the  stomach  will  not  tolerate  the  extreme  doses. — K.] 
The  same  remedy  should  also  be  given  afterward,  for  a  long  time,  in  smaller 
doses.  Where  there  is  no  benefit  at  all  after  twenty  or  thirty  inunctions,  there  is 
little  prospect  of  any  appreciable  improvement.  In  favorable  cases,  the  mercury 
often  begins  to  produce  some  effect  after  the  fifth  or  sixth  inunction ;  and  it  may 
cause  astonishingly  rapid  improvement.  Potassic  iodide  alone  is  sufficient  for  the 
milder  cases  only,  where  there  is  merely  headache,  trigeminal  neuralgia,  or 
paralysis  confined  to  the  motores  oculi. 

In  many  cases  some  symptomatic  treatment  is  also  required.  Narcotics,  appli- 
cations to  the  head,  electricity,  baths,  etc.,  are  employed,  as  in  other  chronic  cere- 
bral diseases,  and  they  often  supplement  very  efficiently  the  specific  remedies. 


CHAPTER  IX. 

PROGRESSIVE   GENERAL   PARALYSIS   OP   THE   INSANE. 

(Paralytic  Dementia.     Paretic  Dementia.     General  Paresis.) 

Preliminary  Remarks. — Although  the  description  of  mental  diseases  is  not 
properly  a  part  of  the  plan  of  this  book,  we  must  nevertheless  make  an  exception 
of  one  disease  of  the  sort,  namely,  the  so-called  progressive  general  paralysis  of 
the  insane,  or  paralytic  dementia,  which  in  medical  parlance  is  often  abbreviated 
into  "general  paralysis."  We  consider  it  advisable  to  make  this  exception,  be- 
cause a  great  part  at  least  of  the  symptoms  of  general  paralysis  are  purely  of  a 
physical  nature,  and  also  because  a  knowledge  of  this  disease,  which  is  so  com- 
mon and  so  fatal  in  its  results,  is  of  the  greatest  importance  for  the  general  prac- 
titioner. 

We  must  thank  the  French  alienists  Boyle  (1822)  and  Calmeil  (1826)  for  the 
first  clinical  descriptions  of  general  paralysis,  by  which  it  was  more  sharply 
differentiated  than  previously  from  other  diseases  which  run  a  like  course.  A 
more  accurate  knowledge  of  the  different  symptoms,  and  the  anatomical  changes 
to  which  the  morbid  symptoms  must  be  referred,  has,  however,  only  of  late  years 
been  rendered  possible  by  the  introduction  of  better  methods  of  investigation. 
Accordingly,  we  must  now  say  that  general  paralysis  is  a  disease  which  may 
attack  the  most  diverse  portions  of  the  whole  central  nervous  system  * — the  brain 
and  spinal  cord — at  the  same  time  or  successively,  but  in  which,  of  course,  we  can 
make  out  certain  rules  as  to  the  predisposition  of  individual  portions  to  disease, 
and  as  to  the  order  of  the  symptoms.  General  paralysis  begins  most  frequently  in 
those  regions  of  the  cerebrum  which  have  an  immediate  relation  to  the  regular 
course  of  the  psychical  and  certain  psycho-motor  processes.  Mental  and  motor 
symptoms  accordingly  form  the  introductory  features  of  the  disease  in  most 
cases.     More  extensive  regions  of  the  central  nervous  system  are  gradually  in- 

*  At  present  hardly  anything  is  known  in  regard  to  a  primary  implication  of  the  peripheral  nerves 
in  the  whole  process  of  general  paralysis.  No  theoretical  objection  can  he  raised  to  the  supposition  of 
such  an  implication. 


PROGRESSIVE  GENERAL  PARALYSIS  OF  THE  INSANE.       7<;i 

volved  in  the  morbid  process,  which  goes  hand  in  hand  with  a  progressive 

degeneration  of  all  the  higher  intellectual  faculties,  while  at  the  same  time 
many  physical  disturbances  dependent  upon  nervous  changes  constantly  in- 
crease. 

iEtiology. — General  paralysis  is  a  common  disease,  and  apparently  demands  a 
heavier  quota  from  the  better  and  more  highly  educated  classes  than  from  the 
lower  classes.  We  may  assume  that,  on  the  average,  one  tenth  of  all  patients 
committed  to  the  insane  asylums  are  general  paralytics.  In  most  patients  the 
beginning  of  the  disease  falls  in  the  period  between  the  thirtieth  and  fiftieth  year. 
The  disease  is  much  rarer  in  advanced  life.  In  young  people  under  twenty  it  has 
hardly  ever  been  observed.  There  is  no  doubt  that  the  male  sex  is  much  more 
frequently  affected  than  the  female,  but  the  number  of  cases  of  general  paralysis 
among  women  is  not  very  small. 

What  is  the  special  caiise  of  general  paralysis  ?  A  generally  acceptable  an- 
swer can  not  be  given;  but  the  theory  is  constantly  gaining  ground,  and  we 
agree  to  it,  from  our  own  experience,  that  by  far  the  most  important  causal  factor 
is  a  previous  syphilitic  infection.  Such  an  infection  can  be  made  out  in  at 
least  seventy-five  per  cent,  of  all  cases.  In  this  regard  precisely  the  same 
conditions  exist,  and,  of  course,  the  same  difficulties  in  the  interpretation  of 
this  relation  are  to  be  considered,  as  we  have  previously  mentioned  in  the 
account  of  the  dependence  of  tabes  dorsalis  on  syphilis  (see  page  632),  a  cir- 
cumstance which  again  is  not  without  significance,  since  intimate  points  of  con- 
nection are  to  be  found  between  tabes  and  general  paralysis  {vide  infra).  If 
we  consider  that  general  paralysis  depends  upon  a  previous  syphilis,  we  have 
an  easy  explanation  of  most  of  the  other  peculiarities  in  the  onset  of  the  disease, 
especially  the  above-mentioned  influence  of  age  and  sex,  the  decidedly  common 
occurrence  of  the  disease  in  persons  in  certain  callings— such  as  artists  and  officers 
— the  frequency  of  the  disease  in  large  cities  in  distinction  from  its  rarer  occur- 
rence in  the  country,  etc. 

Besides  the  aetiological  factors  named,  which,  in  our  opinion,  are  the  most 
important,  all  other  "  causes  "  of  general  paralysis  may  well  be  regarded  as  merely 
predisposing.  Mental  overexertion  has  the  greatest  significance,  especially  if  it 
be  associated  with  psychical  irritation.  In  merchants,  civil  officers,  etc.,  who  suffer 
from  general  paralysis,  such  a  previous  overexertion  can  often  be  made  out.  In 
some  cases  injury  to  the  head  or  insolation  is  claimed  to  be  the  cause.  Hereditary 
predisposition  to  nervous  diseases  plays  perhaps  a  certain  part,  in  the  origin  of 
general  paralysis,  but  by  no  means  a  very  large  one. 

Clinical  History. — General  paralysis  usually  begins  so  slowly  and  gradually 
that  a  definite  period  for  its  beginning  can  hardly  ever  be  given.  In  addition,  it 
is  often  clear,  at  a  period  when  the  disease  is  already  fully  developed,  that  certain 
early  symptoms,  whose  nature  was  at  first  not  correctly  recognized,  ought  to  have 
been  regarded  as  the  initial  symptoms. 

The  first  symptoms  of  the  disease  in  the  psychical  domain  usually  consist  of 
the  gradual  appearance  of  a  change  in  the  whole  nature  and  in  the  mental  indi- 
viduality of  the  patient ;  wherein,  however,  the  mental  disturbance  usually  shows 
from  the  start  the  character  of  weakness— that  is,  of  a  lessened  capability  of  psy- 
chical exertion.  The  patient's  ordinary  mental  work  no  longer  goes  on  as  easily 
as  before.  His  memory  is  uncertain,  and  there  are  marked  forgetfulness  and 
inattentiveness,  which  were  previously  quite  impossible  for  hhn  to  exhibit.  The 
patient  is  often  disorderly  in  his  dress,  and  violates  the  ordinary  social  rules  of 
decency  and  morality.  Since  his  judgment  as  to  the  value  and  significance  of 
things  is  uncertain,  he  commits  purposeless  actions,  wastes  money,  commits  crimes, 
is  dissolute,  etc.     In  these  respects,  too,  the  increasing  mental  dullness  often  ap- 


762  DISEASES  OF  THE  NERVOUS  SYSTEM. 

peal's,  since  the  patient  becomes  incapable  of  any  higher  intellectual,  aesthetic 
enjoyment,  and  since  the  nobler  sway  of  feeling  finally  becomes  chilled,  and  can 
no  longer  exert  any  lasting  influence  upon  his  actions.  Besides  all  these  signs  of 
beginning  mental  weakness,  we  often  notice,  on  the  other  hand,  an  abnormal 
irritability.  The  patient  easily  becomes  agitated,  or  gets  angry;  but  these  humors 
rapidly  pas's  away  without  leaving  a  lasting  impression.  We  easily  understand 
how  this  change  in  the  whole  personality  of  the  patient  must  distress  and  alarm 
his  family,  since  the  relatives  at  first  can  not  understand  at  all  why  the  patient  is 
now  "  so  different  from  what  he  was." 

In  the  first  period  of  the  disease  a  subjective  feeling  of  illness  is  frequently 
present.  The  patient  himself  notices  that  his  mental  capacity,  especially  his 
memory,  is  diminished,  and  he  very  often  becomes  extremely  anxious  on  this 
account.  It  frequently  happens  that  certain  subjective  sensations  are  also  noticed 
a  feeling  of  confusion  in  the  head,  pressure  in  the  head,  dizziness,  rheumatoid 
pains,  etc.  The  sleep  is  disturbed,  as  a  rule,  and  also  the  appetite  and  the  digestion. 
If  such  a  patient  comes  to  the  physician  with  his  complaints,  it  unfortunately  only 
too  often  happens  that  he  is  in  the  beginning  regarded  as  "  neurasthenic,"  and  is 
treated  accordingly. 

Careful  observation,  however,  may  even  now  usually  discover  the  disease  with 
certainty.  The  beginning  mental  disturbance  is  usually  more  apparent  to  the 
family  than  to  the  physician,  who  has  not  known  the  patient  before  and  who  sees 
him  only  cursorily,  but  it  can  usually  easily  be  confirmed  on  a  somewhat  more 
searching  examination  of  the  patient.  We  generally  succeed  best  by  making 
the  patient  reckon ;  he  often  makes  the  greatest  mistakes  in  simple  examples  in 
multiplication ;  especially  does  he  forget  to  add  numbers  carried  in  the  mind,  etc. 

Certain  motor  symptoms,  however,  which  usually  come  on  in  the  early  stages 
of  the  disease,  are  of  the  greatest  diagnostic  significance,  especially  peculiar  dis- 
turbances of  speech  and  handwriting.  The  paralytic  disturbance  of  speech  shows 
itself  first  in  the  form  of  stumbling  over  syllables  {Silbernstolpern),  or  literal 
ataxia.  The  individual  sound  (in  distinction  from  bulbar  paralysis)  can  be  pro- 
nounced quite  correctly,  but  the  combination  of  different  sounds  in  the  whole 
word  causes  increasing  difficulties.  It  is  a  good  plan,  in  order  to  recognize  the 
first  beginnings  of  this  difficulty,  to  have  the  patient  pronounce  a  few  difficult 
words,  such  as  "third  riding  artillery  brigade,"  ''representative  government," 
"  initiative,"  "  electricity,"  etc.  We  often  hear  "  artralleriry  "  instead  of  "  artillery," 
and  like  blunders.  In  the  later  stages  of  the  disease  the  speech  is  sometimes 
almost  wholly  incomprehensible.  We  also  observe  other  more  complicated  apha- 
sic  disturbances,  such  as  paraphasia,  persistent  repetition  of  the  same  word,  etc. 
In  such  cases  the  patients  are  sometimes  no  longer  able  to  read  any  sentence 
correctly.  They  at  times  put  in  entirely  different  words,  so  as  to  make  utter 
nonsense;  but  they  do  not  notice  it  themselves.  The  abnormal  associated  move- 
ments of  the  facial  muscles  on  speaking  are  also  often  to  be  observed,  and  are 
very  characteristic.  The  voice  of  general  paralytics  often  loses  its  power  of 
modulation  and  becomes  weak  and  rough — symptoms  'which  depend  upon  a 
defective  innervation  of  the  vocal  cords.  The  change  in  the  handwriting,  to 
be  observed  in  general  paralytics,  is  even  more  characteristic  than  the  disturbance 
of  speech  (see  Fig.  106).  This  is  at  first  purely  of  a  motor  nature;  the  letters  are 
uncertain,  irregular,  and  tremulous.  A  psychical  factor,  however,  also  shows 
itself;  single  letters  are  omitted,  the  dot  on  the  i  and  the  marks  of  punctuation 
are  forgotten,  the  patient  ceases  to  keep  on  the  lines,  or  leave  a  free  margin,  etc. 
As  the  disease  advances,  the  disturbance  in  the  handwriting  gradually  increases, 
so  that  the  writing  may  finally  become  wholly  illegible,  and  may  consist  merely 
of  senseless  scratches. 


PEOGEESSIVE  GENERAL  PARALYSIS  OF  THE  INSANE.       7GÜ 

Besides  the  changes  in  the  speech  and  the  handwriting,  which  we  have  just 
briefly  described,  other  physical  disturbances  arc  often  quite  early  symptoms,  and 
prove  in  how  many  parts  of  the  nervous  system  at  once  the  disease  may  begin  its 
work  of  destruction.  Tbe  condition  of  the  pupils  especially  is  of  importance  in 
diagnosis.  They  are  often  unequal,  and  also  show  a  reflex  immobility  (see  page 
642)  in  a  large  number  of  cases,  especially  in  those  in  which  other  tabetic  symp- 
toms develop  (vide  infra).  Transitory  ocular  paralyses  are  at  times  early  symp- 
toms.    Not  infrequently  we  find  quite  early  changes  in  the  tendon  reflexes,  either 


^d^ 


ßrt  A^-    O^tJ^r^M^/^^A^K 


Fig.  106.— Examples  of  handwriting  in  general  paralysis.  Attempts  made  by  patients  in  the  Danvers 
Lunatic  Hospital  to  write  "  God  save  the  Commonwealth  of  Massachusetts."  Besides  the  motor  dis- 
turbance, the  frequent  omission  of  certain  letters  will  be  noticed,  e.  g.,  "  Masschuetts  "  for  "Massa- 
chusetts."   In  3  and  4  the  handwriting  is  almost  wholly  illegible. 

absence  of  the  patellar  reflex  (a  tabetic  symptom)  or  an  increase  (beginning  spastic 
paralysis  of  the  legs).  The  association  of  reflex  immobility  of  the  pupils  with  an 
increase  of  the  patellar  reflex  is  not  uncommon.  In  the  distribution  of  the 
sensory  nerves  we  may  mention  as  repeatedly  observed  symptoms,  neuralgia, 
attacks  of  migraine,  and  finally  optic  atrophy,  the  latter  usually  as  one  symptom 
of  a  co-existing  tabes. 

We  can  not  give  a  generally  applicable  account  of  the  further  course  of  general 
paralysis,  since  it  may  differ  decidedly  in  this  respect.  In  what  follows  we  can 
point  out  only  the  main  features  of  the  different  types  of  the  disease,  and,  in 
particular,  we  will  sketch  only  very  briefly  the  groups  of  mental  symptoms. 

We  often  say  that  those  cases  belong  to  the  "  classical  form  "  of  general  paraly- 
sis where  an  initial  "  stage  of  depression  "  with  a  melancholy  tendency  is  followed 
by  a  second  stage  of  "  maniacal  exaltation."  This  is  the  stage  where  the  delusions, 
which  are  already  quite  pronounced,  assume  more  and  more  the  character  of 
"  grand  ideas,"  and  thus  exhibit  the  "  delusions  of  grandeur  "  which  have  for  a  long 
time  been  generally  regarded  as  ominous.  The  first  signs  are  often  found  in  the 
patient's  statements  that  he  is  now  much  better,  that  he  is  "  very  well,"  that  he 


704  DISEASES  OF  THE  NERVOUS  SYSTEM. 

feels  "very  strong,"  etc.  These  delusions,  however,  often  assume  gradually  a 
more  exaggerated  form ;  the  patient  considers  himself  enormously  rich,  he  owns 
thousands  of  palaces,  millions  of  dollars,  has  made  the  greatest  inventions,  con- 
siders himself  the  Emperor  Napoleon,  Christ,  a  "  higher  God,"  etc.  Any  judgment 
as  to  the  absurdity  of  these  ideas,  and  as  to  the  sad  contrast  between  his  claims 
and  the  reality,  has  already  become  impossible  to  him;  bat,  of  course,  there  are 
even  now  occasional  remissions  in  this  condition,  when  the  patient  is  clearer  and 
recognizes  temporarily  the  morbid  character  of  his  delusions. 

We  must  not  think,  however,  by  any  means,  that  the  delusion  of  grandeur  is 
necessarily  an  invariable  symptom  in  general  paralysis.  In  many  cases  (the  so- 
called  "  depressive  "  form  of  general  paralysis)  the  initial  melancholic-hypochon- 
driacal  condition  continues.  The  delusions  that  appear  possess  the  same  coloring; 
the  patient  claims  that  he  can  no  longer  eat,  that  he  is  poisoned,  that  he  no  longer 
has  a  head  or  an  arm,  that  he  is  very  small  ("  delire  micromaniaque  "),  etc.  Some- 
times acute  and  severe  conditions  of  anxiety  come  on.  In  other  cases,  again  (the 
agitated  or  maniacal  form  of  general  paralysis),  there  are  states  of  violent  excite- 
ment, in  which  the  patient  raves  loudly,  cries,  and  tries  to  destroy  whatever 
falls  in  his  way.  Such  states  sometimes  alternate  with  delusions  of  grandeur. 
Finally,  we  not  infrequently  see  cases  which,  in  their  mental  relations,  present 
simply  the  symptoms  of  a  mental  enfeeblement  gradually  increasing  to  complete 
dementia,  without  ever  showing,  in  any  notable  form,  states  of  excitement,  the 
development  of  delusions,  etc. 

While  the  intellectual  life  steadily  goes  to  utter  ruin  in  the  ways  just  stated, 
the  physical  disturbances  of  the  disease,  as  a  rule,  gradually  advance  in  a  more 
severe  degree.  In  many  cases  ataxia  of  the  extremities  develops,  and  also  loss 
of  sensibility  and  vesical  disturbances — in  short,  the  symptoms  of  tabes.  In  these 
cases  the  tendon  reflexes  are  almost  always  lost,  and  the  pupils  are  often  immobile. 
In  other  rarer  cases,  however,  there  is  actual  paralysis  first  in  the  lower  and  then  in 
the  upper  extremities.  In  these  cases  the  tendon  reflexes  are  often  increased,  so 
that  the  picture  of  "  spastic  paralysis  "  develops.  Again,  in  other  cases  bulbar 
symptoms  appear,  such  as  disturbances  in  swallowing  or  masticatory  paralysis, 
and  also  ocular  paralyses,  usually  as  a  part  of  the  tabetic  symptom-complex,  etc. 

Peculiar  attacks,  which  are  among  the  commonest  and  most  characteristic 
symptoms  of  general  paralysis,  are,  however,  of  special  interest,  and  sometimes 
even  of  marked  importance  in  diagnosis.  These  "  paralytic  attacks "  in  their 
milder  degrees  sometimes  appear  even  in  comparatively  early  stages  of  the  dis- 
ease. Then  they  usually  consist  of  attacks  of  vertigo,  an  obscuring  of  conscious- 
ness, or  even  a  loss  of  consciousness,  coming  on  quite  suddenly,  and  lasting  from 
a  few  minutes  to  half  an  hour  or  more,  and  they  are  very  often  associated  with 
mild  hemiplegic  or  monoplegia  symptoms.  We  very  often  see,  besides  the  vertigo, 
a  temporary  feeling  of  weakness  in  the  right  arm,  associated  with  a  marked  apha- 
sic  disturbance  of  speech.  To  this  there  is  often  added  some  slight  twitching 
in  the  affected  extremities  or  in  the  face.  In  the  further  course  of  the  disease  the 
attacks  usually  increase,  and  are  termed  apoplectiform  or  epileptiform  paralytic 
attacks,  according  as  the  conditions  of  paralysis  or  spasm  predominate.  The  epi- 
leptiform attacks  may  often  be  repeated  with  great  frequency — thirty  or  forty 
attacks  a  day  or  more — during  which  time  the  patient  remains  in  an  unconscious 
state.  If  the  patients  gradually  return  to  consciousness,  sometimes  only  after  a 
week  or  two,  we  very  often  see,  as  a  result  of  such  severe  attacks,  a  permanent 
impairment  of  the  general  condition,  an  increase  of  the  dementia,  etc. 

The  other  organs,  apart  from  the  nervous  system,  are  only  secondarily  impli- 
cated in  the  morbid  process.  It  may  be  mentioned  briefly  here  that  formerly,  for 
a  long  time,  stress  was  laid  upon  certain  changes  in  the  pulse,  the  pulsus  tardus 


PROGRESSIVE  GENERAL  PARALYSIS   OF  THE  INSANE.       705 

especially  being  thought  to  be  characteristic;  but  the  numerous  investigations  of 
the  pulse  have  so  far  not  given  us  any  significant  or  sure  results. 

The  temperature  as  a  rule  is  approximately  normal,  or  often  somewhat  sub- 
normal, but  very  marked  changes  in  the  temperature  occur  in  connection  with 
the  paralytic  attacks — sometimes  elevations  and  sometimes  very  deep  declines. 

The  whole  duration  of  the  disease  is  in  some  cases  only  a  few  mouths  (the 
"  galloping"  form  of  general  paralysis),  usually  it  is  two  or  three  years,  and  some- 
times much  more.  The  most  rapidly  fatal  form  is  that  in  which  there  is  very 
soon  a  marked  emaciation  and  a  rapid  loss  of  strength  as  a  result  of  the  sleepless- 
ness, the  constant  unrest,  and  the  refusal  of  food.  In  other  cases  death  ensues 
from  the  gradual  and  general  loss  of  strength,  or  in  a  paralytic  attack;  or,  finally, 
as  is  frequently  the  case,  from,  the  onset  of  secondary  conditions,  such  as  severe 
bedsores,  pyelo-cystitis,  tuberculosis,  intestinal  diseases,  etc. 

Pathological  Anatomy  and  Nature  of  the  Disease.— Considering  the  great  diffi- 
culty of  an  accurate  microscopic  examination  of  the  brain,  it  is  not  strange  that 
our  knowledge  of  the  pathological  anatomy  of  general  paralysis  is  still  very  defect- 
ive. If  we  except  occasional  immaterial  changes  in  the  skull,  such  as  hyperostoses 
and  the  like,  or  in  the  meninges,  such  as  hematoma  of  the  dura  or  secondary 
thickening  of  the  pia  over  atrophied  portions  of  the  brain,  the  first  striking  and 
at  any  rate  most  important  anomaly  seems  to  be  the  atrophy  of  the  brain  which 
affects  chiefly  the  anterior  half,  especially  the  frontal  lobes.  In  this  region  the 
convolutions  are  very  much  diminished,  and  the  fissures  are  wider ;  the  weight  of 
the  anterior  portion  of  the  brain  may  be  reduced  to  one  fourth  or  one  third  of  the 
normal.  If  we  examine  the  convolutions  microscopically  we  find  that  the  dimin- 
ution of  the  whole  organ  depends  chiefly  upon  a  loss  of  nervous  elements.  The 
cortex  usually  shows  the  greatest  changes.  In  fresh  cases  we  sometimes  see  the 
signs  of  a  mild  "  inflammation " — that  is,  we  find  vascular  dilatation  and  little 
disseminated  foci  of  round  cells  about  the  vessels,  but  the  changes  in  the  nerv- 
ous elements  themselves  are  far  more  important,  and  consist  essentially  in  a  degen- 
erative atrophy.  We  must  mention  especially  that  in  the  cortex  of  the  frontal 
lobes,  especially  marked  in  the  straight  convolution  and  in  the  island  of  Reil,  and 
also  in  other  portions,  we  can  make  out  with  certainty,  by  the  aid  of  good  meth- 
ods of  examination,  a  very  considerable  loss  of  the  fine  medullary  nerve-fibers, 
mainly  those  which  run  parallel  with  the  surface,  and  hence  are  termed  "  associ- 
ation-fibers "  (Tuczek) ;  but  signs  of  degeneration  and  atrophy  are  very  often  to  be 
seen  in  the  ganglion-cells  themselves.  The  destruction  of  the  nervous  elements  is 
regarded  by  many  investigators  as  secondary,  since  they  lay  the  chief  stress  upon 
the  marked  changes  in  the  interstitial  tissue,  such  as  increase  of  the  connective 
tissue,  numerous  spider-cells,  or  thickening  of  the  vascular  walls,  which  are  almost 
always  to  be  found  in  old  cases,  and  hence  they  speak  of  an  interstitial  encephalitis 
(Mendel).  We  ourselves,  with  Tuczek,  Wernicke,  and  others,  are  much  more  in- 
clined to  the  theory  that  we  have  to  do  mainly  with  a  primary  process  of  degen- 
erative atrophy  of  the  nerve-fibers  and  nerve-cells,  to  which  the  increase  of  the 
connective  tissue  is  only  a  secondary  addition. 

The  anatomical  affection  in  general  paralysis,  moreover,  is  by  no  means  limited 
to  the  cerebral  cortex.  We  can  often  make  out  the  loss  of  fibers  in  the  deeper 
parts  also,  in  the  white  substance,  and  the  central  ganglia.  The  co-existing 
changes  in  the  spinal  cord,  first  accurately  described  by  Westphal,  and  since  then 
recognized  as  almost  constant,  are  of  especial  interest.  They  usually  consist  of 
fascicular  systemic  degeneration  of  the  lateral  columns  (the  pyramidal  tract),  or 
the  posterior  columns.  A  large  part  of  the  physical  disturbances  of  general  para- 
lytics, such  as  tabetic  symptoms  or  spastic  paralysis  {vide  supra),  are  certainly  due 
not  to  the  cerebral  disease,  but  to  these  accompanying  changes  in  the  spinal  cord. 


766  DISEASES  OF  THE  NERVOUS  SYSTEM. 

Accordingly,  we  believe  that,  according  to  onr  present  knowledge,  we  can 
best  conceive  tbe  nature  of  general  paralysis  in  tbe  following  way:  By  tbe  action 
of  certain  injurious  influences,  wbicb  usually  seem  to  stand  in  some  connection 
with,  syphilis  (see  page  632),  there  is  a  gradually  progressive  destruction  of  nerve- 
tissue  in  the  most  diverse  portions  of  the  nervous  system.  The  clinical  symptoms 
must  naturally  differ  according  to  the  significance  and  function  of  the  affected 
fibers  or  cells.  As  a  rule,  certain  cortical  regions  of  the  cerebrum  are  first  dis- 
eased. Tbe  disturbances  of  speecb  are  probably  dependent  upon  the  loss  of  fibers 
in  the  left  island  of  Reil,  the  disturbances  of  intelligence  upon  tbe  destruction  of 
fibers  in  the  frontal  lohes.  We  may  also  make  out  corresponding  anatomical 
changes,  either  cerebral  or  spinal,  as  an  explanation  of  the  later  motor,  tabetic,  and 
other  symptoms ;  but  in  many  cases  the  order  in  which  the  different  sections  are 
affected  varies  considerably.  We  have  seen  in  a  previous  section  (see  page  645) 
that  the  whole  process  may  begin  with  a  spinal  disease,  especially  tabes  dor- 
salis,  to  which  the  paralysis  is  "added"  later;  but  we  must  understand  that  the 
two  conditions  are  wholly  analogous  to  and  co-ordinate  with  each  other.  Both 
are  parts  of  the  same  degenerative  process,  which  can  accomplish  its  work  of 
destruction  in  the  most  diverse  regions  of  the  nervous  system. 

No  coarse  anatomical  lesions  can  be  made  out,  as  a  rule,  to  explain  the  para- 
lytic attacks,  but  it  is  very  probable  that  they  depend,  at  least  in  great  part,  upon 
the  changes  in  the  motor  central  convolutions. 

Diagnosis.— Since  the  diagnosis  of  beginning  general  paralysis  is  of  the  great- 
est practical  importance,  we  will  once  more  mention  briefly  all  those  symptoms 
which  are  especially  to  be  considered  in  diagnosis:  Striking  alteration  in  the 
behavior,  rapid  and  motiveless  change  in  the  disposition,  disturbances  of  mem- 
ory, loss  of  intelligence  (failures  in  reckoning,  etc.),  the  characteristic  changes 
in  the  speech  and  handwriting,  and  finally  the  somatic  symptoms  which  often 
co-exist:  difference  in  the  pupils,  immobility  of  the  pupils,  loss,  or,  more  rarely, 
increase  of  the  tendon  reflexes,  and  mild  paralytic  attacks,  such  as  vertigo,  distur- 
bance of  speech,  temporary  disturbance  of  motion  in  one  arm,  etc. 

We  would  also  mention,  as  especially  common  and  disastrous  mistakes,  that 
the  symptoms  of  general  pai'alysis  are  often  misunderstood  at  first,  and  are  regarded 
as  the  signs  of  immorality,  the  failure  of  the  sense  of  duty,  etc.  It  also  fre- 
quently happens  that  general  paralysis  is  at  first  regarded  as  simple  neurasthenia 
or  hypochondriasis,  and  treated  accordingly. 

As  a  rule,  general  paralysis  can  be  certainly  distinguished  from  other  organic 
nervous  diseases  by  careful  attention;  but  of  course  we  must  add  that  in  some 
cases  cerebral  tumors,  syphilis  of  the  cerebral  arteries,  and  especially  certain  cases 
of  multiple  sclerosis,  may  show  a  type  of  disease  very  like  general  paralysis. 

Prognosis. — The  prognosis  of  general  paralysis,  like  that  of  all  chronic  degen- 
erative conditions  of  the  central  nervous  system,  is  very  unfavoi'able.  At  present 
we  know  of  only  a  small  and  decreasing  number  of  actual  recoveries,  but  there  are 
many  cases  where  there  is  a  temporary  improvement  in  the  condition,  a  "  remis- 
sion," sometimes  of  a  considerable  degree  and  lasting  a  long  time.  The  earlier  the 
patient  comes  under  proper  care  and  treatment  the  sooner  may  we  hope  for  such 
a  favorable  turn.  Of  course,  as  we  have  said,  relapses  of  the  disease  almost 
always  come  on  later.  Those  cases  especially  are  to  be  regarded  as  unfavorable 
in  which  frequent  paralytic  attacks  come  on  early,  in  which  other  physical  symp- 
toms, especially  of  a  spinal  nature,  soon  set  in,  and  in  which  the  whole  nutrition 
of  the  body  rapidly  suffers. 

Treatment. — As  soon  as  the  disease  is  recognized,  the  first  and  imperatively 
necessary  injunction  must  be  to  remove  the  patient  from  all  physical  and  intel- 
lectual exertion  as  well  as  from  all  mental  excitement.     The  patient  must  there- 


CHRONIC  HYDROCEPHALUS.  7<;t 

fore,  if  possible,  withdraw  from  business,  which  up  to  that  time  he  may  have  tried 
to  carry  on.  His  methods  of  life  and  his  diet  must  be  regulated,  and  every  excess 
must  be  forbidden.  For  the  cases  which  even  at  first  are  associated  with  states 
of  great  mental  excitement,  the  commitment  to  a  proper  asylum  is  often  most 
urgently  to  be  recommended,  while  for  cases  that  during  their  course  show  simple 
mental  weakness,  care  at  home  is  often  sufficient. 

In  regard  to  the  treatment  of  the  disease  itself,  we  should  advise  inunction  with 
mercurial  ointment,  especially  if  we  can  discover  a  previous  syphilitic  infection. 
As  a  rule,  we  ought  not  to  expect  much  success  from  this  any  more  than  in  tabes 
(see  page  647),  but  we  may  perhaps  check  the  advance  of  the  disease.  We  should 
therefore  try  the  antisyphilitic  treatment  chiefly  in  the  initiai  stages  of  the  disease. 
We  may  combine  the  internal  use  of  iodide  of  potassium  with  the  inunction. 

Furthermore,  we  should  try  tepid  baths,  with  cool  sponging,  and  also  a  cautious 
application  of  electricity  (galvanization  of  the  head  and  spinal  cord),  and,  of  inter- 
nal remedies,  ergotine  especially.  We  need  not  go  more  fully  here  into  the 
numerous  symptomatic  details. 


CHAPTER  X. 
CHRONIC  HYDROCEPHALUS. 

iEtiology  and  Pathology. — Repeated  mention  has  been  made  in  preceding 
chapters  of  the  occurrence  of  dropsy  in  the  ventricles  as  a  sequel  to  other  cerebi'al 
diseases,  such  as  meningitis  and  tumors.  Besides  this  "  secondary  hydrocephalus," 
a  collection  of  fluid  in  the  ventricles  may  be  a  symptom  of  an  apparently 
idiopathic  primary  disease.  This  is  observed  most  of  all  in  the  newborn,  or  at 
least  in  young  children. 

Little  is  known  with  certainty  about  the  causes  of  chronic  hydrocephalus.  The 
assumption  is  very  frequently  made  that  the  condition  is  the  result  of  an  inflam- 
mation of  the  ependyma  of  the  ventricle,  which  itself  occurs  either  before  birth  or 
very  soon  after,  but  the  autopsy  often  fails  to  support  this  idea.  There  is  equally 
slight  objective  evidence  that  there  is  a  stasis  due  to  mechanical  obstruction. 
Syphilis  and  dipsomania  have  been  regarded  as  predisposing  causes  ;  whether 
justly  or  not,  is  uncertain.  It  has  been  repeatedly  observed  that  the  disease  has 
attacked  several  children  of  a  single  family. 

The  most  important  physical  sign  of  hydrocephalus  in  children  is  enlargement 
of  the  head.  The  circumference  of  the  skull  may  even  in  the  first  year  of  life  be 
sixty  to  eighty  centimetres.  Usually  the  frontal  bones  and  the  parietal  eminences 
are  especially  prominent.  The  cranium  becomes  gradually  almost  as  thin  and 
translucent  as  paper.  The  fontanelies  and  sutures  gape  widely.  The  brain  is 
flattened  out,  so  as  to  seem  almost  like  a  bag,  filled  with  the  hydrocephalic  fluid. 
In  well-marked  cases  the  entire  thickness  of  the  hemispheres  is  frequently  not 
more  than  an  inch.  The  space  within,  containing  the  serous  effusion,  represents 
the  enormously  distended  ventricles,  particularly  the  lateral  ventricles,  although 
the  third  and  fourth  ventricles  are  quite  often  distended  also.  The  walls  of  the 
ventricles  are  often  strewn  with  minute  granulations,  or  they  present  a  reticular 
hypertrophy.  The  hydrocephalic  fluid  usually  has  the  appearance  of  colorless 
serum,  and  contains  a  very  slight  amount  of  albumen,  if  any.  The  specific  gravity 
is  about  1004  to  1006.  The  amount  of  fluid  may  be  a  quart  or  more;  but,  of 
course,  there  is  great  variation  in  this  respect  in  different  cases. 

Congenital  hydrocephalus  is  often  associated  with  other  peculiarities  or  defects 
in  the  structure  of  the  brain,  which  we  can  not  mention  here. 


708  DISEASES  OF  THE  NERVOUS  SYSTEM. 

Clinical  History. — Sometimes  a  child  is  born  with  hydrocephalus  so  far  devel- 
oped as  to  occasion  dystocia.  Usually,  however,  the  parents  notice  nothing  pecul- 
iar about  the  child  for  some  weeks.  Then  they  are  alarmed  by  the  gradual  swell- 
ing of  the  head.  As  a  basis  for  determining  abnormal  size,  we  may  mention  that 
under  normal  conditions  the  circumference  of  the  head  at  birth  is  about  forty  centi- 
metres, at  the  end  of  a  year  about  forty -five  centimetres,  and  from  that  age  to  puberty 
there  is  a  gradual  approach  to  a  circumference  of  about  fifty  centimetres.  The  pos- 
sible dimensions  in  chronic  hydrocephalus  have  been  already  stated.  The  increase 
in  circumference  is  often  quite  rapid,  amounting  in  a  fortnight  or  three  weeks  to 
one  or  two  centimetres.  Usually  the  swelling  is  tolerably  symmetrical ;  but  some- 
times the  greater  increase  is  in  the  antero-posterior  diameter,  making  the  skull 
dolichocephalic.  At  times  the  rate  of  expansion  may  be  particularly  rapid,  and 
then  at  other  times  it  may  seem  to  be  suspended.  That  the  fontanelles  and  sutures 
remain  widely  open  has  already  been  mentioned ;  sometimes  it  is  even  possible  to 
get  fluctuation  through  them.  An  intravascular  murmur  can  now  and  then  be 
heard  in  the  head,  but  it  has  no  great  importance  with  regard  to  diagnosis.  The 
veins  are  often  so  greatly  distended  as  to  form  a  bluish  network  underneath  the 
scalp.  The  face  remains  small,  in  striking  contrast  with  the  great,  heavy  cranial 
portion  of  the  head.  The  head  almost  always  hangs  over  forward  from  its  weight. 
The  eyes  generally  look  down,  partly  because  the  roof  of  the  oi'bit  is  depressed, 
and  partly  because  of  impairment  of  the  nervous  supply  to  the  motores  oculi. 

A  very  important  symptom  is  the  defective  intellectual  development  of  hydro- 
cephalic children.  They  can  not  learn  to  talk  well,  if  at  all.  If  they  play,  it 
is  in  a  silly  manner.  They  can  not  concentrate  their  attention  upon  anything, 
and  they  are  heedless  and  dirty.  It  must,  however,  be  mentioned  that  sometimes, 
in  spite  of  considerable  hydrocephalus,  the  patient  now  and  then  evinces  an  unex- 
pected activity  of  mind — thus,  he  gradually  becomes  able  to  distinguish  the  differ- 
ent objects  and  individuals  about  him. 

There  is  almost  invariably  motor  disturbance  also.  The  legs,  more  rarely  the 
arms,  are  decidedly  paretic,  or  there  may  be  even  complete  paraplegia.  There  are 
usually  spastic  symptoms  and  increased  tendon  reflexes.  Few  patients  learn  to 
walk  or  stand  alone.  The  arms  seldom  present  any  great  paresis,  but  their  move- 
ments often  betray  an  awkwardness  and  uncertainty  suggestive  of  ataxia.  It  is 
noteworthy  that  sensation  al  most  always  remains  intact.  At  least  the  patient  reacts 
vigorously  to  the  prick  of  a  pin,  etc.  Of  the  special  senses,  sight  is  most  frequent- 
ly affected ;  choked  disk  and  atrophy  of  the  optic  nerve  have  been  observed  repeated- 
ly. Symptoms  of  motor  irritation  are  of  very  frequent  occurrence,  such  as  gener- 
al convulsions  an d  spasm  of  the  glottis.  General  nutrition  is  pretty  well  maintained 
in  many  cases,  but,  as  a  rule,  hydrocephalic  children  are  atrophic  and  ill  developed. 

The  chronic  hydrocephalus  of  children  almost  always  terminates  unfavorably. 
Only  a  few  patients  survive  the  fifth  year,  although  now  and  then  striking  excep- 
tions occur.  Death  is  generally  the  result  of  marasmus ;  or  a  convulsive  seizure 
may  prove  fatal.  The  possibility  of  recovery  has  not  yet  been  demonstrated.  The 
progress  of  the  disease  may,  however,  be  arrested,  and  the  child  continue  for  years 
in  statu  quo. 

Hydrocephalus  in  adults  is  a  very  rare,  chronic,  and  apparently  idiopathic  disease. 
Its  cause  again  is  assumed  to  be  a  chronic  inflammation  of  the  ventricular  ependyma. 
The  symptoms  are  sometimes  very  like  those  of  a  tumor  of  the  brain,  and  sometimes 
there  is  a  remarkable  absence  of  characteristic  cerebral  disturbance,  except  that 
spastic  paralysis  of  the  extremities  (compare  page  663)  is  gradually  developed. 

Diagnosis. — A  pronounced  case  of  congenital  hydrocephalus  can  be  recognized 
without  difficulty,  inasmuch  as  the  excessive  size  of  the  head  betrays  the  disease 
upon  the  first  glance.     Less  extreme  cases  may  indeed  be  somewhat  obscure,  and 


MENIERE'S  DISEASE.  7<;<j 

we  have  especially  to  avoid  confounding  the  condition  in  question  with  rachitic 
enlargement  of  the  skull.  We  should  always,  therefore,  take  into  consideration 
the  intellectual  powers,  the  presence  or  absence  of  motor  disturbances,  and  other 
similar  symptoms,  as  well  as  the  cranial  peculiarities.  In  the  hydrocephalus  of 
adults  there  is  often  no  enlargement  whatever,  so  that  a  diagnosis  can  hardly  ever 
be  declared  positively. 

Treatment. — Thus  far,  no  remedy  has  been  applied  with  success  in  chronic 
hydrocephalus.  The  following  may  be  tried  :  Applications  of  mercurial  oint- 
ment and  of  tincture  of  iodine  to  the  scalp,  methodical  compression  of  tbe  skull, 
and  iodide  of  potassium  internally.  The  hydrocephalic  fluid  has  often  been  drawn 
off,  to  a  certain  extent,  by  tapping,  but  with  merely  temporary  benefit,  if  any. 

Hence  we  confine  ourselves  chiefly  to  hygienic  and  symptomatic  treatment. 


CHAPTER  XI. 

MENIERE'S   DISEASE. 
(  Vertigo  ab  aure  Iwsa.    Labyrinthine  Vertigo.) 

In  1861,  Meniere,  a  French  physician,  first  called  attention  to  a  peculiar  affection 
which  sometimes  results  from  chronic  aural  disease  and  is  characterized  mainly 
by  excessive  vertigo  and  loud  tinnitus  aurium.  At  first  the  symptoms  appear  in 
distinct  paroxysms.  These  are  ushered  in  by  a  shrill  ringing  in  the  ears,  which 
is  often  compared  to  the  whistling  of  a  locomotive,  and  which  is  perceived  in  but 
one  ear.  At  the  same  time,  or  shortly  after,  comes  on  a  very  pronounced  dizzi- 
ness, of  a  unique  sort.  The  patient  has  a  feeling  as  if  his  whole  body  were  mov- 
ing, as  if  he  were  falling  forward  or  were  whirling  around.  Consciousness  is 
unimpaired,  but  the  patient  feels  very  bad,  the  skin  is  pale  and  cool,  and  the  face 
is  bathed  in  cold  perspiration.  Frequently  there  is  vomiting  toward  the  close  of 
the  attack.     The  first  paroxysms  are  of  brief  duration. 

As  the  disease  progresses  the  attacks  become  more  and  more  frequent,  and  at 
last  the  vertigo  may  be  constant,  being  extremely  annoying  to  the  patient  and 
perhaps  confining  him  to  bed.  Even  now  there  are  occasional  paroxysmal  ex- 
acerbations of  the  disorder,  usually  ushered  in  by  the  shrill  tinnitus.  The  tokens 
of  chronic  aural  disease  on  one  side,  or  less  frequently  on  both  sides,  also  persist. 
Sometimes  there  is  purulent  otorrhcea;  often  the  aural  speculum  reveals  lesions 
of  the  drum  or  of  the  middle  ear;  and  almost  invariably  there  is  more  or  less 
deafness  on  the  affected  side.  This  condition  may  persist  for  years,  until  finally 
it  ceases  of  its  own  accord,  after  the  deafness  on  that  side  becomes  complete. 

We  possess  scanty  information  as  to  the  origin  of  these  subjective  phenomena. 
That  they  are  due  to  a  disease  of  the  internal  ear  (labyrinth)  can  scarcely  be 
doubted ;  and  it  is  further  probable  that  in  every  case  the  semicircular  canals  are 
involved.  Numerous  experimental  investigations  have  demonstrated  that  these 
last-named  structures  bear  a  part  in  maintaining  the  equilibrium  of  the  body. 
Acquaintance  with  this  variety  of  vertigo  is  valuable  to  a  nervous  specialist,  inas- 
much as  Meniere's  disease  has  been  more  than  once  confounded  with  epilepsy  and 
disease  of  the  cerebellum  and  other  parts  of  the  brain. 

Treatment  is  not  wholly  unavailing.  Charcot  has  discovered  that  the  persist- 
ent use  of  quinine  almost  always  gives  great  relief,  and  may  even  completely  cure 
the  disease.  Eight  to  fifteen  grains  (grm.  0"5-l)  of  quinine  should  be  given  daily, 
in  two  or  three  doses,  and  continued  for  at  least  several  weeks.  The  particulars 
of  such  special  treatment  of  the  ear  as  may  be  necessary  must  be  sought  elsewhere. 
49 


770  DISEASES  OF  THE  NERVOUS  SYSTEM. 


VI. — Neuroses  without  known  Anatomical  Basis. 


CHAPTER  I. 

EPILEPSY. 

{Falling  Sickness.     Morbus  sacer.) 

iEtiology. — Epilepsy  is  a  peculiar  disease  of  rather  frequent  occurrence,  the 
main  symptom  of  which  is  paroxysmal  loss  of  consciousness.  In  typical  cases 
the  unconsciousness  is  associated  with  violent  general  convulsions ;  but  there  are 
many  anomalous  and  rudimentary  forms  of  epilepsy  without  any  symptoms  of 
motor  irritation.  "  Genuine  epilepsy  "  is  a  functional  neurosis — that  is,  with  our 
present  means  of  investigation  we  can  discover  no  constant  objective  lesion  of  the 
nervous  system  as  its  basis.  It  is,  indeed,  true  that  attacks  similar  to  those  of  true 
epilepsy  not  infrequently  occur  in  the  course  of  tumor,  syphilis,  and  other  diseases 
which  do  present  an  anatomical  lesion ;  but  such  attacks  are  merely  symptomatic, 
and  are  therefore  termed  "  epileptiform,"  in  distinction  from  the  genuine  epileptic 
paroxysms.  [Convulsions  may  also  be  due  to  lead  encephalopathy  (vide  infra). 
-K.] 

Of  the  actual  causes  of  epilepsy  we  know  nothing.  We  are  acquainted  only 
with  certain  factors  which  are  favorable  to  the  development  of  the  disease,  and  are 
to  be  regarded,  therefore,  as  predisposing  or  exciting  causes.  Heredity  is  decidedly 
the  most  important  of  these.  About  one  third  of  all  cases  of  epilepsy  occur  in 
persons  who  have  inherited  a  nervous  diathesis,  and  one  or  more  of  "whose  blood- 
relations  have  suffered  from  diseases  of  the  nervous  system.  It  should  not  be 
understood  that  we  must  find  other  cases  of  genuine  epilepsy  in  the  family,  in 
order  to  establish  the  fact  of  congenital  predisposition.  The  question  is  merely 
whether  the  ancestors  have  exhibited  a  general  tendency  to  nervous  disease.  The 
more  accurate  and  careful  our  investigations,  the  offener  shall  we  find  among  the 
relatives  of  the  patient  instances  of  nervous  trouble — sometimes  genuine  epilepsy, 
sometimes  insanity,  hysteria,  or  general  "  nervousness. "  Of  course  these  "  nervous 
families  "  present,  besides  those  that  are  actually  ill,  others  who  are  more  or  less 
peculiar  and  odd,  and  yet  others  who  have  extraordinary  talents,  although  fre- 
quently somewhat  ill-balanced.  It  is  said  that  the  children  of  parents  who  are 
related  to  each  other  are  somewhat  predisposed  to  epilepsy,  as  well  as  to  other 
nervous  diseases;  but  certainly  this  factor  is  very  rarely  of  importance.  Perhaps 
dipsomania  in  the  parents  is  somewhat  more  prejudicial  in  this  regard.  It  is  said 
to  have  been  repeatedly  observed  that  children  begotten  while  the  father  was 
intoxicated  became  epileptic. 

There  are  other  influences  which  are  assumed  to  have  setiological  importance, 
but  whether  justly  or  not  is  difficult  to  decide.  Alcoholic  excesses  can  seldom  act 
in  this  way  (although  epilepsy  is  said  to  attack  absinthe-drinkers  in  France  quite 
frequently).  Venereal  excesses  probably  have  still  less  importance.  It  should 
also  be  borne  in  mind  that  not  infrequently  excesses  in  these  directions  are  the 
result  of  neurotic  tendencies  already  existing.  Syphilis  has  no  direct  connection 
with  genuine  epilepsy.  Epileptiform  convulsions  may,  as  we  have  seen,  be  symp- 
tomatic of  syphilis,  being  due  to  the  cerebral  lesion  caused  (vide  page  758)  by  this 
latter  disease.     Certain  factors  may  determine  the  onset  of  epilepsy,  although  they 


EPILEPSY.  Y7l 

can  not  be  said  to  cause  the  disease.  Such  are  overexertion  of  mind  or  body, 
repeated  emotional  disturbance,  certain  general  conditions  of  the  system,  such  as 
anaemia  or  malnutrition,  on  tbe  one  hand,  and  plethora  on  the  otber;  and,  in 
particular,  acute  febrile  diseases,  such  as  scarlet  fever,  measles,  and  gastritis,  j  In 
some  cases  abnormal  putrefactive  processes  in  the  small  intestines  seem  to  act  as 
the  exciting-  causes  of  the  individual  attacks. — K.]  Another  important  point  is  that 
the  first  attack  is  sometimes  brought  on  by  great  mental  excitement,  especially 
fright.  But  here,  too,  it  is  probable  that  the  terror  is  merely  the  exciting  cause, 
a  tendency  to  the  disease  already  pre-existing.  We  must  also  be  on  our  guard 
against  confounding  genuine  epilepsy  with  the  convulsive  form  of  hysteria  (q.  v.), 
which  very  frequently  develops  after  fright. 

In  some  instances  there  is  an  evident  connection  between  epilepsy  and  a  pre- 
vious injury  to  the  head,  as  from  a  fall,  blow,  or  cut.  At  a  certain  interval  after 
the  trauma,  attacks  begin  which  seem  precisely  like  those  of  genuine  epilepsy. 
This  is  known  as  "traumatic  epilepsy."  But  these  are  not  cases  of  genuine  epi- 
lepsy, inasmuch  as  there  is  really  some  anatomical  lesion  of  the  cortex  cerebri 
which,  in  some  way  as  yet  unknown,  causes  irritation  of  the  motor  centers  of  the 
cortex  (vide  infra).  It  is  often  the  case  that  this  sort  of  epileptiform  attacks  is 
peculiar  in  that  the  convulsions  are  at  first  unilateral,  or  confined  to  a  single  limb, 
corresponding  to  the  seat  of  the  injury  in  the  opposite  cerebral  hemisphere. 

"  Keflex  epilepsy "  remains  to  be  mentioned.  This  name  is  applied  to  cases 
where  each  convulsive  attack  seems  to  be  excited  by  reflex  influence  originating 
in  some  one  part  of  the  body.  Most  cases  have  followed  traumatic  injury  of 
peripheral  nervous  trunks  (retained  splinters,  or  scars),  and  have  ceased  upon 
removal  of  the  exciting  cause.  Other  causes  are  new  growths  in  the  nerves, 
foreign  bodies  in  the  ear,  otitis,  intestinal  parasites,  and,  apparently,  diseases  of 
the  female  sexual  organs.  But  it  seems  probable  that  sufferers  from  these  attacks 
have  had  a  tendency  to  disease  of  the  nervous  system.  We  must  hesitate  to  rank 
reflex  epilepsy  in  the  same  class  with  the  genuine  form.  In  former  treatises 
"  reflex  epilepsy  "  has  certainly  very  often  been  confused  with  traumatic-hysterical 
spasms  (vide  infra,  the  chapter  on  traumatic  neuroses). 

Both  the  traumatic  and  the  reflex  varieties  of  epilepsy  have  repeatedly  been 
the  object  of  experimental  investigation.  Brown-Sequard  has  shown,  by  a  great 
number  of  experiments,  that  epilepsy  can  be  excited  in  rabbits  by  injuries  to  the 
medulla,  the  spinal  cord,  and  the  sciatic,  as  well  as  other  peripheral  nerves.  A 
certain  time  after  the  operation  the  animals  undergo  spontaneous  convulsive 
paroxysms.  These  occur  at  frequent  intervals  for  a  long  time,  and  may  be  volun- 
tarily excited  at  any  time  by  irritation  of  a  certain  portion  of  the  skin  called  the 
"  epileptogenous  zone."  An  interesting  observation  in  this  connection  has  been 
made  by  Brown-Sequard,  which  is  that  sometimes  the  progeny  of  these  animals, 
who  have  been  made  epileptic,  suffer  from  spontaneous  epilepsy.  Westphal 
induced  epilepsy  in  guinea  pigs  by  blows  upon  the  skull.  Immediately  after  the 
blow  general  convulsions  occurred,  but  soon  entirely  ceased.  Afterward,  how- 
ever, there  were  repeated  epileptiform  attacks.  Westphal  thought  that  the  causa- 
tive lesion  in  these  instances  was  the  minute  haemorrhages  which  were  found  in 
the  upper  part  of  the  cervical  division  of  the  cord  and  in  the  medulla. 

Further  experiments  bearing  upon  the  same  subject  will  be  discussed  later  on. 

Clinical  History. — In  describing  the  symptoms  of  epilepsy,  we  shall  first  con- 
sider the  various  forms  of  the  epileptic  paroxysm,  and  then  describe  the  general 
course  of  the  disease. 

1.  The  typical  epileptic  paroxysm  is  usually  described,  for  the  sake  of  greater 
clearness,  as  made  up  of  several  stages.  First  is  the  prodromal  stage,  or,  accord- 
ing to  Galen's  expression,  still  in  vogue,  the  stage  of  the  epileptic  aura  (aura= 


Y72  DISEASES  OF  THE  NERVOUS  SYSTEM. 

breath).  Not  infrequently,  however,  there  is  no  aura  whatever,  the  convulsions 
coming-  on  without  warning-.  But  in  many  cases  the  prodromata  are  well  marked, 
and  are  repeated  with  remarkable  regularity  and  similarity  before  each  individual 
attack,  although  the  different  cases  of  epilepsy  differ  greatly  as  to  the  special 
phenomena  of  the  aura  occurring  in  each. 

The  best  manner  in  which  to  distinguish  the  various  forms  of  aura  is  accord- 
ing to  the  nature  of  the  nervous  phenomena,  whether  sensory,  motor,  vasomotor, 
or  psychical.  Of  these  the  most  frequent  is,  beyond  a  doubt,  the  sensory.  Here 
we  have  peculiar  paresthesia?,  beginning  in  an  arm  or  leg,  or  perhaps  in  the 
region  of  the  heart  or  stomach,  and  thence  usually  "mounting  to  the  head."  It 
is  seldom  that  the  peculiar  sensation  is  actually  like  a  ''breath"  or  puff  of  air. 
The  aura  which  proceeds  from  the  epigastrium  is  sometimes  associated  with  a 
very  disagreeable  feeling  of  oppression  and  anxiety,  and  often  also  with  nausea 
and  vomiting.  The  aura  may  be  referred  to  the  nerves  of  special  sense.  In  cer- 
tain instances  the  patient  perceives  an  unpleasant  odor,  which  he  likens  to  some 
familiar  one.  An  aura  of  taste  also  occurs,  but  it  is  very  rare.  An  optical  aura 
is  much  more  frequent,  consisting  in  a  subjective  sensation  of  color  or  light  (usu- 
ally a  sensation  of  red  appears  first),  in  an  apparent  increase  or  diminution  of  the 
size  of  surrounding  objects,  or  finally  in  actual  hallucinations  of  vision,  such  as 
beholding  all  sorts  of  human  or  brute  shapes.  An  auditory  aura  is  not  very 
rare:  it  produces  a  sudden  feeling  of  deafness  in  one  ear,  or  various  subjective 
sounds,  like  whistling,  humming,  or  roaring. 

The  motor  aura  takes  the  form  of  mild  premonitory  contractions,  affecting  the 
head,  face,  arm,  or  leg.  There  may  be  aphasic  disturbance  at  the  same  time;  or 
we  may  observe  symptoms  of  irritation  of  the  unstriped  muscles  (strangling,  or 
a  desire  to  go  to  stool).  Sometimes  there  are  prodromal  vasomotor  phenomena, 
where  the  aura  consists  in  a  sensation  of  cold  or  warmth,  often  associated  with 
excessive  pallor  or  redness  of  the  face  or  hands.  An  attack  may  be  ushered  in  by 
chilliness,  perspiration,  or  palpitation . 

Finally,  the  name  of  psychical  aura  is  applied  to  an  initial  impairment  of  con- 
sciousness, with  vertigo,  confusion  of  thought,  etc.  A  particularly  frequent  form 
for  this  to  assume  is  excessive  mental  uneasiness  and  excitement. 

Various  forms  of  aura  are  not  infrequently  seen  in  combination. 

The  aura  lasts  sometimes  only  a  few  seconds.  It  may  persist  long  enough  for 
the  patient,  who  knows  from  experience  what  is  coming,  to  lie  down  or  take 
other  precautionary  measures  {vide  infra).  In  some  few  cases  the  aura  may  last 
hours,  and  even  days.  This  is  especially  true  of  the  psychical  variety.  Some- 
times the  aura  passes  away  without  being  succeeded  by  any  true  epileptic  fit ;  but 
it  is  usually  followed  by  the  second  stage  of  the  attack — the  convulsive  stage. 

The  convulsions  almost  invariably  begin  abruptly.  Perhaps  there  is  no  aura, 
or  only  a  very  brief  one,  before  the  patient  falls  suddenly  to  the  ground,  usually 
on  his  face,  although  sometimes  on  the  side  or  back.  Consciousness  is  entirely 
suspended.  Insensibility  is  complete,  and  often  the  patient  sustains  severe  injury 
from  his  fall.  Some  patients  utter  a  loud  "  epileptic  cry  "  at  the  commencement 
of  the  attack,  but  they  are  already  entirely  unconscious. 

The  convulsive  stage  begins  with  a  brief  period  of  general  tonic  spasm  of  the 
muscles.  The  head  is  usually  strongly  extended,  the  teeth  are  pressed  firmly 
together,  the  trunk  is  curved  backward  in  opisthotonos,  the  extremities  are  ex- 
tended, and  the  fingers  are  clinched  over  the  flexed  thumb.  Inasmuch  as  the 
respiratory  muscles  participate  in  the  seizure,  breathing  stops,  and  the  original 
pallor  of  the  face  soon  gives  place  to  deep  cyanosis.  This  general  tonic  convul- 
sion ordinarily  is  but  brief,  perhaps  fifteen  to  thirty  seconds.  It  is  followed  by  the 
second  period  of  the  convulsive  stage — that  of  the  clonic  convulsions.     The  facial 


EPILEPSY.  773 

muscles  now.  exhibit  the  most  violent  contortions;  the  eyeballs  roll,  or  occasion- 
ally present  a  conjugate  deviation  toward  one  side;  the  tongue  is  thrust  out  and 
retracted  convulsively;  the  head  beats  violently  against  the  floor;  and  the  mus- 
cles of  the  arms,  legs,  and  trunk  undergo  the  severest  clonic  spasms.  The  pupils 
are  probably  contracted  for  a  short  time  at  first,  but  during  the  convulsive  stage 
they  are  widely  dilated  and  do  not  react  at  all.  The  pulse  is  somewhat  accel- 
erated, but  not  greatly.  The  temperature  is  normal,  or  elevated  a  small  fraction 
of  a  degree.  The  cutaneous  reflexes  are  still  suspended  directly  after  an  attack; 
but  the  tendon  reflexes  are  generally  somewhat  exaggerated,  although  sometimes 
they  also  are  diminished  or  absent.  Not  infrequently  an  involuntary  dejection 
takes  plaee  during  the  fit,  or  the  bladder  is  emptied;  and  in  men  there  may  be  a 
seminal  emission.  During  these  violent  convulsions  the  body  is  often  severely 
injured.  The  tongue  is  frequently  bitten.  The  venous  stasis  is  so  extreme  that 
sometimes  minute  haemorrhages  occur  into  the  conjunctiva,  the  skin  of  the  face, 
and  other  parts. 

The  convulsive  stage  usually  lasts  several  minutes.  Then  the  contractions 
cease,  often  after  a  deep,  long-drawn  sigh ;  and  the  patient  passes  into  the  third 
stage,  of  post-epileptic  coma.  He  lies  unconscious,  but  his  respiration  grows 
quiet,  and  the  cyanosis  vanishes.  Gradually  the  coma  yields  to  slumber,  which 
may  persist  for  some  hours;  but  some  patients  remain  only  a  very  brief  time  in 
this  stage,  and  recover  from  their  attack  with  surprising  rapidity.  It  is,  however, 
not  infrequently  the  case  that  for  some  days  after-pains  are  felt ;  there  are  head- 
ache, languor,  and  exhaustion,  and  mental  despondency  and  irritability.  For 
some  time  there  may  be  severe  pain  in  the  muscles,  particularly  those  of  the 
trunk.  There  may  be  slight  paresis  of  one  limb  or  one  side  of  the  body  after  an 
attack,  but  this  speedily  vanishes  again  in  cases  of  pure  epilepsy.  In  the  mine 
first  passed  after  the  seizure  is  often  found  a  trace  of  albumen,  and  perhaps  a  few 
hyaline  casts.  Not  infrequently  there  is  also  decided  polyuria  for  some  time  sub- 
sequent to  the  fit. 

2.  The  Milder,  Rudimentary  Forms  of  Epileptic  Seizure.  Petit  Mai. — Be- 
sides these  violent  paroxysms  just  delineated  {•'grand  mal"),  there  are  very  often 
witnessed  in  epilepsy  milder  attacks  of  so-called  "petit  mal."  Sometimes  there 
is  only  a  transitory  dizziness,  or  slight  faintness,  or  perhaps  a  brief  loss  of  con- 
sciousness, but  without  accompanying  symptoms  of  motor  irritation.  These 
milder  attacks  may  or  may  not  be  preceded  by  an  aura.  Cases  have  been  seen 
repeatedly  where  the  patient  suddenly  pauses  in  the  midst  of  conversation,  card- 
playing,  piano-playing,  or  other  occupation,  stares  absently  for  a  moment,  and 
then,  with  equal  abruptness,  goes  on  with  what  he  was  doing,  as  if  nothing  had 
happened.  In  other  instances  the  patient  pursues  his  occupation  during  this 
brief  suspension  of  consciousness.  For  example,  if  seized  while  upon  the  street, 
he  walks  on  mechanically,  but  takes  the  wrong  turning,  or  goes  into  a  strange 
house,  when  suddenly  he  comes  to  himself  and  wonders  to  find  himself  where  he 
is.  Cases  of  "  sudden  somnolence  "  are  also  almost  all  of  them  ascribable  to  epi- 
lepsy. There  are  all  sorts  of  transitional  forms  between  the  slight  attack  of 
vertigo  and  the  typical  epileptic  fit,  Not  infrequently  the  patient  falls  down 
unconscious,  but  he  has  only  a  slight  twitching  of  the  face  or  arm,  and  in  a  few 
minutes  is  entirely  himself  again. 

[The  medico-legal  bearings  of  epilepsy,  in  its  mild  as  well  as  in  its  severe  form, 
are  very  important,  but  they  can  be  only  alluded  to  here.] 

3.  Epileptoid  Conditions. — Cases  of  petit  mal  are  generally  rudimentary  forms 
of  the  typical  epileptic  paroxysm,  and  consist  merely  of  a  simple  impairment  of 
consciousness,  possibly  associated  with  slight  motor  symptoms ;  but  in  the  epilep- 
toid state  the  character  of  the  typical  epileptic  attack  is  almost  indistinguishable. 


774  DISEASES  OF  THE  NERVOUS  SYSTEM. 

The  disturbance  is  paroxysmal,  and  it  can  often  be  shown  to  be  connected  with 
genuine  epileptic  seizures,  else  its  undoubted  relation  to  epilepsy  would  never 
have  been  recognized.  The  greatest  practical  importance  attaches  to  Saint's 
"psychical  equivalents  of  epilepsy."  These  are  attacks  of  mental  disturbance, 
which  either  immediately  succeed  a  typical  epileptic  fit  (u post-epileptic  insanity") 
or  occur  independently.  The  patient  is  completely  deranged,  and  may  do  the 
strangest  things — may  strip  himself,  steal,  jump  into  the  water,  or  commit  incen- 
diarism. Here  the  mind  may  be  said  to  be  only  clouded,  as  compared  with  other 
instances  where  there  is  violent  psychical  excitement,  associated  with  terror, 
frightful  hallucinations,  and  resultant  maniacal  excitement.  Not  infrequently 
the  patient  is  led  to  acts  of  violence  against  those  about  him.  In  the  young  the 
attack  may  take  a  peculiar  form:  the  child  runs  about  in  a  peevish  way,  collects 
all  sorts  of  things  together,  makes  strange  motions,  etc.  Almost  always  the 
patient,  on  recovering  consciousness,  remembers  nothing,  or  almost  nothing,  of 
what  has  happened.  Numerous  and  valuable  particulars  upon  this  subject,  and  a 
consideration  of  its  great  medico-legal  importance,  must  be  sought  in  text-books 
on  insanity. 

Another  form  of  epileptoid  attack  is  the  epileptoid  sweating  of  Emminghaus 
a  spontaneous  outbreak  of  excessive  perspiration  in  epileptics,  which  may  or  may 
not  be  associated  with  impairment  of  consciousness. 

General  Course  of  the  Disease. — In  a  large  majority  of  cases  epilepsy  begins 
before  the  thirtieth  year.  Often  the  disease  appears  in  early  youth,  and  sometimes 
in  even  the  earliest  years.  Many  a  child  has  "  convulsions  from  teething,"  which 
later  on  are  seen  to  have  been  epileptic.  It  is  only  in  rare  instances  that  the  first 
appearance  of  trouble  occurs  in  advanced  life. 

It  is  impossible  to  give  any  general  rule  as  to  the  frequency  of  the  paroxysms. 
Different  cases  differ  very  much.  There  are  persons  who  during  their  whole  life 
have  no  more  than  three  or  four  seizures,  at  intervals  of  ten  or  fifteen  years,  while 
in  most  cases  there  is  an  attack  every  two  to  eight  weeks.  In  severe  types  the  fits 
may  even  recur  daily.  One  very  often  sees  certain  variations  in  the  course  of  the 
disease ;  at  some  periods  the  intervals  between  the  attacks  will  be  longer,  and  at 
others  shorter.  In  severe  cases  the  patient  may  have  for  several  days  very  f reqixent 
seizures,  so  that  he  does  not  regain  consciousness  at  all  between  them.  This  is 
termed  the  epileptic  state  (etat  de  mal,  status  epilepticus).  The  condition  is  quite 
rare.     It  is  often  fatal,  death  being  ushered  in  by  a  great  rise  of  temperature. 

External  influences  sometimes  affect  the  frequency  of  epileptic  attacks.  Alco- 
holic or  sexual  excess,  mental  excitement,  and  physical  overexertion  almost 
always  exert  a  malign  influence.  An  opposite  effect  is  often  experienced  where 
a  quiet  life  is  led,  with  every  attention  paid  to  hygiene  and  pure  air.  In  women, 
the  appearance  of  the  catamenia  is  not  infrequently  the  signal  for  the  occurrence 
of  an  attack.  In  many  instances  the  disease  begins  with  the  first  establishment  of 
menstruation.  Sometimes,  however,  epileptic  girls  grow  better  when  they  arrive 
at  puberty.  Pi*egnancy  sometimes  increases  and  sometimes  diminishes  the  fre- 
quency of  the  paroxysms.  Intercurrent  diseases  seem  frequently  to  exert  a  bene- 
ficial influence  upon  the  frequency  of  the  attacks. 

There  is  a  practical  distinction  between  diurnal  and  nocturnal  epilepsy.  Many 
patients  have  attacks  only  during  the  day,  while  others  again  have  them  only  at 
night.  A  case  of  purely  nocturnal  epilepsy  may  go  on  for  a  long  while  unsus- 
pected, particularly  if  the  patient  sleep  alone.  He  seldom  has,  on  the  next 
morning,  the  slightest  recollection  of  his  attack  during  the  night.  He  usually 
perceives,  however,  from  a  confused  feeling  in  his  head,  or  from  certain  in- 
juries such  as  a  bitten  tongue,  or  from  the  disordered  state  of  the  bed,  that  some- 
thing must  have  happened  to  him  during  the  night.     In  some  cases  of  nocturnal 


EPILEPSY.  775 

epilepsy  the  patient  wakes  up  out  of  sleep  before  he  enters  into  the  epileptic  state 
of  unconsciousness.  Probably  he  is  aroused  by  the  aura.  Besides  cases  where 
the  fits  occur  during  the  day  or  the  night  only,  mixed  forms  arc  frequently  seen. 

With  regard  to  the  occurrence  of  the  different  varieties  of  epileptic  seizure,  all 
sorts  of  combinations  are  possible.  Many  cases  never  have  any  but  the  typical 
convulsions;  but  in  many  others  there  are  also  a  greater  or  less  number  of  attacks 
of  petit  mal.  The  latter  may  even  be  for  a  long  period  the  sole  indication  of  the 
disease.  Often  there  are  no  epileptoid  conditions  whatever,  while  in  other  in- 
stances the  "  psychical  equivalents  "  are  the  most  prominent  feature  of  the  dis- 
order. 

During  the  interval  between  the  individual  attacks  many  epileptics  seem  per- 
fectly well,  both  physically  and  mentally.  They  are  not  infrequently,  to  be  sure, 
somewhat  peculiar  and  nervously  excitable,  or  again  dull  and  lethargic;  but  this 
does  not  by  any  means  apply  to  them  all.  Many  epileptics,  and  particularly  such 
as  have  comparatively  infrequent  paroxysms,  are  very  capable;  and  history 
furnishes  numerous  examples  of  eminent  men  who  suffered  from  this  disease — for 
instance,  Cassar,  Mahomet,  Eousseau,  and  Napoleon  I. 

Much  effort  has  been  devoted  to  the  discovery  of  "signs  of  physical  degener- 
acy "  in  epileptics.  Relying  upon  numerous  measurements,  Benedikt  believes 
that  a  majority  of  epileptics  exhibit  craniometric  anomalies,  such  as  asymmetry  of 
the  cranium,  macrocephalia,  or  steepness  of  the  vertex.  It  is  also  not  unusual  to 
meet  with  anomalies  of  the  auricles,  teeth,  or  hands  *  in  such  cases.  And,  indeed, 
all  peculiarities  of  this  sort  are,  in  general,  more  frequently  observed  in  neuro- 
pathic families  than  in  healthy  ones. 

When  the  disease  has  lasted  some  time,  and  particularly  if  the  attacks  come  at 
very  short  intervals,  the  general  condition  of  the  patient  often  undergoes  a 
gradual  but  marked  change.  This  rule  is  by  no  means  invariable.  The  mind 
becomes  more  and  more  affected;  the  intellect  grows  feeble;  memory  grows 
weaker,  and  occasionally  there  is  at  last  dementia.  In  such  cases  the  body  also 
suffers.  There  are  emaciation,  paresis,  tremor,  and  other  persistent  disturbances 
of  cerebral  origin. 

Duration. — Epilepsy  must  be  termed  a  life-long  disease.  To  be  sure,  it  is  no 
rare  thing  for  the  paroxysms  to  cease  and  not  return  for  years.  But  one  can 
never  rest  satisfied  that  all  trouble  is  at  an  end ;  some  cause  or  other  may  excite 
another  attack  after  a  long  interval.  In  general,  an  epileptic  has  a  shorter  life- 
expectancy  than  healthy  persons,  especially  as  he  may  be  carried  off  by  chronic 
pulmonary  or  other  intercurrent  disease. 

The  prognosis  is  obvious  from  what  has  been  already  said.  The  individual 
seizure  is  only  exceptionally  dangerous  of  itself.  Often  the  so-called  "  status  epi- 
lepticus  "  ends  fatally,  as  above  stated.  In  general,  those  cases  may  be  called  the 
most  favorable  where  the  separate  paroxysms  are  infrequent  and  mild ;  but  even 
here  the  disease  may  suddenly  assume  an  aggravated  form.  With  regard  to  the 
distinction  between  nocturnal  and  diurnal  epilepsy,  the  nocturnal  is,  in  our 
opinion,  the  milder  of  the  two. 

Pathology. — The  very  fact  that  in  the  intervals  between  attacks  the  patient 
often  betrays  no  sign  of  disease,  shows  that  epilepsy  can  not  be  due  to  auy  per- 
sistent macroscopic  lesion  of  the  tissues.  Indeed,  in  many  cases  nothing  is  found 
at  the  autopsy,  or,  at  most,  changes  which  can  not  be  regarded  as  essential,  such  as 
osteosclerosis  of  the  cranium  or  thickening  of  the  cerebral  meninges.  Epileptic 
subjects  who  were  during  life  decidedly  demented  usually  present  atrophy  of  the 
hemispheres.     Meynert  states  that  changes   in   the   pes  hippocampi  major  are 

*  We  have  lately  seen  an  epileptic  man  who  had  six  fingers  on  each  hand. 


776  DISEASES  OF  THE  NERVOUS  SYSTEM. 

noticeably  frequent  in  epilepsy;  but  tbese  changes  are  not  at  all  constant,  and 
their  significance  remains  to  be  established. 

We  must  therefore,  for  the  present,  be  content  to  assume  that  the  cause  of  the 
epileptic  seizure  is  an  intermittent  functional  condition  of  irritation.  A  natural 
question  is,  Where  shall  Ave  locate  this  irritation,  and  what  may  be  its  nature? 
The  opinion  was  long  current  that  the  medulla  oblongata  must  be  regarded  as  the 
true  seat  of  the, disease.  Schröder  van  der  Kolk  was  the  first  to  express  this 
opinion.  It  afterward  received  support  from  the  experimental  investigations  of 
Nothnagel,  who  demonstrated  that  irritation  of  a  particular  spot  ("convulsive 
center";  in  the  pons,  in  rabbits,  invariably  excites  general  convulsions.  Never- 
theless, most  pathologists  have  now  abandoned  this  view,  because  experiment  and 
clinical  observation  indicate  with  increasing  distinctness  that  the  origin  of  epi- 
leptic convulsions  is  to  be  sought  in  the  cortex  cerebri.  The  clinical  evidence  is 
the  invariable  combination  of  convulsions  and  impairment  of  consciousness ;  the 
circumstance  that  the  milder  and  the  masked  forms  of  epilepsy,  now  known  to  be 
intimately  related  to  the  time  epileptic  convulsions,  also,  almost  without  excep- 
tion, indicate  psychical  disturbance;  that  attacks,  the  symptoms  of  which  are  per- 
fectly analogous  with  those  of  epilepsy,  are  often  found  to  be  the  result  of  ana- 
tomical lesions  of  the  cerebral  cortex;  and,  finally,  that  these  convulsions  in  man 
and  the  convulsions  of  "cortical  epilepsy"  {vide  infra),  experimentally  produced 
in  animals,  extend  over  the  different  groups  of  muscles  in  a  way  which  corre- 
sponds precisely  with  the  anatomical  position  of  the  different  motor  centers  in  the 
cortex  (Hughlings  Jackson).  For  example,  if  the  convulsion  begins  in  the  dis- 
tribution of  the  facial  nerve,  it  extends  from  this  point  to  the  arm  before  it  affects 
the  leg. 

There  is  also  experimental  evidence  that  epileptic  paroxysms  are  of  cortical 
origin.  A  great  number  of  observers  (Hitzig,  Ferrier,  Albertoni,  Luciani,  Franck, 
and  Pitres)  have  proved  that  electrical  irritation  of  the  motor  regions  of  the  cortex 
in  animals  will  produce  epileptiform  convulsions.  Unverricht  has  made  some  of 
the  latest  and  most  thorough  investigations  in  regard  to  this  point  upon  dogs.  He 
found  that  when  a  motor  center  is  stimulated  the  convulsions  spread  from  the 
corresponding  group  of  muscles  to  others  in  a  way  which  corresponds  precisely 
to  the  anatomical  position  of  the  separate  centers.  If  one  of  the  centers  in  the 
cortex  be  destroyed,  the  convulsions  of  the  corresponding  muscles  cease  at  once. 
This  proves  that  the  motor  centers  must  be  intact  in  order  to  render  the  occur- 
rence of  epileptic  seizures  possible.  Just  how  the  stimulation  extends  from  one 
center  to  another  we  have  as  yet  no  certain  information.  Probably  it  travels 
horizontally  through  the  cortex. 

We  see,  therefore,  that  in  all  probability  the  seizures  hi  man  also  originate  in 
the  cortex  of  the  brain.  The  phenomena  of  the  aura  are  likewise  referable  to 
some  stimulation  of  the  cortex,  probably  of  the  sensory  region  in  most  cases,  as  in 
the  optical  aura.  The  starting  point  of  the  irritation  is  probably  usually  in  the 
motor  cortex,  but  it  dees  not  seem  impossible  that  an  irritation  developing  in  the 
posterior  cortical  regions  may  extend  secondarily  to  the  anterior  motor  portion  of 
the  cortex  (Unverricht).  The  manner  in  which  the  irritation  is  created  is  as  yet 
entirely  conjectural.  Kussmaul  and  Tenner  proved  that  epileptiform  convulsions 
can  be  excited  by  a  general  cerebral  anaemia;  and  this  fact  was  the  main  founda- 
tion for  the  assumption  that  the  genuine  epileptic  convulsions  are  also  due  to  a 
temporary  cerebral  anaemia,  caused,  it  may  be,  by  local  vasomotor  constriction. 
Definite  proof  has  not  yet  been  furnished  on  this  point.  In  the  artificial  epilepsy 
which  Unverricht  produced,  and  that  also  which  Magnan  excited  by  absinthe,  the 
cortex  of  the  brain  was  not  strikingly  anaemic. 

Diagnosis. — Most  cases  of  epilepsy  are  easily  recognizable.     It  needs  only  to  be 


EPILEPSY.  777 

borne  in  mind  that  epileptiform  convulsions  may  also  occur  as  a  symptom  of 
cerebral  diseases  which  do  have  an  anatomical  basis,  such  as  tumor,  abscess,  mul- 
tiple sclerosis,  and  hydatids.  As  a  rule,  however,  such  diseases  are  readily  distin- 
guished by  the  state  of  the  patient  between  the  seizures,  or  by  the  further  course 
of  the  illness.  It  should  also  be  understood  that  unilateral  convulsions,  or  such 
as  are  confined  to  a  single  member  (Jacksonian  epilepsy,  vide  .supra,  page  714), 
are  usually  not  true  epilepsy,  but  symptoms  of  some  circumscribed  affection  of  the 
cortex.  The  differentiation  from  hysterical  convulsions  (q.  v.)  is  seldom  difficult. 
Weight  should  be  laid  on  the  general  character  of  the  attack,  the  complete  loss  of 
consciousness  in  epilepsy,  the  dilatation  of  the  pupils,  which  do  not  react  to  light, 
the  initial  pallor  not  infrequently  observed,  and  the  late  cyanosis  of  the  face.  It 
is  mainly  the  same  factors  which  will  enable  us  to  detect  simulated  epilepsy.  Here, 
also,  there  is  an  absence  of  those  bodily  injuries,  such  as  a  bitten  tongue,  which 
are  often  so  characteristic  of  the  genuine  disease. 

Treatment. — Although  no  remedy  is  capable  of  working  a  certain  and  perma- 
nent cure  of  epilepsy,  yet  a  favorable  influence  can  be  exerted  upon  the  disease  in 
many  ways,  so  as  to  lessen  the  frequency  and  severity  of  the  paroxysms,  and  to 
avert  many  of  their  evil  results. 

In  the  first  place,  regimen  is  of  great  importance.  Any  excessive  exertion  of 
mind  or  body  must  be  forbidden.  Temperance  must  be  exercised  in  eating  and 
drinking.  Alcohol,  strong  coffee,  and  tea,  can  be  used  only  moderately;  nor  is 
too  much  smoking  permissible.  The  diet  should  be  simple  and  unirritating,  and 
vegetable  rather  than  animal.  It  is  said  that  in  some  cases  decided  improvement 
has  been  brought  about  by  confining  the  patient  to  milk  and  vegetables.  In 
summer  the  patient  should  live  quietly  in  the  country  or  the  mountains.  We 
have  also  the  individual  constitution  to  consider:  a  weak  and  anaemic  person 
must  have  iron  and  abundant  nourishment;  and  a  full-blooded,  corpulent  indi- 
vidual should  drink  the  natural  aperient  waters,  and  live  abstemiously. 

Proceeding  to  the  treatment  of  the  disease  itself,  we  shall  rarely  find  any  cause 
to  remove ;  although,  in  a  few  cases  of  reflex  epilepsy,  the  excision  of  old  scars, 
the  extraction  of  foreign  bodies,  or  trephining  the  skull,  where  the  disease  has 
followed  an  injury,  have  brought  about  permanent  recovery.  In  genuine  typical 
epilepsy  we  have  no  such  indications  to  fulfill,  and  we  must  have  recourse  to  such 
treatment  as  experience  shows  can  influence  favorably  the  outward  manifesta- 
tions of  the  disease.  [In  Jacksonian  epilepsy  the  cortical  center  of  the  initial 
spasm  of  the  convulsion  has  been  excised  a  number  of  times,  even  when,  after 
trephining,  it  appeared  healthy.  The  center  should  be  carefully  determined,  after 
the  brain  is  exposed,  by  faradic  stimulation  of  the  cortex.  In  some  cases  relief 
has  been  obtained,  and  the  convulsions  have  ceased  for  a  considerable  period.  It 
is  too  early  to  speak  of  the  ultimate  results,  but  in  some  cases  the  attacks  have 
finally  recurred  in  equal  severity. — K.] 

Among  symptomatic  remedies,  potassic  bromide  has  an  undisputed  right  to 
the  first  place.  It  was  first  recommended  by  Locock  in  the  year  1853.  It  should 
be  the  first  thing  tried  in  any  severe  case.  Apparently  it  acts  by  directly  lower- 
ing the  sensitiveness  of  the  motor  centers  of  the  cortex  to  irritation.  Rather 
large  doses  are  requisite.  Beginning  with  about  one  drachm  (grin.  4-5)  a  day,  we 
may  find  it  advisable  to  increase  up  to  two  or  two  and  one  half  drachms  (grm. 
8-10).  It  may  be  prescribed  in  water  (1  to  10  or  15),  or  in  powders  which  the 
patient  himself  is  to  dissolve  in  water,  sweetened  if  desired.  The  remedy  in 
almost  all  cases  needs  to  be  used  for  months  and  years,  and  it  is  therefore  often 
advisable  for  the  patient  to  buy  a  half  pound  or  a  pound  and  weigh  it  out  himself 
into  the  proper  doses.  It  should  always  be  taken  in  a  good  deal  of  water,  say  half 
a  tumbler  or  more,  to  avoid  irritating  the  stomach.    The  total  amount  for  the  day 


778  DISEASES  OF  THE  NERVOUS  SYSTEM. 

is  usually  divided  into  two  or  three  portions;  but  the  whole  may  he  dissolved  in 
a  large  amount  of  water  and  drunk  gradually  through  the  day.  The  bromides  of 
sodium  and  ammonium  are  also  frequently  employed.  They  have  the  advantage 
of  disturbing  the  stomach  less  than  does  the  potassium  salt.  It  is  a  good  way  to 
combine  the  different  bromides — for  instance,  bromide  of  sodium  and  bromide  of 
ammonium,  of  each  10  parts;  distilled  water,  200  parts:  three  tablespoonfuls  a 
day  in  water.  It  is  well  to  combine  the  various  bromides.  Erlenmeyer  strongly 
recommends  a  mixture  of  two  parts  of  potassic  bromide  with  one  each  of  sodic  and 
of  amnionic  bromide. 

In  using  the  bromides,  persistence  is  necessary  for  at  least  months,  and  often, 
with  occasional  interruptions,  for  years,  if  benefit  is  to  be  obtained.  In  case  there 
are  unpleasant  symptoms  due  to  the  remedy,  such  as  excessive  acne,  muscular 
lassitude  and  tremor,  cardiac  weakness,  dyspepsia,  impotence,  or  melancholy,  we 
must  diminish  the  dose,  or  even  omit  the  medicine  for  a  time.  Many  patients  are 
greatly  annoyed  by  pustules  due  to  the  bromide ;  this  can  sometimes  be  avoided 
by  giving  Fowler's  solution  at  the  same  time.  If  the  attacks  are  decidedly 
abated,  the  dose  may  be  gradually  diminished,  to  be  increased  again,  however;  if 
there  be  any  tendency  to  a  relapse. 

Recourse  to  other  remedies  is  seldom  had,  unless  potassic  bromide  fails,  or  for 
some  cause  must  be  discontinued.  We  may  then  try  valerian  in  powder,  8-30  gr. 
(grm.  0-5-2)  several  times  a  day,  or  as  an  infusion.  It  is  a  very  good  plan  to  give 
patients  who  are  taking  bromide  a  cup  or  two  of  valerian  tea  at  bedtime.  Bella- 
donna may  also  be  exhibited,  or  a  pill  of  atropine,  gr.  TJ„  (grm.  0"0005),  three  to 
five  times  a  day;  or  zinc  oxide  in  the  dose  of  one  to  three  grains  (grm.  0-05-0"20), 
perhaps  combined  with  a  grain  of  extract  of  belladonna,  and  fifteen  grains  of 
valerian,  as  a  powder,  three  times  a  day.  Thei'e  are  also  many  other  remedies  of 
doxibtful  efficacy :  curare,  hyoscine,  the  root  of  artemisia  vulgaris,  ammonio-cupric 
sulphate,  nitrate  of  silver,  and  arsenic. 

Electricity  is  apparently  beneficial  in  occasional  instances,  and  may  be  tried  in 
connection  with  other  remedies.  The  galvanic  current  should  be  cautiously 
applied  to  the  head  and  the  sympathetic  nerves.  Still  greater  benefit  is  some- 
times obtained  from  a  carefully  conducted  cold-water  cure.  Cold  sponging  with 
friction  at  night  helps  most  cases,  and  it  is  sometimes  very  advisable  to  send  the 
patient  in  summer  to  some  appropriate  establishment  for  cold-water  treatment. 

Treatment  during  the  Paroxysm. — In  most  cases  we  can  do  little  during  the 
seizure  except  to  take  such  precautionary  measures  as  common  sense  suggests. 
We  possess  no  means  of  suppressing  an  attack  when  once  under  way;  nor, 
indeed,  is  it  often  dangerous.  In  individual  instances  the  patient  finds  out  from 
experience  some  method  to  cut  short  the  paroxysm  during  the  aura.  For 
instance,  there  are  cases  where  tightly  bandaging  or  vigorously  rubbing  the  part 
in  which  the  aura  originates  will  avert  the  convulsions.  A  number  of  cases  have 
also  been  known  where  the  ingestion  of  a  generous  quantity  of  common  salt  dur- 
ing the  aura  (usually  in  these  instances  starting  from  the  epigastrium)  has  had 
the  same  effect.  A  patient  of  our  own,  whose  attacks  began  with  a  feeling  of  rec- 
tal tenesmus,  maintained  that  she  could  almost  invariably  suppress  the  convul- 
sions by  promptly  going  to  stool,  if  she  had  time  and  opportunity.  It  was  for- 
merly a  frequent  manoeuvre  to  seek  to  ward  off  the  attack  by  compressing  the 
carotids ;  but  this  usually  fails.  Berger  recommends  the  inhalation  of  nitrite  of 
amyl  at  the  commencement  of  the  fit,  having  repeatedly  seen  benefit  follow  its  use. 

In  the  "  status  epilepticus,"  narcotics  are  the  most  deserving  of  trial,  and  in 
particular  chloroform  or  ether  given  by  inhalation.  Amyl  nitrite  may  also  be  of 
service. 

[It  is  sometimes  desirable  to  withhold  the  knowledge  that  he  is  an  epileptic 


INFANTILE  CONVULSIONS  (ECLAMPSIA  INFANTUM;.  770 

from  the  patient,  whose  ordinary  life  should  be  interfered  with  as  little  as  is 
possible. 

Especially  in  cases  characterized  by  headache  and  heat  in  the  head,  Brown- 
Sequard  finds  the  application  of  ice  directly  to  the  back  of  the  neck  and  between 
the  shoulders  useful.] 

APPENDIX. 

INFANTILE  CONVULSIONS    (ECLAMPSIA  INFANTUM). 

Convulsions  in  childhood  are  of  such  frequency  and  importance  as  to  justify 
brief  special  mention  here. 

Every  practitioner  learns  from  experience  that  the  young  are  especially  pre- 
disposed to  convulsions.  Probably  this  is  partly  due  to  excessive  reflex  excita- 
bility of  the  brain  in  childhood.  Thus  children  not  infrequently  undergo  con- 
vulsions under  circumstances  in  which  adults  would  very  rarely  have  them. 
They  sometimes  are  seen  in  children  in  the  beginning  of  acute  febrile  diseases, 
such  as  pneumonia,  scarlet  fever,  and  measles.  They  also  occur  from  indigestion, 
particularly  when  the  stomach  has  been  overloaded ;  sometimes  on  account  of 
teething;  or  because  of  intestinal  worms.  Here  they  are  in  all  probability  of 
reflex  origin. 

Convulsions  may  occur  in  very  early  life  without  ascertainable  cause.  In 
many  cases  they  are  really  the  commencement  of  epilepsy,  as  is  seen  afterward. 
Again,  they  may  be  due  to  some  actual  lesion  in  the  brain.  For  example,  if  one 
recalls  the  initial  stage  of  the  acute  poliomyelitis  and  acute  encephalitis  of  children 
(vide  pages  668  and  744),  it  will  not  seem  unlikely  that  many  rapidly  fatal  cases  of 
"convulsions"  are  really  instances  of  the  diseases  mentioned.  This  point  has  not 
yet  been  at  all  satisfactorily  investigated  by  pathologists.  At  any  rate,  it  does  not 
seem  satisfactory  to  us  to  regard  the  "  oedema  of  the  meninges  "  found  in  such 
cases  as  an  independent  disease  and  the  sufficient  cause  of  death.  Often  convul- 
sions occur  suddenly  in  children  and  then  cease,  never  to  recur,  without  our 
being  able  to  find  any  explanation  of  the  attack.  Experience  shows  that  rachitic 
children  are  especially  liable  to  suffer  from  eclampsia — possibly  because  of  cranial 
rachitic  changes  (?). 

The  symptoms  of  the  eclamptic  attacks  are  on  the  whole  analogous  with  those 
of  epileptic  paroxysms.  The  child's  eyes  become  staring  and  fixed,  and  there 
are  tonic  and  clonic  spasms  of  the  face,  trunk,  and  extremities.  Such  seizures 
may  continue  for  days  with  brief  intermissions.  In  such  cases  the  prognosis  is 
dubious,  particularly  if  the  child  be  weakly,  but  it  is  by  no  means  absolutely  bad. 
The  cause  and  the  significance  of  the  convulsions  can  seldom  be  determined 
immediately. 

Symptomatic  treatment  consists  in  applying  cold  to  the  head,  wet  packs,  sina- 
pisms on  the  chest  and  the  calves  of  the  legs,  and  perhaps  an  enema  (to  which 
vinegar  may  be  added).  These  measures  generally  answer  for  mild  cases.  If  the 
fits  are  very  frequent  and  violent,  we  may  allow  even  small  children  to  inhale 
chloroform,  often  with  great  advantage.  A  dessertspoonful  is  to  be  poured  upon 
a  handkerchief  and  administered  cautiously. 

Of  course,  we  must  also  try  to  discover  and  remove  the  cause.  The  attacks 
due  to  overloading  the  stomach  usually  occur  in  not  very  young  children,  and  ai*e 
apt  to  be  greatly  benefited  by  a  prompt  emetic  or  purge. 

[A  bath  at  a  temperature  of  90°-95°,  while  cool  water  is  applied  to  the  head, 
seems  often  to  be  of  service ;  if  the  child  be  exhausted  by  diai'rhoea,  the  cold  to  the 
head  should  be  omitted.     In  a  teething  child  it  can  do  no  harm,  and  it  sometimes 


780  DISEASES  OF  THE  NERVOUS  SYSTEM. 

has  a  very  marked  beneficial  effect  to  lance  the  gums  thoroughly.  Enemas  con- 
taining chloral  with  or  without  bromide  of  potash  are  more  used  in  this  country 
than  is  chloroform  by  inhalation. 

A  drop  of  nitrite  of  amyl  by  inhalation  is  said  by  Eustace  Smith  to  exert  a  con- 
trolling effect  on  the  muscular  movements.] 


CHAPTER  II. 

CHOREA. 

{Chorea  Minor.    St.  Yitus's  Dance.) 

iEtiology.—  Centuries  ago  the  name  chorea  (dance)  was  applied  mainly  to 
those  strange  states  of  "  dancing  mania  "  which  were  endemic  in  certain  places, 
being  due  to  excessive  mental  excitement  and  to  the  innate  propensity  to  imita- 
tion. The  specific  for  this  condition  was  held  to  be  a  pilgrimage  to  some  shrine 
of  St.  Vitus.  At  the  present  time,  however,  chorea  is  used  to  designate  a  perfectly 
definite  disease,  of  which  the  characteristic  symptom  is  the  appearance  of  certain 
peculiar  motor  phenomena  due  to  irritation  of  the  nervous  centers.  It  is  some- 
times called  chorea  minor,  in  contradistinction  from  what  was  formerly  termed 
chorea  major  or  magna.  This  latter  is,  however,  not  a  genuine,  independent  dis- 
ease, but  a  manifestation  of  hysteria  (q.  v.),  or  apparently  in  many  instances  of 
epilepsy. 

Chorea  proper  is  mainly  a  disease  of  children.  It  occurs  most  often  between 
the  fifth  and  fifteenth  years,  although  it  may  be  seen  both  earlier  and  later. 
There  is  a  slightly  greater  liability  to  it  in  girls  than  in  boys.  Hereditary  neuro- 
pathic tendencies  are  also  a  factor  iu  its  aetiology,  but  not  a  very  important  one.* 

As  to  causation,  in  many  cases  nothing  definite  can  be  made  out.  Mental  ex- 
citement, as  from  fright,  seems  in  some  few  instances  to  favor  the  onset  of  the 
trouble.  It  is  also  certain  that  the  imitative  impulse  will  often  lead  to  choreic 
movements  in  healthy  children  who  come  in  contact  with  choreic  patients,  but  it 
is  doubtful  whether  this  "  imitative  chorea  "  can  be  regarded  as  true  chorea.  There 
is  a  very  interesting  connection  between  chorea  and  acute  articular  rheumatism. 
Although  the  statement  of  certain  authors,  that  almost  every  case  of  acute  ai'ticular 
rheumatism  in  children  is  followed  by  chorea,  is  far  too  strong,  yet  this  sequence 
is  comparatively  frequent.  Chorea  is  sometimes  seen  also  in  children  who  have 
a  mild  form  of  chronic  rheumatism,  or  in  such  as  have  valvular  cardiac  disease, 
whether  preceded  by  articular  rheumatism  or  not.  [Some  observers  claim  that 
there  is  an  increased  amount  of  uric  acid  in  the  urine  of  patients  with  chorea,  the 
acid  diminishing  as  the  chorea  subsides. — E.]  Here  chorea  is  seen  as  a  sequel  to 
an  infectious  disease ;  perhaps  this  is  a  hint  of  the  light  in  which  we  should  view 
apparently  idiopathic  cases  of  chorea.  [Lewis,  having  studied  1,383  attacks  of 
chorea  and  673  of  acute  articular  rheumatism,  finds  that  the  fewest  attacks  of 
chorea  occur  in  October  and  November,  the  greatest  number  in  March  and  April. 
The  greatest  number  of  attacks  of  rheumatism  occur  in  April,  the  smallest  in 
the  autumn.  The  frequency  of  attacks  of  both  diseases  seems  related  to  the  num- 
ber of  storm-centers  which  passed  within  four  hundred  miles  of  the  localities 
studied,  and  to  the  mean  actual  barometer  and  mean  relative  humidity.     Over- 

*  The  so-called  hereditary  or  Huntington's  chorea  is  a  special  disease.  Choreic  movements  appear 
in  many  members  of  the  same  family  in  several  generations,  and  at  an  advanced  age,  from  thirty  to 
forty.     The  disease  is  incurable,  and  often  leads  to  mental  deterioration. 


CHOKEA.  781 

study,  acting  with  meteorological  conditions,  may  be  a  predisposing  but  not  an 
exciting  cause  of  chorea. — K.] 

Women  are  particularly  liable  to  chorea  during  pregnancy.  Chorea  gravi- 
darum is  most  frequent  in  youthful  Primiparae. 

Clinical  History. — Chorea  usually  begins  gradually,  and  without  any  special 
prodromata.  Sometimes,  however,  there  are  prodromal  symptoms,  chiefly  a  cer- 
tain mental  depression  and  irritability,  with  indisposition  to  intellectual  effort. 
There  may  be  slight  rheumatic  pains  or  anorexia,  and  other  evidences  of  constitu- 
tional disturbance. 

Ordinarily,  the  peculiar  motor  disturbances  are  the  first  thing  to  attract  the 
attention  of  the  patient  or  its  parents.  There  are  involuntary  and  irrepressible 
movements  in  the  most  diverse  groups  of  muscles.  Both  single  contractions  and 
also  complicated  movements  occur,  independently  of  the  will,  and  in  all  parts  of 
the  body,  now  in  one  place,  now  in  another,  sometimes  in  a  single  member,  and 
sometimes  in  several  at  once.  The  movements  may  be  made  in  rapid  succession, 
or  may  be  separated  by  long  intervals  of  quiet.  The  facial  muscles  may  be 
involved,  causing  an  occasional  wrinkling  of  the  brow  or  distortion  of  the  mouth. 
The  eyes  or  the  eyelids  may  also  exhibit  involuntary  movements.  The  pupils 
are  frequently  dilated.  If  the  patient  be  asked  to  protrude  his  tongue  and  keep  it 
quiet,  it  will  often  be  involuntarily  withdrawn  into  the  mouth  or  thrust  to  one 
side.  The  tongue  may  even  be  sufficiently  affected  to  impair  speech.  The  laryn- 
geal muscles  have  also  been  observed  to  make  choreic  movements.  The  arms  are 
frequently  the  most  affected  of  any  part ;  they  are  twisted,  fleered,  elevated,  put 
behind  the  back — in  short,  moved  in  every  conceivable  way.  The  trunk  is  gener- 
ally but  little  disturbed  in  the  milder  cases,  but  in  severe  ones  the  whole  body 
participates.  The  patient  stands  up,  lies  down  again,  turns  upon  his  side,  etc. 
The  legs  are  seldom  as  much  disturbed  as  the  arms  and  face,  but  slight  move- 
ments of  the  lower  limbs  are  very  frequent — the  foot  is  thrust  forward  or  ex- 
tended, the  knee  is  flexed,  and  so  on.  In  general,  it  may  be  said  to  be  character- 
istic of  chorea  that  the  abnormal  motor  irritation  usually  affects  a  considerable 
number  of  muscles  simultaneously,  thus  exciting  all  sorts  of  combined  movements; 
and,  secondly,  that  choreic  movements,  for  the  most  part,  are  not  short  twitches, 
but  take  place  in  a  manner  decidedly  similar  to  that  of  voluntary  movements. 

The  vigor  of  the  movements  varies  greatly  in  different  cases.  At  first  they 
may  be  too  slight  for  the  unpracticed  eye  to  catch.  Many  children  in  an  incipient 
stage  of  chorea  are  unjustly  punished  at  school  because  they  write  ill  or  do  not 
sit  quietly.  Many  cases  are  mild  throughout,  never  having  very  severe  disturb- 
ance. Others,  though  considerably  annoyed,  can  nevertheless  walk  or  stand 
alone.  In  the  severest  cases,  however,  the  whole  body  is  continually  in  active 
motion.  The  patient  throws  himself  about  in  bed,  and  all  the  extremities  exhibit 
constant  violent  and  irregular  movements.  The  ingestion  of  food  is  extremely 
difficult,  sleep  is  disturbed,  and  the  patient's  flesh  and  strength  are  rapidly  and 
greatly  diminished. 

Further,  each  individual  case  presents  variations  in  severity  at  different  times. 
If  the  patient  be  left  quietly  to  himself,  the  contractions  are  comparatively  very 
slight.  As  soon  as  he  is  conscious  of  being  watched  or  as  soon  as  any  one  speaks 
to  him,  his  condition  usually  becomes  much  worse.  During  sleep  the  choreic 
movements  cease  altogether. 

In  many  cases  all  the  voluntaiw  muscles  are  involved ;  but  sometimes  the  dis- 
ease is  limited  to  certain  groups  of  muscles.  Very  frequently  the  disturbance  is 
mainly  unilateral  (hemichorea) ;  the  opposite  side  of  the  body  then  exhibits  few 
involuntary  movements,  or,  it  may  be,  none.  As  already  stated,  the  face  and 
npper  extremities  are  often  more  affected  than  the  trunk  and  lower  limbs. 


782  DISEASES  OF  THE  NERVOUS  SYSTEM. 

These  motor  disturbances  often  constitute  the  sole  or  the  predominant  symp- 
tom of  chorea.  There  is  hardly  ever  muscular  weakness  or  paralysis.  It  is 
remarkable  how  little  feeling  of  fatigue  there  usually  is,  despite  the  incessant 
activity.  In  a  few  cases  only,  of  genuine  chorea,  have  we  seen  actua]  paresis, 
affecting,  for  instance,  one  arm,  or  in  hemichorea  the  same  half  of  the  body. 
Sensation  is  unimpaired.  The  reflexes  do  not  exhibit  striking  peculiarities.  The 
tendon  reflexes  we  have  sometimes  found  to  be  noticeably  diminished,  although 
in  other  instances  they  were  normal.  There  may  be  isolated  spots  in  the  spinal 
column  tender  on  pressure,  but  this  is  not  at  all  constant.  That  chorea  may  be 
complicated  by  arthritis  and  valvular  cardiac  disease  has  ah'eady  been  stated. 
Some  caution  should  be  exercised  in  making  a  diagnosis  of  cardiac  lesion  here,  for 
experience  shows  that  choreic  patients  are  apt  to  have  functional  murmurs  and 
slightly  irregular  cardiac  action.  [Osier  has  found  that  the  endocarditis  of  chorea 
is  very  apt  to  lead  to  organic  valvular  disease.  Of  110  choreic  patients  that  he 
examined  more  than  two  years  after  the  attack,  54  presented  signs  of  organic 
heart  disease. — K.]  The  temperature  is  not  elevated,  in  spite  of  the  constant 
muscular  contractions,  nor  is  the  amount  of  urea  excreted  by  the  kidneys  in- 
creased. 

Slight  mental  disturbance  is  frequently  observed.  The  patient  is  often  rude, 
peevish,  capricious,  incapable  of  mental  exertion,  irritable,  and  inclined  to  tears; 
but  any  great  or  permaneut  impairment  of  intellect  is  very  exceptional  indeed. 

The  entire  process  generally  occupies  several  months.  In  mild  cases,  however, 
recovery  may  ensue  at  the  end  of  a  few  weeks,  while,  on  the  other  hand,  cases 
may  last  a  year  or  even  longer.  Variations  in  the  intensity  of  the  chorea  are 
often  witnessed.  These  are  sometimes  spontaneous,  and  sometimes  are  due  to 
outward  influences.  Even  when  the  disease  is  apparently  extinguished,  we  must 
be  prepared  for  a  possible  relapse.  The  disease  may  appear  repeatedly  in  the 
course  of  a  few  years,  in  such  a  way  that  it  is  not  easy  to  determine  whether  the 
different  attacks  are  relapses  or  new  illnesses.  The  protracted  cases  are,  as  a  rule, 
comparatively  mild ;  and  many  cases  that  begin  with  great  violence  end  compara- 
tively early.  In  adults,  however,  we  have  met  with  some  rather  severe  cases  which 
were  very  chronic,  and  seemed  at  last  to  become  stationary. 

The  termination  of  chorea,  in  the  great  majority  of  cases,  is  favorable.  Now 
and  then  severe  cases  do  occur  which  end  in  death.  In  these  the  choreic  move- 
ments are  extremely  violent.  The  patient  is  tossed  about  in  his  bed,  and  can  eat 
little  and  sleep  none.  We  have  ourselves  observed  three  such  cases,  in  girls  four- 
teen to  seventeen  years  of  age,  which  proved  fatal  within  the  first  two  or  three 
weeks.  Two  died  from  general  exhaustion  and  collapse,  and  the  third  from 
gangrene  affecting  numerous  cutaneous  traumatic  lesions,  which  had  occurred 
despite  every  possible  precaution. 

Nature  of  the  Disease.— All  cases  of  genuine  cherea  thus  far  examined  by 
pathologists  have  failed  to  furnish  any  lesions  which  can  be  regarded  as  essential. 
In  the  three  cases  above  mentioned  the  autopsy  revealed  absolutely  nothing 
abnormal  in  the  central  nervous  system.  We  are  at  present,  therefore,  obliged  to 
classify  chorea  as  a  "  neurosis  " — that  is.  as  a  disease  that  produces  functional  dis- 
turbances, for  which  latter  there  is  no  anatomical  basis  known  to  us.  The  symp- 
toms themselves  show  that  the  disorder  must  affect  principally  some  motor  region 
of  the  nervous  system ;  but  just  which  motor  region  is  involved  can  at  present 
only  be  conjectured.  It  seems  very  probable,  however,  that  the  true  seat  of  chorea 
is  to  be  sought  in  the  brain.  In  the  first  place,  the  frequent  occurrence  of  hemi- 
chorea would  indicate  this ;  as  would  also  the  fact  that  slight  mental  anomalies 
are  frequently  combined  with  chorea;  and,  finally,  "choreiform"  movements  may 
occur  as  the  sole  symptom  of  undoubted  cerebral  disease,  as  in  post-hemiplegic 


CHOREA.  783 

hemichorea.  We  have,  however,  no  hint  as  to  whether  the  motor  regions  in- 
volved are  those  located  in  the  cortex,  or  others.  The  surmise  has  quite  of  ten 
been  expressed  that  chorea  is  due  to  embolism  of  a  mild'  type;  but,  in  our  opinion, 
this  view  lacks  proof  entirely,  and  is  even  improbable.  As  already  said,  it  may  be 
that  the  connection  existing  between  chorea  and  acute  articular  rheumatism  will 
throw  some  light  upon  the  nature  of  the  former  disease. 

[Money  has  produced  choreic  movements  in  dogs  by  the  injection  of  starch 
into  the  carotids,  thus  causing  embolism  of  minute  cerebral  vessels.] 

Diagnosis. — The  diagnosis  is  almost  always  easy,  and  it  can  often  be  made  at  a 
glance.  The  motor  symptoms  of  athetosis,  paralysis  agitans,  and  of  alcoholic, 
senile,  saturnine,  and  mercurial  tremor  are  so  characteristic  as  to  be  readily  dis- 
tinguished from  the  movements  of  chorea.  It  is  not  difficult  to  perceive  the 
difference  between  genuine  idiopathic  chorea  and  the  symptomatic  choreiform 
movements  occasioned  by  some  other  cerebral  lesion. 

Prognosis. — As  has  been  stated,  the  prognosis  is  almost  invariably  favorable, 
although  the  disease  may  prove  very  tedious.  The  possibility  of  relapses  should 
be  borne  in  mind.  The  prognosis  is  doubtful  only  in  the  worst  cases  of  acute 
chorea,  where  there  is  great  and  rapid  failure  of  the  general  health. 

Treatment. — Even  in  mild  cases  the  patient  must  be  kept  from  school  and  at 
home,  in  order  to  avoid  all  unnecessary  excitement  from  ridicule  and  the  like. 
If  the  chorea  be  only  moderately  severe,  it  is  not  necessary  that  the  child  should 
be  in  bed;  we  may  even  allow  moderate  exercise  in  the  open  air.  Where  the 
motions  are  violent,  we  should  seek  to  guard  the  patient  from  self -in  jury  by  means 
of  pillows  and  cushions. 

Among  the  remedies  recommended  for  chorea,  the  chief  place  is  occupied  by 
arsenic  and  potassic  bromide.  Arsenic  in  particular  seems  often  to  be  of  value. 
We  give  Fowler's  solution  in  water ;  beginning  with  five  drops,  two  or  three  times 
a  day,  we  gradually  increase  to  eight  or  ten  drops.  [In  severe  cases  much  larger 
doses  may  be  given.  It  should  be  pushed  up  to  twenty  drops  or  more,  stopping 
for  twenty-four  hours  if  symptoms  of  poisoning  appear,  and  beginning  again  at 
the  same  dose.  It  should  be  freely  diluted. — K.]  In  children  under  six,  the  dose 
should  be  made  somewhat  smaller.  If  the  child  be  anasmic,  iron  may  be  given 
in  addition;  or,  if  there  be  great  restlessness  and  loss  of  sleep,  narcotics  may  also 
be  administered.  Antipyrine,  in  doses  of  seven  to  fifteen  grains  (grm.  0 -5-1-0) 
several  times  a  day,  is  sometimes  of  distinct  service  in  severe  cases.  We  may 
also,  especially  if  arsenic  fail,  try  bromide  of  potassium  in  large  doses,  a  drachm 
(grm.  3-5)  a  day.  Numerous  other  drugs  have  been  recommended :  oxide  of  zinc, 
valerianate  of  zinc,  nitrate  of  silver,  and  sulphate  of  copper.  At  present  they  are 
very  rarely  used ;  but  Riess  has  lately  recommended  physostigmine,  one  sixth  to 
one  third  of  a  grain  a  day  (grm.  0-001-0-002),  best  subcutan eously.  [Sulfonal, 
three  to  five  grains  (grm.  0-2-0*4)  three  times  a  day,  acts  well,  as  an  adjuvant  to 
arsenic,  in  cases  where  there  is  much  excitement.  Exalgine,  two  or  three  grains 
(grm.  0-l-0'2)  three  times  a  day,  has  recently  been  recommended. — K.]  If  the  dis- 
ease occur  as  a  sequel  of  articular  rheumatism,  we  may  try  salicylic  acid.  Nar- 
cotics should  be  employed  very  cautiously  in  chorea.  Although  chloral  has  been 
recently  recommended  for  grave  cases,  there  are  instances  known  where  this 
remedy  has  been  followed  by  unfortunate  results. 

Hydrotherapeutics  of  a  mild  kind  do  good,  and  can  easily  be  carried  out  in 
most  instances.  Thus,  we  may  use  lukewarm  baths,  a  wet  pack,  or  gentle  spong- 
ing with  water  at  72°-82°  (18°-22°  R.)  to  great  advantage. 

Electricity  may  also  be  tried.  A  feeble  current  of  galvanic  electricity  is  ap- 
plied to  the  head  (in  the  region  of  the  motor  centers),  or  the  spinal  cord  is  gal- 
vanized.    If  there  be  points  along  the  spinal  column  where  pressure  causes  pain, 


784:  DISEASES  OF  THE  NERVOUS  SYSTEM. 

it  is  said  to  be  an  excellent  plan  to  apply  the  anode  to  them ;  hut  the  results  of 
electrical  treatment  are  seldom  very  brilliant. 

In  the  chorea  of  pregnancy,  which  sometimes  is  a  very  violent  disease,  the 
same  remedies  may  be  employed.  If  they  do  no  good,  artificial  delivery  may 
be  required;  after  which,  as  we  have  ourselves  once  observed,  there  may  be  a 
rapid  abatement  of  all  symptoms. 


CHAPTER  III. 

PARALYSIS  AGITANS. 

(Shaking  Palsy.     ParTcinsoii's  Disease.) 

.ffitiology. — In  1817  Parkinson  described  for  the  first  time  a  disease  which  he 
named  the  "shaking  palsy."  It  is  not  of  very  frequent  occurrence,  and  as  yet 
little  has  been  ascertained  with  regard  to  its  Eetiology.  In  most  cases  it  develops 
very  gradually,  without  any  demonstrable  cause.  It  almost  always  attacks  elderly 
persons,  being  very  rare  before  the  thirty -fifth  year.  Sex  does  not  seem  to  exert 
any  great  predisposing  influence.  Hereditary  neuropathic  tendencies  can  indeed 
bs  traced  in  some  instances,  but  are  certainly  of  less  potency  in  paralysis  agitans 
than,  for  instance,  in  epilepsy.  Special  exciting  causes  have  sometimes  been  ob- 
served, such  as  catching  cold,  violent  emotional  excitement,  and  traumatic  influ- 
ences, among  the  latter  injury  to  the  nerves,  burns,  etc.  Berger  reports  two  cases 
where  the  first  symptoms  appeared  after  an  acute  febrile  disease  (typhoid  fever). 

Clinical  History. — Paralysis  agitans  has  two  characteristic  symptoms,  viz.,  (1) 
peculiar  evidences  of  motor  irritation,  evinced  by  tremor,  and  (2)  a  condition  of 
stiffness  and  persistent  shortening  of  certain  muscles,  consequent  upon  which  is  a 
series  of  peculiar  motor  phenomena. 

The  trembling  is  generally  the  earliest  symptom  to  attract  the  patient's  atten- 
tion. It  usually  begins  in  the  hands,  especially  in  the  right  hand,  and  then 
gradually  involves  the  arm  and  leg  on  the  same  side,  next  tbe  other  arm  and 
leg,  and  finally,  in  well-marked  cases,  the  entire  body.  The  form  of  tremor  is 
very  characteristic.  There  are  rapid,  uniform,  oscillatory  movements  of  varying 
extent.  The  tremor  is  usually  greatest  in  the  hands  and  arms.  At  the  same  time 
the  thumbs  and  half-flexed  fingers  exhibit  a  movement  which  suggests  spinning 
or  pill-rolling.  The  forearm  is  generally  flexed  and  extended  in  rapid  alterna- 
tion, but  it  is  always  very  difficult  to  determine  just  what  muscles  contract.  With 
regard  to  the  trunk,  it  is  often  a  question  whether  its  tremor  is  of  independent 
origin,  or  due  merely  to  the  motion  of  the  extremities.  Charcot  states  that  the 
head  and  the  facial  muscles  are  never  implicated,  but  there  is  doubt  about  this 
point.  We  ourselves,  as  well  as  other  observers,  have  repeatedly  seen  independ- 
ent tremor  of  the  head.  As  to  the  face,  the  muscles  about  the  chin  seem  to  suffer 
chiefly. 

The  trembling  of  paralysis  agitans  is  almost  continuous.  It  may,  indeed,  cease 
for  a  moment  in  a  limb,  but  only  to  recur  immediately.  The  quieter  the  patient 
is,  in  mind  and  body,  the  less  violent  are  the  movements.  If  he  is  excited,  or 
begins  to  speak,  or  is  watched,  the  tremor  at  once  becomes  exaggerated,  and  may 
be  violent  enough  to  jar  the  whole  body  vehemently.  Active  motion  does  not  in- 
tensify the  tremor.  On  the  contrary,  it  may  often  be  observed  that  the  trembling 
abates  when  the  muscles  undergo  vigorous  voluntary  contraction,  as  when  a 
weight  is  lifted,  or  the  hand  of  another  is  firmly  gi'asped. 


PARALYSIS  AG  IT  ANS. 


785 


The  second  symptom  is  almost  more  characteristic  than  the  first.  It  consists  of 
a  peculiar  rigidity  of  the  muscles.  We  generally  notice,  even  in  the  face,  pecul- 
iar tension  of  the  muscles.  This  often  produces  a  stolidity  of  expression,  so  that 
the  emotions  are  less  clearly  depicted  than  upon  the  countenance  of  a  healthy  per- 
son. The  head  gradually  becomes  more  and  more  flexed.  When  the  disease  das 
lasted  some  years,  the  chin  may  even  rest  upon  the  sternum.  The  muscles  of  the 
trunk  and  extremities  also  stiffen  gradually,  and  lead  to  peculiar  and  almost 
pathognomonic  appearances.  The  body  is  bent  over  forward;  the  arms  cling  to 
the  trunk,  and  are  flexed  at  the  elbow-joint ;  the  fingers  are  flexed,  especially  at 
the  metacarpophalangeal  joint;  the  thumbs  rest  against  the  fingers,  as  if  holding 
a  pen,  or  else  are  flexed  inward  upon  the  palm;  and  the  legs  are  somewhat  bent 
at  the  knee.  The  accompanying  picture  (Fig.  107)  is  from  the  photograph  of  a 
patient  who  was  for  a  long  time  under  observation  at  the  clinique  in  Leip.sic,  and 
gives  a  good  representation  of  the  characteristic  posture. 

The  stiffness  of  the  muscles  also  operates  to  impair  motion  in  various  ways.  In 
particular  all  movements  of  the  trunk  are  greatly  impeded.  In  advanced  cases 
the  patient  can  not  get  upon  his  feet,  if  he  is  lying  in  bed,  without  help.  Inasmuch 
however,  as  the  muscular  strength  usually  remains 
good  (vide  infra),  he  requires  to  exert  but  a  slight  trac- 
tion upon  some  helping  hand  in  order  to  attain  an  erect 
posture.  On  the  other  hand,  the  patient  is  often  utterly 
unable  to  turn  in  bed  from  one  side  to  the  other.  In 
severe  cases,  therefore,  it  is  often  necessary  to  alter  the 
patient's  position  several  times  in  a  night,  especially  as 
lying  long  in  one  attitude  makes  him  feel  very  uneasy. 
If  the  patient  is  in  a  chair,  he  can  not  get  up  of  him- 
self, because  it  is  impossible  for  him  tp  bend  his  body 
forward  in  the  necessary  manner;  but  with  just  a  little 
help  he  can  stand  up,  and  is  then  able  to  walk  alone  or 
even  to  run.  Then,  since  the  flexion  of  the  trunk  for- 
ward brings  the  center  of  gravity  forward  also,  and  the 
trunk  can  not  be  sufficiently  bent  backward,  he  is  apt 
to  "  get  a-going,"  so  that  he  can  not  stop  until  hebrings 
up*  against  a  post  or  a  wall.  If  such  a  patient,  with  a 
considerable  degree  of  anteflexion  and  rigidity  of  the 
trunk,  is  slightly  pushed  from  behind,  he  will  have  to 
start  into  a  run  to  avoid  falling.  This  phenomenon  is 
termed  "  propulsion."  A  push  backward,  which  brings 
the  center  of  gravity  behind  the  point  of  support,  is 
very  likely  to  make  such  a  patient  fall,  as  he  will  sel- 
dom succeed  in  moving  backward  fast  enough  to  re- 
cover his  balance  (retropulsion).  Both  propulsion  and 
retropulsion  are  conceived  by  Charcot  to  be  "  forced 
movements "  (see  page  541)  in  the  strict  sense  of  the 
term.  We  are,  however,  convinced,  as  the  result  of 
numerous  observations,  that  these  phenomena  can  in 
every  case  be  explained  simply  by  the  mechanical  con- 
ditions arising  from  displacement  of  the  center  of 
gravity.  Again,  the  reason  why  many  patients  are  prone  to  keep  their  arms  be- 
hind them  as  they  walk  is  that  such  a  position  contributes  slightly  toward  bring- 
ing the  center  of  gravity  farther  backward. 

The  movements  of  the  extremities  are  less  impaired  than  those  of  the  trunk, 
but  they  often  betray  a  certain  slowness  and  stiffness  of  motion.     The  strength  of 
50 


Fig.  107.— Characteristic  position 
of  the  body  in  paralysis  agi- 
tans. 


786  DISEASES  OF  THE  NERVOUS  SYSTEM. 

the  inuscJes  may  be  preserved  for  a  long  while,  hut  often  there  is  at  last  evident 
pai'esis.  Even  in  the  early  stages  of  the  disease  the  muscles  may  become  easily 
fatigued.  The  impairment  of  facial  expression  has  already  been  referred  to.  In 
many  cases  the  muscles  of  the  eye  also  seem  to  participate  in  the  rigidity,  making 
it  difficult  for  the  eye  in  reading  to  follow  rapidly  along  each  line,  or  to  pass  from 
the  end  of  one  line  to  the  commencement  of  the  next.  [The  voice  is  often  affected ; 
the  patient  talks  in  a  high-pitched  monotone. — K.] 

The  muscular  rigidity  is  almost  more  characteristic  of  paralysis  agitans  than  is 
the  tremor.  Indeed,  there  would  seem  to  be  cases,  as  we  have  ourselves  observed, 
where,  at  least  for  a  time,  the  posture  of  the  patient  is  typical,  and  yet  there  is  no 
trembling.  Such  cases  might  be  called  paralysis  agitans  sine  agitatione.  In 
uncomplicated  cases  all  other  nervous  functions  remain  perfectly  normal.  Sensa- 
tion is  never  impaired.  Sometimes  some  pain  is  felt  at  the  commencement  of  the 
disease,  particularly  in  the  shoulders.  There  is  no  striking  disturbance  of  reflex 
action  nor  of  the  bladder.  In  a  few  cases  of  paralysis  agitans,  cerebral  and  men- 
tal symptoms  have  been  observed ;  but  they  are  so  rare  tbat  it  is  impossible  to 
say  whether  they  belong  to  the  disease  or  are  merely  accidental  complications.  It 
is  also  noteworthy  that  many  patients  complain  of  a  subjective  feeling  of  excess- 
ive warmth.  The  internal  temperature  is  normal ;  but  it  is  said  that  the  tem- 
perature of  the  surface  of  the  body  is  frequently  somewhat  elevated.  Sometimes 
there  is  a  tendency  to  excessive  perspiration.  [Mosse  and  Banal  have  found  that 
the  excretion  of  urea  and  the  total  excretion  of  phosphoric  acid  is  increased  in 
paralysis  agitans,  but  that  the  excretion  of  imperfectly  oxidized  phosphoric  acid  is 
diminished,  thus  showing  that  there  is  increased  combustion. — K.] 

The  disease  runs  a  very  chronic  course,  perhaps  for  twenty  years  or  more. 
From  the  first,  it  keeps  on  slowly  but  gradually  developing.  The  symptoms 
rarely  exhibit  marked  alterations  of  mildness  and  severity,  but  for  long  periods 
the  progress  of  the  disease  may  be  apparently  arrested.  Recovery  has  never  yet 
been  observed.  The  final  and  fatal  termination  is  not  brought  about  by  the  dis- 
ease itself,  but  is  due  to  some  intercurrent  affection  or  to  general  marasmus.  The 
original  of  the  above  picture  came  to  a  pitiable  end  by  tumbling  face  downward 
into  a  puddle  of  water.     He  could  not  get  up,  and  was  drowned. 

Nature  of  the  Disease. — The  true  nature  of  the  disease  is  unknown.  Inasmuch 
as  the  disorder  is  purely  a  motor  one,  the  corresponding  lesions  must  be  sought 
somewhere  in  the  motor  system.  As  yet,  however,  post-mortem  examinations  of 
the  nervous  system,  even  with  the  microscope,  have  revealed  no  definite  changes. 
We  must,  therefore,  confess  that  we  have  even  had  a  doubt  whether  it  is  justifi- 
able to  claim  that  paralysis  agitans  is  an  affection  of  the  nervous  system  at  all,  or 
whether  it  may  not  possibly  be  of  purely  muscular  origin.  Certainly  it  would 
not  be  impossible  for  abnormal  processes  in  the  muscles  to  excite  the  tremor  and 
tonic  contraction.  But,  as  has  been  said,  there  is  at  present  no  ground  for  decid- 
ing this  question ;  we  would  merely  suggest  it. 

[Borgherini  has  found,  at  the  autopsy  of  a  case  of  paralysis  agitans,  an  increase 
in  the  nuclei  of  the  vessels  of  the  brain  and  cord,  with  changes  in  their  caliber, 
and  hyperplasia  of  the  interstitial  tissue  affecting  the  nerve-elements,  the  hyper- 
plasia being  most  marked  in  the  motor  tract.  The  gray  axis  and  the  white  matter 
of  the  pons,  medulla,  and  cord  were  affected.  An  increase  of  connective  tissue 
was  noted  also  in  the  muscles. — K.] 

Diagnosis. — Any  typical  case  of  paralysis  agitans  can  be  easily  and  certainly 
recognized.  The  important  factors  are  the  peculiar  tremor,  the  characteristic  car- 
riage, and  the  rigidity  of  the  muscles  of  the  trunk  and  extremities.  It  was  for- 
merly a  difficult  matter  to  distinguish  between  paralysis  agitans  and  multiple 
sclerosis ;  but  to-day  the  peculiarities  of  the  two  diseases  are  better  known,  and 


ATHETOSIS.  787 

confusion  is  seldom  possible.  The  character  of  the  tremor  varies  in  the  two.  In 
paralysis  agitans  it  persists  even  when  the  patient  is  quiet,  and  it  is  decidedly  oscil- 
latory. The  motion  in  multiple  sclerosis  (q.  v.)  is  almost  always  an  intention 
tremor  only,  and,  what  is  of  still  greater  importance  in  distinguishing  between 
them,  the  general  appearances  of  the  two  diseases  are  essentially  unlike. 

Treatment. — As  has  already  been  implied  above,  we  possess  no  means  of  con- 
trolling the  disease.  In  most  cases,  therefore,  the  treatment  is  confined  to  general 
hygienic  measures.  Good  may  be  done  by  lukewarm  baths  of  considerable  dura- 
tion, and  by  gentle  massage  of  the  muscles.  Among  internal  remedies  Erb  has 
lately  recommended  hyoscine,  as  having  the  most  palliative  and  soothing  in- 
fluence. It  is  best  given  subcutaneously,  and  we  must  always  begin  with  very 
small  doses,  as  otherwise  unpleasant  symptoms,  such  as  vertigo,  headache,  etc., 
may  arise.  We  inject  a  twentieth  to  a  twelfth  of  a  grain  (mgr.  J— J)  in  aqueous 
solution  (solution  of  hyoscine  muriate,  1  to  1,000,  seven  to  fifteen  minims).  If  well 
borne  we  can  cautiously  increase  the  dose.  [Atropine  has  recently  shown  good 
results,  especially  when  given  subcutaneously.— K.]  Arsenic,  ergotine,  potassic 
bromide,  physostigmine,  and  curare  may  also  be  tried.  If  electricity  is  to  do  any 
good  at  all,  the  case  must  be  a  recent  one.  It  is  said  that  in  some  instances 
stretching  of  the  nerves  has  diminished  the  tremor  considerably ;  but  our  own 
observations  would  not  lead  us  to  recommend  the  procedure  in  this  disease. 


CHAPTEE  IV. 
ATHETOSIS. 

In  1871  the  American  neurologist  Hammond  described  under  the  name  of  athet- 
osis (uderos,  without  fixed  position)  a  peculiar  symptom  of  irritation  of  the  motor 
centers,  differing  in  a  characteristic  manner  from  all  other  forms  of  involuntary 
movements,  including  the  epileptiform  and  choreic.  The  movements  of  athetosis 
(see  page  541)  are  often  very  complicated  and  peculiar.  The  part  affected  by  them 
is  in  continuous  unrest.  If  the  facial  muscles  (usually  those  of  the  lower  divis- 
ion of  the  facial  nerve)  and  the  muscles  of  mastication  be  attacked,  the  face  and 
mouth  are  constantly  being  twisted  and  distorted.  If  the  tongue  suffer,  as  in 
one  case  which  we  saw,  speech  is  difficult  and  indistinct.  If  the  muscles  of  the 
back  of  the  neck  be  implicated,  the  head  is  usually  drawn  backward  or  to  one 
side,  and  is  turned  and  twisted  in  all  sorts  of  ways.  Most  charactei'istic  of  all, 
however,  are  the  movements  exhibited  by  the  hand  and  fingers  when  affected. 
The  fingers  are  incessantly  being  separated,  extended,  flexed,  and  intertwined, 
assuming  the  oddest  positions.  The  accompanying  pictures  may  serve  to  illustrate 
this"  (vide  Fig.  108).  The  character  of  the  movements  reveals  that  the  interossei 
must  be  chiefly  involved.  It  is  a  very  frequent  result  of  the  unceasing  stretching 
of  the  articular  ligaments  of  the  fingers  that  at  last  the  articulations  become 
relaxed  to  such  a  degree  as  to  permit  of  hyperextension  of  the  fingers,  which  it  is 
impossible  for  a  healthy  person  to  imitate.  The  arms  are  generally  less  severely 
affected  than  the  hands;  and  in  the  lower  limbs  the  trouble  is  not  often  so  severe 
as  in  the  upper.  The  toes  may,  however,  exhibit  motions  analogous  to  those  of 
the  fingers. 

Although  in  general  the  movements  are  continuous,  their  vigor  frequently 
varies.  Thus  they  almost  always  are  aggravated  if  the  patient  becomes  excited. 
During  sleep  they  generally  cease,  although  in  certain  instances  they  have  per- 
sisted even  then,  only  being  diminished.     When  voluntary  motions  are  being 


788 


DISEASES   OF  THE  NERVOUS  SYSTEM. 


made  they  ordinarily  grow  feebler ;  but  they  may.  on  the  contrary,  become  exag- 
gerated, taking  the  form  of  sympathetic  movements. 

We  must  distinguish  between  genuine  idiopathic  athetosis  and  a  symptomatic 

form,  which  also  occurs. 


Symptomatic  athetosis 
is  seen  in  various  nervous 
diseases.  The  first  obser- 
vations reported  by  Ham- 
mond were,  most  of  them, 
made  in  cases  of  epilepsy, 
or  the  severe  psychoses, 
and  the  like.  By  far  the 
most  frequent  source  of  the 
phenomenon,  however,  is 
hemiplegia,  producing 

what  is  known  as  post- 
hemiplegic chorea,  or  bet- 
ter, post-hem  iplegic  hemi- 
athetosis.  This  is,  to  be 
sure,  a  very  rare  sequel  to 
the  ordinary  hemiplegia  of 
elderly  persons,  but  follows 
rather  infantile  paralysis 
of  cerebral  origin  (vide  p. 
744).  Some  traces  of  athet- 
osis are  seen  in  a  majority 
of  the  cases  of  infantile 
hemiplegia. 

Idiopathic  athetosis  is 
rare.  Here  the  peculiar 
movements  are  the  chief, 
if  not  the  sole,  symptom  of 
disease.  A  few  cases  of 
this  sort  have  been  re- 
ported where  the  athetosis 
began  without  known 
cause,  and  usually  was  lim- 
ited to  some  one  region. 
It  attacked  elderly  individ- 
uals who  were  previously 
healthy.  Of  especial  im- 
portance is  an  apparently 
congenital  form  of  atheto- 
sis, dating  from  the  earli- 
est infancy.  Of  this  we 
have  ourselves  seen  several 
instances,  which  closely 
resembled  one  another. 
The  condition  is  a  perma- 
nent one,  not  progressive, 
nor,  on  the  other  hand, 
capable  of  any  great  amelioration.  The  movements  are  almost  always  most  pro- 
nounced in  the  face,  head,  and  fingers.     There  are  no  other  nervous  disturbances, 


Fig.  108.— Example  of  the  position  of  the  fingers  in  the  movements  of 
athetosis  (personal  observation). 


TETANY.  789 

neither  paralysis  nor  impairment  of  sensation.  The  intelligence  of  the  patient 
may  or  may  not  be  below  par. 

Of  the  nature  of  athetosis,  or  the  locality  or  nature  of  the  irritation,  we  possess 
no  information  as  yet.  It  is  extremely  probable  that  the  lesion  is  in  every  case  a 
cerebral  one.  Perhaps  it  is  in  the  cortex.  In  symptomatic  athetosis  we  find 
post  mortem  the  changes  caused  by  the  original  trouble.  In  idiopathic  athetosis 
no  changes  have  thus  far  been  reported.  In  a  case  of  our  own  which  came  to 
autopsy,  absolutely  nothing  abnormal  was  found  in  the  brain.  The  patient  was 
an  elderly  female,  who  displayed  typical  movements  of  the  arm  and  hand. 

It  is  not  yet  known  whether  recovery  is  possible.  A  certain  amount  of  improve- 
ment sometimes  follows  the  administration  of  Fowler's  solution,  bromide  of  potas- 
sium, or  galvanism. 


CHAPTER  V. 

TETANY. 

(Intermittent  Tetanus.     Tetanilla.) 

iEtiology. — Tetany,  a  name  originating  with  Corvisart,  is  applied  to  a  peculiar 
neurosis,  characterized  mainly  by  paroxysmal  tonic  convulsions  in  certain  groups 
of  muscles.  The  disease  attacks  by  preference  children  and  young  adults  between 
fifteen  and  thirty  years  of  age.  The  physiological  processes  peculiar  to  the  female 
sex  seem  to  have  an  especial  tendency  to  excite  the  disorder.  It  is  comparatively 
so  frequent  in  nursing  women  that  Trousseau  has  called  it  ^contracture  des 
nourrices. " 

Among  exciting  causes,  catching  cold  deserves  particular  mention.  Hence  the 
earlier  observers  describe  the  disease  as  "  intermittent  contracture  of  rheumatic 
origin."  In  other  cases  the  disorder  has  appeared  as  a  sequel  to  other  acute  dis- 
eases, such  as  typhus  or  typhoid  fever,  smallpox,  and  intestinal  troubles.  A  very 
remarkable  fact  was  pointed  out  by  N.  Weiss — namely,  that  tetany  is  apt  to  fol- 
low operative  extirpation  of  goitre.  No  explanation  of  this  has  yet  been  discov- 
ered. Reports  from  various  quarters  give  color  to  the  idea  that  tetany  may 
sometimes  be,  to  a  certain  extent,  epidemic.  It  must  be  confessed,  however,  that 
it  is  somewhat  doubtful  whether  the  attacks  referred  to  were  genuine  tetany. 
We  are  also  inclined  to  believe  that  endemic  influences  may  promote  its  occur- 
rence» At  any  rate,  the  published  accounts  would  seem  to  indicate  that  tetany  is 
much  more  frequent  in  Heidelberg  (Erb,  F.  Schul tze),  Breslau  (Berger ),  and 
Vienna  (N.  Weiss),  than  in  Leipsic,  for  instance,  where  it  is  one  of  the  very  rarest 
nervous  diseases. 

Clinical  History. — The  paroxysm  of  tetany  usually  has  certain  prodromata, 
consisting  of  slight  general  discomfort  and  pain,  and  of  a  feeling  of  weakness  and 
stiffness,  most  marked  in  the  arms.  These  symptoms  last  some  hours  (at  least) 
before  the  true  convulsive  stage  begins.  The  upper  extremities,  aud  more  par- 
ticularly the  fingers,  almost  always  suffer  first;  and  then,  after  the  arms,  the 
lower  extremities  become  involved.  The  spasm  usually  affects  the  toes  before  it 
seizes  upon  the  other  parts  of  the  leg.  The  symptoms  are  almost  invariably 
bilateral  and  symmetrical.  Exceptionally,  the  disturbance  commences  in  a  lower 
limb,  or  is  confined  to  one  side  of  the  body.  In  most  cases  the  flexor  muscles  are 
predominantly  affected,  giving  rise  to  very  characteristic  postures.  The  fingers 
are  in  apposition  with  one  another,  and  placed  as  if  holding  a  pen,  or,  as  Trous- 
seau says,  as  if  the  hand  were  about  to  be  thrust  into  the  vagina,  during  labor. 


790  DISEASES  OF  THE  NERVOUS  SYSTEM. 

The  hands  are  flexed,  the  elbows  are  also  slightly  flexed,  and  the  upper  arm  in 
severe  cases  is  pressed  against  the  chest.  In  the  lower  extremities,  the  toes  are 
flexed,  and  the  feet  are  in  the  posture  of  talipes  equinus.  The  muscles  of  the 
thigh  rarely  suffer.  The  same  is  true  of  the  trunk,  face,  and  diaphragm.  The 
main  characters  of  a  typical  attack,  such  as  has  just  been  sketched,  apply  to  all 
but  a  few  cases. 

The  intensity  .of  the  tonic  spasm  is  very  great.  The  affected  muscles  feel  as 
hard  as  a  board,  and  are  usually  rather  sensitive  to  pressure.  The  attack  some- 
times coutinues  only  a  few  minutes,  but  not  infrequently  it  may  occupy  several 
hours  or  days.  As  a  rule,  there  are  no  disturbances  of  sensation  or  other  addi- 
tional nervous  phenomena.  There  is  no  impairment  of  consciousness.  In  a  few 
instances  slight  cederaatous  swelling  has  been  observed,  and  also  profuse  perspira- 
tion. The  temperature  is  normal  or  slightly  elevated,  but  the  pulse  is  often 
quite  rapid. 

When  the  attack  ceases,  which  it  always  does  gradually,  and  never  suddenly, 
the  patient  feels  perfectly  well,  save  for  a  slight  pain  and  stiffness  in  the  mus- 
cles. But  even  in  the  interval  between  the  paroxysms  there  are  usually  some 
few  objective  symptoms,  which  have  a  most  important  bearing  on  the  pathology 
of  tetany.  In  the  first  place,  the  peripheral  nerves  are  generally  abnormally 
sensitive  to  electricity.  The  complete  demonstration  of  this  fact  we  owe  to  Erb. 
The  weakest  current  will  produce  frequently  violent  contractions.  In  an  analo- 
gous way,  the  nerves  react  to  unusually  slight  mechanical  stimulation.  This  is 
often  peculiarly  marked  in  the  facial  nerve,  as  Chvostek  and  N.  Weiss  have 
shown.  Thus,  if  the  face  be  vigorously  stroked  from  above  downward,  almost  all 
of  the  muscles  contract  energetically,  one  after  the  other.  The  direct  mechanical 
excitability  of  the  muscles,  on  the  other  hand,  is  not  increased  (F.  Schultze). 

Another  very  characteristic  symptom  was  discovered  by  Trousseau — "  Trous- 
seau's sign."  It  is  found  in  most  cases,  although  not  in  all,  and  is  this:  a  fresh 
paroxysm  can  at  any  time  be  artificially  excited  by  pressure  upon  the  larger 
arteries  and  nerves  of  the  arm  (particularly  the  median  nerve  and  the  brachial 
artery).  It  is  not  definitely  known  how  compression  accomplishes  this.  Berger 
found  that  mechanical  or  electrical  irritation  of  certain  painful  points  situated 
along  the  spinal  column  produces  the  same  result. 

The  frequency  of  the  attacks  varies  greatly  in  individual  cases.  As  a  rule, 
there  are  several  paroxysms  daily ;  but  the  intervals  may  last  for  days,  or  again 
may  be  almost  inappreciable.  The  entire  duration  of  the  disease  is  generally  sev- 
eral weeks.  It  is  noteworthy  that  when  the  paroxysms  grow  less  frequent  and 
violent  there  is  also  a  gradual  diminution  in  the  hypersensitiveness  of  the  nerves 
and  in  the  reaction  to  Trousseau's  test.  As  long  as  these  symptoms  persist, 
spontaneous  attacks  are  also  possible. 

The  termination  of  tetany  is  almost  always  favorable.  No  essential  anatomical 
lesions  have  yet  been  detected.  The  symptoms  leave  us  in  doubt  whether  the  dis- 
ease affects  the  peripheral  nerves  or  the  nervous  centers. 

Diagnosis. — The  diagnosis  is  not  difficult  if  we  only  consider  carefully  the 
symptoms  presented,  the  nature  of  the  paroxysms,  and  the  other  phenomena  above 
enumerated.  Similar  conditions  may  result  from  ergotine-poisoning,  or  from  cer- 
tain occupations,  as  in  "  cobbler's  cramp,"  but  the  differential  diagnosis  is  usually 
easy.  The  peculiar  tonic  spasms  of  young  children  are  not,  in  our  opinion,  to  be 
regarded  as  tetany ;  they  have  already  been  described  {vide  page  576)  under  the 
name  of  arthrogryposis,  and  are  characterized  by  persistent  tonic  contracture,  not 
paroxysmal,  and  most  pronounced  in  the  distribution  of  the  ulnar  nerve  on  both 
sides ;  and  in  them  there  is  no  abnormal  sensitiveness  of  the  nerves  to  mechanical 
stimuli. 


TETANUS.  791 

Treatment. — The  main  treatment,  besides  general  hygienic  measures,  is  elec- 
tricity. The  stabile  current  is  passed  upward  through  the  nerves  affected;  the 
galvanic  current  is  also  applied  to  the  spinal  cord,  and  the  anode  is  applied  to  the 
various  nerve-trunks,  with  the  cathode  on  the  sternum.  This  last  procedure  some- 
times dissipates  a  spastn  actually  present.  Internal  remedies,  such  as  bromide  of 
potassium,  arsenic,  and  belladonna,  rarely  produce  brilliant  results.  Berger  was 
successful  in  some  cases  with  subcutaneous  injections  of  curare.  Tepid  baths,  and 
cold  sponging  with  friction  cautiously  employed,  and  applied  especially  to  the 
back,  often  aid  treatment  materially. 


CHAPTER  VI. 

TETANUS. 

(Lock-jaw.) 


iEtiology. — There  are  two  chief  exciting  causes  of  this  disease,  as  are  indicated 
by  the  names  rheumatic  tetanus  and  traumatic  tetanus.  The  rheumatic  vai'iety 
results  from  catching  cold,  or  getting  a  thorough  wetting,  or  some  similar  mishap. 
The  other  occurs  in  persons  who  have  some  open  wound,  whether  from  injury  or 
operation.  There  is  no  ground  for  establishing  tetanus  neonatorum  as  a  third  dis- 
tinct form.  Cases  to  which  this  name  has  been  applied  are  invariably  connected 
with  the  falling  off  of  the  cord,  and  are  therefore  instances  of  traumatic  tetanus. 
In  a  few  instances  it  is  impossible  to  discover  what  has  been  the  immediate  occa- 
sion of  the  disease ;  such  cases  are  classed  as  idiopathic  tetanus. 

With  us  tetanus  is  a  comparatively  rare  disease.  It  is  noteworthy  that  people 
who  have  to  do  with  horses  are  quite  often  affected  (Verneuil).  In  the  tropics  it 
is  much  more  common.  Negroes  are  well  known  to  be  peculiarly  liable  to  it. 
Men  are  much  oftener  attacked  than  women.  Tetanus  has  been  seen  as  an 
endemic  and  also  as  an  epidemic.  This  has  been  most  frequent  in  times  of  war, 
and  is  in  part  due  to  the  unfavorable  influence  of  certain  external  circumstances, 
such  as  bad  weather  or  bad  hygienic  surroundings.  Traumatic  tetanus  comes  on 
after  injuries  of  the  fingers,  hands,  and  lower  extremities. 

All  these  facts  must  previously  have  led  to  the  thought  that  tetanus  was  a 
specific  infectious  disease,  but  we  have  only  recently  succeeded  in  establishing  an 
actual  foundation  for  this  suspicion.  Rosenbach  cultivated  from  the  wound  of 
a  man  who  died  of  tetanus  a  special  form  of  bacillus  which  Nicolaier  had  formerly 
found  in  garden  earth.  These  bacilli  are  distinguished  by  a  little  head  at  one  end 
(spur).  If  a  small  amount  of  these  bacilli  be  injected  under  the  skin  of  mice,  the 
most  violent  tetanic  spasms  ensue  in  the  animals  thus  treated.  Since  the  develop- 
ment of  the  bacteria  remains  limited  to  the  seat  of  the  wound  or  the  injection,  it 
is  a  priori  probable  that  the  spasms  are  not  excited  immediately  by  the  bacilli,  but 
by  a  chemical  poison  produced  by  them  during  life.  In  fact,  Brieger  has  lately 
succeeded  in  producing  several  alkaloid-like  substances  from  tetanus-cultures,  so- 
called  toxines,  which  he  terms  tetanine,  tetanotoxine,  and  spasmotoxine.  All  these 
substances  are  violent  poisons,  and,  like  strychnine,  provoke  the  most  violent 
tetanic  spasms  in  the  animals  experimented  on. 

It  is  still  uncertain  whether  the  tetanus  bacilli  enter  the  body  only  through 
injuries  of  the  skin,  or  in  other  ways. 

Clinical  History. — In  rheumatic  tetanus  the  symptoms  usually  begin  soon  after 
exposure  to  the  exciting  cause.  There  may  be,  however,  an  interval  during  which 
the  patient  feels  perfectly  well,  or  at  most  has  only  certain  mild  and  indefinite 


792  DISEASES  OF  THE  NERVOUS  SYSTEM. 

premonitory  symptoms,  such  as  languor  and  headache.  Similar  prodromata  may 
occur  in  the  apparently  idiopathic  cases. 

Traumatic  tetanus  seldom  begins  immediately  after  the  injury  has  been 
received.  Several  days  or  even  weeks  may  intervene  previous  to  the  outbreak  of 
the  disease.  Here,  too,  there  may  be  mild  prodromata  for  a  brief  period  preceding 
the  graver  phenomena.  The  patient's  wound  presents  no  specific  appearances. 
Tetanus  may  be  associated  with  either  slight  or  severe  injuries,  whether  treated 
carelessly  or  kept  aseptic. 

The  symptoms  of  the  disease  proper  are  the  same  in  both  rheumatic  and 
traumatic  tetanus.  They  usually  begin  gradually.  Ordiuai'ily,  the  first  thing 
noticed  is  a  feeling  of  rigidity  and  tension  in  the  muscles  of  the  face,  lower  jaw, 
and  back  of  the  neck.  The  stiffness  spreads  by  degrees  to  the  m  uscles  of  the  back 
and  abdomen.  The  disease  is  sometimes  completely  developed  in  a  few  hours,  but 
sometimes  not  till  after  several  days. 

The  persistent  tension  of  the  facial  muscles  gives  the  countenance  a  strange 
immobility.  The  brow  is  usually  wrinkled,  and  the  corners  of  the  mouth  are 
often  drawn  back  in  a  "  sardonic  grin.:'  Most  prominent  of  all  is  the  tonic  spasm 
of  the  masseters,  or  trismus.  The  teeth  are  so  firmly  pressed  together  that  it 
finally  becomes  impossible  to  open  the  mouth  more  than  one  or  two  millimetres. 
The  eyes  are  staring,  the  pupils  usually  contracted.  The  muscles  at  the  back  of 
the  neck  draw  the  head  somewhat  backward,  and  it  is  immovable.  The  spinal 
column  is  bent  forward,  so  that  the  trunk  is  convex  anteriorly,  permitting  the 
hand  to  be  passed  between  it  and  the  bed — opisthotonos.  The  epigastrium  and  the 
anterior  part  of  the  abdomen  are  flat.  The  abdominal  muscles  are  as  hard  as  a 
board.  The  lower  limbs  may  be  rigidly  extended,  but  the  arms  generally  can  be 
quite  freely  moved.  Convulsive  dysphagia,  as  seen  in  hydrophobia  (q.  v.),  may 
occur,  but  it  is  rare  (vide  infra). 

In  many  cases  the  continuous  tonic  spasm  is  occasionally  interrupted  by  sud- 
den and  irregular  paroxysms,  during  which  all  the  affected  muscles  become  still 
more  tense.  In  severe  cases  this  gives  the  whole  body  a  violent  shock,  and  makes 
the  opisthotonos  even  more  pronounced.  In  a  very  bad  case  the  paroxysms  are 
very  frequent ;  in  a  mild  case  they  are  rare  or  almost  indistinguishable.  Some- 
times they  are  apparently  spontaneous,  and  sometimes  they  are  evidently  of  reflex 
origin,  being  superinduced  by  external  irritation.  In  severe  cases  the  cause  may 
be  comparatively  insignificant,  such  as  a  slight  jar  or  noise. 

If  there  are  other  nervous  derangements,  little  is  known  about  them — partly, 
no  doubt,  because  it  is  seldom  possible  to  make  an  extended  examination  of  the 
patient.  Sensation  is  said  to  have  been  impaired  in  some  instances,  but  in  others 
it  is  perfectly  normal.  The  muscles  affected  by  the  spasms  are  usually  the  seat 
of  severe  pain.  The  cutaneous  reflexes  are  almost  always  greatly  exaggerated. 
In  two  cases  which  we  saw  very  recently,  the  patellar  reflex  was  much  increased, 
and  in  one  there  was  distinct  ankle-clonus.  Paralysis  is  extremely  exceptional. 
There  is  often  profuse  perspiration.     The  intellect  remains  perfectly  unclouded. 

There  is  a  special  form  of  tetanus  which  must  be  briefly  mentioned.  It  was 
first  described  by  E.  Rose,  and  is  called  "hydrophobic  tetanus,"  or  "cephalic 
tetanus."  It  occurs  only  in  connection  with  injuries  situated  in  the  distribution 
of  the  cranial  nerves — that  is,  in  the  face  and  head — and  is  characterized  in  most 
cases  by  violent  spasm  of  the  pharynx  and  oesophagus.  This  is  in  addition  to  the 
other  ordinary  phenomena  of  tetanus.  The  disease  in  many  ways  reminds  one  of 
hydrophobia.  Another  characteristic  point  is  that  in  most  cases  there  is  facial 
paralysis  on  the  injured  side. 

Tetanus  seldom  gives  rise  to  disturbances  referable  to  the  internal  viscera.  In 
one  case,  however,  in  the  Leipsic  hospital,  croupous  pneumonia  and  acute  nephri- 


TETANUS.  793 

tis  came  on  a  few  days  before  the  end.  Often  there  are  dyspnoea  and  a  most 
harassing  sense  of  thoracic  oppression — symptoms  due  mainly  to  the  convulsive 
rigidity  of  the  muscles,  by  which  the  thorax  is  constantly  maintained  in  the 
position  it  normally  assumes  during  inspiration.  Expectoration  is  impeded;  and, 
finally,  there  may  be  such  an  accumulation  of  secretions  in  the  mouth  and  air- 
passages  as  to  cause  a  secondary  diffuse  bronchitis,  or  an  inhalation  pneumonia. 
Another  occasional  source  of  extreme  dyspnoea  is  spasm  of  the  glottis. 

The  pulse  often  remains  normal  for  a  long  while,  but  it  is  usually  accelerated, 
not  infrequently  reaching  120  or  160  beats  a  minute  in  severe  cases.  Such  a  pulse 
is  small,  and  may  be  somewhat  irregular.  The  temperature  is  at  first  usually 
normal,  or  slightly  elevated.  Later. it  is  almost  sure  to  rise;  and,  as  Wunderlich 
pointed  out,  it  is  often  very  high  shortly  before  death— for  instance,  107°  to  111° 
(42°-44°  C).  It  is  not  rare  for  the  temperature  to  keep  on  rising  for  a  short  time 
after  death.  No  explanation  of  this  terminal  elevation  of  temperature  has  yet 
been  furnished.  It  can  not  be  the  result  of  the  increased  production  of  heat  oc- 
casioned by  the  muscular  spasm,  for  in  earlier  stages  the  most  violent  convulsions 
are  unattended  by  any  such  change.  Authorities  are,  therefore,  inclined  to  assume 
that  at  the  last  there  is  a  paralysis  of  the  centers  which  regulate  the  warmth  of 
the  body,  just  as  is  seen  in  other  severe  nervous  disorders,  such  as  meningitis,  in- 
jury to  the  cervical  portion  of  the  cord,  and  uraemia. 

Interesting  observations  have  been  made  with  regard  to  tissue-metamorphosis 
during  tetanus.  The  excretion  of  urea  is  not  increased.  This  fact  agrees  well 
with  Voit's  view,  that  muscular  activity  has  no  connection  with  the  breaking  down 
of  albuminoids.  Senator  failed  to  find  any  increase  of  kreatine  and  kreatinine  in 
the  urine.  Probably  the  production  of  carbonic  dioxide  is  abnormally  large  in 
tetanus.  At  least,  physiological  considerations  would  strongly  indicate  this,  al- 
though it  has  not  yet  been  actually  demonstrated.  Occasionally  traces  of  albumen 
and  sugar  have  been  detected  in  the  urine.  There  is  usually  obstinate  constipa- 
tion, probably  due  to  the  persistent  rigidity  of  the  abdominal  muscles ;  and,  indeed, 
micturition  is  not  a  little  impeded  from  the  same  cause. 

It  may  be  said,  in  regard  to  the  general  course  of  the  disease,  that  there  are 
severe  and  mild  forms  of  the  disease.  What  has  been  said  above  applies  mainly  to 
the  severe  form.  In  this,  all  the  symptoms  reach  their  extreme  violence  in  a  few 
days,  the  paroxysms  occur  in  quick  succession,  and  death  usually  takes  place  within 
a  week  or  two.  The  fatal  result  is  brought  about  by  the  suspension  of  respii^ation 
and  by  cardiac  failure.  Of  course,  the  extreme  difficulty  of  taking  an  adequate 
amount  of  food  has  an  unfavorable  influence.  The  bad  cases  seldom  outlast  the  first 
week.  If  they  do,  there  is  some  slight  hope  of  recovery;  the  paroxysms  may 
gradually  become  less  frequent  and  less  severe,  until  they  finally  cease  altogether. 
The  severe  form,  however,  so  rarely  ends  favorably  that  the  prognosis  is  always 
very  grave.  The  mild  form,  on  the  contrary,  usually  runs  a  much  more  favor- 
able course.  In  it,  all  the  symptoms  are  from  the  first  much  less  severe.  Often 
there  is  only  more  or  less  trismus,  accompanied  by  no  marked  spasm  in  the 
muscles  of  the  trunk,  if  any  at  all.  There  is  little  constitutional  disturbance. 
The  temperature  is  normal ;  and  the  prognosis  is  rather  favorable.  The  disease 
may  sometimes  drag  on  for  some  weeks,  but  it  often  ends  in  complete  recovery. 
It  must  not  be  forgotten,  however,  that  what  at  first  seems  a  mild  case  may 
develop  into  the  severe  form. 

The  anatomical  changes  in  the  nervous  system  in  fatal  cases  are  almost  wholly 
negative.  Any  small  haemorrhages,  etc.,  have,  if  they  be  present,  only  a  second- 
ary significance. 

Diagnosis. — In  most  cases,  tetanus  can  be  easily  recognized  from  the  peculiar 
convulsions  and  the  general  aspect  of  the  disease.     It  might  be  confounded  with 


794  DISEASES  OF  THE  NERVOUS  SYSTEM. 

acute  meningitis,  for  this  may  cause  rigidity  of  the  neck  and  back;  but  here 
there  are  usually  certain  cerebral  symptoms  also  present,  such  as  headache  and 
impairment  of  consciousness;  and,  on  the  other  hand,  in  tetanus,  trismus  is  an 
almost  constant  phenomenon,  although  exceptional  in  meningitis.  Strychnine 
poisoning  produces  convulsions  similar  to  those  of  tetanus,  but  they  generally 
affect  the  extremities  in  a  more  marked  degree.  Hydrophobia  is  distinguished 
from  tetanus  by  the  aetiology,  the  absence  of  trismus,  the  predominance  of  the 
pharyngeal  convulsions,  and  the  gi^eater  distinctness  of  the  individual  paroxysms. 

Where  trismus  is  the  only  symptom,  we  must  guard  against  mistaking  for 
tetanus  the  symptomatic  rigidity  of  the  jaws  which  occurs  with  severe  sore  throat, 
diseases  of  the  teeth,  or  inflammation  of  the  maxillary  articulation. 

Treatment. — There  is  no  specific  method  of  treating  tetanus.  In  accordance 
with  the  view  above  mentioned  as  to  the  nature  of  the  disease,  we  have  em- 
ployed, repeatedly,  large  doses  of  salicylic  acid.  This  seemed  to  work  well  in  one 
case,  but  in  others  it  did  not.  We  must  therefore  rely  mainly  on  symptomatic 
remedies,  with  the  aim  of  preserving  life  until  a  spontaneous  cure  takes  place. 
For  this  purpose,  narcotics  are  apparently  to  be  preferred ;  and  among  them  the 
best  are  opium  in  large  doses,  and  chloral,  of  which  thirty  grains  (grm.  2)  should 
be  given  two  or  three  times  a  day,  and  the  amount  gradually  increased.  If 
deglutition  be  very  difficult,  the  chloral  may  be  given  per  anum.  Bromide  of 
potassium  should  also  be  mentioned  (at  least  two  and  a  half  to  four  drachms, 
grm.  10-15,  daily),  and  calabar-bean  (a  sixth  of  a  grain  of  extract  of  physo- 
stigmine,  grm.  0-01,  three  to  five  times  a  day).  The  above  remedies  diminish  the 
irritability  of  the  nervous  centers.  In  curare  we  possess  a  means  of  lowering  the 
excitability  of  the  terminations  of  the  motor  nerves  in  the  muscles.  It  has  there- 
fore been  employed  by  many,  but  by  few  with  success.  It  is  difficult  to  say  what 
the  dose  of  curare  is,  inasmuch  as  the  strength  of  different  samples  varies.  The 
best  way  is  to  determine  the  strength  of  the  solution  to  be  employed  by  experi- 
menting on  some  animal.  Usually  a  one-per-cent.  solution  of  curare  in  water  is 
employed,  and  an  amount  equal  to  one  quarter  of  the  contents  of  a  Pravaz's 
syringe  is  injected,  the  dose  being  gradually  and  cautiously  increased.  [Such  a 
syringe  contains  about  thirteen  minims  (0-8  grm.).] 

It  is  very  desirable  to  put  the  patient  by  himself  in  a  darkened  and  quiet 
chamber.  Nourishment  should  be  liquid,  and  lukewarm  stimulants,  such  as 
alcohol  and  camphor,  should  be  given  from  the  first.  Protracted  warm  baths 
may  be  given  cautiously.  We  know  from  personal  observation  that  such  baths 
are  very  grateful  to  some  patients. 

It  need  hardly  be  said  that  in  traumatic  tetanus  the  primary  wound  should 
receive  careful  attention.  Since,  according  to  recent  investigations,  the  tetanus 
bacilli  remain  limited  in  their  growth  to  the  seat  of  the  wound,  it  may  be  indi- 
cated in  the  beginning  of  tetanus,  if  possible,  to  amputate  the  wounded  part  or 
to  excise  the  wound.  Of  course,  from  present  experience  we  can  not  promise  a 
successful  result.     Otherwise  the  treatment  is  the  same  as  in  rheumatic  tetanus. 


CONGENITAL  MYOTONIA.  795 

CHAPTER  VII. 

CONGENITAL    MYOTONIA. 

( Thomsen' s  Disease.) 

In  1876,  Thomsen,  a  Sleswick  physician,  described  a  peculiar  disease  which  up 
to  that  time  had  escaped  observation.  He  had  had  experience  of  it  in  himself  and 
numerous  members  of  his  own  family.  Thomsen  called  it  "tonic  convulsions  of 
the  voluntary  muscles,"  an  appropriate  but  somewhat  clumsy  name,  for  which 
we  suggested  instead  "congenital  myotonia."  Apparently  the  disease  is  very 
infrequent;  but  a  considerable  number  of  cases  have  already  been  reported  in 
Germany,  France,  and  Italy. 

The  disease  seems  to  be  congenital;  at  least,  the  symptoms  invariably  date 
from  the  earliest  infancy.  It  is  very  often  hereditary;  and  males  seem  to  suffer 
oftener,  and  also  more  severely,  than  do  females.  The  essential  symptom  of 
myotonia  is  this:  whenever  any  voluntary  muscle  has  been  inactive  for  a  time 
and  is  then  made  to  contract,  it  falls  into  a  state  of  more  or  less  persistent  con- 
traction, a  mild  sort  of  tetanus,  so  that  it  can  not  be  immediately  relaxed.  It  is 
obvious  how  this  would  interfere  with  any  series  of  motions,  and  make  voluntary 
movement  difficult.  The  patient  is  not  paralyzed  at  all,  but  he  has  a  feeling  of 
great  resistance  to  be  overcome  in  performing  any  act.  Quick  and  accurate 
motions  are  often  out  of  the  question,  so  that,  for  instance,  the  patient  can  not 
perform  military  duty.  It  is  noteworthy  that  the  stiffness  temporarily  disappears 
after  the  patient  has  been  moving  his  muscles  for  some  time.  On  going  upstairs, 
the  first  steps  are  often  very  stiff  and  laborious,  while  succeeding  ones  grow  easier 
and  easier.  Mental  excitement  invariably  exerts  a  very  unfavorable  influence, 
exaggerating  the  stiffness  of  the  muscles. 

Upon  physical  examination,  the  observer  is  usually  struck  by  the  extraordinary 
development  of  the  muscles.  The  size  of  the  extremities,  in  particular,  almost 
deserves  the  term  "  genuine  muscular  hypertrophy,"  although  the  strength  is  not 
always  proportionately  great.  It  is  a  remarkable  fact  that,  upon  direct  electrical 
irritation  of  the  muscles,  the  contraction  outlasts,  in  most  cases,  the  passage  of  the 
current.  This  is  also  true,  although  less  marked,  when  the  electricity  is  applied 
to  the  motor  nerves.  Erb  has  also  observed,  during  the  stabile  application  of  the 
galvanic  current,  wavelike  contractions  starting  from  the  cathode  and  passing 
one  after  another  over  the  muscles  toward  the  anode.  The  direct  mechanical 
excitability  of  the  muscles  is  sometimes  normal,  but  sometimes  increased.  The 
idio-muscular  contractions  {vide  page  546)  are  especially  apt  to  be  increased.  The 
reflexes,  sensation,  and,  indeed,  all  other  nervous  phenomena,  are  normal. 

These  facts  render  it  very  probable  that  the  cause  of  the  disease  is  to  be  sought 
in  the  muscle  itself,  and  that  myotonia  is  due  to  a  congenital  peculiarity  of  the 
muscular  system.  Erb  reports  that,  upon  microscopic  examination  of  minute 
particles  of  muscular  tissue  which  were  excised,  he  found  marked  hypertrophy  of 
individual  muscular  fibers,  and  an  increase  in  the  number  of  nuclei  in  the  sar- 
colemma.* 

*  [In  a  recent  treatise  Erb  admits  only  twenty-three  typical  cases  known  at  present.  His  investi- 
gations show  that  on  voluntary  movement  there  are  protracted  contractions  of  the  muscles  lasting 
from  five  to  thirty  seconds;  these  he  terms  myotonic  disturbances  of  motion.  Mechanical  excita- 
bility of  the  nerves  is  perhaps  diminished;  faradic  excitability  of  the  nerves  is  normal,  but  a  sudden 
increase  of  the  current  may  excite  protracted  contraction ;  galvanic  excitability  is  nearly  normal,  but 
a  succession  of  shocks  may  produce  the  tonic  contraction.  The  mechanical  excitability  of  the  mus- 
cles is  increased,  a  touch  with  the  finger  being  enough  to  excite  tonic  contraction.    Faradic  excitability 


?96  DISEASES  OF  THE  NERVOUS  SYSTEM. 

The  disease  persists  through  life.  The  patient  gradually  becomes  accustomed 
to  it,  and  learns  to  conceal  his  misfortune  as  much  as  possible.  There  may  be  no 
constitutional  disturbance.  Sometimes  there  is  melancholia.  Therapeutic  efforts 
have  not  yet  been  attended  with  much  success.  We  might  try  cold  sponging, 
with  friction,  gentle  massage,  and  methodical  exercise  of  the  muscles. 

[Eulenburg  describes  a  congenital  family  affection,  which  he  calls  congenital 
paramyotone,  allied  to  myotonia,  where  tonic  spasm  was  produced  by  cold.  Gow- 
ers  has  found  the  association  of  tonic  spasm  with  ataxia — ataxic  paramyotone. — K.] 


CHAPTER  VIII. 
CATALEPSY. 

Formerly  catalepsy  was  regarded  as  a  special  form  of  disease,  but  at  present  the 
opinion  is  almost  universally  held  that  it  is  merely  a  symptom  of  several  different 
diseases.  As  was  mentioned  on  page  541,  "cataleptic  rigidity"  is  a  term  descrip- 
tive of  that  peculiar  condition  of  the  muscles  in  which  the  limbs  maintain  invol- 
untarily any  position  which  the  observer  puts  them  into.  If  we  change  the  posi- 
tion of  the  members  which  are  cataleptic,  the  patient  does  not  make  the  slightest 
effort  to  alter  the  posture  in  which  we  leave  them,  however  strange  and  awkward, 
and  apparently  insupportable,  it  may  be.  The  limbs  may  be  moved  in  this  way 
almost  like  wax,  and  have  therefore  been  said  to  exhibit  a  "  waxy  flexibility." 

No  real  explanation  of  the  cataleptic  state  has  been  given.  We  have  not  yet 
advanced  beyond  the  study  of  the  circumstances  under  which  it  appears,  and  of 
the  associated  phenomena.  As  has  been  said,  the  tonic  muscular  spasm  of  cata- 
lepsy is  never  very  great,  being  little  more  than  suffices  to  overcome  gravity  and 
maintain  the  limb  in  the  posture  given  to  it.  This  shows  that  there  must,  in  every 
case,  be  a  due  proportion  in  the  vigor  of  the  contractions  of  antagonistic  muscles ; 
and  this  relative  force  must  vary  with  every  change  of  position.  How  this  con- 
tinuous and  remarkable  regulation  of  motor  nervous  energy  takes  place  is  an 
unanswered  question.  Perhaps  reflex  action  has  something  to  do  with  it.  A 
further  interesting  point  is,  that  changes  of  position  induced  by  electrical  stimula- 
tion of  the  nerves  or  muscles  are  not  permanent;  when  the  stimulus  ceases  to  act, 
the  limb  falls  back  into  its  old  place. 

Catalepsy  occurs  oftenest  as  a  symptom  of  hysteria.  In  this  case  it  is  usually 
associated  with  other  disturbances,  chief  among  which  are  impairment  of  con- 
sciousness and  anaesthesia.  The  anaesthesia  is  especially  marked  in  the  muscles. 
For  example,  the  patient  will  stand  for  an  hour  with  arms  extended,  and  yet 
experience  not  the  slightest  sensation  of  weariness.  At  last,  however,  the  arms 
sink  slowly  clown.  Closely  allied  to  hysterical  catalepsy  is  hypnotic  catalepsy,  a 
condition  which  can  be  artificially  produced  by  certain  procedures  (see  the  next 
chapter)  in  many  hysterical  subjects  at  will.     Charcot  has  reported  cases  where 

is  very  marked  ;  the  muscles  are  quickly  relaxed  after  weak  currents,  but  a  sudden  increase  produces 
protracted  contractions.  Galvanic  excitability  is  increased  quantitatively,  anodic  and  catliodic  closure 
contractions  appearing  with  currents  of  one  or  two  milliamperes ;  qualitatively  both  poles  react  alike. 
The  wavelike  contractions  mentioned  above  are  very  characteristic.  Erb  has  given  the  name  of 
myotonic  reaction  (MyR)  to  these  electrical  phenomena.  Hereafter,  he  thinks,  a  tap  with  the  percus- 
sion hammer  and  a  few  cathodic  closure  contractions  will  suffice  to  establish  the  diagnosis.  Besides 
the  anatomical  changes  above  mentioned,  Erb  also  finds  that  the  cross-section  of  the  individual  mus- 
cular fiber  is  rounded  instead  of  polygonal,  like  the  normal  fiber,  and  that  the  interstitial  tissue  is 
increased.     In  one  case  he  found  a  striking  vacuolization  of  the  individual  fibers. — Teans.] 


HYSTERIA.  797 

the  lethargy  of  hypnotism  could  in  variably  be  transformed  into  catalepsy  by  open- 
ing the  previously  closed  eyes.  These  cases  also  presented,  in  addition  to  the 
catalepsy,  the  strange  phenomenon  called  "  suggest  ion."  If  tbe  patient  were  put 
into  any  posture  associated  with  some  definite  mental  conception  (such,  for  exam- 
ple, as  the  attitude  of  prayer,  or  that  assumed  in  terror,  or  to  express  detestation ), 
then  the  corresponding  thoughts  would  come  into  the  mind,  as  a  hallucination, 
but  with  all  the  vividness  of  reality.  Ample  proof  of  this  was  visible  in  the 
expression  of  the  face  and  in  the  whole  bearing  of  the  subject.  An  analogous 
fact  has  been  observed  by  Duchenne,  Lasegue,  and  ourselves — namely,  that  some- 
times a  hysterical  person  can  be  brought  into  the  cataleptic  state  by  artificial  clo- 
sure of  the  eyes  (compare  what  is  said  in  the  next  chapter  about  hysterical  anaes- 
thesia). 

Catalepsy  is  also  seen  in  many  psychoses,  particularly  in  certain  grave  forms 
of  melancholia  known  as  melancholia  attonita  and  katatonia,  and  sometimes  in 
progressive  general  paralysis.  (For  particulars  see  works  on  insanity.)  The  cata- 
leptic state  may  also  develop  in  connection  with  grave  organic  cerebral  disease,  as 
in  meningitis  and  apoplectic  coma.  It  may  finally  be  mentioned  in  passing  that 
quite  well-marked  catalepsy  is  sometimes  observed  in  young  children  of  one  or 
two  years  when  they  are  ill.  Probably  they  fall  into  a  sort  of  stupor ;  or  often  it 
seems  that  they  are  rendered  hypnotic,  as  it  were,  by  the  presence  of  strangers. 

Catalepsy  has  been  regarded  as  a  special  disease  in  those  very  rare  cases  where 
otherwise  healthy  persons  are  liable  to  "cataleptic  fits."  The  condition  comes  on 
suddenly,  unprovoked,  and  passes  off  spontaneously  after  a  variable  length  of  time. 
It  is,  however,  very  probable  that  these  cases  are  either  hysterical  or  epileptoid, 
and  deserve  to  be  classed  with  genuine  epilepsy. 

Prognosis  and  Treatment. — Since  catalepsy  is  a  symptom  of  so  many  different 
diseases,  it  is  impossible  to  make  any  general  statements  with  regard  to  prognosis 
or  therapeutics.  The  reader  may  gain  some  light  from  the  remarks  on  the  treat- 
ment of  hysteria  in  the  next  chapter. 


CHAPTER   IX. 
HYSTERIA. 

./Etiology  and  Definition.— It  is  impossible  to  give  a  definition  of  hysteria  that 
shall  be  at  once  brief  and  accurate,  for  the  aspects  of  the  disease  are  so  manifold 
that  there  is  no  one  symptom  which  can  be  called  pathognomonic  or  even 
universally  characteristic.  Hysteria  is  therefore  symptomatically  not  a  well- 
rounded  morbid  unit,  but  the  nature  of  all  those  pathological  conditions  which 
we  term  hysterical  may  very  well  be  regarded  from  a  single  point  of  view. 
Hysteria  thus  has  its  peculiarities  and  its  rules  like  any  other  disease.  Only 
because  its  laws  have  been  sought  elsewhere  than  where  they  really  are,  has  the 
claim  often  been  made  in  the  past  that  the  morbid  symptoms  of  hysteria  were 
subject  to  no  law. 

The  fundamental  condition  for  a  right  understanding  of  hysteria  seems  to  be 
that  we  should  free  ourselves  from  the  old  untenable  idea  that  hysteria  is  a  "gen- 
eral functional  disease  of  the  whole  nervous  system,  where  now  this  and  now  that 
portion  of  it  may  be  disturbed  in  its  functions."  We  regard  hysteria  as  a  disease 
which  relates  to  the  cerebral  activity  immediately  associated  with  the  psychical 
processes — that  is,  if  you  will,  with  a  psychosis,  but  in  the  broader  sense  of  the 
word;  the  disturbance  affects  not  only  the  normal  course  of  the  psychical  pro- 


798  DISEASES  OF  THE  NERVOUS  SYSTEM. 

cesses,  but  also  their  association  with  the  purely  corporeal  processes  of  innervation. 
The  starting  point  of  the  disturbance,  however,  is  always,  in  its  final  relation,  in 
the  psychical  sphere,  although,  as  we  shall  see  later,  the  occasion  of  the  psychical 
change  is  often  to  be  sought  in  material  processes. 

Starting  from  this  standpoint  we  may  note  the  following  characteristic  marks 
of  hystericalaffections : 

1.  All  hysterical  disturbances,  no  matter  how  severe  the  functional  nervous 
derangement  attributable  to  them,  are  without  visible  anatomical  basis.  The  best 
proof  of  this  is  the  fact  that  any  case,  however  alarming,  may  recover  completely 
in  a  very  short  time. 

2.  The  hysterical  affection  is  very  often  intimately  associated  with  exciting 
causes  of  a  psychical  nature.  Not  only  is  its  appearance  and  incipiency  most 
closely  linked  with  emotional  excitement,  but  later  on  the  mind  is  the  main  if 'not 
the  only  channel  through  wbich  causes  can  operate  to  change  the  condition  of  the 
patient,  whether  favorably  or  unfavorably. 

3.  It  is  therefore  evident  that  the  origin  of  all  hysterical  disturbances  must  be 
sought  in  the  most  central  portions  of  the  nervous  system — those  regions  which 
are  most  directly  concerned  in  the  mental  processes.  Hysterical  phenomena  are, 
however,  exhibited  in  all  parts  of  the  nervous  system,  so  far  as  these  depend  upon 
psychical  processes  or  may  be  altered  by  them.  The  symptoms  of  hysteria  are 
therefore  more  manifold  than  those  of  almost  any  other  disease.  Although  so 
manifold,  certain  symptoms  predominate  with  such  frequency  as  to  be  character- 
istic of  hysteria,  and  therefore  to  be  regarded  as  especially  valuable  in  diagnosis. 
Following  Charcot,  we  term  such  symptoms  "hysterical  stigmata."  These  symp- 
toms are  most  constantly  present,  and  therefore  they  can  easily  be  found  at  any 
time. 

4.  Besides  the  permanent  symptoms— the  "  stigmata  " — we  see  in  many  cases 
of  hysteria  peculiar  nervous  attacks.  These  are  also  highly  characteristic  of 
hysteria,  since  they  come  on  in  forms  which  are  seen  in  no  other  disease ;  but  there 
are  also  patients  who  suffer  from  hysteria  who  nevertheless  are  never  visited  by 
attacks.  The  possibility  of  the  occurrence  of  an  attack  is,  however,  always  present. 
Very  often  the  attacks  are  provoked  by  easily  discoverable  psychical  causes. 

After  this  brief  introduction,  turning  to  the  aetiology,  psychical  causes,  as  has 
been  said,  are  of  first  importance.  In  numerous  instances  hysteria  comes  on  as 
an  immediate  sequel  to  violent  emotional  excitement  or  to  a  "  psychical  trauma," 
if  we  may  use  such  an  expression.  Hysterical  convulsions  or  paralysis  may  be 
excited  by  great  terror  or  violent  anger  or  any  unusual  agitation.  Here  the 
efficient  cause  is  often  hidden  by  some  attendant  circumstance.  If,  for  example, 
a  woman  falls  into  the  water,  or  gets  burned,  or  tumbles  downstairs,  and  there- 
upon develops  hysteria,  the  mistake  is  often  made  of  ascribing  the  disease  to 
catching  cold,  or  to  the  injury  received,  although  really  it  was  the  mental  excite- 
ment which  produced  it.  Only  in  severe  traumatic  concussion  of  the  whole  body 
may  the  partly  physical  symptoms  of  commotio  cerebri  and  commotio  spinalis  be 
united  with  the  psychical  shock.  There  then  develop  peculiar  morbid  conditions 
which  we  term  traumatic  neuroses  and  which  are  closely  related  to  hysteria.  We 
will  speak  of  them  particularly  in  the  last  chapter  of  this  section.  Purely  hys- 
terical conditions,  such  as  anaesthesia,  hyperesthesia,  contracture,  paralysis,  etc., 
may  also  arise  from  slight  local  injuries.  What  is  very  remarkable  in  such  cases 
is,  tbat  the  special  attendant  circumstances  at  the  time  of  the  psychical  disturb- 
ance often  influence  the  localization  of  the  hysterical  phenomena:  that  part,  to 
which  attention  was  particularly  directed  at  the  time,  not  infrequently  becomes, 
later  on,  the  seat  of  the  nervous  disturbance.  In  hysterical  joint-affections  (page 
528)  the  cause  not  infrequently  proves  to  have  been  an  injury  to  the  particular 


HYSTERIA.  790 

joint  now  suffering  from  hysteria.  A  young1  girl,  who  was  awakened  at  night  by 
the  smoke  of  her  burning  mattress,  arid  who  bad  a  severe  laryngitis  from  inhaling 
the  vapors,  exhibited  later  an  indubitably  hysterical  paralysis  of  the  vocal  cords. 
In  the  case  of  another  girl,  who  in  jumping  from  a  carriage  fell  upon  her  side, 
we  afterward  saw  hemianesthesia  of  the  same  side.  Many  such  instances  could 
be  cited. 

Certain  hysterical  cases,  therefore,  have  for  their  obvious  cause  a  single  occa- 
sion of  mental  agitation;  but  in  many  others  the  disease  is  not  thus  abruptly 
excited.  As,  in  poisoning,  we  can  distinguish  between  the  sudden  action  of  a  large 
dose  and  chronic  cases  where  minute  amounts  of  poison  are  absorbed  daily  for  a 
long  period,  so  hysteria  may  come  on  not  only  after  a  single  violent  shock,  but 
also  as  the  final  consequence  of  psychical  influences  insignificant  of  themselves, 
but  potent  because  of  their  frequent  repetition  or  persistency.  It  is  in  cases  of  this 
sort  that  the  causes  do  not  become  evident  to  the  physician  until  he  has  gained  the 
entire  confidence  of  his  patient;  for  the  root  of  the  trouble  is  often  entwined  about 
the  most  private  affairs.  Anxiety,  sorrow,  disappointed  expectations,  abandoned 
hopes,  and,  in  brief,  everything  which  can  depress  and  overwhelm  the  mind — 
these  are  factors  which  may  at  last  excite  the  functional  nervous  derangements  of 
hysteria. 

Finally,  we  must  state  that  hysteria  may  often  develop  without  any  specially 
noticeable  cause.  We  see  this  particularly  in  young  people  with  a  marked 
hereditary  nervous  taint.  Here  the  ordinary  daily  demands  upon  the  central 
nervous  system  sometimes  suffice  to  disturb  in  a  measure  its  normal  equilibrium. 

There  are  still  other  causes.  The  blow  which  brings  a  feeble  body  to  the 
ground  rebounds  without  effect  from  a  massive  frame.  Exactly  the  same  may 
be  said  of  the  "blows"  to  which  the  nervous  system  is  subjected.  Few  entirely 
escape  these  influences,  but  there  are  some  "  strong  natures "  who  resist  the 
psychical  assault  without  wavering,  while  others  have  a  feebly  resistant  nervous 
organization  and  are  overpowered.  We  see,  therefore,  that  the  predisposition 
of  different  individuals  to  diseases  of  the  nervous  system  varies.  This  fact  is  a 
very  important  one  in  the  pathogenesis  of  all  functional  nervous  disorders.  In 
what  this  predisposition  consists  we  do  not  know,  being  acquainted  only  with  its 
results  and  with  some  of  its  causes. 

In  many  cases  this  predisposition  is  hereditary.  Hysteria  is  prominent  among 
those  neuroses  which  attack  different  members  of  a  family — one  suffering  from 
one  disease  and  another  from  another  (vide  page  770).  It  is  also  possible  to 
acquire  such  a  predisposition.  At  least  it  may  be  developed  and  fostered,  on  the 
one  hand,  or,  on  the  other,  checked  and  repressed.  In  these  directions  physical  as 
well  as  psychical  factors  are  of  importance.  Anything  which  weakens  the  con- 
stitution diminishes  the  resistant  power  of  the  nervous  system.  Among  psychical 
influences,  nothing  favors  the  development  of  hysterical  tendencies  more  efficiently 
than  does  a  bad  education.  Hysteria  is  often  ascribable  to  an  irritability  and  fee- 
bleness of  the  nervous  system  thus  engendered.  The  whims  of  the  child  are  not 
controlled,  its  will  is  not  strengthened,  nor  its  energy  developed ;  its  imagination 
is  unsuitably  and  excessively  stimulated,  or  its  intellectual  powers  are  overtaxed 
and  prematurely  ripened. 

It  is  well  known  that  hysteria  occurs  more  frequently  in  the  "  feebler  "  female 
sex  than  among  men;  but  it  is  by  no  means  a  rare  thing  for  men  to  exhibit 
hysterical  convulsions,  paralysis,  contracture,  or  other  well-marked  disturbances. 
Most  cases  occur  between  puberty  and  the  end  of  middle  life.  It  is  not  very  rare 
to  see  pronounced  hysteria  in  children,  especially  such  as  are  over  eight  or  ten 
years  old.  The  disease  very  frequently  begins  to  develope  a  year  or  two  previous 
to  puberty.     Nationality  and  race  also  seem  to  exert  some  influence— for  instance, 


800  DISEASES  OF  THE  NERVOUS  SYSTEM. 

the  severer  forms  of  hysteria  are  decidedly  more  frequent  in  France  than  in  Ger- 
many; and  the  Jewish  race  are  particularly  subject  to  the  disease. 

One  matter  remains  to  be  considered  with  regard  to  aetiology,  to  which  a 
greatly  exaggerated  importance  was  formerly  ascribed.  It  is  the  influence  of  dis- 
ease of  the  sexual  organs.  The  very  name  "  hysteria  "  (varipa  =  uterus)  reveals 
what  the  old  view  was,  namely,  that  hysteria  invariably  originated  in  disease  of 
the  female  genitals.  Not  to  speak  of  the  fact  that  the  disease  occurs  in  men  and 
children,  an  unprejudiced  consideration  of  the  matter  will  show  that  the  above 
assumption  is  entirely  groundless  even  in  regard  to  women.  A  large  number  of 
hysterical  women  present  no  anomaly  of  their  sexual  organs:  and  even  if  the  lat- 
ter be  diseased,  we  are  not  justified  in  at  once  assuming  that  the  hysteria  is  second- 
ary to  the  sexual  disorder.  In  these  cases,  also,  we  usually  find,  on  careful  inquiry, 
that  psychical  causes  have  been  at  work;  and  these  are  incomparably  more  potent 
in  exciting  hysteria  than  is  malposition  of  the  uterus  or  constriction  of  the  cervical 
canal.  It  is  true,  however,  that  disease  of  the  genital  organs  may  depress  the 
spirits  more  than  some  other  diseases  would,  and  so  indirectly  promote  hysterical 
disturbances.  In  the  same  indirect  way,  menstruation,  pregnancy,  and  confine- 
ment exert  an  important  influence  upon  the  development  and  course  of  hysteria. 
Sexual  excesses  or  total  abstinence  from  sexual  indulgence  also  produce  their 
effects  indirectly  through  the  mind. 

The  Symptoms  and  Manifestations  of  Hysteria. 

Considering  the  great  differences  in  the  external  morbid  symptoms  under 
which  hysteria  may  manifest  itself,  it  is  not  easy  to  give  in  a  brief  summary  a 
superficial,  intelligible,  and  yet  accurate  description  of  its  clinical  manifestations. 
We  believe  that  we  can  best  attain  this  end  by  speaking  first  of  the  most  impor- 
tant and  most  frequent  of  the  single  symptoms  of  hysteria,  by  descinbing  next 
the  hysterical  attacks,  and  finally  by  trying  to  evolve  a  general  picture  of  the 
disease. 

1.  The  Hysterical  Stigmata,  especially  the  Sensory  Anaesthesia  and  Hyperes- 
thesia.— In  every  case  where  the  diagnosis  of  hysteria  has  already  been  established 
or  where  it  is  to  be  confirmed,  we  must  examine  the  patient  for  certain  symptoms, 
which,  as  we  have  said,  are  so  common  in  hysteria,  and  in  part  so  peculiar  to 
it,  that  by  themselves  they  are  often  of  decisive  diagnostic  significance.  These 
symptoms  are  termed  "hysterical  stigmata."  A  knowledge  of  them  is  the  more 
important  for  the  physician  in  that  we  often  detect  them  only  by  a  special  exami- 
nation directed  to  that  end.  Patients  only  exceptionally  inform  us  as  to  these 
symptoms.  It  is  not  at  all  unusual  for  patients  to  have  no  inkling  of  their  exist- 
ence until  after  an  examination. 

The  most  important,  because  the  commonest,  of  these  hysterical  signs  relate  to 
sensibility.  The  more  carefully  we  examine,  the  more  rarely  will  we  meet  with  a 
case  of  severe  hysteria  in  which  in  some  sensory  region  we  do  not  find  manifest 
disturbances,  especially  a  diminution  of  sensibility.  We  must  therefore  test 
accurately  not  only  the  sensibility  of  the  whole  surface  of  the  body,  but  also  the 
functions  of  all  the  other  senses  (sight,  hearing,  smell,  and  taste). 

The  sensory  disturbances  of  the  skin  must  first  be  mentioned.  Not  infrequently 
we  find  a  diminution  of  sensibility  over  the  whole  surface  of  the  body,  especially 
a  more  or  less  complete  analgesia.  In  such  cases  we  can  stick  a  pin  in  deeply  any- 
where, or  pierce  a  fold  of  skin  with  a  pin,  without  the  patient's  complaining  of 
pain.  As  is  well  known,  it  often  happens  that  hysterical  patients,  in  order  to  ap- 
pear interesting  or  from  some  other  reason,  produce  upon  themselves  deep  injuries 
and  wounds;  this  is  almost  always  connected  with  the  patient's  analgesia.     Very 


HYSTERIA.  801 

often,  however,  the  anaesthesia  is  not  general,  but  it  is  limited  to  a  definite  region. 
We  find  complete  anaesthesia  of  one  arm  or  leg,  or  we  find  on  the  trunk  or  the 
extremities  single  areas  of  anaesthesia,  in  which  the  anaesthetic  parts  are  bounded 
by  the  normally  sensitive  skin;  these  areas  may  take  all  possible  forms,  and  may 
often  be  very  peculiar.  The  sensibility  to  pain  is  almost  always  the  most  disturbed 
when  the  other  forms  of  cutaneous  sensibility  may  be  quite  unaffected,  but  changes 
in  the  sensibility  to  temperature,  pressure,  etc.,  may  also  occur.  It  may  be  added 
that  in  the  severer  forms  of  anaesthesia  the  deeper  parts  may  also  be  insensitive,  so 
that  the  so-called  muscular  sense  is  absent,  and  patients  with  their  eyes  shut  have 
not  the  slightest  idea  of  the  position  of  the  anaesthetic  limbs. 

Besides  cutaneous  anaesthesia,  disturbances  in  the  sensibility  of  the  other  sen- 
sory organs  (other  u  sensory  anaesthesias")  are  among  the  commonest  signs  of 
hysteria.  Sometimes  the  patients  say,  when  asked,  that  they  see  indistinctly  and 
dimly.  If  we  examine  the  eyes  we  often  find  a  loss  of  visual  acuteness  and  a 
rapidly  induced  fatigue  on  using  them.  A  limitation  of  the  visual  field  is  the 
most  characteristic  sign — that  is,  an  anaesthesia  of  the  peripheral  portions  of  the 
retina.  The  degree  of  this  limitation  sometimes  shows  manifest  differences  for 
the  different  colors.  Hysterical  achromatopsia  is  a  common  symptom — that  is,  a 
partial  or  complete  loss  of  the  color  sense.  According  to  Charcot,  in  the  hysterical 
the  perception  of  violet  usually  first  disappears,  then  green,  and  lastly  blue  and 
yellow ;  but  we  must  not  hold  too  strictly  to  all  these  rules ;  for,  although  the 
French  investigators  are  otherwise  deserving  of  great  praise  in  adding  to  our 
knowledge  of  hysteria,  in  this  respect  they  seem  decidedly  too  schematic,  and  to 
have  generalized  too  rashly.  Diminution  of  the  auditory  acuteness  in  one  or  both 
ears  is  also  not  uncommon.  Anaesthesia  of  smell  and  taste  is  still  more  common. 
Salt,  quinine,  vinegar,  sugar,  etc.,  either  excite  no  sensation  of  taste  at  all,  or  the 
tongue  is  anaesthetic  for  one  or  another  of  these  substances.  The  same  holds  for 
the  sense  of  smell.  All  these  symptoms  are  especially  important  in  diagnosis,  be- 
cause in  organic  diseases  they  are  relatively  much  rarer  in  such  a  degree  than  in 
hysteria. 

The  sensory  anaesthesias  above  described  may  of  course  be  combined  in  various 
ways  in  different  cases,  but  none  of  these  combinations  is  so  characteristic  and 
individual  as  hysterical  hemianesthesia,  a  symptom-complex  which  occurs  almost 
solely  in  hysteria,  and  is  therefore  of  distinct  diagnostic  value. 

Hysterical  hemianaesthesia  is  one  of  the  most  common  symptoms  of  profound 
hysteria.  It  must  often  be  sought  for,  inasmuch  as  the  patient  herself  frequently 
has  no  suspicion  of  its  existence  until  her  attention  is  called  to  it.  It  seems  just 
as  if  one  half  of  the  body  had  been  entirely  lost  to  consciousness ;  the  patient  does 
not  know  whether  it  is  or  is  not  capable  of  feeling. 

In  a  typical  and  fully  developed  case  the  hemianaesthesia  does  actually  affect 
just  one  half  of  the  body.  There  are  rudimentary  forms;  but  in  these  complete 
ones,  the  boundary  between  the  anaesthetic  parts  and  the  parts  retaining  normal 
sensitiveness  accurately  corresponds  to  the  median  line  of  the  body.  The  skin  on 
the  affected  side  is  entirely  insensible  to  the  prick  of  a  needle  or  to  heat.  Often 
it  seems  somewhat  blanched,  and  its  blood-vessels  seem  to  be  constricted;  at  least 
the  skin  very  often  bleeds  surprisingly  little  if  wounded.  The  mucous  membranes 
upon  the  abnormal  side  are  all  equally  anaesthetic,  including  the  conjunctiva,  that 
half  of  the  buccal  cavity  and  of  the  tongue.  The  deeper  parts,  such  as  the  mus- 
cles and  joints,  are  also  almost  invariably  anaesthetic.  The  patient  can  no  longer 
fesl  in  what  position  the  limbs  of  the  affected  side  are ;  and  if  they  are  moved 
passively,  no  sensation  is  communicated  to  her.  The  organs  of  special  sense  are 
usually  involved.  Hearing  is  impaired  upon  the  affected  side;  the  corresponding 
half  of  the  tongue  can  not  taste;  the  corresponding  nostril  can  not  smell;  and 

51 


802  DISEASES  OF  THE  NERVOUS  SYSTEM. 

sight  upon  that  side  is  affected  in  a  peculiar  manner.  There  is  no  heniiopia,  but 
a  total  amblyopia,  or  possibly  amaurosis.  If  the  amaurosis  be  not  complete,  we 
find  at  least  a  limitation  of  the  visual  field  and  the  signs  of  the  above-mentioned 
achromatopsia. 

Apart  from  other  hysterical  symptoms  with  which  hemianaesthesia  as  well  as 
all  the  other  sensory  anaesthesias  may  be  associated,  we  must  mention  here  one 
symptom  which  is  in  close  relation  to  anaesthesia,  and  which  was  first  described  by 
Duchenne  under  the  name  of  "  loss  of  muscular  sense "  (perte  de  la  conscience 
musculaire) .  The  patient,  whose  arm,  for  example,  is  anaesthetic,  can  not  move 
it  if  she  closes  her  eyes,  although  with  open  eyes  she  can  move  it  as  well  as  ever. 
When  the  eyes  are  shut  the  arm  remains  motionless  in  the  position  it  has  pre- 
viously occupied.  If  its  position  be  altered  by  passive  motion,  the  new  position  is 
maintained  with  equal  persistency.  There  is,  with  the  eyes  shut,  pronounced 
catalepsy.  Duchenne  referred  this  peculiar  symptom  to  the  loss  of  a  special 
sense  which  he  termed  "  muscular  sense  "  {conscience  musculaire).  According  to 
our  present  conception  of  hysteria  it  would  be  more  correct  to  regard  the  symptom 
as  pui'ely  psychical. 

The  much-discussed  and  peculiar  symptoms  of  transfer,  as  well  as  metalloscopy 
and  allied  symptoms,  will  be  mentioned  below.  » 

Thus  far  we  have  spoken  only  of  anaesthesia,  but  we  very  often  find  in  the  hys- 
terical certain  hyperaesthetic  regions.  These  hyperaesthesias  are  so  characteristic 
that  we  must  reckon  them  among  the  hysterical  stigmata,  and  must  therefore  look 
for  them  in  every  case.  Sometimes  the  physician's  attention  is  called  to  these  places 
because  they  are  the  seat  of  constant  slight  or  severe  pain.  In  other  cases  the  ten- 
derness appears  only  upon  pressure.  The  hyperaesthesia  may  be  so  great  that  the 
patient  can  scarcely  bear  the  slightest  touch.  Of  course,  the  hyperaesthesia  is  very 
closely  connected  with  the  condition  of  the  patient's  attention.  If  the  thoughts  be 
diverted,  even  firm  pressure  is  often  not  at  all  noticed.  We  see  clearly,  then,  that 
we  usually  have  to  do  here  with  a  "psychical  hyperaesthesia." 

The  hyperaesthetic  spots  are  either  quite  extensive  or  quite  circumscribed,  or 
even  limited  to  one  definite  spot.  They  may  lie  near  to  or  in  the  midst  of  anaes- 
thetic areas.  They  are  relatively  rarest  in  the  extremities  and  more  common  on 
the  head  and  trunk,  especially  on  the  sternum,  on  the  sides  of  the  chest,  under  the 
mammae,  etc.  Most  common,  and  therefore  especially  characteristic,  is  the  hyper- 
aesthesia of  the  vertebral  column,  and,  in  women,  of  the  lower  abdominal  region 
.("  ovarian  pain,"  "  ovarie  ").  The  latter  term  is  convenient  but  by  no  means  cor- 
rect, since  really  we  have  only  a  tenderness  of  the  soft  parts  generally,  which  is  at 
once  noticeable  on  deep  pressure,  and  we  do  not  have  solely  or  chiefly  a  tender- 
ness of  the  ovary.  We  usually  find  "  ovarie  "  only  on  one  side,  offener  on  the  left 
than  on  the  right.  Analogous  symptoms  in  men— tenderness  in  the  groins  or  the 
testicles— are  less  common.  Hyperaesthesia  of  the  vertebral  column,  hysterical 
"  spinal  irritation,"  is  even  more  important  for  diagnosis  than  ovarie.  The  hyper- 
aesthesia affects  either  the  whole  spine  or  merely  single  portions  of  it,  often  only 
single  vertebrae.  It  may  attain  so  high  a  degree  that  the  slightest  touch  of  the 
skin  over  the  vertebrae,  or  somewhat  deep  pressure,  may  cause  the  liveliest  outcries 
and  shrinking.     This  symptom  is  almost  pathognomonic  of  hysteria. 

The  relations  which  these  hyperaesthetic  regions  have  to  the  hysterical  attacks 
are  very  important,  and  they  have  therefore  procured  for  them  the  name  of  "hys- 
terogenous  zones."  We  will  speak  further  on  this  point  in  describing  the  hyster- 
ical attacks. 

Hyperaesthesia  in  other  sensory  regions— abnormal  sensitiveness  of  the  eye,  ear, 
etc.— also  occurs.  Thus  certain  cases  of  hysterical  blepharospasm  seem  to  be  due 
to  an  immoderate  sensitiveness  to  light.     Unusually  sharp  hearing  is  noted,  espe- 


HYSTERIA.  803 

cially  during  the  hysterical  attacks.     Here,  too,  belongs  the  aversion  of  many 
patients  to  certain  smells  and  tastes,  and  the  like. 

2.  Hysterical  Paralysis.  —  Hysterical  paralysis  is  frequently  an  immediate 
sequel  to  some  violent  mental  excitement  (for  example,  "paralysis  from  fright ''); 
but  it  may  come  on  gradually.  Hysterical  paralysis  is  indubitably  of  central 
origin.  It  is  a  paralysis  of  the  will.  The  patient  has  lost  the  power  to  will  a 
contraction  of  the  affected  muscles.  One  always  has  the  feeling  that  the  patient 
could  move  the  paralyzed  limb  perfectly  well  if  she  only  desired  to;  but  she  can 
not  bring  the  will  to  bear  on  it,  and  this  inability  is  the  real  trouble.  It  also 
seems  a  remarkable  circumstance  that  hysterical  paralysis  often,  but  of  course 
not  always,  affects  only  certain  combined  movements.  Many  patients,  for  in- 
stance, can  move  their  legs  very  well  in  bed,  but  they  can  not  walk  a  step.*  We 
have  seen  a  hysterical  writing  paralysis ;  the  right  arm  was  not  paralyzed,  but  it 
utterly  refused  to  make  any  attempt  to  write. 

The  extremities  are  most  frequently  paralyzed,  particularly  the  lower  limbs; 
but  hemiplegia  is  not  especially  rare.  A  very  common  manifestation  is  loss  of  the 
power  to  walk.  The  patient  lies  in  bed  or  on  a  sofa,  and  sometimes  while  thus 
reclining  she  can  flex  and  extend  the  legs  very  well ;  but  as  soon  as  she  is  urged 
to  stand  up  or  walk,  the  knees  double  up,  the  patient  begins  to  tremble,  the  respira- 
tion grows  rapid  and  convulsive,  and  there  is  not  the  slightest  effort  made  to  move 
the  legs.  If  only  one  leg  be  paralyzed,  the  gait  is  often  very  peculiar  and  char- 
acteristic. The  sound  limb  makes  long  strides,  while  the  paralyzed  one  is  held 
perfectly  rigid,  and  often  is  dragged  along  with  a  loud  shuffling  sound.  The  arms 
are  much  less  often  affected.  The  facial  muscles  are  hardly  ever  paralyzed.  We 
once  saw  hysterical  diplopia. 

In  regard  to  the  more  precise  form  of  the  paralysis,  both  flaccid  and  spastic 
paralyses  occur  in  hysteria.  In  many  cases  of  hysterical  paralysis  the  tendon 
reflexes  may  be  so  exaggerated — nay,  there  may  even  be,  as  we  have  repeatedly 
seen,  such  a  lively  foot  phenomenon — that  one  is  at  first  disposed  to  think  of  actual 
spinal  paralysis.  In  other  cases,  as  in  paralysis  of  an  arm,  the  paralyzed  limb 
hangs  down  completely  flaccid.  The  paralyzed  parts  are  often  at  the  same  time 
completely  anaesthetic  (a  circumstance  which  may  often  be  distinctive  in  diag- 
nosis), but  in  other  cases  they  are  normally  sensitive  or  even  hyperaesthetic. 

Hysterical  paralysis  of  the  vocal  cords  is  seen  very  often.  The  voice  is  gener- 
ally lost  suddenly,  and  the  patient  can  talk  only  in  a  whisper — hysterical  aphonia. 
On  laryngoscopic  examination,  we  are  often  struck,  at  the  outset,  by  the  anaes- 
thesia of  the  pharynx  and  its  lack  of  reflex  excitability.  We  find  no  trace  of  any 
anatomical  lesion  of  the  cords,  but  merely  that  they  are  paretic.  The  glottis  can 
not  be  completely  closed,  and  sometimes  the  vocal  cords  actually  grow  wider 
apart  upon  every  effort  at  phonation.  The  patient  then  speaks  exclusively  in  a 
whisper.  Hysterical  mutism  quite  rarely  follows  hysterical  aphonia.  The  patients 
entirely  lose  voluntary  control  of  their  speech  apparatus,  and  finally  become  com- 
pletely dumb. 

Hysterical  paralysis  of  the  pharynx  and  oesophagus  is  much  less  frequent. 
If  there  be  dysphagia,  it  is  often  not  an  easy  matter  to  determine  whether  it  is  due 
to  paralysis  or  to  spasm. 

3.  Hysterical  Contractures. — Contractures  may  occur  as  isolated  phenomena, 
or  in  combination  with  other  symptoms,  such  as  anaesthesia  or  paralysis.     They 

[*  This  inability  to  stand  or  walk,  with  the  preservation  of  good  strength  and  co-ordination  in  the 
legs  when  sitting  or  standing,  and  the  persistence  of  power  to  execute  certain  less  usual  movements, 
such  as  hopping  on  one  foot,  has  been  termed  by  Blocq  astasia-abasia.  It  is  often  associated  with 
hysteria,  but  it  may  exist  independently  of  it. — K.] 


804 


DISEASES  OF  THE  NERVOUS  SYSTEM. 


are  caused  by  unusually  strong  tonic  muscular  contractions.  The  starting-  point 
of  the  irritation  is  certainly  in  the  central  nervous  system.  Sometimes  the  con- 
tractures are  temporary,  hut  often  they  are  characterized  by  their  intensity  arid 
their  great  persistency.  The  extremities  suffer  most  frequently,  although  the 
trunk  or  the  hack  of  the  neck  may  be  affected.  In  the  hands  and  feet,  especially 
in  the  toes,  flexor  contractures  predominate,  but  in  the  larger  joints  extensor  con- 
tractures are  the  rule.  Although  many  varieties  occur,  single  forms  of  contracture 
are  especially  characteristic.  As  an  example,  we  will  refer  to  the  accompanying 
illustration  (Fig.  109). 

The  relations  of  hysterical  contractures  to  the  articular  neuralgias  have  already 

been  mentioned  (p.  529).  They  may  occur  in 
a  hemiplegic,  paraplegic,  or  monoplegic  form. 
They  often  follow  a  hysterical  convulsive  at- 
tack (vide  infra).  All  hysterical  contractures 
disappear  completely  in  chloroform  narcosis 
W  ^IKp  and  in  deep  sleep. 

4.  Vasomotor  Disturbances.  Secretory  Dis- 
turbances. Symptoms  in  the  Internal  Organs. 
— Besides  the  sensory  and  motor  symptoms 
just  described,  other  symptoms  occur  in  hys- 
teria which  fall  under  the  domain  of  the  vas- 
omotor and  secretory  nerves.  The  signifi- 
cance of  many  of  these  symptoms  is,  of  course, 
not  yet  clear. 

In  the  first  place  abnormal  anaemia  or  ab- 
\  normal  fullness  of  the  vessels  (a  cool,  pale  skin 

in  the  one,  a  hot,  red  skin  in  the  other)  is  not 
infrequent,  and  points  to  vasomotor  influences. 
Since  we  know  that  the  vascular  nerves  are 
influenced  in  a  high  degree  by  the  emotions, 
ir,.nm   we  can  probably  assume  a  central  origin  for 

Fig    109.  —  Hysterical  contracture.       riom  r  j  & 

Bourneville  and  RegnarcTs  iconographie   these  symptoms.     Haemorrhages  from  inter- 

de  la  Salpetriere).  ,  ,        n        ,  -,    .  ,-, 

.  nal  organs  are  harder  to  explain;  they  are 
apparently  not  uncommon  in  hysteria,  and  they  have  often  been  explained  by 
"nervous  vasomotor  influences,"  but  in  our  opinion  we  must  be  extremely 
guarded  in  such  an  assumption.  We  most  frequently  see  hysterical  haemateuiesis 
or  hysterical  haemoptysis— that  is,  the  evacuation  of  blood  from  the  mouth,  either 
with  cough  or  with  more  of  a  strangulation.  Inexperienced  physicians  have 
thus  often  been  led  to  a  false  belief  in  dangerous  pulmonary  disease  or  gastric 
ulcer ;  but  if  we  look  more  closely  we  shall  find  that  the  blood  evacuated  is  of  a 
clear  raspberry-red  color,  is  mixed  with  a  good  deal  of  mucus  and  saliva,  and  is 
of  a  thin  fluid  consistency.  The  whole  amount  is  seldom  more  than  two  or  three 
ounces  (grm.  50-80).  If  we  inquire  more  carefully  as  to  its  origin,  we  can  usually 
find  a  source  for  the  blood  in  the  gums  or  in  the  oral  or  pharyngeal  mucous  mem- 
brane. There  are  often  spasmodic  chokings  or  hiccoughs,  by  which  a  haemor- 
rhage of  the  mucous  membrane  is  mechanically  produced.  It  is  also  certain 
that  in  many  cases  intentional  deception  on  the  part  of  the  patients  may  lie  at 
the  bottom  of  the  haemorrhage.  We  must  be  especially  cautious  in  haemorrhages 
from  the  genitals,  from  the  skin,  from  the  palms  in  the  "stigmatized,"  etc. 

Finally,  among  the  vasomotor  disturbances  we  must  mention  one  symptom 
whose  significance,  in  our  opinion,  has  not  yet  been  satisfactorily  explained — we 
mean  hysterical  fever.  In  severe  hysteria,  especially  at  the  time  of  severe  attacks 
and  psychical  disturbances,  other  observers,  and  we  ourselves,  have  repeatedly  seen 


HYSTERIA.  805 

high  febrile  temperatures,  106°  (41°  0.)  and  more;  and  these  temperatures  come 
on  in  a  very  irregular  manner.  In  none  of  the  cases  under  our  own  observation, 
however,  could  we  wholly  exclude  the  possibility  of  simulation — that  is,  of  pro- 
ducing a  rise  of  the  mercury  by  rubbing  and  pressing  on  the  thermometer.  In 
all  the  measurements  we  made  ourselves  in  the  rectum  the  temperature  was 
normal,  while  the  high  fever  was  always  said  to  occur  in  our  absence.  We  there- 
fore recommend  great  caution  with  reference  to  this  point. 

Anomalies  of  the  secretory  and  excretory  organs  have  also  been  met  with  in 
hysteria.  Many  patients  have  a  remarkably  dry  skin,  while  others  sometimes 
perspire  very  freely.  The  secretion  of  saliva  is  subject  to  similar  modifications. 
Very  remarkable  observations  have  been  made  in  a  few  cases  with  regard  to  hys- 
terical ischuria ;  for  days  only  a  very  small  amount  of  urine  has  been  passed, 
although  there  has  been  no  retention.  In  one  case  of  this  sort,  observed  by 
Charcot,  there  was  violent  vomiting  at  the  same  time,  and  the  vomitus  con- 
tained a  comparatively  large  amount  of  urea  (vicarious  excretion).  Hysterical 
polyuria  occurs  more  frequently  than  ischuria.  A  large  amount  of  very  light- 
colored  urine  of  low  specific  gravity  is  excreted.  This  polyuria  is  in  many 
instances  merely  the  result  of  excessive  ingestion  of  liquids.  Polydipsia  (exces- 
sive thirst)  is  a  very  frequent  symptom  in  hysteria,  particularly  at  the  close  of 
a  fit. 

The  digestive  disturbances  which  many  patients  have  are  mainly  such  as  have 
already  been  discussed  on  page  400,  under  the  head  of  "  nervous  affections  of  the 
stomach."  Colicky  pains,  obstinate  constipation,  occasional  diarrhoea,  and  similar 
symptoms,  are  by  no  means  rare.  Hysterical  tympanites  also  deserves  mention. 
It  is  due  to  the  accumulation  of  a  large  amount  of  air  and  gas  in  the  prima?  viae. 
This  may  be  in  part  the  result  of  a  sort  of  paresis  of  the  muscular  coat  of  the 
stomach  and  intestines,  but  another  frequent  cause  is  the  swallowing  of  large 
amounts  of  air.  Perhaps  the  patient  does  this  on  purpose.  The  prominence  and 
tension  of  the  abdominal  walls  may  be  so  considerable  as  to  simulate  grave  dis- 
eases, such  as  peritonitis,  or  a  tumor,  or  pregnancy.  Doubts  of  this  sort  can  always 
be  dispelled  by  inducing  anaesthesia  with  chloroform.  It  is  possible  to  remove 
the  gas  completely  in  a  short  time  by  pressing  upon  the  abdomen,  or  by  introduc- 
ing a  long' tube  through  the  rectum. 

Sometimes  there  are  symptoms  referable  to  the  genital  organs.  It  has  been 
already  pointed  out  that  too  much  prominence  was  formerly  given  to  the  influence 
of  sexual  diseases  in  exciting  hysteria.  It  is  also  true  that  nervous  derangements 
of  the  genital  organs  may  be  among  the  symptoms  of  hysteria.  In  this  way  pain 
and  hyperesthesia  may  be  occasioned,  and  possibly  many  instances  of  dysmenor- 
rhea and  leucorrhoea  have  a  similar  origin.  We  can  also  readily  understand 
that  sexual  relations  often  influence  very  excitable,  hysterical  individuals  to  no 
slight  extent,  as  indeed  is  very  frequently  betrayed  by  the  character  of  their  hal- 
lucinations and  their  utterances  when  delirious. 

5.  General  Mental  and  Bodily  Constitution  of  the  Hysterical.— If  we  regard 
hysteria  as  a  disease  which  is  largely  psychical,  which  is  the  only  correct  view,  it 
will  not  seem  strange  if  the  whole  mental  constitution  and  nature  of  the  patient 
show  special  peculiarities.  In  many  cases,  therefore,  the  psychical  condition  of 
the  hysterical  is  so  characteristic  that  the  physician  can,  from  the  patient's  nature 
and  demeanor,  form  his  conclusions  as  to  the  form  of  her  disease. 

Hysterical  persons  are  irritable  and  emotional,  easily  depressed,  sensitive» 
whimsical,  and  subject  to  violent  extremes  of  feeling.  They  are  inclined  to  exag- 
gerate their  sufferings,  exact  a  great  deal  of  attention,  and  are  anxious  to  excite 
sympathy.  They  have  little  energy  or  force  of  will,  but  they  are  sly  and  obsti- 
nate in  carrying  out  any  pet  desire.     Again,  they  can  be  very  amiable  and  attrac- 


806  DISExVSES  OF  THE  NERVOUS  SYSTEM. 

tive  if  they  take  the  fancy.  They  are  almost  iuvariahly  clever.  It  is  comparatively 
exceptional  to  see  hysteria  in  dull  and  stupid  persons. 

This  brief  sketch  represents  many  cases,  as  we  have  said,  hut  not  all.  Such 
patients  very  frequently  present  no  very  great  disturbances,  but  complain  merely 
of  all  sorts  of  general  derangements,  sometimes  of  one  kind  and  sometimes  of 
another,  and  yet  are  able  to  perform  their  daily  duties  tolerably  well.  A  case  of 
paralysis,  contracture,  or  other  important  localized  hysterical  trouble  may  not 
present  any  marked  mental  peculiarities.  Either  there  are  none,  or,  if  they  exist, 
the  patient  conceals  them  from  the  physician. 

With  regard  to  the  general  physical  constitution  of  hysterical  subjects,  it  has 
already  been  mentioned  that  any  bodily  weakness  favors  the  development  of  the 
disease ;  and  yet  hysteria  is  by  no  means  confined  to  the  ill-nourished,  weakly, 
and  anaemic.  On  the  contraiy,  many  patients  seem  to  be  in  blooming  health  and 
well  nourished.  In  a  severe  case  of  hysteria,  however,  the  effects  of  the  disease 
on  general  nutrition  may  be  very  distinct.  Little  food  is  ingested,  sleep  is  dis- 
turbed, digestion  is  affected  (vide  infra),  and  the  bodily  health  is  gradually 
undermined. 

HYSTERICAL  ATTACKS,   CONDITIONS  OF  SPASM,   ETC. 

While  the  symptoms  thus  far  described  are  largely  of  a  permanent  character, 
paroxysmal  nervous  symptoms  are  also  very  common  in  hysteria.  The  diagnosis 
of  the  entire  morbid  condition  is  often  made  certain  by  the  onset  of  such  hysterical 
attacks,  which  are  often  very  characteristic,  and  their  significance  is  readily  per- 
ceived by  the  experienced  physician.  There  are  some  cases  of  hysteria  which  run 
their  course  entirely  free  from  these  attacks,  where  there  are  only  certain  per- 
manent nervous  symptoms,  such  as  paralysis,  contractures,  anaesthesia,  etc. ;  but 
there  are  also  other  patients  in  whom  the  hysterical  attacks  dominate  the  whole 
scene,  and  are  sometimes  the  only  manifestations  of  the  disease.  A  hysterical  at- 
tack is  not  infrequently  the  beginning  of  the  trouble,  especially  in  those  cases 
where  the  disease  is  excited  by  fright,  etc.,  and  where  the  attack  follows  immedi- 
ately upon  the  psychical  excitement. 

In  regard  to  the  severity  and  the  variety  of  the  hysterical  attacks,  they  are  so 
manifold  that  an  exhaustive  account  of  all  the  possibilities  can  not  here  be  given; 
but  certain  features  and  details  are  so  common  in  them,  and  recur  so  often,  that  a 
consideration  of  them  is  often  in  itself  sufficient  for  a  correct  diagnosis. 

The  mildest  form  of  the  hysterical  attack  consists  of  the  development  of  a  feel- 
ing of  distress,  anxiety,  vertigo,  and  especially  of  a  loss  of  voluntary  control  of 
the  body.  The  patient  sinks  on  a  bed  or  chair,  closes  the  eyes,  and  becomes  inca- 
pable of  action  or  speech.  Mild  symptoms  of  motor  irritation  usually  ensue,  most 
commonly  an  acceleration  of  respiration,  general  tremor,  winking  of  the  eyes, 
etc.  Mild  spastic  symptoms  in  the  pharyngeal  muscles  and  the  diaphragm  are  not 
'  uncommon.  There  is  very  often  a  lively  palpitation  during  the  attack.  The  face 
is  sometimes  quite  red,  but  in  other  cases  pale. 

In  such  mild  attacks  any  impartial  observer  has  distinctly  the  impression  that 
the  patient  is  humoring  her  inclinations.  If,  therefore,  she  be  encouraged,  or  if 
cold  water  be  thrown  in  the  face  or  on  the  back  without  too  great  regard  for  her 
feelings,  she  usually  soon  regains  her  will-power  and  rapidly  recovers. 

In  an  unbroken  series  these  mildest  forms  of  attack  pass  over  into  the  severer 
types,  where  the  clouding  of  consciousness  is  greater  and  the  symptoms  of  motor 
irritation  are  more  severe.  Complete  loss  of  consciousness,  so  common  in  epilepsy, 
is  scarcely  seen  in  hysterical  seizures,  but  there  is  very  often  a  marked  clouding  of 
consciousness,  and  in  the  severe  forms  morbid  alterations  of  consciousness  (vide 
infra).     If  hysterical  attacks  occur  which  resemble  those  of  epilepsy  ("  hystero- 


HYSTERIA. 


807 


epilepsy  "),  we  must  think  of  the  possibility  of  a  combination  of  the  two  diseases; 
but  usually  the  form  of  the  hysterical  convulsion  is  essentially  different  from  that 
of  the  epileptic.  In  severe  hysterical  convulsions  the  convulsive  movements  are 
more  varied,  more  extensive,  and  more  complicated  than  in  epilepsy.  The  arms 
make  thrashing  and  thrusting-  movements,  and  often  apparently  quite  well-co- 
ordinated movements.  Patients  strike  the  bed,  and  sometimes  their  own  bodies, 
with  the  clenched  fist;  they  seize  objects,  such  as  the  bedclothes  or  furniture,  and 
cling-  fast  to  them.  We  also  see  clonic  or  tonic  flexor  and  extensor  spasms  in  the 
legs.  The  eyes  almost  always  converge  or  are  turned  to  one  side,  and  they  often 
roll.  The  lids  are  lightly  closed  or  occasionally  open.  There  is  almost  always 
trismus,  and  there  is  often  grinding  of  the  teeth.  The  trunk  usually  twists  and 
turns  the  most.  The  patient  often  thrusts  her  head  hard  against  the  wall  or  the 
bed.  The  whole  body  may  assume  positions  which  a  healthy  person  can  scarcely 
imitate  without  special  practice.  The  best  known,  and  in  fact  one  of  the  com- 
monest and  most  characteristic,  is  the  arched  position  (arc  de  cercle),  of  which  the 
accompanying  illustration  (Fig.  110)  gives  an  idea. 


Fig.  110.— Hysterical  arc  de  cercle  (Bourneville  and  Regnard). 

Many  patients  rest  for  a  time  on  the  floor  supported  only  by  the  head  and  toes. 
At  intervals  they  sling  or  roll  their  bodies  to  and  fro,  drum  on  the  floor  with  their 
legs,  throw  themselves  into  the  air,  etc.  Any  one  who  has  once  seen  such  a  "  grand 
hysterical  convulsion  "  will  never  forget  the  picture. 

A  different  but  still  common  form  of  hysterical  convulsion  is  characterized  by 
a  pronounced  implication  of  the  respiratory  muscles.  The  attack  begins  with  a 
spasmodic  acceleration  of  respiration,  and  the  breathing  becomes  shorter  and  more 
rapid.  We  have  ourselves  counted  two  hundred  respirations  a  minute.  Other 
peculiar  spasms  of  the  respiratory  muscles,  which  occur  in  this  way  only  in  hys- 
teria, are  also  common;  hiccough,  loud  sobbing,  grunting,  etc.  The  muscles  of 
the  pharynx  are  usually  implicated  in  producing  these  noises.  Of  course,  all  these 
spasmodic  conditions  may  be  joined  in  the  most  varied  ways  with  spasms  of  the 
trunk  and  the  extremities. 

One  of  the  most  essential  factors  which  often  gives  the  most  characteristic 
stamp  to  the  grand  hysterical  attack,  is  the  relation  which  the  spasms  often  have 
to  certain  co-existing  abnormal  conditions  of  consciousness.  During  the  attack 
the  patient  is  usually  not  unconscious,  but  she  is  under  the  dominion  of  inner 
morbid  delusions,  and  these  often  mirror  themselves  in  the  outward  movements. 
The  patient  is  wholly  dominated  by  a  definite  circle  of  ideas ;  she  has  hallucinations, 
and  passes  through  some  frightful  or  exciting  event.  All  this  is  most  strikingly 
manifested  in  her  movements  and  her  expression.  Hence,  in  an  attack  the  face 
often  expresses  terror,  rage,  threatening,  concupiscence,  serenity,  etc.  Very  often 
the  internal  excitement  breaks  forth  in  words,  and  there  is  actual  hysterical 


808  DISEASES  OF  THE  NERVOUS  SYSTEM. 

delirium,  the  most  marked  emotional  utterances,  etc.  The  patients  often  talk 
continually  to  themselves,  usually  vei*y  rapidly,  with  frequeut  repetitions  of  the 
same  phrase  or  word.  We  can  often  succeed  in  giving  the  delirium  a  definite 
direction  by  questioning  the  patient,  or  converse  regularly  with  the  patient  during 
an  attack,  but  usually  the  pure  motor  spasms  again  set  in,  or  persist  for  some  time 
in  a  tonic  form. 

We  can  not  go  further  into  the  numerous  details  of  the  symptoms  of  the  grand 
attack  ("  gran  de  liysterie  "),  for  an  accurate  knowledge  of  which  we  must  thank 
the  observations  of  Charcot  and  the  school  of  La  Salpetriere  in  Paris  (Bourneville 
and  Regnard,  P.  Richer).  The  descriptions  of  the  French  authors  apply  to  the 
grand  hysteria  not  infrequently  seen  in  Germany.  In  regard  to  the  whole  picture 
of  the  attack  the  French  neurologists  distinguish  several  periods  which  corre- 
spond in  general  with  the  above-described  conditions.  The  first  period  consists  of 
severe  epileptiform  convulsions  apparently  associated  with  loss  of  consciousness. 
Then  comes  the  period  of  "contortions  and  grand  movements"  (clown ismus), 
and  finally  the  period  of  plastic  positions  and  passionate  attitudes  (attitudes  pas- 
sionelles).  The  short  and  very  significant  expressions  of  this  scheme  are  of  prac- 
tical value,  but  in  our  experience  we  can  only  rarely  expect  sharply  defined 
"  periods  "  in  the  individual  case ;  the  grand  hysterical  attack  is  rather  composed 
in  the  most  varied  ways  of  the  different  symptoms  above  mentioned. 

There  remains  one  essential  relation  in  order  to  complete  the  picture  of  the  hys- 
terical attack,  and  that  is  the  "  suggestibility  "  of  the  patient,  which  is  so  peculiarly 
characteristic  of  hysteria.  By  ".suggestion"  we  mean  the  artificial  production 
of  a  definite  psychical  state,  or  a  physical  state  dependent  on  the  mind,  by  arous- 
ing the  appropriate  ideas.  In  the  general  characteristics  of  the  mental  constitu- 
tion of  many  hysterical  persons  we  have  already  had  to  point  out  how  much  and 
how  often  such  patients  let  themselves  be  dominated  by  their  imaginations.  Sug- 
gestion is  merely  the  artificial  fostering  of  this  psychical  peculiarity  and  its  special 
application.  The  more  we  try  to  foster  and  preserve  this  peculiarity,  the  more  we 
leave  uncorrected  the  false  ideas  which  the  patients  have,  the  better  we  succeed  at 
last  in  making  the  patients  merely  a  shuttlecock  for  their  ideas.  Hence  the  phy- 
sician's daily  experience  teaches  that,  as  suggestion  experiments  are  repeated,  the 
patients  more  easily  become  susceptible  to  them,  so  that  finally  we  can  actually  "  do 
everything  with  them."  There  can  scarcely  be  any  difference  of  opinion  as  to 
whether  such  an  experiment  without  restraint  is  medically  and  morally  permissi- 
ble ;  and  even  the  fostering  of  suggestion  for  therapeutic  purposes  is  a  two-edged 
sword  whose  action  is  not  always  rigidly  within  the  physician's  control. 

Suggestion  is  most  easy  during  the  hysterical  attack  itself,  especially  in  those 
forms  where  the  patients  speak,  hear,  and  answer.  As  soon  as  we  give  the  sub- 
stance of  the  patient's  ideas  a  definite  direction,  and  tell  them  in  a  convincing 
tone  that  they  are  in  a  garden  or  a  wood,  picking  flowers  or  fruit,  that  they  are 
attacked,  bound,  lying  on  the  edge  of  a  precipice  or  the  water,  etc.,  we  see  in  their 
bearing  and  speech  that  they  think  they  are  actually  experiencing  all  these  con- 
ditions in  their  delirium  and  hallucinations.  The  emotional  utterances  of  fear, 
terror,  joy,  or  aversion  are  then  often  expressed  with  astonishing  art.  In  the  same 
way  we  can  suggest  paralyses,  contractures,  or  anaesthesias.  The  most  interesting 
feature  of  it  all  is,  that  when  the  attack  is  over  every  trace  of  recollection  of  what 
happened  during  it  is  lost.  The  same  patients  who  just  now  were  so  much  excited 
by  some  definite  idea,  a  few  seconds  later,  when  the  attack  has  ceased  of  itself  or 
has  artificially  been  brought  to  an  end  (vide  infra),  know  nothing  more  about  it. 
They  have  not  even  a  vanishing  recollection  like  that  of  a  dream  about  what  they 
have  just  said  and  done,  even  if  it  be  expressly  described ;  but  it  is  still  more  re- 
markable that  during  the  following  attack  they  often  remember  very  well  what 


HYSTERIA.  809 

they  have  experienced  actually  or  in  their  imaginations  in  the  past  attack.  In 
such  cases  we  can  actually  speak  of  "  double  consciousness."  ]  'rocesses  of  tbecon- 
scious  waking  life,  however,  often  remain  in  the  consciousness  during  the;  attack. 
We  often  see  that  the  actual  event  (scene  of  terror,  etc.)  which  has  given  rise  to  the 
first  onset  of  the  attacks,  is  often  gone  through  with  anew  in  the  delirium  of  sub- 
sequent attacks. 

Hypnotic  symptoms  are  closely  allied  to  the  processes  in  suggestion.  We  can 
not  give  here  a  complete  review  of  this  field,  which,  as  is  well  known,  has  been  so 
much  studied  of  late.  The  tendency  of  human  nature  to  mysticism  and  the  influ- 
ence of  suggestions,  which  may  be  of  value  not  only  with  the  patients  but  even  with 
the  investigating  physicians,  are  the  reasons  why  the  false  and  the  true  have  often 
been  mixed  in  the  study  of  hypnosis.  We  can  say  only  that  one  great  advance  is 
now  generally  recognized,  and  that  is,  that  most  persons  of  scientific  training  have 
abandoned  the  hypothesis,  once  frequently  accepted,  of  a  special  "  magnetic 
power  "  (animal  magnetism),  by  which  the  "  magnetizers  "  could  put  their  •'  medi- 
ums "  into  the  "  magnetic  sleep  "  or  other  abnormal  conditions. 

Hypnosis  is  nothing  more  than  the  intentional  artificial  production  of  a  hyster- 
ical attack,  or  a  hysterical  psychosis  by  suggestion — that  is,  by  the  action  of  definite 
ideas  on  the  person  to  be  hypnotized.  Therefore,  only  those  persons  can  be  hyp- 
notized in  whom,  these  ideas  have  a  strong  enough  influence.  No  man  can  be 
hypnotized  to  whom  the  nature  of  hypnosis  is  clear.  The  essential  featui'e  of  all 
hypnotic  procedures  is  merely  to  produce  in  the  most  lively  way  possible  the  idea, 
"  It  will  happen  as  the  hypnotizer  says."  All  other  things — the  fixation  of  the  eyes 
on  bright  objects,  the  vibrations  of  a  tuning-fork,  etc. — are  side  issues,  and  serve 
merely  to  support  the  suggestion.  In  all  easily  hypnotizable  persons  the  mere 
closure  of  the  eyes  and  the  remark,  u  Now  go  to  sleep,"  are  enough  to  produce  the 
hypnotic  sleep.  Patients  (and  here  we  may  actually  speak  of  "  patients  ")  reach 
this  suggestibility,  of  course,  only  after  they  have  often  been  hypnotized ;  for  the 
offener  the  same  action  of  an  idea  is  produced  the  more  easily  it  occurs — a  law 
which  follows  also  from  many  other  experiments  in  the  psychical  domain.  The 
different  forms  of  hypnosis  are  not  distinguishable  from  the  various  hysterical 
conditions.  Hypnosis  is  artificial  hysteria,  and  from  this  alone  we  note  the 
danger  of  all  hypnotic  experiments  as  soon  as  they  are  practiced  by  the  ignorant. 
In  this,  too,  it  has  often  been  shown  that  we  can  not  become  free  again  from  the 
spirits  which  we  call  up.  The  French  physicians  (Richer)  distinguish  four  chief 
forms  of  the  hypnotic  state,  which  show,  however,  many  transitions:  1.  The  cata- 
leptic state,  in  which  the  limbs  r'etain  all  the  positions  artificially  given  them  (see 
the  previous  chapter).  2.  The  state  of  "  suggestion,"  of  artificially  produced  hallu- 
cinations. If  we  put  the  body  passively  into  certain  positions  corresponding  to 
definite  acts,  we  can  produce  in  the  patient  all  the  appropriate  ideas  with  the  dis- 
tinctness of  an  hallucination.  To  this  category  belong  the  well-known  hypnotic 
exhibitions  where  hypnotized  adult  men  toss  babies,  eat  raw  potatoes  with  an 
expression  of  enjoyment,  etc.  3.  The  lethargic  state,  that  is,  a  state  of  apparent 
unconsciousness,  with  the  eyes  closed,  the  muscles  completely  relaxed,  and  a 
marked  increase  of  excitability  in  the  muscles  and  nerves.  A  light  pressure  or  a 
slight  blow  on  a  nerve,  like  the  facial,  suffices  to  put  all  the  muscles  supplied  by 
it  into  a  tetanic  contraction  which  outlasts  the  irritation.  4.  By  certain  manip- 
ulations (for  instance,  rubbing  over  the  parietal)  we  can  change  the  lethargic  state 
into  one  of  hysterical  somnambulism.  The  patients  remain  half  unconscious,  but 
answer  automatically  questions  which  ai^e  put  to  them,  obey  orders  given  to  them, 
and  sometimes  show  certain  sensory  hyperassthesias.  We  see  that  all  these  forms 
are  precisely  identical  with  the  different  forms  of  the  hysterical  attack.  Only  the 
increased  mechanical  excitability  of  muscles  and  nerves  is  not  yet  fully  explained. 


810  DISEASES  OF  THE  NERVOUS  SYSTEM. 

May  not  suggestions — that  is,  ideas  which  lead  to  unconscious  voluntary  muscular 
contractions — also  play  a  part  here  ? 

We  have  thus  far  omitted  to  dwell  upon  an  important  point  in  the  description 
of  the  hysterical  attack — namely,  the  relation  to  it  of  "  hysterogenous  zones," 
We  have  mentioned  above  how  often  in  hysterical  patients  certain  parts  of  the 
body  (the  ovarian  region,  the  sides  of  the  chest,  etc.)  are  extremely  sensitive  to 
pressure.  It  is  by  no  means  uncommon  that,  in  spite  of  the  patient's  resistance, 
somewhat  longer  pressure  on  such  a  spot  may  excite  a  hysterical  attack.  On  the 
other  hand,  we  sometimes  succeed  in  causing  an  existing  attack  to  cease  by  pressure 
on  the  same  zone.  We  are  of  the  opinion  that  in  these  manipulations  also  ideas 
become  potent  as  connecting  links. 

Finally,  we  must  add  that  there  are  also  milder  forms  of  hysterical  spasm 
which  are  limited  to  a  definite  muscular  region,  and  are  not  associated  with  any 
marked  clouding  of  consciousness.  There  are,  for  example,  isolated  spasms  of  the 
muscles  of  the  neck,  isolated  respiratory  spasms  (spasmodic  cough,  etc.),  and  iso- 
lated spasms  in  the  arms  and  legs ;  the  laryngeal  muscles  may  also  be  affected 
(hysterical  spasms  of  the  glottis).  Spasms  of  the  diaphragm  and  other  muscles  of 
inspiration  are  quite  common  under  the  form  of  hysterical  hiccough,  which  may 
sometimes  last  in  the  severest  way  for  days  or  weeks.  To  spasmodic  conditions  in 
the  muscles  of  the  pharynx  and  oesophagus  we  refer  the  well-known  symptom  of 
so-called  globus  hystericus :  the  patients  feel  as  if  a  ball  were  moving  up  and 
down  in  the  throat. 

We  sometimes  see  spasmodic  conditions  which  come  on  in  a  clonic  fashion,  or 
in  single  twitchings  in  this  or  that  muscular  territory ;  sometimes  affect  sym- 
metrical groups  of  muscles;  are  not  associated  with  disturbances  of  consciousness; 
cease  during  sleep,  and  are  often  easily  cured  by  appropriate  mental  treatment. 
Such  conditions  have  been  described  under  special  names  as  special  diseases — 
electrical  chorea,  paramyoclonus  multiplex,  or  myoclonia.  In  our  opinion,  most 
of  these  cases,  if  not  all,  are  undoubtedly  hysterical  (see  pages  573  and  576). 

General  Course  of  the  Disease. — Our  description  of  the  symptomatology  of  hys- 
teria has  been  confined  to  the  most  important  and  frequent  phenomena;  and  yet 
even  this  meager  outline  shows  what  an  infinite  variety  of  shapes  the  disease 
assumes.  1.  In  one  class  of  cases  there  are  no  severe  symptoms  whatever.  The 
patient  merely  displays  the  general  mental  condition  characteristic  of  hysteria: 
she  is  easily  excited,  prone  to  make  much  of  her  ills,  has  all  sorts  of  symptoms, 
such  as  pain,  palpitation,  dyspepsia,  and  dyspnoea,  and  these  are  aggravated  by 
mental  excitement,  while  at  other  times  they  may  so  nearly  vanish  that  the  patient 
does  not  appear  to  be  ill.  2.  A  second  class  of  cases  has  more  severe  disturbance, 
coming  on  after  some  unfavorable  psychical  influence.  The  patient  may  have 
displayed  a  general  hysterical  tendency  previously,  or  may  have  seemed  perfectly 
well.  Here  we  may  observe  all  the  symptoms  above  enumerated  and  described. 
There  may  be  paralysis,  spasm,  contracture,  anaesthesia,  or  paresthesia.  The  indi- 
vidual symptoms  may  persist  obstinately  for  weeks  and  months;  but  again  they 
may  vanish  on  a  sudden  or  give  place  to  other  disturbances.  Psychical  influences 
are  unmistakably  potent,  not  merely  in  the  incipient  stage  but  also  in  the  further 
course  of  the  disease.  Any  aggravation  of  the  symptoms  is  usually  referable  to 
emotional  excitement.  This  is  particularly  true  of  the  hysterical  convulsions. 
In  many  cases,  almost  every  fresh  paroxysm  is  due  to  anger,  terror,  or  some  simi- 
lar cause.  3.  The  third  class  comprises  the  most  severe  forms  of  hysteria,  with 
those  nervous  disturbances  briefly  outlined  above.  They  are  as  complicated  as 
they  are  puzzling,  and  form  manifold  combinations  with  all  the  other  hysterical 
phenomena,  including  anaesthesia,  contracture,  and  paralysis. 

The  entire  duration  of  the  disease  varies  greatly.     The  true  root  of  all  evil  is 


HYSTERIA.  811 

the  abnormal  excitability  of  the  nervous  system,  which  always  remains  in 
unstable  equilibrium;  and  often  it  is  not  possible  to  cure  tliis.  If  not,  the  trouble 
lasts  almost  indefinitely.  New  manifestations  of  the  disease  succeed  to  periods  of 
apparently  perfect  health.  Usually  the  symptoms  do  not  abate  till  quite  late  in 
life.  There  are,  however,  many  instances  of  complete  and  permanent  relief. 
This  favorable  termination  is  more  especially  to  be  hoped  for  where  the  patient 
comes  into  suitable  and  appropriate  conditions  of  life,  having  some  regular  occu- 
pation which  is  not  exposed  to  all  sorts  of  unfavorable  psychical  influences.  Many 
cases  of  hysterical  disturbance,  in  previously  healthy  children  or  young  adults, 
and  due  to  some  distinct  cause,  terminate  comparatively  soon,  and  never  recur. 
It  is  never  possible,  however,  to  be  sure  that  there  will  be  no  relapse,  inasmuch  as 
a  single  appearance  of  hysteria  shows  unmistakably  that  the  nervous  system  is 
abnormally  vulnerable  to  external  impressions  and  the  mental  emotions  excited 
by  them. 

Diagnosis. — An  experienced  physician  is  seldom  greatly  puzzled  by  hysterical 
affections.  Although  the  disease  may  at  first  simulate  some  grave  organic  disor- 
der, a  careful  physical  examination  and  continued  observation  will  almost  invari- 
ably disclose  the  true  character  of  the  case.  In  the  first  place,  there  are  never 
any  such  symptoms  as  would  absolutely  prove  the  existence  of  some  organic 
lesion.  For  example,  we  never  find  atrophy  or  loss  of  electrical  reaction  in  con- 
nection with  hysterical  paralysis.  Secondly,  many  symptoms  are  characteristic 
of  hysteria  and  are  never  seen  in  any  other  disease.  Such  are  numerous  forms 
of  convulsions,  and  hemianassthesia  with  amblyopia  of  one  eye.  Above  all,  we 
should  regard  the  whole  psychical  behavior  of  the  patient,  the  influence  exerted 
upon  her  by  emotional  disturbances,  and  the  aetiology  of  the  illness — for  instance, 
if  caused  by  some  mental  excitement  or  emotion.  The  discovery  of  specific  hys- 
terical symptoms,  the  so-called  hysterical  stigmata,  sensory  anaesthesias,  hyster- 
ogenous  zones,  etc.,  are  especially  important.  Many  symptoms  of  hysteria,  espe- 
cially certain  forms  of  spasm  and  hemianesthesia,  are  in  themselves  so  character- 
istic that  from  them  alone  a  correct  diagnosis  can  be  made. 

Treatment. — What  has  been  said  about  the  aetiology  of  hysteria  at  once  sug- 
gests a  possible  method  of  prophylaxis.  A  watchful  eye  will  often  detect,  even  in 
childhood,  the  signs  of  abnormal  nervous  excitability,  and  in  such  a  case  the 
parent  will  make  it  his  duty  to  impose  a  suitable  physical  and  mental  regimen, 
that  graver  disturbances  may  be  averted. 

If  hysteria  be  already  developed,  the  first  and  most  important  treatment  is 
mental.  There  could  be  no  greater  mistake  than  to  deride  the  patient  or  treat 
her  as  a  malingerer ;  for  hysteria  is  a  disease,  and  its  symptoms  are  just  as  inde- 
pendent of  any  conscious  volition  on  the  part  of  the  patient  as  those  of  any  other 
disease.  It  is,  however,  absolutely  essential  to  carry  out  the  moral  training, 
which  the  physician  must  institute  with  all  the  proper  strictness  and  energy, 
because  in  this  way  alone  can  any  good  be  accomplished.  Sometimes  this  most 
important  indication  can  be  fulfilled  only  after  the  patient  has  been  withdrawn 
from  the  over-anxious  and  over-assiduous  parents  or  relatives,  and  like  unfavor- 
able influences.  In  such  cases,  treatment  in  some  institution  will  often  be  vastly 
better  than  the  best  care  at  home ;  and  our  own  experience  leads  us  to  recommend 
most  urgently  that  the  eventual  necessity  o.f  removal  to  an  asylum  should  be 
constantly  borne  in  mind  with  regard  to  aggravated  cases.  Often  the  mere  dread 
of  removal  to  such  a  place  has  a  favorable  mental  influence. 

Proper  moral  treatment  achieves  comparatively  the  best  results  where  there  is 
hysterical  paralysis.  When  we  are  once  certain  that  the  paralysis  is  due  to 
hysteria,  the  patient  must  be  instructed  how  to  regain  by  practice  the  lost  power 
of  the  will  over  the  paralyzed  muscles.     If  the  paralysis  affect  the  lower  extremi- 


812  DISEASES  OF  THE  NERVOUS  SYSTEM. 

ties,  as  it  usually  does,  the  patient  must  be  set  on  her  feet,  regardless  of  all  her 
opposition  and  complaints,  and  kindly  but  most  firmly  required  to  try  to  walk. 
Of  course,  at  first  she  must  be  well  supported.  This  exercise  must  be  methodically 
gone  through  with  several  times  a  day.  Gradually  the  patient's  gait  becomes 
more  and  more  secure.  She  regains  confidence  in  her  own  ability,  and,  having 
once  begun  to  improve,  visually  makes  rapid  progress  toward  complete  recovery. 
Every  experienced  physician  can  recall  numerous  instances  where  hysterical 
paralysis  which  had  lasted  weeks  and  months  was  cured  in  a  few  days  by 
tbis  mode  of  treatment.  Faradization  of  the  muscles,  cold  sponging,  with  friction 
and  bathing,  are  excellent  adjuvants;  and  the  disagreeable  element  in  these  pro- 
cedures of  itself  stimulates  the  patient  to  make  every  possible  exertion  to  regain 
the  use  of  her  limbs. 

When  tbere  is  hysterical  paralysis  of  the  vocal  cords,  a  similar  training  will 
be  found  both  practicable  and  efficient.  Electricity  is  also  of  great  value.  It  may 
be  applied  externally  or  within  the  larynx.  Often  tbe  patient,  terrified  by  the 
sudden  pain  it  causes,  recovers  her  voice  at  once. 

The  treatment  of  hysterical  contractures  consists,  first,  in  an  effort  to  loosen 
up  the  contracture  by  massage  and  energetic  passive  motion.  Faradism  will  be 
found  of  assistance  here  also.  In  order  to  maintain  the  ground  thus  gained,  the 
patient  must  be  induced  to  exercise  the  muscles  regularly  by  making  voluntary 
movements. 

The  treatment  of  hysterical  spasmodic  conditions  often  causes  greater  difficul- 
ties. In  many  cases  a  sharp  sensory  irritation,  douching  with  cold  water,  or  a 
cold  bath  with  cold  shower-bath,  suffices  to  restore  the  energy  of  the  patient's 
will,  which  is  necessary  to  regain  control  over  the  muscles  and  thus  check  the 
spasms.  The  dread  of  the  repetition  of  the  bath  does  its  part  in  warning  the  pa- 
tients from  giving  themselves  up  unresistingly  to  a  repetition  of  the  attack.  The 
electric  current  (strong  faradism  during  the  attack)  may  also  act  favorably  in  the 
same  way.  The  action  of  such  measures,  however,  very  often  gradually  weakens, 
the  patients  become  accustomed  to  the  cold  baths,  and  they  remain  without 
effect. 

The  milder  varieties  of  hysterical  convulsion,  such  as  hysterical  hiccough  or 
cough,  are  often  controlled  by  a  stern  reproof.  It  is  precisely  in  these  cases  that 
the  moral  effect  of  transfer  to  some  institution  frequently  causes  the  abrupt  disap- 
pearance of  symptoms  which  have  lasted  for  months.  The  severe  hysterical 
attacks  are  often,  of  course,  peculiarly  obstinate,  and  they  may  resist  for  months, 
and  even  years,  the  most  intelligent  treatment. 

Hysterical  anaesthesia  is  best  treated  with  the  faradic  wire-brush.  Tbis  vigor- 
ous irritation  restores  the  anaesthetic  parts  to  the  domain  of  consciousness.  It 
should  be  said,  however,  that  these  cases  may  prove  obstinate  or  relapse. 

The  most  difficult  of  all  hysterical  cases  to  treat  are  those  where  the  symptoms 
are  not  strongly  pronounced,  but  where  there  is  a  general  hysterical  condition,  ex- 
pressing itself  in  a  multitude  of  nervous  derangements,  such  as  palpitation,  dyspep- 
sia, and  general  debility,  or  in  purely  subjective  symptoms,  or  in  emotional  tend- 
encies. Such  patients  are  often  advanced  in  years,  so  that  little  is  to  be  hoped 
for  from  moral  training;  and  their  circumstances  may  be  unfavorable  without 
our  being  able  to  remedy  the  situation.  Even  here,  however,  the  physician  may 
greatly  benefit  the  patient  by  means  of  psychical  influences,  if  he  once  gains  her 
complete  confidence.  It  will  also  be  found  advantageous  to  employ  such  remedies 
as  invigorate  the  nervous  system  (see  the  next  chapter) ;  electricity  should  be 
given,  either  in  the  form  of  general  faradization,  or  the  faradic  brush  applied  to  the 
back  and  shoulders,  or  the  galvanic  current  applied  to  the  spinal  column  and  the 
sympathetic  nerve ;  and  of  still  greater  importance  is  a  methodical  cold-water  treat- 


HYSTERIA.  813 

ment,  either  by  sponging,  or  bathing,  or  douches.     Such  patients  are  often  vastly 
improved  by  sea-bathing  in  summer,  or  by  going  to  the  mountains. 

The  numerous  internal  remedies  for  hysteria  are  also  of  more  use  in  these 
general  conditions  than  where  there  are  marked  nervous  disturbances  in  special 
parts  of  the  body.  In  the  latter,  internal  remedies  do  good  only  indirectly  and 
subjectively,  and  about  in  proportion  to  the  confidence  of  the  patient  in  the  vir- 
tues of  the  medicine.  This  is  the  explanation  of  the  frequent  cases  of  rapid 
recovery  after  taking  homoeopathic  and  "  electro-homceopathic "  remedies,  and 
those  still  more  marvelous  cures  effected  by  means  of  holy  water  and  relics. 

Among  the  "antihysterical "  agents  contained  in  our  medical  thesaurus,  asafceti- 
da,  valerian,  and  castoreum  are  the  most  famous:  but  probably  few  would  at  the 
present  day  claim  that  they  possess  any  specific  virtues.  Perhaps  the  preparations 
of  valerian  are  the  most  useful  where  there  is  hysterical  excitement,  as  evinced  by 
convulsions  or  palpitation.  Bromide  of  potassium,  arsenic,  and  other  medicines 
which  ordinarily  exert  a  favorable  influence  upon  the  nerves,  seldom  accomplish 
any  permanent  good  in  hysteria,  although  often  prescribed.  Narcotics  do  little 
good,  and  may  do  much  harm.  It  is  easy  to  develop  the  morphine  habit  in  such 
patients. 

If  hysteria  be  Complicated  by  some  actual  oi"ganic  disease,  the  latter,  of  course, 
demands  special  treatment.  Great  benefit  is  hoped  for  by  many  from  the  cure  of 
any  uterine  complaint  which  may  be  present.  Cases  are  known  where  grave  hys- 
terical disturbance  has  vanished  upon  dilatation  of  a  constricted  cervical  canal  or 
rectification  of  a  displacement;  but  there  are  numerous  other  instances  on  record 
where  gynaecological  treatment  has  proved  entirely  unavailing.  It  may  also  be 
questioned  whether,  in  the  successful  cases,  the  main  benefit  was  not  due  to  sub- 
jective influences.  Hegar  has  removed  the  ovaries  in  a  few  severe  cases,  but  the 
operation  is  not  yet  fully  established.  At  any  rate,  it  is  justifiable  only  when  the 
ovaries  are  known  to  be  in  an  abnormal  condition.  Friedreich  claims  to  have  had 
excellent  results  from  energetic  cauterization  of  the  clitoris.  We  do  not  believe 
that  in  this  he  will  have  many  imitators. 

In  general,  we  may  certainly  maintain  that  all  methods  of  treatment  of  hys- 
teria are  efficient  only  when  associated  with  the  necessary  psychical  factor.  Hence 
any  prescription,  no  matter  how  senseless  it  seems,  may  have  the  greatest  effect 
as  soon  as  the  patient  "'  believes  in  it " — that  is,  as  soon  as  the  psychical  action  of 
this  belief  is  manifest.  Hence  we  may  say  that  in  hysteria,  as  a  rule,  treatment 
either  produces  rapidly  a  brilliant  success  or  ic  has  no  effect  at  all. 

We  must  here  mention  two  methods  of  treatment  which  have  lately  been  much 
discussed — metallotherapy  and  treatment  by  hypnosis. 

In  regard  to  metallotherapy  a  French  physician,  named  Burq,  discovered 
years  ago  that  by  laying  plates  of  metal  upon  a  cutaneous  surface  affected  by  hys- 
terical anaesthesia  a  remarkable  result  is  sometimes  produced.  Almost  at  once 
sensation  is  restored  to  the  immediate  region,  and  often  to  a  much  larger  area. 
Most  of  the  cases  have  been  those  of  hysterical  hemianaesthesia.  It  is  not  every 
kind  of  metal  which  will  prove  effective,  nor  will  the  same  kind  affect  all  patients. 
It  is  said  that  iron  is  most  frequently  efficient ;  but  sometimes  copper,  zinc,  or  gold 
is  required.  The  process  of  determining  the  metal  essential  to  each  individual 
case  Burq  called  "  metalloscopy  " ;  and  he  stated  that  this  metal  would  also  have 
the  same  effect  if  given  internally !  In  1876  a  committee  appointed  by  the  Pari- 
sian Societe  de  Biologie  tested  these  statements,  at  least  with  regard  to  the  external 
application  of  metals — the  idea  of  their  internal  administration  having  been  pretty 
much  abandoned — and  confirmed  them.  Charcot  also  discovered  manv  remarkable 
facts  of  a  similar  nature,  which  likewise  soon  received  universal  substantiation. 
The  most  remarkable  of  these  phenomena  is  known  as  transfer.     The  return  of 


814  DISEASES  OF  THE  NERVOUS  SYSTEM. 

sensation  to  the  anaesthetic  area,  as  a  result  of  applying  a  metal  plate,  is  accom- 
panied by  a  simultaneous  development  of  anaesthesia  upon  the  opposite,  pre- 
viously normal  side,  in  an  exactly  corresponding  place.  Sometimes  sensation 
oscillates  from  one  side  to  the  other  and  back  again,  so  that  now  one  half  of  the 
body  and  now  the  other  is  alternately  sensitive  or  anaesthetic.  If  the  metal  be 
placed  at  the  start  upon  the  normal  skin,  that  part  becomes  anaesthetic,  while  the 
corresponding  part  upon  the  opposite  side  of  the  body  regains  its  former  normal 
condition. 

It  has  also  been  discovered  that  other  hysterical  symptoms  exhibit  analogous 
phenomena.  Transfer  can  sometimes  be  observed  in  hysterical  amblyopia,  achro- 
matopsia, deafness,  loss  of  smell  and  taste,  contractures,  and  paralysis.  Such 
transfers  may  be  induced  by  various  means  other  than  metal  plates.  These  are 
classed  as  aesthesiogenous  remedies,  and  include  large  magnets,  feeble  galvanic 
currents,  and  static  electricity.  Vibrating  tuning  forks  and  sinapisms  have  also 
produced  similar  results.  Hence  it  seems  to  us  to  be  an  undoubted  conclusion 
that  the  whole  of  the  group  of  symptoms  just  described  has  no  peculiar  place. 
They  are  simply  the  results  of  suggestion,  produced  once  more  by  ideas.  The 
similarity  of  the  test  as  performed  by  the  physician  produces  the  similarity  of  the 
symptoms  that  ensue. 

Of  late  the  treatment  of  hysteria  by  hypnosis  has  acquired  a  far  greater  prac- 
tical significance  than  metallotherapy ;  it  is  a  mode  of  treatment  which  has  been 
practiced  most  extensively  by  the  "  school  of  Nancy "  (Bernheim).  If,  during 
hypnosis,  morbid  states  can  be  produced  by  suggestion,  it  naturally  follows  that 
morbid  states  can  also  be  cured  by  suggestion.  If  by  many  well-known  successes 
the  hypnotizing  physician  has  at  the  outset  acquired  the  patient's  confidence,  as 
relics  have  the  confidence  of  believers,  the  most  beautiful  results  can  of  course  be 
attained  in  this  way.  There  is  no  special  peculiar  principle  in  the  hypnotic  treat- 
ment. Any  other  efficient  mode  of  treating  hysteria  rests  on  the  same  conditions  and 
pi'esumptions.  Hypnosis  has  only  the  one  great  consequence,  that  it  is  artificially 
produced  as  a  severe  abnormal  mental  state  in  a  patient  who  previously  had  not 
spontaneously  falien  into  this  state.  In  that  lies  the  sequel,  which  of  course  need 
not  always  be  permanent,  but  which  often  enough  has  been  most  severe:  the 
attempt  to  hypnotize  a  patient  who  is  suffering  from  a  slight  hysterical  affection 
has  not  infrequently  been  followed  by  the  onset  of  a  severe  hysterical  attack. 
The  mischance  will  seldom  happen  to  the  physicians  and  magnetizers  who  prac- 
tice hypnotism  as  a  specialty,  because  their  psychical  influence  on  their  patients 
is  usually  greater  from  the  outset;  but  we  should  consider  it  a  misfortune  if 
hypnosis  should  come  into  too  general  use.  That  in  this  way  apparently  the 
most  wonderful  cures  can  often  be  obtained,  is  perfectly  wTell  established  and  not 
at  all  surprising;  but  the  same  cures  can  also  be  obtained  in  other  ways,  with- 
out running  the  risk  of  producing  first  that  of  which  you  would  cure  your  patient, 
for  to  hypnotize  means  to  make  hysterical.  Furthermore,  it  is  not  hard  to 
prophesy  that,  as  the  knowledge  of  the  peculiar  nature  of  hypnosis  becomes  gen- 
eral, it  will  lose  its  halo  with  the  patient,  and  with  that  it  will  lose  its  healing 
power. 


NEURASTHENIA.  815 

CHAPTER  X. 

NEURASTHENIA. 

(Nervous  Debility.) 

When  studying  the  disorders  of  the  spinal  cord,  it  will  be  remembered  that  we 
found  one  group  of  symptoms  which  did  not  rest  upon  any  discoverable  anatomical 
basis,  but  which  were  merely  functional  (vide  page  G05).  In  some  part  due  to  abnor- 
mal excitability  of  the  nervous  system,  but  mainly,  however,  the  result  of  impaired 
vigor,  this  condition  was  denominated  "nervous  weakness."  Perfectly  analogous 
phenomena  may  originate  in  the  brain,  and  are  named  cerebral  neurasthenia,  in 
contrast  with  spinal  neurasthenia.  In  most  instances  we  meet  with  both  cerebral 
and  spinal  symptoms,  and  must  therefore  call  the  disease  cerebro-spinal,  or  general, 
neurasthenia. 

The  American  neurologist  Beard  was  the  first  to  recognize  the  importance  of 
this  disease  and  to  give  it  its  present  name.  Beard  was  at  first  inclined  to  believe 
that  neurasthenia  was  mainly  an  "  American  disease  " ;  but  this  is  by  no  means 
the  case,  inasmuch  as  sufferers  from  neurasthenia  form  a  very  important  contin- 
gent among  the  patients  of  German  specialists.  Neurasthenia  is  certainly  one  of 
the  most  frequent  and  important  nervous  diseases  from  a  practical  standpoint,  nor 
is  its  study  by  any  means  devoid  of  scientific  interest. 

Causation. — A  full  list  of  the  causes  of  neurasthenia  would  include  almost  all 
those  influences  which  in  any  way  act  unfavorably  upon  the  nervous  system. 
Most  of  these  have  been  enumerated  on  page  606.  Where  the  disease  is  mainly 
of  the  cerebral  form,  excessive  brain-work  contributes  very  largely  to  its  produc- 
tion, particularly  when  combined  with  certain  kinds  of  excitement.  The  mer- 
chant is  liable  to  it,  whose  bold  ventures  subject  him  to  deep  anxiety  and  eager 
hope;  and  the  politician,  who  is  incessantly  agitated  by  party  strifes;  and  like- 
wise the  artist  or  scholar,  whose  ambition  gives  him  no  rest.  In  all  these  cases 
the  nervous  system  finally  becomes  exhausted— that  is,  neui'asthenia  is  established. 
Even  here,  however,  neuropathic  tendencies  come  into  play,  for  some  are  crushed 
by  a  burden  which  others  can  bear.  In  very  many  instances  this  liability  to  the 
disease  is  inherited;  in  others  it  is  acquired  (vide  page  606). 

As  was  mentioned  under  spinal  neurasthenia,  hypochondria  frequently  assumes 
an  important  role  in  these  cases.  It  not  only  exaggerates  the  existing  symptoms, 
but  it  contributes  others  of  its  own.  In  this  we  find  one  essential  difference  be- 
tween neurasthenia  and  genuine  hysteria.  In  the  latter,  however  much  com- 
plaint there  may  be,  a  genuine  hypochondriacal  tendency  is  extremely  rare. 
Hypochondria  becomes  even  the  essential  factor  in  those  melancholy  forms  of 
neurasthenia  which  so  often  result  from  onanism  or  other  sexual  abuses.  This 
same  element  is  also  probably  the  main  one  in  the  strikingly  frequent  cases  of 
neurasthenia  in  physicians. 

The  symptoms  of  spinal  neurasthenia  have  been  already  briefly  described,  so 
that  we  may  here  confine  our  remarks  chiefly  to  the  still  more  important  cerebral 
symptoms.  Most  frequent  among  these  is  a  subjective  sensation  of  pressure  in 
the  head.  Patients  give  a  very  various  description  of  this  sensation.  Essentially, 
however,  it  is  a  feeling  of  pressure  and  numbness,  and  makes  the  patient  doubt 
whether  he  is  in  the  full  possession  of  his  intellectual  powers.  The  pressure  is 
sometimes  chiefly  frontal  and  sometimes  occipital ;  it  may  rise  to  the  height  of 
actual  pain,  this  being  frequently  associated  with  marked  hypereesthesia  of  the 
scalp. 

Associated  with  this  pressure  there  is,  as  we  have  just  intimated,  in  many  cases 
a  sense  of  incapacity  for  any  methodical  intellectual  effort,  an  intellectual  debility 


816  DISEASES  OF  THE  NERVOUS  SYSTEM. 

often  rendering  the  patient  entirely  incapable  of  performing  the  duties  of  his 
vocation.  He  can  no  longer  write  or  read  for  any  length  of  time,  these  pursuits 
being  further  interfered  witb,  in  some  cases,  by  a  feeling  of  weakness  and  pressure 
in  the  eyes  themselves  (neurasthenic  asthenopia).  A  very  important  symptom  is 
loss  of  sleep.  This  symptom  is  in  many  cases  the  most  annoying  of  any,  and 
makes  the  patient  importunate  for  relief.  There  is  almost  sure  to  be  depression  of 
spirits ;  the  patient  does  not  believe  that  he  will  ever  recover,  and  gives  voice  to 
the  most  melancholy  predictions.  Beard  has  called  attention  to  peculiar  condi- 
tions of  anxiety  sometimes  observed  in  neurasthenic  patients.  Tbe  sufferer  dreads 
to  go  into  society,  or  to  mingle  with  a  crowd,  or  to  be  subjected  to  any  physical 
jar.     Vertigo  is  also  frequent,  but  is  rarely  very  severe. 

The  lack  of  intellectual  energy  is,  in  most  cases  of  any  severity,  accompanied 
by  decided  bodily  weakness.  This,  too,  would  often  seem  to  be  of  cerebral  origin, 
and  consequent  upon  deficient  innervation  of  the  muscles  by  the  nervous  centers. 
The  patient  can  not  walk  far  without  becoming  weary,  is  incapable  of  any  great 
manual  effort,  and  in  some  cases  feels  so  weak  that  he  does  not  like  to  leave  his 
chamber,  and  passes  most  of  his  time  in  bed  or  on  the  sofa.  The  various  bodily 
functions  may  be  interfered  with.  The  appetite  is  diminished,  the  bowels  consti- 
pated, the  skin  is  dry,  and  the  circulation  feeble  in  the  extremities,  so  that  there  is 
in  many  cases  constant  complaint  of  cold  hands  and  feet.  Sometimes  the  secre- 
tions are  increased  in  amount  rather  than  diminished.  There  is  salivation  or  pro- 
fuse perspiration.  There  may  also  be  palpitation  of  nervous  origin.  [In  most 
cases  of  neurasthenia  there  is  defective  metabolism.  The  urine  is  scanty,  the  uric 
acid  increased  relatively  to  the  urea,  and  in  sexual  neurasthenia  there  may  be  an 
excess  of  indican.     Many  neurasthenics,  however,  drink  very  little. — K.] 

There  are  numerous  other  nervous  phenomena  occasioned  by  neurasthenia, 
which  we  need  not  here  describe  with  great  minuteness.  Some  of  them  are  most 
marked  in  the  "spinal  form"  of  the  disease;  such  are  pain  in  the  back,  spinal 
irritation,  paresthesia  and  pain  in  the  extremities,  and  sexual  derangements. 
Sometimes,  however,  these  symptoms  appear  to  be  rather  of  psychical — that  is,  of 
cerebral — origin.  Nervous  dyspepsia  is  frequently  conjoined  with  neurasthenia; 
it  has  already  been  described  on  page  400. 

The  general  course  of  the  disease  is  almost  always  chronic.  In  the  milder 
cases  there  is  little  outward  evidence  of  derangement;  the  patient  endeavors  to 
hide  his  troubles,  as  his  indefinite  symptoms  seldom  gain  much  sympathy,  and  are 
apparently  contradicted  by  his  well-nourished  and  healthy  appearance.  In  the 
severe  cases,  however,  the  patient's  vigor  is  so  much  impaired  that  the  disease 
acquires  a  grave  aspect  even  for  others  than  the  patient,  and  fills  them,  as  well  as 
him,  with  infinite  anxiety.  The  course  of  the  disease  is  apt  to  be  varied  by  alter- 
nate improvement  and  relapse. 

Prognosis. — It  is  difficult  to  make  a  general  statement  as  to  the  termination  of 
cases  of  neurasthenia.  The  disease  is  never  actually  dangerous,  nor  does  its  exist- 
ence often  prepare  the  way  for  more  severe  secondary  nervous  disease.  And  yet 
the  nervous  constitution  of  many  neurasthenic  patients  is  such  that  complete 
recovery  can  not  be  attained.  There  are,  however,  numerous  cases,  especially 
such  as  have  resulted  from  a  special  exciting  cause,  which  can  be  removed,  where 
permanent  and  complete  recovery  ensues.  In  other  cases  the  symptoms  can  be 
so  far  abated  that  the  patient  is  practically  well,  although  not  entirely  free  from 
discomfort. 

Diagnosis. — Neurasthenia  can  usually  be  detected  without  difficulty,  •  but  the 
establishment  of  the  diagnosis  requires  the  exclusion  of  organic  lesions  of  the 
nervous  system.  Every  case,  therefore,  must  be  submitted  to  a  thorough  and 
careful  examination.     Grave  cerebral  diseases,  such  as  incipient  tumors  or  general 


NEURASTHENIA.  Si  7 

paralysis,  have  been  repeatedly  mistaken  for  neurasthenia.  One  important  point 
in  diagnosis  is  the  aetiology,  including  both  the  outward  circumstances  and  the 
presence  or  absence  of  a  constitutional  predisposition  to  nervous  diseases.  Hys- 
teria has  certainly  many  points  in  common  with  neurasthenia,  but  it  is  essentially 
an  entirely  different  disease.  In  neurasthenia  we  find  none  of  those  innumerable 
localized  nervous  disturbances  which  we  saw  in  the  preceding  chapter  to  be  so 
well  marked  in  hysteria;  nor  do  we  ever  observe  in  neurasthenia  that  rapid  onset 
and  sudden  disappearance  of  the  symptoms,  nor  their  abrupt  development  as  a 
consequence  of  some  violent  emotional  excitement.  A  severe  case  of  neurasthenia 
is  decidedly  the  graver  disease  of  the  two,  at  least  in  this  sense,  that  it  represents 
a  far  more  profound  functional  disturbance  of  the  nervous  system  than  does  hys- 
teria. On  the  other  hand,  certain  special  symptoms,  such  as  convulsions  or 
paralysis,  may  be  more  severe  in  hysteria  than  in  neurasthenia. 

Treatment. — As  in  hysteria,  so  also  in  neurasthenia,  moral  treatment  is  of 
prime  importance;  but  here  it  must  be  of  a  different  kind  than  in  hysterical 
cases.  The  neurasthenic  requires  sympathy.  He  must  be  repeatedly  examined 
by  the  physician.  Every  fresh  examination,  at  the  end  of  which  the  physician 
is  able  to  assure  him  of  the  absence  of  any  serious  objective  change,  has  a  most 
quieting  and  beneficial  effect  upon  the  patient.  In  so  far  as  hypochondriasis  is  a 
prominent  symptom,  this  moral  influence  may  alone  restore  the  patient  to  health. 

Where  the  neurasthenia  rests  on  some  other  basis  than  mere  hypochondriasis 
we  must,  in  addition  to  moral  treatment,  employ  remedies  which  have  a  tendency 
to  invigorate  the  entire  nervous  system.  In  order  to  bring  about  any  permanent 
improvement,  the  treatment  must  be  methodical  and  long  continued,  so  that  the 
patient  may  remain  under  the  personal  influence  of  the  physician  for  a  consider- 
able length  of  time.  Moral  training  is  always  an  important  and  indeed  an  essen- 
tial part  of  the  treatment  of  nervous  debility. 

.  In  any  methodical  course  of  treatment,  regimen  is  of  great  importance.  The 
rules  laid  down  must  be  carefully  adapted  to  the  special  circumstances  of  each 
individual.  Severe  mental  labor  must  be  forbidden,  and  mental  excitement 
avoided.  The  diet  depends  upon  the  individual  case.  For  a  corpulent  patient, 
treatment  calculated  to  diminish  obesity  will  sometimes  be  followed  by  decided 
improvement  in  the  general  condition  and  in  bodily  vigor.  In  those  frequent 
instances  where  the  patient  is  pale  and  thin,  and  very  likely  oppressed  by  nervous 
dyspepsia  (see  page  400),  we  should,  on  the  other  hand,  make  vigorous  efforts  to 
improve  nutrition.*  Definite  instructions  must  be  given  in  order  that  the  patient 
may  ingest  a  proper  amount  of  food.  Milk,  butter,  fresh  meat,  eggs,  and  simple 
puddings  are  appropriate  articles  of  diet.  Often  the  weight  and  strength  both 
improve  rapidly.  Any  large  amount  of  alcohol  or  of  tobacco  should  be  forbidden. 
Tea  and  coffee  may  be  taken  in  moderation,  if  the  patient  is  accustomed  to  then' 
use.  In  regard  to  bodily  exercise,  we  must  again  be  guided  by  the  condition  of 
the  individual.  We  would  most  earnestly  warn  the  physician  from  the  error, 
frequently  committed,  of  driving  weakly  and  debilitated  persons  to  take  long 
walks.  For  such,  bodily  rest  is  much  more  desirable;  and  fresh  air  may  be 
enjoyed  at  the  same  time,  if  the  patient  sits  out  of  doors  or  drives.  The  sluggish 
and  corpulent,  on  the  other  hand,  often  require  an  increased  amount  of  exercise. 


*  Playfair,  Weir  Mitchell,  and  certain  other  neurologists,  have  built  up  a  special  "method"  of 
treating  neurasthenia  and  allied  conditions  of  nervous  exhaustion;  this  consists  in  "overfeeding"  the 
patient — that  is,  in  introducing  as  large  an  amount  of  nourishment  as  possible  into  the  system  at  the 
same  time  that  complete  bodily  and  mental  rest  is  secured.  Faradic  electricity  and  massage  are  also 
daily  employed.  This  mode  of  procedure  is  certainly  excellent  in  many  cases,  but  it  must  not  be 
regarded  as  universally  applicable.  There  are  cases  of  neurasthenia  for  which  it  is  not  suitable. 
52 


818  DISEASES  OF  THE  NERVOUS  SYSTEM. 

It  is  a  good  plan  in  many  instances  to  employ  the  Swedish  movement  cure,  or 
similar  gymnastic  exercises. 

Less  general  remedies  are  electricity  and  hydropathic  treatment.  Electricity 
is  warmly  praised  by  many  patients.  The  galvanic  current  is  generally  employed, 
and  is  applied  either  over  the  sympathetic  nerve  or  along  the  spinal  cord.  Its 
use  demands  great  caution.  The  current  should  not  be  too  strong,  and  there 
should  be  no  abrupt  changes  in  it.  Galvanism  applied  to  the  head  is  seldom 
well  borne.  Another  very  valuable  mode  of  treatment  was  first  practiced  by 
Beard  and  Rockwell,  and  consists  in  general  faradization.  The  patient  is  almost 
completely  stripped,  and  places  both  feet  upon  a  large,  flat  electrode,  wbile  the 
various  parts  of  tbe  body  are  stroked  with  another  large  sponge  electrode;  in 
place  of  this  second  electrode  the  u  electrical  hand  "  of  the  physician  may  be  em- 
ployed. The  physician  takes  the  second  electrode  in  his  left  hand  and  allows  the 
current  to  pass  through  his  own  body.  Various  institutions  have  lately  begun 
to  employ  electrical  baths;  these  also  often  seem  to  produce  good  results.  In 
addition  to  peripheral  galvanization  and  faradization  of  the  nerves  and  muscles,  it 
is  also  advantageous  to  employ  the  faradic  wire-brush,  particularly  on  the  back 
of  the  neck,  along  the  spinal  column,  and  over  the  shoulders  and  thighs. 

The  hydro-therapeutic  treatment  may  be  quite  well  carried  out  at  the  patient's 
home,  but  a  severe  case  will  be  better  off  in  some  well-conducted  institution.  Cold 
sponging,  douches,  hip-baths,  lukewarm  baths  (or  swimming),  are  all  employed. 
Douches  must  not  be  applied  to  the  head.  If  there  is  sexual  disturbance,  hip-baths 
of  cold  water  are  advisable.  They  should  not  be  taken  at  night.  Douching  of  the 
genitals  and  loins  is  also  excellent.  Subsequently  sea-bathing  will  prove  extremely 
beneficial  for  many  patients.  "We  would  recommend  the  seashore  especially  for 
emaciated  and  anaemic  subjects,  who  are  frequently  greatly  benefited  by  the  im- 
proved appetite  and  rest  thus  obtained.  If  the  patient  be  well  nourished,  on  the 
other  hand,  a  journey  on  foot  through  the  mountains,  if  made  cautiously,  may  be 
very  valuable. 

In  neurasthenia,  internal  remedies  should  be  given  only  as  indicated  by  the 
symptoms.  If  there  is  anaemia,  iron,  quinine,  or  Fowler's  solution  is  prescribed; 
if  there  is  dyspepsia,  some  stomachics,  such  as  dilute  hydrochloric  acid,  pepsin,  or 
some  bitter.  The  constipation  should  be  overcome  mainly  by  diet.  A  valuable 
adjuvant  is  massage  of  the  abdomen ;  and,  indeed,  massage  is  coming  to  be  re- 
garded as  a  valuable  tonic  for  the  whole  system  where  there  is  nervous  disturbance. 
It  is  especially  appropriate  where  there  are  painful  sensations  in  the  nerves  and 
muscles,  and  may  here  be  combined  with  electricity.  When  there  are  vasomotor 
symptoms  (a  feeling  of  heat,  congestion,  palpitation),  we  often  prescribe  ergotine, 
four  to  six  one-grain  (grin.  0"05)  pills  a  day.  In  all  states  of  nervous  irritation 
bromine  preparations  are  much  used,  a  powder  of  potassic  and  sodic  bromides,  or 
bromine  water.  In  nervous  headaches,  and  also  in  other  nervous  states,  anti- 
pyrine  often  has  a  good  effect.    Antifebrine  and  phenacetine  act  in  the  same  way. 

The  treatment  of  the  wakefulness  which  results  from  neurasthenia  deserves  a 
brief  mention.  In  the  first  place,  we  would  warn  the  physician  against  the  abuse 
of  chloral  and  morphine.  The  attempt  should  always  first  be  made  to  secure 
sleep  by  a  rational  general  treatment,  or  by  some  less  injurious  remedies.  Often 
a  warm  bath  for  half  an  hour  at  bedtime  soothes  the  patient  and  brings  him 
sleep ;  and  in  other  cases  a  wet  cloth  laid  upon  the  head  or  back  of  the  neck  pro- 
duces the  same  favorable  result.  Patients  often  report  that  general  faradization 
at  bedtime  is  an  excellent  soporific.  Sometimes  a  moderate  dose  of  alcohol  is 
efficient— for  instance,  a  glass  of  beer  or  good  wine  taken  before  going  to  bed.  If 
none  of  these  means  avail,  our  next  resort  should  be  the  bromide  of  potassium. 
Very  likely  small  doses  of  this  have  only  a  subjective  effect,  but  there  can  be  no 


THE  TRAUMATIC  NEUROSES.  819 

doubt  that  a  large  dose,  say  about  a  drachm  (grm.  3-5)  in  a  glass  of  water,  does 
have  a  direct  tendency  to  produce  sleep.  We  may  also  mention  extract  of  can- 
nabis indica;  the  preparation  known  as  cannabinum  tannicum,  five  to  ten  grains 
(grm.  0'2-0-5);  paraldehyde,  about  a  drachm  (grm.  3-5)  at  night;  and  urethane, 
twenty  to  forty -five  grains  (grm.  1*5-3)  in  water  at  bedtime.  Paraldehyde  has  a 
very  disagreeable  taste.  Kast  has  lately  recommended  sulphonal,  twenty  to  thirty 
grains  (grm.  1/5-2)  in  a  large  amount  of  water,  in  soup  or  tea,  two  or  three 
hours  before  bedtime.  These  various  remedies  seldom  give  great  satisfaction. 
and  we  must  therefore  rely  mainly  on  general  treatment. 


CHAPTER  XL 
THE  TRAUMATIC   NEUROSES. 

As  an  appendix  to  the  last  two  chapters  on  hysteria  and  neurasthenia,  we  must 
now  speak  of  a  series  of  morbid  states  which  are  at  any  rate  closely  related  to  the 
above-mentioned  affections,  but  which  yet  show  certain  peculiarities.  We  have 
to  do  here  with  nervous  symptom-complexes  which  come  on  as  a  result  of  a  severe 
concussion  of  the  whole  body,  or  sometimes  after  a  more  circumscribed  injury  of 
a  definite  part  of  the  body,  and  hence  are  termed  "traumatic  neuroses."  By  the 
term  "neurosis"  we  would  imply  that  the  nervous  symptoms  produced  by  the 
trauma  do  not  depend  upon  coarse  material  injuries  of  the  nervous  system,  but 
upon  finer  changes  not  yet  made  out  anatomically. 

Considering  first  those  conditions  which  arise  from  severe  general  concussion 
of  the  body,  they  were  first  observed,  especially  after  railway  accidents,  by  English 
and  American  physicians,  and  given  the  name  of  "  railway  spine  "  or  "  railway 
brain."  It  was  soon  proven,  of  course,  that  precisely  the  same  morbid  symptoms 
may  arise  after  other  injuries. 

The  type  of  disease  is  very  characteristic.  Usually  the  original  trauma  (over- 
turn, collision,  etc.)  is  so  great  that  immediately  after  it  the  well-known  symptoms 
of  commotio  cerebri  or  commotio  spinalis  ensue  with  more  or  less  severity — loss 
of  consciousness,  general  paralysis  of  the  extremities,  collapse,  small  and  slow 
pulse,  cool  skin,  pallor  of  the  face,  dyspnoea,  vomiting,  retention  of  urine,  etc. 
Such  cases  may  terminate  fatally  in  a  few  hours  with  no  material  visible  change 
in  the  brain  or  cord  to  be  found  at  the  autopsy.  In  other  cases  the  first  severe 
shock  passes  off  and  a  series  of  objective  and  subjective  disturbances  remain,  which 
may  persist  for  a  long  time,  and  which  often  do  not  disappear  even  after  years  have 
passed.  It  is  these  subsequent  states  which  deserve  the  name  of  general  traumatic 
neurosis.  It  is  worthy  of  note  that  these  appear  not  only  after  severe  injuries, 
but  also  after  mild  ones  in  which  the  initial  symptoms  of  commotion  were  not 
especially  marked.  We  will  return  to  this  point  in  speaking  of  the  nature  of  the 
traumatic  neurosis. 

The  severe  initial  symptoms  of  commotion  cease  in  a  few  days,  or  even  sooner. 
The  patient  recovers,  tries  to  get  up,  and  the  improvement  goes  on  to  a  certain 
degree ;  but  a  number  of  symptoms  remain  which  do  not  disappear,  and  which 
diminish  or  wholly  take  away  the  victim's  capacity  for  work.  If  we  examine  such 
patients  we  find  no  signs  of  material  injury  either  in  the  nervous  system  or  in  any 
other  internal  organ.  What  first  strikes  us  is  a  peculiar  psychical  change.  The 
patients  are  dull,  depressed,  disinclined  to  any  occupation,  and  have  no  more 
pleasure  in  intercourse  with  their  families  and  friends.  They  brood  constantly 
over  their  accident  and  its  results.     The  sleep  is  disturbed  and  often  rendered  un- 


820  DISEASES  OP  THE  NERVOUS  SYSTEM. 

easy  by  dreams.  Of  other  subjective  symptoms  we  must  mention  especially  pains 
in  the  part  which  was  hurt ;  these  are  commonest  in  the  back,  the  sacral  region, 
the  sides  of  the  chest,  the  hips,  etc.  They  also  complain  of  headache,  vertigo, 
dullness,  dim  vision,  tinnitus,  spots  before  the  eyes,  loss  of  appetite,  etc.  Objective 
examination  often  shows  a  general  motor  weakness.  Many  patients  can  walk  quite 
well  alone,  but  they  are  soon  fatigued;  others  walk  only  slowly  and  stiffly  with 
support,  complaining  of  pain  in  the  back  on  walking,  and  therefore  holding  the 
hand  on  the  back,  etc.  The  nutrition  of  the  muscles  is  usually  good.  The  elec- 
trical excitability  of  nerves  and  muscles  is  completely  normal.  Examination  of 
the  sensibility  may  reveal  very  important  changes,  which  are  of  value  in  diag- 
nosis. This  examination  must  always  extend  to  all  the  sensory  organs.  The 
skin  over  almost  the  entire  body  is  often  very  insensitive  to  painful  irritations, 
pin-pricks,  the  electric  current,  etc.  There  is  analgesia.  In  some  places  we  find 
complete  anaesthesia,  which  may  affect  an  entire  extremity  or  only  circumscribed 
parts  of  the  extremities  and  the  trunk.  The  boundary  between  the  anaesthetic 
and  the  normally  sensitive  parts  is  usually  quite  sharply  defined,  and  the  arrange- 
ment is  often  very  peculiar.  Sometimes  the  skin  is  peculiarly  insensitive  to  cer- 
tain irritants  (heat,  cold,  etc.),  or,  on  the  other  hand,  it  is  peculiarly  sensitive. 
Examination  of  the  eyes  sometimes  shows  loss  of  visual  acuteness,  limitation  of 
the  visual  field,  and  imperfect  color  perception.  Very  often  the  hearing  is  poor 
on  one  or  both  sides.  The  smell  is  often  much  blunted,  and  the  taste  completely 
lost,  so  that  even  quinine,  vinegar,  and  similar  strongly  tasting  substances  no 
longer  excite  any  sensation  of  taste. 

Besides  the  symptoms  of  impairment  of  sensation  and  motion  just  described, 
we  often  find  also  symptoms  of  sensory  and  motor  irritation.  Pain  in  the  head, 
spots  before  the  eyes,  and  tinnitus,  have  been  mentioned  above.  Hyperesthesia  of 
the  skin  is  more  characteristic — tenderness  of  the  vertebral  column,  and  particu- 
larly great  tenderness  of  such  parts  of  the  body  as  were  most  affected  by  the  origi- 
nal injury.  Among  the  symptoms  of  motor  irritation  we  may  mention  muscular 
contraction  and  muscular  rigidity,  again  most  common  in  the  limbs  most  affected 
by  the  injury.  A  marked  tremor  is  also  very  common.  The  reflexes  differ  in 
different  cases ;  they  are  often  much  increased.  Among  the  trophic  changes  we 
may  mention  that  the  hair  may  turn  gray  or  fall  out.  Marked  muscular  atrophy 
occurs  only  in  the  more  local  traumatic  neuroses  {vide  infra). 

If  we  ask  after  the  cause  and  the  special  nature  of  this  peculiar  affection,  char- 
acterized chiefly  by  psychical  disturbances,  sensory  anaesthesia,  and  motor  weak- 
ness, two  chief  factors  are  to  be  considered.  First,  a  purely  physical  factor,  the 
concussion  of  the  nervous  system.  That  such  a  cause  can  produce,  without  coarse 
anatomical  injury,  the  severest  functional  injury  to  the  nervous  system,  is  beyond 
a  dotibt;  and  if  the  most  threatening  symptoms  can  come  on  immediately  after 
the  concussion,  it  is  certainly  not  to  be  regarded  as  impossible  that  permanent  re- 
sults may  be  left  after  the  concussion  which  form  the  basis  of  the  later  symptoms 
of  the  traumatic  neurosis.  Furthermore,  a  purely  psychical  factor  is  undoubtedly 
to  be  considered.  A  great  fright  is  associated  with  the  injury.  The  accident 
readily  excites  a  fear  of  an  incurable  illness,  with  permanent  incapacity  for  work 
and  for  earning  a  living.  The  perplexity  and  frequent  contentions  about  sick 
funds,  insurance  societies,  and  claims  for  damages,  do  their  part  in  keeping  the 
patient  disturbed.  These  factors  also  bring  about  a  state  which  has  the  closest 
points  of  contact  with  general  nervousness,  neurasthenia,  and  hypochondria.  In 
the  individual  case  it  is  often  scarcely  possible  sharply  to  separate  the  results  of 
the  material  injury  from  this  mental  activity. 

In  many  patients — and  then  the  causes  are  purely  psychical — the  morbid  symp- 
toms that  follow  the  injury  follow  closely  the  type  of  hysteria.    Then  we  should 


THE  TEAUMATIC  NEUROSES.  821 

speak  not  of  a  traumatic  neurosis  but  of  traumatic  hysteria.  We  have  already 
said,  in  the  chapter  on  hysteria  (vide  supra),  that  this  is  very  common.  We 
must  regard  most  of  the  cases  of  "local  traumatic  neurosis"  as  hysterical.  We 
see  not  very  rarely,  after  injuries  which  affect  one  limb,  nervous  disturbances  in 
the  injured  arm  or  leg  which  can  not  possibly  be  due  to  a  local  injury  of  the 
nerve — flaccid  paralysis,  anaesthesia,  contracture,  hyperesthesia,  etc.  We  have 
already  learned  to  recognize  these  conditions  either  in  the  chapter  on  articular 
neuralgia  (vide  page  528),  or  in  the  previous  chapter.  Here,  too,  the  psychical 
factor  involved  in  the  injury  certainly  plays  the  most  important  part  in  the  aeti- 
ology. 

We  should,  however,  at  present  still  distinguish  the  special  traumatic  neurosis 
from  all  these  states,  although  we  must  admit  that  we  can  not  draw  a  sharp 
boundary  between  the  traumatic  neurosis  and  hysteria,  that  both  states  are  cer- 
tainly closely  allied,  and  that  the  two  may  also  be  combined.  Theoretically,  how- 
ever, we  can  make  this  distinction,  that  in  the  genuine  traumatic  neurosis  the 
pui'ely  physical  factor  of  material  concussion  is  of  aetiological  significance. 

In  regard  to  the  course  of  the  true  general  traumatic  neurosis  almost  all  ob- 
servers agree  that  it  is  protracted.  In  fact  it  is  practically  important  to  know  that 
most  of  the  severe  cases  of  this  sort  are  not  capable  of  complete  recovery.  The 
patient's  complaints  and  troubles  persist  for  years  without  becoming  much  worse, 
but  also  without  any  marked  improvement ;  but  the  course  is  often  still  more  un- 
favorable, since  the  patient's  mental  powers  may  show  a  progressive  decline,  and 
complete  dementia  may  finally  develop. 

The  treatment  of  the  traumatic  neurosis  is  based  on  the  same  principles  that 
we  have  studied  in  the  two  previous  chapters,  in  speaking  of  the  treatment  of  hys- 
teria and  neurasthenia.  Great  stress  is  to  be  laid  on  exerting  a  favorable  mental 
influence  on  the  patient.  The  most  useful  remedies  besides  are  the  electric  cur- 
rent (galvanization  of  the  spine,  galvanization  and  faradization  of  the  muscles  and 
nerves,  and  the  faradic  brush),  and  also  baths  and  rubbing,  and  internal]}7  qui- 
nine, iron,  and  strychnine. 

[It  hardly  seems  proper  to  regard  the  "  traumatic  neurosis  "  as  a  single  morbid 
state.  In  some  cases  the  symptoms  point  definitely  to  an  affection  of  the  cord, 
and  the  mental  symptoms  are  absent.  Here  the  patient  complains  of  pain,  weak- 
ness of  the  legs,  and  disturbances  of  the  sphincters ;  the  sensibility  may  be  dimin- 
ished, and  the  reflexes  are  exaggerated.  The  most  marked  changes  in  the  cord 
have  been  found  in  the  lateral  columns.  In  other  cases  the  symptoms  are  clearly 
those  of  grand  hysteria,  but  such  cases  are  rare  in  America.  In  many  cases  the 
symptoms  are  chiefly  neurasthenic.  In  yet  a  fourth  class  there  are  more  pro- 
nounced symptoms  of  mental  and  physical  failure;  anaesthesia  is  marked,  the 
muscular  strength  is  slight,  and  the  symptoms  mentioned  above  are  pronounced. 
These  cases  may  terminate  fatally  after  a  few  years,  and  are  probably  cases  of 
diffuse  sclerosis  of  the  brain  and  cord.  Traumatic  lumbago  is  a  common  compli- 
cation.— K.l 


DISEASES   OP   THE   KIDNEYS,   THE   PELVIS   OP 
THE   KIDNEY,    AND   THE   BLADDER. 


SECTION   I. 
Diseases  of  the  Kidneys. 


CHAPTER  I. 

GENERAL  PRELIMINARY   REMARKS  UPON  THE   PATHOLOGY   OF 

RENAL  DISEASE. 

Although  some  knowledge  of  the  occurrence  and  significance  of  renal  affections 
had  been  acquired  even  by  the  older  physicians,  still  the  service  of  having  pointed 
out  the  frequency  of  these  diseases,  and  of  having  clearly  recognized  their  most 
important  anatomical  forms  and  their  chief  clinical  symptoms,  belongs  undoubt- 
edly to  the  English  physician  Richard  Bright,  who  was  born  in  1788  and  died  in 
1858,  as  physician  in  ordinary  to  Queen  Victoria.  Bright's  first  work  on  this  sub- 
ject appeared  in  the  year  1827.  In  this  he  brought  forward  the  special  discovery 
that,  in  many  cases  of  general  dropsy,  which  are  associated  with  the  secretion  of 
an  albuminous  urine,  a  primary  affection  of  the  kidneys  must  be  regarded  as  the 
special  cause  of  the  disease.  Since  then,  the  disease  described  by  him  has  been 
almost  universally  called  "  Bright's  disease  "  ("  Morbus  BrigMii "),  a  name  still 
much  employed,  but  in  whose  stead  the  anatomical  terms  would  be  more  proper, 
since  many  forms  were  previously  classed  under  it  which,  according  to  our  more 
accurate  present  knowledge,  must  be  separated. 

Bright's  statements  were  either  confirmed  or  expanded  in  subsequent  times  by 
many  other  observers.  Christison,  Osborne,  and  R.  Willis  in  England,  and  Rayer 
and  M.  Solon  in  France,  were  the  chief  students  of  renal  diseases.  Frerichs  pub- 
lished the  first  great  work  in  Germany  in  the  year  1851.  His  division  of  Bright's 
disease  into  three  different  "  stages,"  based  on  Reinhardts  histological  investiga- 
tions, was  for  a  long  time  quite  generally  accepted,  until  gradually  further  clinical 
experience  showed  that  it  was  untenable.  A  more  accurate  division  of  renal  dis- 
eases was  first  opposed  to  it  in  England  (Johnson,  S.  Wilks,  and  others),  and  then 
in  Germany  (Traube,  Bartels).  Under  the  incentive  of  these  labors,  especially  the 
work  of  Bartels  in  1871,  renal  pathology  thus  fell  into  a  doubtful  classification, 
with  which  the  facts  of  experience  could  be  harmonized  only  by  force.  Only  of 
late  years  has  a  natural  theory  of  renal  diseases,  derived  from  general  pathological 
observations,  at  last  become  accepted — a  theory  which  is  based  chiefly  upon  the 
anatomical  work  of  Weigert,  but  which  may  also  be  brought  into  complete  har- 
mony with  the  data  of  clinical  observation. 

The  chief  reason  why  the  kidneys  are  so  often  diseased,  either  alone  or  in  con- 
junction with  other  organs,  is  to  be  found  in  the  fact  that  the  body  must  eliminate 


REMARKS  UPON   THE  PATHOLOGY  OF  RENAL  DISEASE.     823 

all  forms  of  injurious  matter,  which,  circulate  in  the  blood,  in  great  part  by  the 
kidneys.  Consequently  the  action  of  any  injurious  substance  is  often  manifested 
chiefly  in  the  kidneys,  since  they  must,  in  a  certain  measure,  be  repaid  for  the  serv- 
ice which  they  do  for  the  rest  of  the  body  by  their  own  disease.  According  to 
their  nature  and  character,  the  injurious  substances,  which  are  here  to  be  con- 
sidered, are  divided  chiefly  into  two  great  groups — the  chemico-toxic  and  the 
organized  infectious  substances.  In  this  way  the  kidneys  may  be  involved  sym- 
pathetically after  the  ingestion  of  many  poisons,  and  also  in  the  great  majority  of 
all  the  infectious  diseases.  In  these  cases,  of  course,  as  we  shall  see  later,  certain 
chemical  and  infectious  poisons  exert  their  action  in  a  particularly  frequent  and 
in  a  particularly  severe  or  definitely  characterized  fashion.  Beside  these  forms  of 
origin  for  many  renal  diseases,  which  are  the  chief  ones  to  be  considered,  we  must 
consider  other  causes  of  disease  which  are  much  rarer.  One  way  in  which  the 
morbific  agents  may  also  enter  is  especially  important — namely,  from  the  lower 
urinary  passages,  the  bladder,  and  pelvis  of  the  kidney  upward  into  the  kidney. 
In  this  way  those  renal  diseases  arise  which  come  on  secondarily  to  cystitis,  pyeli- 
tis, etc.  Finally,  of  course,  disturbances  of  circulation  and  mechanical  traumatic 
injuries  may  also  make  themselves  manifest  in  the  kidneys. 

The  clinical  symptoms  which  are  caused  by  the  different  forms  of  renal  dis- 
ease, and  which  serve  for  its  recognition,  are  referable  only  in  very  small  part 
directly  to  the  diseased  organ  itself.  In  renal  diseases  characteristic  subjective  local 
symptoms — like  local  pain — are  but  rare,  and  the  anatomical  position  and  the 
physiological  conditions  of  the  kidney  make  it  almost  impossible  to  discover  any 
changes  in  their  size,  their  physical  consistency,  etc.,  by  a  direct  objective  exam- 
ination. In  the  diagnosis  of  renal  diseases  we  are  therefore  confined  chiefly  to 
the  investigation  of  two  groups  of  symptoms :  in  the  first  place,  to  the  examination 
of  the  secretion  from  the  kidneys,  the  urine,  whose  character,  as  we  know  by 
experience,  may  be  materially  altered  when  there  is  renal  disease ;  and,  in  the 
second  place,  to  the  discovery  of  certain  phenomena  in  other  portions  of  the  body, 
which  are  immediately  dependent  upon  the  renal  affection.  Since  both  the  patho- 
logical changes  in  the  urine,  and  the  symptoms  in  other  organs  occurring  in  renal 
affections,  have  much  in  common  in  almost  all  the  forms  of  renal  disease,  it  is 
advisable  first  to  describe  the  main  features,  at  least,  of  the  general  symptomatology 
of  renal  diseases.  We  shall  then  be  obliged,  in  the  following  special  chapters,  to 
mention  only  the  precise  circumstances  of  the  occurrence  and  onset  of  each 
symptom ;  the  general  significance  of  the  symptoms  being  already  known. 

1.  Albuminuria. 

The  most  constant  symptom,  and  one  which  in  many  cases  first  of  all.  and 
often  even  alone,  renders  the  diagnosis  of  a  renal  affection  possible  with  complete 
certainty,  is  albuminuria — that  is,  the  appearance  of  albumen,  and  especially  of 
serum  albumen  and  serum  globuline  (paraglobuline),  in  the  urine.  From  recent 
investigations  (Leube,  Für  bringer,  and  others)  we  know  that  in  some  cases  the 
urine  may  contain  a  very  slight  amount  of  albumen  even  in  healthy  persons, 
especially  after  physical  exertion,  in  emotional  disturbances,  etc.  These  rare 
exceptions,  however,  do  not  invalidate  the  correctness  of  the  assertion  that  when 
a  definite  amount  of  albumen  is  persistently  eliminated  by  the  urine  it  must  be 
regarded  as  something  pathological. 

The  detection  of  albumen  in  the  urine  for  clinical  purposes,  wherein  no  regard 
need  be  paid  to  the  separation  of  serum  albumen  and  serum  globuline,  is  per- 
formed almost  exclusively  by  means  of  the  so-called  heat  test.  If  the  urine  is 
cloudy,  it  must  be  filtered  before  heating.  The  reaction  of  the  urine  must  always 
be  tested  first.     If  it  is  acid,  as  it  usually  is,  the  urine  is  heated  in  a  test-tube  with- 


824  DISEASES   OF  THE  KIDNEYS. 

out  any  further  addition.*  If  the  reaction  of  the  urine  is  neutral  or  alkaline, 
we  acidify  it,  before  heating,  with  a  few  drops  of  acetic  acid.  If  the  urine  contains 
albumen,  a  decided  flocculent  precipitate  of  coagulated  albumen  appears  on  heat- 
ing it.  We  can  make  a  mistake  only  where  there  is  an  alkaline  reaction  in  the 
urine,  which  sometimes  happens  in  neutral  or  very  faintly  acid  urine,  owing  to 
the  escape  of  carbonic  acid  during  the  heating,  and  the  consequent  precipitate  of 
phosphates,  especially  of  calcic  phosphate.  In  order  not  to  mistake  such  a  pre- 
cipitate of  phosphates  for  a  precipitate  of  albumen,  it  is  necessary,  after  the  urine 
has  been  heated  for  a  short  time,  to  add  to  the  precipitate,  if  present,  nitric  acid  (an 
excess  does  no  harm).  A  precipitate  of  phosphates  is  dissolved  at  once,  but  a 
precipitate  of  albumen  usually  becomes  thicker  and  more  compact.  We  can 
measure  the  amount  of  albumen  contained  in  the  urine  approximately  by  the 
height  of  the  settled  precipitate  on  the  bottom  of  the  test-tube.  We  often  speak  of 
"one  half  or  one  fourth  of  the  volume  being  albumen,"  but  we  can  not  state 
any  definite  relation  between  this  estimate  of  the  volume  and  the  precise  amount 
of  albumen.  Of  other  tests  for  albumen  we  will  mention  here  the  very  accurate 
one  with  ferrocyanide  of  potassium  and  acetic  acid.  If  we  add  acetic  acid  to  a 
urine  containing  albumen,  and  then  add  drop  by  drop  a  solution  of  ferrocyanide 
of  potassium,  a  very  distinct  precipitate  of  albumen  is  at  once  formed. 

If  we  have  found  out  that  the  urine  certainly  contains  albumen,  we  must  then 
decide  whether  we  have  really  a  true  renal  albuminuria — that  is,  whether  a  urine 
already  albuminous  is  secreted  in  the  kidneys,  or  whether  the  albumen  is  not 
mixed  with  a  perfectly  normal  or  at  least  non-albuminous  urine  later,  in  the  kid- 
neys themselves  or  in  the  urinary  passages,  the  pelvis  of  the  kidney,  or  the  bladder 
(spurious,  accidental  albuminuria).  Such  a  spurious  albuminuria  occurs  when 
the  urine  is  contaminated  with  blood  (as  in  haemorrhages  from  the  kidneys,  the 
pelvis  of  the  kidney,  the  bladder,  or  the  urethra),  or  with  pus  (in  pyelitis,  cystitis, 
etc.).  In  these  cases,  of  course,  the  albumen  contained  in  the  serum  of  the  blood 
or  pus  is  found  in  the  urine.  Spurious  albuminuria  is  usually  easily  recognized, 
since  the  presence  of  pus  or  blood  in  the  urine,  which  is  shown  by  the  appear- 
ance of  the  urine  or  upon  microscopic  examination  (red  blood-corpuscles,  pus-cor- 
puscles), points  with  immediate  certainty  to  the  origin  of  the  albuminuria.  Beside 
that,  the  amount  of  albumen  in  these  cases  is  usually  but  slight,  and  corresponds 
to  the  amount  of  pus  or  blood  in  the  urine.  A  disproportion  in  this  respect  must 
excite  the  suspicion  whether,  beside  the  spurious  albuminuria,  there  is  not  perhaps 
at  the  same  time  an  affection  of  the  kidneys  causing  a  true  renal  albuminuria. 
The  determination  of-  this  point  is  not  always  perfectly  easy,  but  we  can  usually 
come  to  a  decision  by  finding  abnormal  morphological  constituents  of  the  urine, 
the  so-called  urinary  casts  (vide  infra),  which  give  indubitable  evidence  of  the 
existence  of  a  disease  of  the  kidneys. 

What  general  pathological  significance  has  the  true  renal  albuminuria,  and 
what  are  the  causes  of  its  origin  ?  According  to  our  present  theories,  the  answer 
to  these  questions  is  simply  this:  Almost  every  pure  albuminuria  is  a  direct 
sign  of  an  abnormal  perviousness  of  the  walls  of  the  glomeruli ;  and  the  patho- 
logical changes,  which  the  glomeruli  undergo  in  the  different  diseases  of  the 
kidney,  have  as  their  immediate  result  this  abnormal  perviousness,  and  the  conse- 
quent transudation  of  albumen  into  the  urine.  The  fact  that  the  easily  filtrated 
serum  albumen  of  the  blood,  as  well  as  the  water,  does  not  pass  through  the 
vascular  loops  of  the  glomeruli,  even  under  normal  conditions,  is  due  entirely  to 
the  circumstance  that  the  capillaries  of  the  Malpighian  bodies  are  not  inserted 
bare  into  the  beginning  of  the  uriniferous  tubules,  but  that  they  are  covered  with 

*  The  lieat-test  becomes  still  more  certain,  but  it  is  rather  more  elaborate,  if  we  first  add  to  the 
urine  a  few  drops  of  acetic  acid  and  about  one  sixth  of  its  volume  of  a  concentrated  solution  of  common 
salt  or  Glauber's  salt,  and  then  heat  it. 


REMARKS  UPON  THE  PATHOLOGY  OF  RENAL  DISEASE.     825 

epithelium.  This  epithelium  of  the  glomeruli  has  the  task  and  the  power  of  pro- 
viding  for  the  retention  of  the  albumen  in  the  blood.  If  it  suffer  a  pathological 
change  in  any  way,  it  loses  this  power,  and  then  the  albumen  passes  into  the  urine 
(Heiden  hain).  The  simplest  experimental  proof  of  this  theory  is  furnished  by  the 
albuminuria  which  appears  whenever  the  supply  of  arterial  blood  to  the  kidney  i  n 
checked  by  a  temporary  constriction  of  the  renal  artery.  The  epithelium  of  the 
glomeruli  thereby  suffers  a  visible  microscopic  change,  as  its  nuclei  are  found  con- 
siderably swollen.  If  the  kidneys  in  this  condition  are  removed  as  rapidly  as 
possible  and  boiled,  according  to  Posner's  suggestion,  we  can  discover  under  the 
microscope  in  the  capsules  of  the  glomeruli  the  albumen  that  is  thus  coagulated 
(Ribbert) — the  most  certain  sign  that  the  passage  of  the  albumen  from  the  blood- 
vessels into  the  urinary  passages  has  in  fact  taken  place  in  the  glomeruli. 

Almost  all  cases  of  albuminuria  may  readily  be  referred  to  analogous  disturb- 
ances of  nutrition  in  the  epithelium  of  the  glomeruli,  whether  they  be  excited  by 
anomalies  of  the  circulation,  like  arterial  anaemia  or  venous  stasis,  by  toxic  or 
infectious  influences  which  have  reached  the  glomeruli,  or  by  any  other  circum- 
stances. In  these  cases  the  changes  in  the  glomeruli  need  not  always  be  of  a 
very  severe  or  irreparable  nature ;  for  we  often  see  a  slight  albuminuria  appear 
under  the  most  different  conditions,  and  rapidly  pass  off  again.  This  is  the  so- 
called  "transitory  albuminuria,"  which  is  seen,  for  example,  in  various  febrile 
affections,  after  slight  intoxications,  after  epileptic  attacks,  or  in  other  severe 
nervous  conditions,  in  lead-colic,  etc.  We  will  show  later,  in  the  separate 
chapters,  how  the  anatomical  changes  which  are  found  in  severe  renal  diseases 
explain  the  occurrence  of  albuminuria. 

The  other  factors,  which  have  also  been  made  answerable  for  the  origin  of 
albuminuria,  are  without  doubt  quite  subordinate  to  the  changes  in  the  epithe- 
lium of  the  glomeruli,  and  at  most  they  can  affect  the  amount  of  albumen 
eliminated.  The  changes  in  the  composition  of  the  blood,  on  which  formerly 
great  stress  was  laid,  especially  the  hydraemia  and  hypalbuminosis  (the  diminished 
amount  of  albumen)  of  the  blood,  have  probably  only  an  indirect  significance, 
since  the  nutrition  of  the  walls  of  the  glomeruli  suffers  in  such  a  faulty  consist- 
ency of  the  blood,  and  this  circumstance  again  is  the  special  cause  of  the  elimina- 
tion of  the  albumen. 

The  significance  of  the  blood-pressure  for  the  occurrence  of  albuminuria  was 
also  formerly  very  much  overrated.  According  to  the  older  hypothesis,  it  was 
believed  that,  in  an  increase  of  the  blood-pressure,  the  molecules  of  albumen  in  the 
blood  could  be  pressed  through  the  filter  formed  by  the  membrane  of  the  glome- 
ruli. This  hypothesis,  which  was  not  based  upon  experiments,  has  been  dis- 
proved, especially  by  the  experiments  of  Runeberg  ;  these  experiments  showed 
that,  in  the  filtration  of  solutions  of  albumen  through  animal  membranes,  a  rise 
in  the  filtration  pressure  was  followed  by  a  decrease,  and  a  fall  in  the  pressure 
by  an  increase  of  the  per  cent,  of  albumen  in  the  filtrate.  Runeberg  attempted 
to  refer  the  origin  of  albuminuria  in  many  cases  directly  to  a  diminution  of  the 
blood-pressure  in  the  renal  vessels;  but  the  attempt,  on  the  ground  of  these  results, 
is  not  sufficiently  justified.  A  diminution  of  the  blood-pressure  hardly  ever  is 
itself  followed  by  albuminuria,  and  the  clinical  facts  which  may  be  brought  to 
support  the  above  hypothesis  may  all  be  explained  by  the  change  in  the  character 
of  the  walls  of  the  glomeruli,  which  is  always  present  at  the  same  time  with  the 
decreased  pressure. 

Although  in  the  preceding  paragraphs  only  the  Malpighian  bodies  have  been 
regarded  as  the  spot  where  the  transudation  of  the  albumen  of  the  blood  into  the 
urine  takes  place,  we  must  also  note  that,  under  some  circumstances,  we  may 
admit  the  possibility  of  a  passage  of  albumen  directly  into  the  tubules  from  the 


826 


DISEASES  OF  THE   KIDNEYS. 


capillaries  that  encircle  the  uriniferous  tubules;  but  we  must  also  necessarily 
assume  in  such  cases  that  there  is  a  disturbance  of  nutrition  in  the  menibranse 
propria?,  or  at  least  in  the  epithelium  of  the  uriniferous  tubules.  Such  an 
assumption  seems  to  explain  the  albuminuria,  according  to  Senator's  experiments, 
in  venous  stasis  in  the  kidneys,  although  in  these  cases  the  epithelium  of  the 
glomeruli  also  suffers  soon,  and  then  becomes  pervious  to  albumen. 

Finally,  we  may  briefly  mention  that  in  some  cases  other  soluble  albuminous 
substances  are  also  found  in  the  urine  in  renal  diseases  as  well  as  serum  albumen 
and  globuline,  especially  paralbumen,  hemialbumose,  etc.,  but  the  presence  of 
these  substances  has  not  yet  attained  any  practical  diagnostic  significance. 

2.  Casts  and  other  Abnormal  Morphological  Constituents  of  the  Urine 

in  Eenal  Disease. 

Beside  albuminuria,  certain  peculiar  morphological  constituents  of  the  urine, 
visible  under  the  microscope,  are  of  especial  importance  for  the  diagnosis  of  renal 
affections — the  urinary  casts,  whose  significance  was  first  correctly  recognized  by 
Henle  in  1842.  These  are  cylindrical  bodies,  whose  breadth  corresponds  to  the 
width  of  the  uriniferous  tubule,  and  whose  length  only  exceptionally  reaches  a 
millimetre,  and  which  must  be  regarded  in  their  chemical  nature  as  consisting 
mainly  of  a  coagulated  albuminous  substance.  To  the  latter  circumstance  we 
owe  their  old  name  of  "fibrine  casts,"  or  "fibrous  casts,"  a  name  which  can 


Fig.  111.— Different  forms  of  casts,  a.  Hyaline  cast  with  occasional  granules,  b.  Hyaline  cast  with  fat- 
drops  and  granular  cells,  c.  Hyaline  cast  with  red  blood-corpuscles  attached,  d.  Hyaline  cast  with 
white  blood-corpuscles  attached,  e.  Epithelial  cast.  /.  Waxy  cast.  g.  Cast  with  a  large  number  of 
fat-drops. 


no  longer  be  used  with  propriety,  since  the  coagulated  albuminous  substance  of 
most  casts  is,  at  any  rate,  not  identical  with  fibrine. 

Since  the  precise  conditions  of  the  occurrence,  and  the  character  of  the  renal 
casts  in  the  different  diseases  of  the  kidneys,  will  be  spoken  of  later,  we  need  dis- 
cuss here  only  the  general  properties,  the  origin,  and  the  significance  of  casts  (see 
Fig.  111). 

1.  Hyaline  Casts. — The  hyaline  casts  are  the  commonest  and  most  important 
form  of  casts,  and,  to  a  certain  extent,  are  the  ground-form  for  different 
varieties.  They  are  perfectly  homogeneous,  clear  as  glass,  colorless,  soft,  and 
flexible.  We  find  them  either  wide  or  narrow,  sometimes  broken  off  short,  some- 
times quite  long,  usually  straight,  but  in  many  cases  partly  curved.  They  are 
easily  stained  with  carmine  or  gentian-violet.  On  heating  the  urine,  they  are  dis- 
solved, but  they  are  quite  resistant  to  acids. 


REMARKS  UPON  THE  PATHOLOGY  OF  RENAL  DISEASE.     827 

The  hyaline  casts  are  very  often  covered  to  a  greater  or  less  extent  with  ail  sorts 
of  deposits,  which  are  usually  affixed  to  the  soft  substance  of  the  cast  in  the  kidney 
itself,  but  which  may  often  be  attached  to  it  later.  These  deposits  may  consist, 
first,  of  red  blood-corpuscles.  This  condition  is  important,  because  it  points  with 
certainty  lo  the  existence  of  haemorrhages  in  the  kidneys  themselves.  Second,  of 
white  blood-corpuscles.  These  are  often  considerably  swollen,  so  that  we  must 
guard  against  mistaking  them  for  epithelium.  Third,  of  renal  epithelium,  which 
may  be  recognized  by  its  size,  its  more  angular  shape,  and  its  nuclei.  Of  course, 
we  often  find  the  epithelium  cloudy  and  granular,  or  shriveled  and  atrophied 
Fourth,  of  fatty  granular  globules — that  is,  both  fatty  degenerated  epithelium 
and  also  white  blood-corpuscles  which  are  filled  with  fat-drops  from  the  fatty 
degenerated  cells.  Fifth,  of  little  granular  masses  whose  nature  can  not  always 
be  easily  recognized.  They  are  either  coagulated  granules  of  albumen,  or  fat- 
drops,*  or  urates,  or  bacteria,  or,  finally,  granules  of  haematoidine,  which  have 
come  from  the  destruction  of  red  blood-corpuscles,  and  are  usually  easily  recog- 
nized by  their  dark,  brownish-yellow  color.  Sixth,  we  rarely  find  in  the  casts 
drops  like  myeline,  as  to  whose  precise  significance  nothing  is  known. 

2.  The  so-called  granular  casts  are  in  most  cases  nothing  but  hyaline  casts 
which  are  completely  covered  with  the  above-mentioned  granular  masses,  but 
sometimes  the  coagulated  masses  of  albumen  or  the  granules  of  haematoidin  may 
themselves  assume  cylindrical  forms. 

3.  The  pure  blood-casts  are  not  very  common.  They  consist  of  coagulated 
blood,  and  form  casts  of  the  uriniferous  tubules  into  which  the  haemorrhage  has 
taken  place. 

4.  The  epithelial  casts  are  composed  exclusively  of  renal  epithelium,  although 
probably  a  hyaline  cast  often  affords  a  basis  for  the  epithelium  to  cling  to. 
The  epithelial  casts  are  visually  easily  recognized,  and  always  point  to  a  marked 
desquamation  of  epithelium  in  the  diseased  kidney.  We  must  guard  against 
mistaking  renal  epithelium  for  swollen  white  blood-corpuscles,  as  we  have 
already  said.  On  the  epithelial  casts  the  single  epithelial  cells  may  also  present 
different  changes,  such  as  granular  opacity,  fatty  degeneration,  or  atrophy. 

5.  The  so-called  waxy  casts  are  almost  always  quite  broad,  uniformly  yellowish, 
opaque  casts,  which  proceed,  perhaps,  from  a  metamorphosis  of  the  albumen  of 
the  hyaline  casts.  Their  special  diagnostic  significance  is  unknown.  At  all 
events,  they  are  not  by  any  means  found  chiefly  in  the  amyloid  kidney,  but  they 
are  found  most  commonly,  comparatively,  in  acute  and  subacute  nephritis. 

Nothing  definite  can  at  present  be  stated  as  to  the  mode  of  origin  of  hyaline 
casts  ;  the  origin  of  the  blood  and  epithelial  casts  is  self-evident.  Hyaline  casts 
are  most  probably  formed  from  the  coagulated  albumen  eliminated  from  the  kid- 
neys, since  the  formation  of  casts  is  almost  always  coincident  with  albuminuria. 
We  can  not  state  definitely  how  far  destroyed  white  corpuscles  or  degenerated 
renal  epithelium  participate  in  the  formation  of  casts. 

The  clinical  diagnostic  significance  of  renal  casts  is  very  great.  They  are,  in 
the  first  place,  always  a  sure  sign  of  the  existence  of  some  renal  disease,  since  in 
normal  urine  casts  are  not  found  at  all,  or,  at  most,  they  are  exceptional  and  are 
present  in  small  numbers.  The  consideration  of  the  special  forms  of  casts,  and  of 
the  deposit  upon  them,  is  also  of  great  diagnostic  importance,  although  from  it  we 
can  never  decide  immediately  upon  the  general  form  of  the  renal  disease,  but  we 
can  recognize  wTith  certainty  the  type  of  special  pathological  processes  in  the  kid- 
neys. The  blood-casts  and  the  red  blood-corpuscles  sticking  to  the  cylinders  point 
to  the  occurrence  of  renal  haemorrhages ;  the  epithelial  casts  to  a  desquamation 

*  It  is  doubtful  whether  the  hyaline  casts  themselves  may  in  part  undergo  fatty  degeneration. 


828  DISEASES  OF  THE  KIDNEYS. 

of  the  epithelium,  in  the  kidneys ;  the  white  hlood-corpuscles  to  an  emigration 
of  the  colorless  cells  from  the  vessels ;  the  fatty  granular  cells  and  the  fat-drops 
to  the  presence  of  processes  of  fatty  degeneration  in  the  kidneys. 

We  have  already  learned  to  recognize  in  a  great  measure  in  the  preceding,  as 
occasional  deposits  on  the  casts,  the  other  morphological  constituents  found, 
heside  the  casts,  in  the  sediment  of  the  urine  in  renal  disease.  Briefly  recapitu- 
lated, they  are  as  follows : 

1.  Red  hlood-corpuscles.  A  large  amount  of  hlood  in  the  urine  (hsematuria)  is 
almost  always  to  he  recognized  hy  its  blood-red  color.  The  presence  of  blood  may 
be  made  out  with  certainty  by  the  microscope,  or  by  Heller's  blood-test.  The  lat- 
ter is  performed  by  heating  the  urine  in  a  test-tube  with  sodic  or  potassic  hydrate. 
The  blood-corpuscles  are  thus  dissolved,  and  the  hsematine  is  precipitated  with  the 
phosphates,  giving  to  the  precipitate  of  the  latter  a  very  characteristic  blood-red 
color.  Finally,  of  course,  the  spectroscope  may  serve  for  the  detection  of  hsema- 
turia.     Hasmoglobinuria  will  be  described  in  a  special  chapter  later. 

2.  White  blood-corpuscles.  Only  when  they  are  also  attached  to  the  casts  can 
we  assume  with  certainty  that  these  come  from  the  kidneys,  and  not  from  the 
lower  portions  of  the  urinary  tract. 

3.  Renal  epithelium. 

4.  Fat-drops  and  fatty  granular  cells. 

5.  Uric-acid  crystals,  urates  and  calcic  oxalate,  bacteria,  etc. 

3.  The  Dropsy  of  Renal  Disease. 

Although  the  changes  in  the  urine  must  be  alone  decisive  in  the  diagnosis 
of  any  renal  disease,  there  are  yet  certain  other  symptoms  which  are  also  due 
immediately  to  the  renal  affection,  and  which  may  first  direct  our  suspicions  to 
the  existence  of  a  disease  of  the  kidneys,  and  consequently  lead  to  a  careful  exami- 
nation of  the  urine.  Among  these  symptoms  the  dropsy  of  renal  disease  is  one  of 
the  commonest  and  most  important.  This  may,  indeed,  quite  frequently  be  en- 
tirely absent,  both  in  acute  and  chronic  nephritis,  and  in  other  diseases  of  the  kid- 
neys ;  but  in  many  cases  it  is  decidedly  prominent  in  the  whole  clinical  picture. 

If  we  ask  what  is  the  reason  of  the  frequent  occurrence  of  dropsy  in  renal  dis- 
ease, the  answer  at  first  does  not  seem  difficult.  Since  the  main  function  of  the 
kidneys  is  to  excrete  water  from  the  body,  and  since,  as  we  shall  see  later,  in  many 
cases  the  diseased  kidney  can  no  longer  fulfill  this  task,  or  it  can  fulfill  it  only  to 
a  slight  degree,  we  are  not,  in  fact,  very  much  out  of  the  way  in  considering  the 
retention  of  water  in  the  body  as  the  main  cause  of  the  consequent  oedema.  Clin- 
ical observation  seems  in  general  to  agree  completely  with  this  assumption.  The 
oedema  in  renal  disease  seldom  appears  until  the  daily  amount  of  urine  has  been 
below  the  normal  for  some  time,  while,  on  the  other  hand,  in  those  cases  where 
the  amount  of  urine  passed  is  normal,  or  even  abnormally  great,  in  spite  of  the 
existing  renal  disease,  the  oedema  is  usually  wholly  absent.  In  individual  cases, 
too,  we  very  often  see  a  decrease  of  the  oedema  associated  with  an  increase  in  the 
amount  of  urine,  and  an  increase  of  the  oedema  associated  with  a  corresponding 
diminution  in  the  excretion  of  urine.  The  pathological  process  accordingly  seems 
to  consist  of  an  accumulation  in  the  body  of  the  water  which  can  not  be  excreted 
from  it,  and  which  transudes  from  the  vessels  and  thus  gives  rise  to  the  develop- 
ment of  oedema. 

On  more  careful  consideration,  however,  there  are  some  objections  to  this 
theory,  which  is  apparently  so  simple.  In  the  first  place,  it  might  be  supposed  that, 
when  there  is  a  retention  of  water,  the  body  must  get  rid  of  the  surplus  water  by 
employing  to  a  greater  degree  the  other  channels  of  elimination  which  are  at  its 
service — the  skin  and  the  intestines.     Since  we  can  never  determine  accurately 


REMARKS  UPON  THE  PATHOLOGY  OF  RENAL  DISEASE.     829 

the  time  when  the  water  first  begins  to  be  retained  in  the  body,  the  clinical  experi- 
ence just  mentioned  may  also  be  thus  interpreted,  that  the  lessened  excretion  of 
urine  is  not  the  cause  of  the  oedema,  but  that,  on  the  contrary,  the  appearance  of 
oedema  is  rather  the  cause  of  the  diminished  elimination  of  water  by  the  kidneys. 
For  many  cases  this  objection  seems  somewhat  artificial,  because  the  anatomical 
changes  in  the  kidneys  must  often,  without  doubt,  have  a  direct  influence  upon 
the  secretion  of  urine  ;  but,  still,  this  can  not  be  entirely  and  conclusively  demon- 
strated. The  results  of  Cohnheim's  and  Lichtheim's  experiments  also  are  not  in 
harmony  with  the  above  theory  of  the  origin  of  oedema.  By  injecting  a  large 
amount  of  a  half-a-per-cent.  solution  of  common  salt  into  the  vascular  system  of 
an  animal  we  can  so  greatly  overload  its  blood  with  water  as  to  produce  an  arti- 
ficial "  hydraemic  plethora,"  and  nevertheless  there  is  not  the  slightest  oedema,  not 
even  when  the  animal's  renal  arteries  are  tied.  In  conclusion,  we  must  also  state 
that  cases  have  been  seen  repeatedly  where  a  complete  anuria  has  existed  for  sev- 
eral days,  as  a  result  of  the  plugging  or  compression  of  the  ureters,  and  where 
there  was  nevertheless  not  a  trace  of  oedema. 

There  seems  to  be,  then,  another  factor  beside  the  retention  of  water  in  the 
body  which  plays  a  part  in  the  origin  of  oedema;  but  it  is  not  easy  to  decide 
what  it  is.  Cohnheim  lays  the  greatest  stress  upon  a  change  in  the  walls  of 
the  vessels,  by  which  they  become  abnormally  pervious  and  permit  the  water 
accumulated  in  the  blood  to  pass  out  into  the  tissues.  This  hypothesis  seems  plau- 
sible, especially  with  reference  to  the  dropsy  in  scarlatinal  nephritis,  and  in  the 
cases  that  arise  after  the  skin  has  been  thoroughly  chilled ;  but  we  must  also  admit 
that  in  many  cases  such  a  vascular  change  has  not  been  certainly  discovered. 

The  discussion  so  far  relates  mainly  to  the  origin  of  the  dropsy  in  the  acute 
and  subacute  forms  of  nephritis.  In  chronic  nephritis  the  oedema,  without  doubt, 
often  arises  in  quite  another  fashion,  especially  as  a  result  of  the  disturbance  of 
compensation  in  the  final  paralysis  of  the  hypertrophied  left  ventricle  {vide  infra). 
This  oedema  is  then  a  true  general  oedema  of  stasis,  and  may  be  regarded  as  analo- 
gous to  the  oedema  in  uncompensated  heart  disease. 

The  special  peculiarities  in  regard  to  the  appearance  of  oedema  hi  the  different 
diseases  of  the  kidney  will  be  described  later.  The  first  signs  of  the  development 
of  dropsy  are  generally  noticed  in  the  skin,  usually  in  the  face,  and  especially  in 
the  eyelids.  The  ankles  and  legs  also  swell,  then  the  scrotum,  the  dependent  parts 
of  the  trunk,  etc.  In  all  severe  cases  the  whole  subcutaneous  cellular  tissue 
finally  takes  part  in  the  dropsy,  so  that  the  whole  body  is  swollen  to  the  utmost 
degree.  We  almost  always  find  at  the  same  time  an  effusion  into  the  cavities  of 
the  body,  hydrothorax,  ascites,  and  finally  even  hydropericardium.  In  some  cases 
the  dropsy  of  the  serous  cavities  may  attain  even  a  high  degree  without  there  being 
very  much  anasarca — that  is,  general  oedema  of  the  skin.  More  rarely  we  see 
cedematous  swelling  in  the  mucous  membranes,  especially  in  the  conjunctiva?,  the 
soft  palate,  and  the  arytseno-epiglottic  ligaments  (oedema  of  the  glottis).  Among 
the  oedemas  of  internal  organs,  oedema  of  the  lungs  has  a  great  practical  signifi- 
cance. The  questions  as  to  the  occurrence  and  significance  of  oedema  of  the  brain 
will  be  spoken  of  below  (see  uraemia). 

In  its  chemical  composition,  the  dropsical  fluid  corresponds  to  a  very  thin 
blood-serum.  The  amount  of  water  is  usually  97  to  98  per  cent.,  the  amount 
of  salts  one  to  one  and  a  half  per  cent.  The  amount  of  albumen  is  usually  very 
slight.     Urea  has  been  repeatedly  found  in  it. 

4.  Uremia. 
If  the  diseased  kidneys  can  no  longer  perform  their  secretory  functions  in  a 
satisfactory  way,  not  only  does  the  elimination  of  water  from  the  body  thereby 


830  DISEASES  OF  THE  KIDNEYS. 

suffer,  but  the  soluble  constituents  of  the  urine,  the  salts,  the  urea,  and  the  other 
final  products  of  tissue  metamorphosis  may  also  be  retained  in  the  blood  and  ac- 
cumulate there.  Hence  we  often  find  the  blood,  in  patients  with  renal  disease,  not 
only  more  watery  than  under  normal  conditions,  so  that  tbe  specific  gi*avity  of 
the  serum  may  fall  from  1030  to  1020,  or  even  lower,  but,  in  almost  all  cases  where 
there  is  a  diminished  excretion  of  urine,  it  is  also  richer  in  urea,  as  many  experi- 
ments have  shown,  and  under  corresponding  conditions  it  is  probably  also  fre- 
quently richer  in  the  other  constituents  of  the  urine. 

This  accumulation  of  the  urinary  constituents  in  the  blood,  and  further,  per- 
haps, in  the  tissues  themselves,  is  the  cause  of  a  class  of  symptoms  which  are  often 
seen  in  diseases  of  the  kidneys,  and  which  are  termed  uraemic  symptoms  or 
uraemia.  It  is  probable  that  the  retention  of  urea  plays  the  main  part  here,  but 
it  is  also  probable  that  the  retention  of  other  constituents  of  the  urine,  perhaps 
the  potassium  salts  chiefly,  is  likewise  not  without  significance.  Many  experi- 
ments have  shown  that,  by  extirpating  the  kidneys  or  by  tying  the  ureters  in 
animals,  we  can  provoke  a  symptom-complex,  characterized  by  vomiting,  con- 
vulsions, and  coma,  which  corresponds  almost  perfectly  to  the  uraemia  of  renal 
disease.  We  almost  always  see  at  the  same  time  a  very  pronounced  anaemia  of 
the  brain  and  cord,  so  that  the  accumulation  of  the  products  of  tissue  metamor- 
phosis seems  to  excite  a  vascular  spasm  (Fleischer).  We  must  also,  perhaps,  con- 
sider this  secondary  cerebral  anaemia  as  well  as  the  direct  toxic  action,  in  studying 
the  origin  of  the  severe  nervous  uraemic  symptoms.  That  large  amounts  of  urea  in- 
jected into  the  blood  of  healthy  animals  usually  have  no  injurious  results,  is  ex- 
plained simply  by  the  fact  that  in  this  case  the  urea  is  very  rapidly  and  completely 
eliminated  again  by  the  kidneys.  If,  when  feeding  an  animal  with  large  amounts 
of  urea,  we  hinder  its  elimination,  as  Voit  has  shown,  by  withholding  water  at 
the  same  time,  uraemic  symptoms  also  appear. 

Clinical  experience  in  most  cases  also  agrees  perfectly  with  the  theory  that 
uraemia  is  caused  by  a  retention  of  urinary  constituents  in  the  body.  In  most 
cases  the  uraemic  symptoms  appear  only  when  the  daily  amount  of  urine  has  pre- 
viously fallen  to  a  very  low  figure,  or  when  the  secretion  of  urine  has  wholly 
ceased  for  several  days.  That  in  these  cases  not  only  the  elimination  of  water, 
but  also  the  elimination  of  an  amount  of  urea  corresponding  to  the  food  taken, 
and  also  the  elimination  of  the  other  urinary  constituents,  is  very  much  dimin- 
ished, is  shown  by  the  experiments  in  regard  to  this  point  made  by  Fleischer  and 
others.  Furthermore,  a  great  increase  of  the  amount  of  urea  in  the  blood  in 
uraemic  patients  has  been  found  in  many  if  not  in  all  cases. 

Of  course  there  can  be  no  question  that  some  clinical  facts  can  not  be  brought 
into  exact  harmony  with  what  has  been  previously  said.  If  cases  are  repeatedly 
reported  in  which  no  uraemic  symptoms  have  appeared  in  spite  of  anuria  for  sev- 
eral days,  it  does  not  prove  too  much,  since  we  can  never  make  an  exact  estimate 
of  the  matter  accumulated  in  the  blood  which  ought  to  have  been  eliminated ; 
for  the  organism  can  certainly  get  rid  of  the  final  products  of  tissue  metamor- 
phosis in  other  ways  than  through  the  kidneys — for  instance,  through  the  skin 
or  the  intestines— and  we  must  also  bear  in  mind  that  different  individuals  show 
a  great  variation  in  tolerating  the  action  of  any  poison  in  the  body.  It  is  harder, 
however,  to  explain  those  cases  which  are  sometimes  seen,  where  uraemic  symp- 
toms suddenly  appear  in  patients  with  renal  disease  without  being  preceded  by 
any  noticeable  diminution  of  the  secretion  of  urine.  In  these  cases  we  must 
assume  that,  in  spite  of  the  abundant  elimination  of  water— that  is,  in  spite  of  a 
normal  amount  of  urine — there  is  a  retention  of  the  solid  constituents.  Such 
cases,  however,  should  always  make  us  consider  whether,  in  renal  disease,  other 
circumstances  than  the  retention  of  urinary  constituents  may  not  give  rise  to  the 


REMARKS  UPON  THE  PATHOLOGY  OF  RENAL  DISEASE.     831 

development  of  severe  nervous  symptoms.  In  some  such  cases  the  appearance  of 
uraemia  coincides  with  the  disappearance  of  the  previously  existing  oedema.  It  has 
therefore  been  conjectured  that,  in  such  cases,  the  blood  all  at  once  becomes  rich 
in  urea  from  the  rapid  absorption  of  the  oedema  fluid  which  contains  urea,  and 
that  therefore  urasmic  symptoms  now  arise,  in  spite  of  the  abundant  elimination 
of  urine  which  at  once  sets  iu.  This  hypothesis  does  not  seem  to  us  very  prob- 
able, since,  as  was  said  above,  very  large  amounts  of  urea  may  be  injected  into  the 
blood  of  animals  with  healthy  kidneys,  without  the  appearance  of  uraemia.  In 
the  cases  above  mentioned  we  must  therefore  still  further  suppose  tbat  nothing 
but  the  water  is  rapidly  passed  off  again  by  the  kidneys,  while  the  solid  constitu- 
ents remain. 

Among  the  other  theories  of  uraemia  which  have  therefore  been  advanced 
to  explain  the  apparent  contradictions  in  the  clinical  observations  mentioned, 
Traube's  theory  must  be  mentioned  especially;  according  to  this,  an  acute  oedema 
of  the  brain  is  the  cause  of  the  uraemic  symptoms.  There  is  no  doubt  that  this 
theory  does  not  apply  to  many  cases  of  uraemia ;  but,  on  the  other  hand,  we  can 
not  claim  that  it  never  finds  an  application.  It  seems  to  us  that,  in  general,  the 
possibility  of  actual  anatomical  changes  in  the  brain  in  renal  disease  has  not  yet 
been  sufficiently  considered  as  a  cause  of  severe  nervous  symptoms,  since  the  fre- 
quent occurrence  of  special  changes  in  the  retina,  which  also  consists  of  nervous 
elements,  is  closely  connected  with  such  a  theory.  In  most  cases  of  uraemia  we 
can,  however,  hold  to  the  original  explanation,  according  to  which  these  symptoms 
owe  their  origin  to  the  retention  of  the  urinary  constituents  in  the  blood ;  but  we 
can  not  exclude  the  possibility  that,  under  some  circumstances,  severe  nervous 
symptoms  may  arise  from  other  causes  in  patients  with  renal  disease,  which  of 
course  do  not  deserve  the  name  of  "  uraemia,"  although  clinically  they  may  greatly 
resemble  it. 

Finally,  we  may  mention  here  the  theory  advanced  by  Frerichs  in  the  year 
1851,  which  at  first  found  much  favor,  but  which  at  present  is  almost  universally 
abandoned.  According  to  this,  the  urea  retained  in  the  blood  was  not  in  itself 
the  cause  of  the  uraemic  symptoms,  but  it  was  changed  into  carbonate  of  ammo- 
nia by  the  action  of  a  ferment  in  the  blood,  and  from  this  the  severe  nervous 
symptoms  arose.  This  theory  is  untenable,  because  carbonate  of  ammonia  is 
scarcely  ever  found  in  the  blood  of  uraemic  patients.  It  is  much  more  probably 
formed  first  in  the  stomach  and  intestinal  canal  of  uraemic  patients  from  the  urea 
there  excreted  (vide  infra),  as  Claude  Bernard,  Treitz,  Voit,  and  others  have 
shown. 

In  regard  to  the  clinical  symptoms  of  uraemia  in  the  individual  case,  they  show 
all  possible  transitions  from  the  mildest  symptoms,  which  are  only  intimated,  up 
to  the  severest  nervous  symptoms,  which  may  be  the  immediate  cause  of  death. 
The  severe  forms  of  uraemia  may  sometimes  come  on  quite  suddenly,  while  iu 
other  cases  they  may  be  preceded  for  a  long  time  by  milder  uraemic  symptoms, 
which  are  then  termed  prodromata.  The  severest  symptoms  may  not  appear  at 
all,  and  the  milder  symptoms  may  exist  alone  for  a  longer  or  shorter  time.  This 
latter  condition  is  called  chronic  uraemia. 

The  milder  uraemic  symptoms,  which  are  observed  either  alone  or  as  precursors 
of  severe  uraemia,  consist  of  headache,  somnolence,  and  mental  stupor,  of  a  pecul- 
iar uneasiness,  or  of  a  feeling  of  anxiety  and  constraint  (sometimes  associated 
with  hurried  respiration),  and  very  often  of  nausea,  spasmodic  eructations,  and  re- 
peated vomiting;  and,  finally,  not  infrequently,  of  various  symptoms  of  motor- 
irritation,  of  slight  twitchings  or  temporary  tonic  rigidity  of  the  face  or  the  ex- 
tremities, etc. 

The  most  characteristic  symptom  of  severe  uraemia  is  the  uraemic  convulsion. 


832  DISEASES  OF  THE  KIDNEYS. 

or  the  so-called  uraemic  eclampsia.  It  corresponds  almost  exactly  in  its  details  to 
the  pure  epileptiform  attack;  it  usually  begins  with  a  short  tonic  stage,  in  which 
the  whole  body  is  generally  in  a  position  of  extension  in  opisthotonos,  and  then 
follow  vigorous  clonic  contractions  in  the  face  and  extremities.  The  face  becomes 
cyanotic,  a  bloody  froth  comes  from  the  mouth,  the  pupils  are  usually  dilated  and 
almost  without  reaction,  the  respiration  is  accelerated  (but  at  times  it  is  intermit- 
ting from  spasm  of  the  respiratory  muscles),  the  pulse  is  small  and  accelerated, 
and  it  can  scarcely  be  felt  in  the  radial  artery,  and  the  temperature  is  sometimes 
raised.  In  other  cases  the  spasm  begins  with  short  jerky  contractions  in  one  ex- 
tremity, as  in  the  arm,  and  then  invades  the  trunk  muscles,  the  face,  and  the  legs. 
One  half  the  body  is  often  more  affected  in  the  attacks  than  the  other.  The  spasms 
visually  cease  in  a  few  minutes,  and  are  followed  by  deep  coma  and  stertor,  which 
last  for  several  hours  or  more.  There  is  only  rarely  a  single  attack.  The  attacks 
are  much  offener  repeated  after  longer  or  shorter  intervals,  so  that  there  may  even 
be  twenty  or  more  in  the  twenty-four  hours,  during  the  whole  of  which  time  a 
complete  loss  of  consciousness  persists.  Severe  and  fully  developed  epileptiform 
attacks  often  alternate  with  slighter  convulsions. 

Some  other  uraemic  symptoms  besides  the  convulsions  have  already  been 
briefly  mentioned,  but  they  merit  a  somewhat  fuller  description. 

The  uraemic  amaurosis  occasionally  seen  is  especially  interesting.  It  is  usually 
left  after  recovery  from  the  convulsions.  Only  rarely  does  it  precede  them  or 
appear  without  them.  It  always  develops  quite  rapidly,  so  that  the  first  disturb- 
ance of  vision  soon  passes  into  complete  blindness.  The  reaction  of  the  pupils  to 
light  is  almost  always  retained,  and  the  ophthalmoscope  shows  a  perfectly  normal 
retinal  image.  From  this  we  can  scarcely  doubt  that  genuine  ursemic  amaurosis 
is  of  purely  central  origin ;  it  is  probably  due  to  a  disturbance  iu  the  cortex  of  the 
occipital  lobe.  Its  prognosis  is  on  the  whole  favorable,  since  the  disturbance  of 
vision  usually  disappears  completely  in  a  day  or  two,  though  sometimes  not  until 
after  a  longer  time.  Anomalies  are  only  rarely  seen  in  the  region  of  the  other 
nerves  of  special  sense,  the  most  frequent,  comparatively,  being  a  difficulty  in 
hearing,  or  even  complete  deafness. 

Other  motor  disturbances,  except  twitchings  and  convulsions,  are  rare.  Only 
in  a  few  cases  have  hemiplegic  or  monoplegic  paralyses,  contractures,  etc.,  been 
observed.  Mental  symptoms  are  more  commou.  Delirium,  and  maniacal  or 
sometimes  melancholic  states,  occasionally  follow  uraemic  coma. 

Those  ursemic  symptoms  have  also  a  great  interest  which  are  to  be  regarded 
as  a  sort  of  self-help  on  the  part  of  the  organism,  since  they  often  lead  to  a  vica- 
rious elimination  of  urea.  The  first  of  these  is  uraemic  vomiting,  which  is  a 
frequent  and  often  an  extremely  obstinate  symptom  both  in  acute  and  chronic 
uraemia.  In  many  cases  it  is  of  central  origin,  and  is  to  be  regarded  as  analogous 
to  the  vomiting  so  frequent  in  different  forms  of  cerebral  disease ;  but  it  is  often 
produced  by  the  irritation  which  the  gastric  mucous  membrane  suffers  from  the 
urea  eliminated,  or  rather  from  the  carbonate  of  ammonia  arising  from  it.  The 
latter  is  always  first  formed  from  the  urea  in  the  stomach  itself,  and  we  find  in 
the  vomitus  of  uraemic  patients  either  the  still  undecomposed  urea  or  the  carbon- 
ate of  ammonia  in  considerable  quantities.  Sometimes  there  is  quite  a  violent 
hiccough  besides  the  vomiting. 

Uraemic  diarrhoea  has  the  same  significance  as  uraemic  vomiting.  It  is  usually 
provoked  by  the  carbonate  of  ammonia  arising  from  the  urea  in  the  intestines. 
The  latter  often  causes  quite  a  severe  catarrhal,  and  even  at  times  a  diphtheritic, 
inflammation  of  the  intestinal  mucous  membrane.- 

Another  way  in  which  the  organism  sometimes  tries  to  get  rid  of  the  amount 
of  urea  accumulated  in  it  is  by  the  sweat-glands.     Schottin  first  described  the 


REMARKS  UPON  THE  PATHOLOGY  OF  RENAL  DISEASE.     833 

remarkable  discovery  of  a  coating1  of  urea  on  the  skin  in  the  uraemia  of  cholera, 
an  observation  which  since  then  has  been  repeatedly  confirmed  in  other  cases  of 
uraemia.  This  coating  is  most  frequently  seen  on  the  face,  especially  on  the  sides 
of  the  nose,  to  which  little  faintly  lustrous  scales  are  seen  sticking  after  the 
evaporation  of  a  clammy  sweat.  Chemical  examination  shows  that  these  scales 
are  urea.  The  excretion  of  urea  is  much  more  rare  in  other  parts  of  the  skin,  but 
perhaps  the  occasional  severe  uraeuiic  itching  of  the  skin  is  due  to  an  irritation 
of  the  cutaneous  nerves  by  some  of  the  constituents  of  the  urine  that  are  ex- 
creted. 

Other  organs  besides  the  skin  and  the  digestive  tract  are  but  rarely  to  be 
considered  as  a  means  of  the  vicarious  elimination  of  urea,  but  Fleischer  was 
once  able  to  discover  considerable  amounts  of  urea  in  the  sputum  of  a  uraemic 
patient. 

In  conclusion,  we  must  describe  the  condition  of  the  pulse,  of  the  temperature, 
and  of  the  respiration  in  uraemia.  The  pulse  is  often  very  slow  before  the  appear- 
ance of  severe  symptoms,  sometimes  48  or  40,  but  it  is  almost  always  tense  and 
hard.  In  chronic  uraemia,  also,  a  moderate  slowness  of  the  pulse  is  not  infre- 
quent. When  uraemic  convulsions  appear,  however,  the  pulse  usually  becomes 
small  and  very  frequent,  especially  in  cases  that  terminate  unfavorably.  The 
temperature  but  rarely  remains  unchanged  in  severe  uraemia.  If  there  are  con- 
vulsions, it  usually  rises  several  degrees,  in  severe  cases  even  to  106°  or  108°  (41  °~ 
42°  C).  We  have  seen  these  high  temperatures,  especially  as  a  terminal  rise  with 
an  unfavorable  issue,  although  there  may  sometimes  be  an  improvement  even  in 
such  cases.  On  the  other  hand,  there  are  also  great  declines  in  temperature,  down 
to  93°  or  91°  (34°-33°  C),  most  frequently  again  as  a  terminal  temperature  of  col- 
lapse, in  cases  which  end  in  deep  coma  without  marked  symptoms  of  motor  irrita- 
tion. We  might  also  mention  the  "  uraemic  chills  "  which  we  have  seen  several 
times — that  is,  a  chill  coming  on  suddenly  along  with  other  uraemic  symptoms, 
with  a  great  increase  of  temperature,  and  followed  by  a  rapid  fall  in  the  tempera- 
ture. The  respiration  in  uraemic  patients  is  sometimes  very  much  accelerated,  and 
is  especially  deep— a  symptom  which  recalls  the  peculiar  breathing  in  diabetic 
coma  {vide  infra).  Certain  severe  attacks  of  dyspnoea  in  patients  with  renal  dis- 
ease have  been  described  as  "uraemic  dyspnoea"  or  "uraemic  asthma";  but  it  is 
not  always  easy  to  decide  whether  this  is  really  a  uraemic  nervous  symptom  in 
these  cases,  since  similar  conditions  of  sudden  dyspnoea  may  depend  upon  insuffi- 
ciency of  the  left  ventricle  or  upon  inflammatory  affections  of  the  lungs. 

In  regard  to  the  general  course  of  uraemia,  we  have  already  spoken  of  the 
different  ways  in  which  it  occurs,  either  coming  on  quite  suddenly  or  announcing 
itself  by  different  prodromata.  In  most  cases  the  special  exciting  cause  of  uraemia 
is  to  be  found  in  a  failure  of  the  renal  activity  caused  by  the  anatomical  lesion  of 
the  kidneys,  either  because  the  glomeruli  are  unable  to  perform  their  functions 
owing  to  the  disease,  or  because  the  uriniferous  tubules  are  considerably  plugged 
by  casts,  or  from  similar  reasons.  In  the  more  chronic  forms  of  nephritis  with 
cardiac  hypertrophy  {vide  infra)  the  activity  of  the  heart  sometimes  plays  a  very 
considerable  part  in  the  occurrence  of  uraemia,  since,  when  insufficiency  of  the  left 
ventricle  sets  in,  the  insufficiency  of  course  leads  to  a  fall  in  the  arterial  pressure 
and  to  a  consequent  diminution  in  the  excretion  of  urine. 

In  regard  to  the  duration  of  uraemic  symptoms  and  to  the  different  forms  and 
ways  in  which  the  various  uraemic  symptoms  may  be  combined  in  the  clinical 
picture,  we  can  give  only  a  few  general  statements.  The  division  of  uraemia  into 
an  acute  and  a  chronic  form,  already  mentioned,  is  generally  very  useful  practi- 
cally. In  the  acute  form  we  usually  have  the  severe  uraemic  symptoms,  especially 
uraemic  convulsions  and  uraemic  coma.  This  condition  usually  lasts  some  days, 
53 


834  DISEASES  OF  THE  KIDNEYS. 

while  chronic  uraemia,  in  which  the  milder  cerebral  symptoms — ursemic  vomiting, 
difficulty  in  breathing,  etc. — are  most  pi'ominent,  may  last  as  many  weeks. 

The  termination  of  uraemia  is  always  doubtful  in  every  severe  case,  but  it  is  by 
no  means  always  unfavorable.  Even  after  coma  lasting  for  several  days,  with 
very  severe  and  often-repeated  convulsions,  the  ursemic  symptoms  may  wholly 
disappear,  while  on  the  other  hand,  of  course,  uraemia  is  by  no  means  a  rare  cause 
of  death  in  the  most  diverse  forms  of  acute  and  chronic  renal  disease.  In  judging 
of  the  individual  case,  the  most  stress  is  to  be  laid  on  the  condition  of  the  pulse, 
the  respiration,  and  the  temperature;  we  must  also  consider,  of  course,  the  char- 
acter of  the  urinary  secretion,  and  especially  the  other  morbid  symptoms  depend- 
ent upon  the  primary  disease. 

5.   The  Changes  in  the  Circulatory  Apparatus  in  Eenal  Disease. 

Although  it  had  not  escaped  Bright's  observation  that  changes  in  the  heart  are 
also  present  in  diseases  of  the  kidney,  this  condition  was  first  generally  known 
when  Traube,  in  1856,  in  a  treatise  which  has  become  famous,  discovered  that  a 
change  in  the  heart  was  very  common  in  certain  renal  affections,  and  thus  gave 
the  chief  impulse  to  the  numerous  clinical  and  experimental  investigations  that 
have  been  made  since  then  as  to  the  connection  between  cardiac  and  renal 
disease. 

This  connection,  generally  considered,  may  be  accounted  for  in  three  ways: 

First,  the  heart  disease  may  without  doubt  be  the  primary  disease,  and.  only 
secondarily  lead  to  a  disease  of  the  kidneys,  as  a  result  of  disturbances  of  circula- 
tion. In  this  way  develop  the  kidney  of  passive  congestion  {vide  infra,  and  page 
300)  and  the  embolic  processes  in  the  kidney  (vide  infra). 

Secondly,  heart  disease  and  renal  affections  may  also  develop  independently  of 
each  other,  as  a  result  of  an  injurious  influence  that  affects  both  organs  at  the  same 
time.  Thus,  for  example,  a  general  arterio-sclerosis  leads  to  cardiac  hypertrophy 
or  to  myocarditis,  and  also  to  a  granular  kidney  (vide  infra),  as  a  result  of  an 
implication  of  the  renal  vessels.  Certain  other  injurious  influences,  such  as  toxic 
and  constitutional  influences,  alcohol,  syphilis,  or  improper  living,  may  also 
cause  a  disease  of  the  heart  and  the  kidneys  at  the  same  time.  Later  on,  if  both 
affections  have  developed,  their  influence  upon  each  other  is  often,  of  course,  con- 
siderable— a  circumstance  which  may  render  our  judgment  as  to  the  condition 
decidedly  difficult. 

In  the  third  place,  finally — and  this  is  the  point  with  which  we  are  here  chiefly 
concerned — the  renal  affection  may  be  the  primary  disease,  and  is  itself  the  cause 
of  a  change  in  the  heart,  and  especially  of  a  secondary  hypertrophy  of  the  left 
ventricle.  At  present  there  can  no  longer  be  any  doubt  of  the  fact  of  this  depend- 
ence. We  also  know  now  that  the  secondary  development  of  cardiac  hypertro- 
phy is  not  confined  to  one  form  of  chronic  nephritis,  the  so-called  contracted 
kidney,  as  was  at  first  believed,  but  that  it  is  almost  as  constant  in  many  other 
forms  of  nephritis.  Opinions  are  at  present  still  much  divided  as  to  the  precise 
nature  of  this  connection,  and  as  to  the  causal  factors  which  act  here,  as  the  fol- 
lowing account  will  show. 

The  theory  which  Traube  himself  advanced  for  the  explanation  of  the  cardiac 
hypertrophy  in  nephritis  was  that,  in  the  first  place,  less  water  is  withdrawn 
from  the  blood  in  nephritis  for  the  formation  of  the  renal  secretion,  and  that,  in 
the  second  place,  the  flow  of  arterial  blood  into  the  venous  system  is  hindered 
by  the  changes  in  the  kidneys.  Both  circumstances  must  raise  the  pressure  in 
the  arterial  system,  and  therefore  gradually  lead  to  cardiac  hypertrophy.  Thus 
formulated,  Traube's  theory  can  not  be  maintained.     The  first  statement  especially 


REMARKS  UPON  THE  PATHOLOGY   OF  RENAL  DISEASE.     835 

is  untenable,  because  in  many  cases  of  chronic  contraction  of  the  kidney  with 
co-existing  cardiac  hypertrophy  there  is  never  a  diminution  of  the  elimination  of 
water  by  the  kidneys,  and,  besides,  this  can  never  of  itself  cause  an  increase  of  the 
arterial  pressure.  The  greatest  stress,  however,  has  lately  been  laid  by  Cohnheim 
on  the  second  factor  in  Traube's  theory — on  the  disturbance  of  circulation  in  the 
kidney — although  he  modifies  the  form  of  Traube's  statement.  Cohnheim  shows 
that  the  hindrance  to  the  circulation  in  the  kidneys,  which  develops  chiefly  from 
disease  of  the  glomeruli,  must  be  followed  by  an  increase  of  arterial  pressure, 
because  the  flow  of  arterial  blood  to  the  kidneys  is  not  lessened  in  nephritis. 
Abnormal  resistance  to  the  circulation  forms  behind  the  little  renal  arteries  into 
which  an  abundance  of  blood  pours,  and  this  may  cause  an  increase  of  the  general 
arterial  pressure. 

This  theory,  however,  is  opposed  by  the  fact  that  even  complete  ligature  of 
both  renal  arteries  does  not  raise  the  arterial  pressure,  because  the  blood  at  once 
escapes  into  other  vascular  regions  which  dilate.  The  place  where  the  contraction 
of  the  caliber  of  the  renal  artery  occurs,  whether  in  the  main  trunk  or  in  the 
terminal  branches,  can  make  no  difference,  because  by  it  only  the  length  of  the 
impeded,  or  rather,  to  a  certain  degree,  of  the  stagnant  blood-column,  is  altered, 
which  is  without  influence  on  the  general  blood-pressure. 

Besides  Traube's  and  Cohnheim's  "  mechanical  theory,"  the  "  chemical  theory  " 
of  cardiac  hypertrophy,  which  was  advanced  in  a  partial  form  by  Bright,  has 
lately  found  many  advocates  (Senator  and  others).  According  to  this,  the  reten- 
tion of  urinary  constituents.,  especially  urea,  in  the  blood  causes  the  increase  of 
arterial  pressure.  Of  course  the  quantitative  changes  to  be  considered  here  are 
comparatively  very  slight,  even  if  we  admit  the  retention  of  urinary  constituents 
in  all  forms  of  renal  disease  which  lead  to  cardiac  hypertrophy,  but  the  possibility 
of  the  final  effect  of  such  slight  but  permanent  influences  can  not  be  questioned. 

We  can  not  at  present  give  a  definite  decision  as  to  the  cause  of  cardiac  hyper- 
trophy in  diseases  of  the  kidneys.  Experiments  to  provoke  hypertrophy  of  the 
left  ventricle  in  animals  by  artificial  disturbances  of  the  circulation  in  the  kid- 
neys, by  feeding  with  urea,  etc.,  have  given  scarcely  any  absolute  and  positive 
results,  so  that  it  seems  needless  to  go  into  them  more  fully  in  this  place.  It  may, 
however,  be  assumed  as  certain  that  the  cause  of  the  increased  arterial  pressure  is 
to  be  found  in  the  renal  affection  itself,  and  that  the  hypertrophy  of  the  left 
ventricle  appears  only  as  a  result  of  the  permanent  increase  of  pressure.  Corre- 
sponding to  this  increase  of  pressure,  the  increased  tension  of  the  arterial  system 
is  often  found  clinically  very  early,  while  the  signs  of  the  consecutive  hypertrophy 
of  the  left  ventricle  gradually  develop  later.  In  the  following  chapters  we  will 
discuss  the  great  compensatory  significance  belonging  to  cardiac  hypertrophy  in 
renal  disease,  and  how  the  condition  of  the  heart  finally  occupies  almost  entirely 
the  center  of  the  whole  morbid  picture. 

The  relation  between  certain  diseases  of  the  vessels  and  diseases  of  the  kidneys 
will  be  spoken  of  in  the  chapter  on  contracted  kidney. 


836  DISEASES  OF  THE  KIDNEYS. 

CHAPTER  II. 

ACUTE    NEPHRITIS. 

(Acute  BrighVs  Disease.) 

iEtiology. — Acute  nephritis,  like  most  of  the  other  forms  of  nephritis,  is  not 
a  disease  whose  aetiology  is  uniform.  The  same  anatomical  change,  which  we 
term  "  nephritis,"  and  which  is  attended  by  about  the  same  morbid  phenomena, 
may  be  excited  by  influences  of  very  different  kinds.  Almost  all  tbese  influences 
have  one  thing  in  common,  namely,  that,  as  we  have  stated  in  the  preceding  chap- 
ter, they  reach  the  kidneys  by  way  of  the  circulation  and  are  here  in  part 
eliminated,  and  thus  exert  their  specific  injurious  action  upon  the  parenchyma  of 
the  kidneys;  but  they  differ  considerably  from  one  another  in  their  precise  chem- 
ical or  biological  nature.  Since  the  pathological  change  in  the  kidneys  depends 
upon  the  amount  of  the  noxious  material,  upon  the  intensity  of  its  action  and  the 
duration  of  its  influence,  we  see  that  the  cases  of  nephritis  that  arise  in  this  way 
must  present  a  perfectly  continuous  series  from  the  mildest  to  the  severest,  from 
those  that  pass  off  rapidly  to  those  that  last  perhaps  for  years  and  years.  The 
history  of  renal  pathology  teaches  us  in  the  plainest  way  that  all  attempts  to 
divide  the  forms  of  nephritis  into  different  clinical  and  pathological  "  varieties  " 
can  not  be  strictly  carried  out.  The  more  scientific  experience  increases,  the  more 
numerous  must  be  the  forms  established,  and  still  we  only  too  frequently  have  to 
assume  all  sorts  of  "  transitional  forms  "  merely  to  bring  the  reality  into  harmony 
with  the  scheme.  It  therefore  corresponds  merely  to  our  practical  needs  if  we 
take  certain  types  from  this  whole  list  and  divide  nephritis  into  vai'ious  groups; 
for,  from  the  nature  of  the  case,  there  can  be  no  question  of  a  sharp  separation  of 
the  various  forms. 

We  accordingly  call  those  inflammatory  renal  affections  acute  nephritis  which 
arise  comparatively  rapidly  from  any  of  the  injurious  influences  soon  to  be  enu- 
merated, and  which  terminate,  after  a  few  days  or  a  few  weeks,  either  fatally  or 
with  recovery.  Acute  nephritis,  on  the  one  hand,  follows  immediately,  without 
any  fixed  boundary,  the  mildest  morbid  changes  in  the  kidney,  which  are  usually 
not  termed  actual  nephritis,  but  simple  "  parenchymatous  degeneration  " ;  while 
on  the  other  hand  it  shows  a  continuous  transition  to  those  forms  which  last  for 
several  weeks  or  months,  or  longer,  and  hence  are  called  subacute  or  subchronic 
nephritis. 

Among  the  causes  of  acute  nephritis  we  must  mention  first  a  large  group 
which  consist  of  infectious  influences  (acute  infectious  nephritis).  In  these  cases 
the  nephritis  usually  develops  as  a  secondary  complicating  disease  upon  an  already 
existing  primary  infectious  disease,  and  may  be  regarded  in  most  cases  as  a  special 
"  localization  "  of  the  specific  morbid  poison  present  in  the  body.  In  other  cases 
there  may  be  chemical  substances  which  act  injuriously ;  these  may  develop  in  the 
body  under  the  influence  of  infection,  be  excreted  by  the  kidneys,  and  thus  exert 
a  morbific  action  on  the  renal  tissue.  There  is  scarcely  a  single  infectious  disease 
in  which  there  may  not  be  occasionally  a  renal  affection  as  a  complication.  We 
observe  these  affections  in  our  experience  much  more  frequently  in  certain  infec- 
tious diseases  than  in  others,  so  that  we  may  rightly  assume  that  certain  infectious 
substances  have  a  special  injurious  relation  to  the  kidneys.  Since  we  have  already 
dwelt  upon  the  occurrence,  the  frequency,  and  certain  peculiarities  of  secondary 
nephritis  in  the  description  of  the  different  infectious  diseases,  a  brief  recapitula- 
tion of  the  facts,  which  have  already  been  for  the  most  part  described,  will  suf- 
fice here. 


ACUTE  NEPHRITIS.  837 

The  infectious  disease  which  most  frequently  gives  rise  to  an  acute  nephritis 
is  scarlet  fever.  As  has  been  shown  previously  (see  page  41),  the  renal  affection 
appears  but  rarely  at  the  beginning  of  the  disease,  and  then  in  a  very  mild  form, 
while  the  special  severe  scarlatinous  nephritis  usually  attains  its  development 
only  toward  the  end  of  the  third  week  of  the  disease.  In  measles,  secondary 
nephritis  is  very  much  rarer  than  in  scarlet  fever;  in  rötheln  it  is  only  of  very 
exceptional  occurrence.  It  is  commoner  again  in  smallpox,  especially  in  the 
severe  haemorrhagic  forms.  In  varicella,  renal  affections  are  very  rare,  but  they 
have  been  occasionally  observed.  They  are  always  of  but  slight  intensity.  In 
typhoid  fever  a  slight  albuminuria  is  very  common,  but  genuine  acute  nephritis 
is  quite  rare.  There  are  some  cases,  however,  where  a  nephritis  appears  very 
early,  and  where  the  other  typhoid  symptoms  are  so  crowded  into  the  background 
by  it  that  it  is  decidedly  more  difficult  to  make  the  diagnosis  of  typhoid ;  this  is 
called  the  "renal  form  of  typhoid  fever."  In  typhus  and  recurrent  fevers  severe 
cases  of  nephritis  are  not  especially  common,  but  they  are  seen  more  frequently 
than  in  typhoid  fever. 

The  nephritis  that  often  comes  on  in  cholera  is  of  great  practical  importance. 
This  is  seen  in  the  earlier  stages,  and  is  especially  one  of  the  most  frequent 
causes  of  the  so-called  cholera  typhoid  (see  page  86).  Of  course  it  may  appear 
questionable  whether  the  renal  affection  here  is  always  of  an  inflammatory 
infectious  nature,  or  develops  only  in  consequence  of  the  disturbance  of  circu- 
lation. 

Nephritis  develops  quite  frequently  in  the  course  of  diphtheria,  especially  in 
severe  cases  of  this  disease ;  but  the  renal  affection  only  rarely  reaches  a  high 


gm  - pj 


Fig.  112.— Acute  nephritis  (scarlatinal,  early  stage).  1.  Bowman's  capsule  :  2.  Glomerulus,  increase  of 
nuclei  and  swelling  of  ground  substance  ;  3,  4.  Hyaline  casts  in  renal  tubes,  the  appearance  of  the 
nuclei  in  places  is  such  as  to  suggest  nuclear  figures.    Obj.  i,  without  eyepiece.    (Eosinated  Logwood.') 

degree.  We  sometimes  see,  however,  very  severe  forms  of  nephritis  in  the  so- 
called  septic  diseases  (septic  nephritis,  see  page  112),  in  acute  ulcerative  endocar- 
ditis and  endocarditis  verrucosa,  and  allied  affections,  such  as  puerperal  fever, 
septic  wounds,  etc.  Among  other  acute  diseases  which,  in  comparatively  rare 
cases,  may  be  accompanied  by  nephritis,  we  may  mention  croupous  pneumonia, 


838  DISEASES  OF  THE  KIDNEYS. 

epidemic  meningitis,  erysipelas,  certain  forms  of  sore  throat,  certain  acute  intesti- 
nal affections,  acute  articular  rheumatism,  aud  tetanus. 

Finally,  acute  nephritis  may  also  develop  in  the  course  of  chronic  infectious 
diseases,  especially  tuberculosis  and  syphilis.  We  have  ourselves  repeatedly  seen 
a  mild  or  even  a  severe  acute  nephritis  come  on  in  the  secondary  stage  of  the 
latter  disease.  A  genuine  acute  nephritis  may  also  arise  in  the  course  of  pul- 
monary tuberculosis,  but  for  the  present  we  can  not  decide  whether  this  is 
directly  connected  with  the  tuberculosis,  or  whether,  as  is  more  probable,  it  arises 
in  consequence  of  the  absorption  of  septic  substances  from  the  contents  of  the 
cavities. 

We  ought  also  to  speak  of  the  acute  nephritis  sometimes  seen  in  patients  with 
pustular  eruptions,  such  as  impetigo,  pustular  eczema,  severe  scabies,  etc.  It  may, 
however,  appear  doubtful  whether  the  cause  of  the  nephritis  is  to  be  sought  in  the 
absorption  of  some  injurious  substance  from  the  diseased  skin,  or  whether  the 
disturbance  of  the  cutaneous  activity  may  not  in  itself  exert  a  deleterious  influ- 
ence on  the  kidneys. 

Besides  the  infectious  forms  of  nephritis  just  described,  there  is  a  second  great 
group,  which  may  be  classed  under  the  general  heading  of  toxic  nephritis.  In 
these  cases  we  are  dealing  with  the  deleterious  action  of  chemical  substances 
which  enter  the  body  from  without  and  are  excreted  from  it  by  the  kidneys.  It 
is  wholly  impossible  to  enumerate  all  the  substances  which  have  this  injurious 
effect ;  we  will  therefore  confine  ourselves  to  mentioning  those  of  the  greatest 
practical  importance.  Among  the  poisons  proper  we  may  mention  the  mineral 
acids,  sulphuric,  hydrochloric,  and  nitric  acids,  oxalic  acid,  phosphorus,  arsenic, 
lead,  and  Chromate  of  potassium.  Among  remedies  used  internally,  which  may 
excite  nephritis  when  given  in  too  great  doses,  we  may  mention  cantharides, 
squills,  balsam  of  copaiba,  turpentine,  salicylic  acid,  and  chlorate  of  potassium. 
It  is  also  very  important  to  know  that  many  remedies  applied  to  the  external  skin 
are  absorbed  by  the  skin,  and  in  this  way  may  reach  the  kidneys  and  excite  severe 
changes  there.  Among  these  are  cantharidal  plaster,  preparations  of  tar,  petro- 
leum, styrax,  naphthol,  and  pyrogallic  acid.  We  must  mention,  in  addition  to 
these,  the  renal  affection  which  may  arise  from  the  too  abundant  use  of  carbolic 
acid  or  iodoform  to  the  surface  of  open  wounds.  Under  some  circumstances 
renal  affections  may  even  arise  in  individual  cases  from  taking  excessive  amounts 
of  certain  foods  and  drinks,  such  as  spices,  alcohol,  or  very  acid  foods. 

In  the  forms  of  acute  nephritis  which  can  not  be  immediately  referred  to 
infectious  or  toxic  influences,  and  whose  number  is  comparatively  small,  we  can 
sometimes  find  no  definite  cause  at  all.  We  then  speak  of  a  primary  idiopathic 
acute  nephritis.  We  are  indeed  justified  in  thinking  of  causes  of  origin  here 
similar  to  those  in  the  cases  previously  described,  but  causes  which  at  present 
escape  direct  detection.  In  other  cases  an  acute  nephritis  immediately  follows 
exposure  to  severe  cold  or  wetting  of  the  skin.  We  can  not  doubt  the  possibility 
of  such  a  connection  after  quite  numerous  and  indubitable  clinical  experiences, 
although  the  exact  conditions  to  be  considered  here  are  still  almost  wholly 
unknown.  We  usually  take  refuge  in  a  rather  noncommittal  reference  to  the 
"  well-known  connection  between  the  activity  of  the  skin  and  of  the  kidneys." 
The  experiments  on  this  point  have  also  confirmed  the  fact  itself,  but  have  fur- 
nished no  precise  explanation  of  its  cause. 

We  have  still  to  mention  the  nephritis  of  pregnancy  {nephritis  gravidarum) 
as  a  special  form  of  acute  nephritis.  This  usually  comes  on  in  the  last  months  of 
pregnancy  in  women  previously  perfectly  healthy,  and  is  decidedly  more  frequent 
in  Primiparae  than  in  the  course  of  later  pregnancies.  The  precise  causes  of  the 
nephritis  of  pregnancy  are  still  very  obscure.    Some  authors  lay  the  blame  on  the 


ACUTE  NEPHRITIS.  839 

pressure  of  the  pregnant  uterus  on  the  renal  vessels,  others  on  its  pressure  upon 
the  ureters,  etc.  (compare  the  text-books  on  obstetrics). 

Finally",  we  must  mention  that  an  acute  nephritis  may  ensue  on  a  chronic 
nepbritis  that  has  existed  for  a  long  time,  perhaps  without  symptoms  (acute  recur- 
rent nephritis  of  Wagner). 

Pathological  Anatomy. — The  anatomical  changes,  which  are  excited  in  the 
kidneys  by  the  causes  mentioned  in  what  has  gone  before,  show  a  continuous  series 
from  the  mildest  to  the  severest  degrees,  according  to  the  intensity  of  the  injurious 
action.  The  mildest  changes,  which,  as  we  have  said,  are  not  called  actual  "  inflam- 
mation," but  usually  simple  parenchymatous  degeneration,  affect  exclusively  the 
parenchyma  of  the  kidney — that  is,  the  epithelium — while  the  interstitial  tissue, 
the  connective  tissue,  and  the  vessels  remain  perfectly  normal.  This  fact  is  espe- 
cially important  since  it  implies  that,  in  almost  all  the  injurious  influences 
acting  on  the  kidneys,  the  specific  renal  parenchyma  itself  is  diseased  first  and 
before  any  other.  On  macroscopic  examination,  the  kidneys  may  show  scarcely 
any  plainly  perceptible  changes,  but  it  sometimes  strikes  the  practiced  eye  that 
the  kidneys  are  a  little  enlarged,  that  the  cortex  on  section  shows  either  a  more 
reddish  -  gray,  dimmed  coloring  (cloudy  swelling),  or  a  more  grayish  -  white, 
yellowish  hue  (fatty  degeneration).  The  microscopic  examination  gives  more 
accurate  information  as  to  the  degree  and  the  extent  of  the  disease.  We  distin- 
guish different  conditions  according  to  the  form  of  change  in  the  epithelium,  of 
which  the  three  following  are  most  important:  1.  Cloudy  Swelling:  It  is  most 
easily  made  out  in  the  epithelium  of  the  cortical  tubules,  but  it  may  also  be  seen 
in  the  epithelium  of  the  glomeruli.  The  cells  swell,  their  contents  become  uni- 
formly granular  and  cloudy,  the  nuclei  swell,  and  finally  disappear.  Such 
changes  are  often  found  in  acute  infectious  diseases,  like  typhoid,  small-pox,  and 
diphtheria.  2.  Fatty  Degeneration :  This  may  proceed  from  the  cloudy  swelling, 
or  may  develop  independently.  Many  fat-drops  appear  both  in  the  cells  of  the 
uriniferous  tubules  and  also  in  the  epithelium  of  the  glomeruli,  and  they  may 
finally  lead  to  the  disintegration  of  the  cells.  Simple  fatty  degeneration  of  the 
kidneys  is  sometimes  found  in  acute  infectious  diseases,  after  certain  poisons, 
like  phosphorus,  and  finally  in  anaemic  conditions.  3.  Necrosis  of  the  Renal 
Epithelium :  The  nuclei  of  the  cells  disappear,  and  the  cells  are  changed  to  clear 
homogeneous  flakes,  while  in  some  cases  they  are  greatly  swollen  ("dropsical 
degeneration  "  of  Nauwerck-Ziegler).  Genuine  epithelial  necrosis  is  found  in  the 
kidneys,  chiefly  after  the  action  of  toxic  substances — like  cantharides,  the  chromic 
and  chloric  salts,  etc.— but  sometimes  also  in  infectious  diseases.  Combinations 
of  simple  necrosis  with  granular  cloudiness  and  fatty  degeneration  are  not  infre- 
quent. Both  the  last-named  states  may  undergo  resolution  if  they  have  not 
reached  a  high  degree.  Otherwise  all  the  degenerations  mentioned  lead  to  the 
destruction  and  disintegration  of  the  cells ;  nevertheless,  a  complete  restoration  is 
possible,  from  the  regeneration  of  new  epithelial  cells  from  epithelium  that  is  still 
present. 

We  term  those  changes  in  the  kidneys  genuine  acute  nephritis,  in  which  not 
only  the  renal  parenchyma  proper,  the  epithelium,  but  also  the  interstitial  tissue, 
especially  the  vessels,  is  affected  ;  so  that  we  can  make  out  the  exudative  changes 
characteristic  of  all  inflammatory  processes — the  escape  of  fluid  and  cells  from  the 
vessels.  In  these  cases  the  different  histological  processes  may  be  combined  in 
the  most  varied  ways,  so  that  the  anatomical  picture  presents  quite  great  variations, 
although  it  is  almost  always  principally  concerned  with  the  same  processes. 

If  we  begin  with  the  histological  lesion  in  acute  nephritis,  in  order  to  learn  to 
recognize  at  once  the  essential  changes,  we  have  first  precisely  the  same  processes 
of  degeneration  in  the  epithelium  which  have  been  already  described,  but  they  are 


840  DISEASES  OF  THE  KIDNEYS. 

\ 

usually  present  here  in  a  more  marked  degree.  In  some  cases  the  simple  ne- 
crotic pi*ocesses  predominate;  in  others,  the  fatty  degeneration.  We  often  find 
degenerated  cells,  and  not  infrequently  a  more  or  less  marked  desquamation  of 
epithelium.  We  see  besides  the  special  inflammatory  changes.  We  find  a  fluid 
inflammatory  exudation,  rich  in  fibrine,  and  therefore  soon  coagulating  in  the  inter- 
stitial connective  tissue,  which  is  dilated  and  swollen  by  it — inflammatory  oedema. 
The  same  exudation  is  also  found  in  the  uriniferous  tubules,  and,  by  the  proper 
methods,  by  alcohol  or  by  boiling  the  fresh  kidney,  the  albuminous  effusion  can 
be  made  out  both  in  the  capsules  of  the  glomeruli  and  in  the  uriniferous  tubules. 
The  interpretation  of  the  exudation  is,  of  course,  made  very  difficult,  or  often 
wholly  impossible,  by  the  presence  of  albuminous  urine  in  the  uriniferous  tubules. 
The  second  characteristic  of  inflammation,  the  "  cellular  exudation  " — that  is,  the 
emigration  of  white  blood-corpuscles — is  also  present.  In  the  interstitial  tissue  we 
find  accumulations  of  round  cells,  usually  distributed  in  foci,  and  white  blood- 
corpuscles  in  greater  or  less  numbers  also  enter  the  interior  of  the  uriniferous 
tubules.  We  often  find  many  hyaline  casts  in  the  lumen  of  the  straight  tubules 
or  of  Henle's  loops,  whose  origin  is,  in  all  probability,  connected  with  the  albu- 
minous exudation  and  the  emigrated  white  blood-corpuscles  (see  page  776).  The 
vessels  themselves  are  often  hyperaemic  and  dilated,  but  in  some  cases  they 
are  compressed  by  the  interstitial  inflammatory  oedema.  It  is  of  special  signifi- 
cance that  in  very  many  cases  there  are  haemorrhages,  either  into  the  interstitial 
tissue  or  into  the  interior  of  the  uriniferous  tubules,  or  even  into  Malpighi's 
capsules. 

All  the  changes  described  are  not  always  found  uniformly  distributed  over  the 
whole  kidney.  Some  parts  are  often  much  diseased,  others  but  slightly,  while 
others  still  are  nearly,  if  not  quite,  intact.  We  may  accordingly  speak  in  indi- 
vidual cases  of  a  diffuse  or  of  a  localized  nephritis,  although  there  are  no  strict 
limits  here. 

If  the  histological  processes  have  been  made  clear,  the  understanding  of  the 
macroscopic  appearance  of  the  inflamed  kidney  is  very  simple.  We  can  under- 
stand that  either  this  or  that  u  form  "  of  acute  nephritis  must  be  present  accord- 
ing to  the  predominance  of  this  or  that  histological  process.  If  an  abundant 
interstitial  exudation  is  present,  the  kidney  is  much  enlarged ;  if  this  exudation 
is  slight,  the  kidney  varies  but  little,  or  not  at  all,  from  its  normal  size,  not- 
withstanding any  other  severe  changes.  In  the  first  case  it  usually  feels  soft, 
from  inflammatory  oedema;  in  the  second  case,  it  is  comparatively  firm.  If 
there  is  a  marked  hyperaemia  of  the  kidney,  it  appears  much  reddened;  if  the 
kidney  is  anaemic,  it  is  paler ;  and  if  an  extensive  fatty  degeneration  is  also  pres- 
ent, it  is  yellowish-white  or  yellow.  If  haemorrhages  are  present,  they  can  easily 
be  recognized  with  the  naked  eye  on  the  outer  surface  beneath  the  capsule  as  dark- 
red  points  that  can  not  be  wiped  away.  We  speak  then  of  an  "  acute  haemorrhagic 
nephritis."  On  section,  the  medullary  substance  is  more  or  less  dilated,  its  normal 
striated  appearance  is  almost  always  obliterated,  and  its  color  shows  the  same 
variations  as  the  outer  sui-face  of  the  kidney.  Since,  as  we  have  said,  the  nephritic 
changes  often  show  not  a  uniform,  but  a  nodular  arrangement,  we  can  understand 
that  the  kidneys  sometimes  have  quite  a  mottled  appearance,  since  hyperaemic  or 
haemorrhagic  red  spots  alternate  with  the  lighter  anaemic  and  the  yellow  fatty- 
degenerated  parts. 

There  are,  accordingly,  cases  of  nephritis  which  show  almost  nothing  abnormal 
to  the  naked  eye,  while,  on  the  other  hand,  there  are  haemorrhagic  and  non- 
haemorrhagic  forms,  appearing  pale,  yellow,  red,  or  variegated,  none  of  which 
can  in  the  essential  features  be  separated  from  one  another,  but  which  are  com- 
bined with  one  another  in  all  conceivable  ways.     The  forms  of  nephritis  that 


ACUTE  NEPHRITIS.  841 

differ  in  aetiology  have,  to  a  certain  degree,  definite  and  characteristic  anatomical 
types,  but  strict  rules  can  not  be  laid  down  in  regard  to  this. 

In  addition,  quite  a  characteristic  anatomical  form  of  acute  nephritis  deserves  a 
brief  mention,  in  which  the  changes  are  almost  exclusively  limited  to  the  glo- 
meruli, and  which  are  therefore  called  glomerulo-nephritis  (Klebs,  Friedländer, 
Ribbert).  In  the  purest  cases  of  this  form,  as  it  is  seen  especially  in  scarlet  fever 
and  also  in  other  infectious  diseases,  we  find  degeneration  and  abundant  des- 
quamation of  the  epithelium  only  in  the  glomeruli  of  the  kidneys;  and  we  usually 
find,  besides,  a  marked  disease  of  the  vessel- walls,  which  swell  and  acquire  a  homo- 
geneous hyaline  appearance.  The  glomerulo-nephritis  can  not  in  its  essentials  be 
perfectly  definitely  separated  from  the  other  forms  of  acute  nephritis,  since  in 
these,  under  some  circumstances,  the  glomeruli  may  first  be  chiefly  affected ;  but, 
as  it  seems,  this  need  not  happen  in  all  cases  by  any  means. 

Clinical  History. — The  most  essential  symptom  of  acute  nephritis  is  the  abnor- 
mal character  of  the  urine.  In  most  of  the  milder,  and  even  in  many  of  the 
severer  cases  of  nephritis,  the  change  in  the  urine  is  the  sole  objective  clinical 
symptom  which  renders  the  diagnosis  possible.  The  physician  must,  therefore, 
make  it  his  practice  to  submit  the  urine  to  repeated  examinations  in  every  case  of 
disease  where  there  is  any  possibility  of  the  presence  of  a  nephritis. 

The  simple  parenchymatous  degenerations  of  the  kidneys,  cloudy  swelling, 
fatty  degeneration,  etc.,  which  we  will  first  briefly  touch  upon,  may  probably 
sometimes  exist  without  being  followed  by  any  discoverable  change  in  the  urine ; 
but  they  often  lead  to  a  slight  albuminuria,  which  is  easily  explained  from  the 
change  in  the  epithelium  of  the  glomeruli.  If,  then,  the  urine  contains  a  slight 
amount  of  albumen  (which  usually  soon  passes  off)  in  the  course  of  any  febrile 
infectious  disease  or  other  affection  (the  so-called  febrile  albuminuria,  etc.),  we  are 
justified  in  assuming  some  of  these  mild  conditions  of  degeneration  in  the  kidneys. 
Usually  the  urine  shows  no  other  peculiarities,  but  sometimes  we  find  in  the 
sediment  a  few  hyaline  casts,  a  few  white  blood-corpuscles,  etc.  As  we  have 
repeatedly  stated,  these  conditions  pass  into  nephritis  proper  without  any  sharp 
limitations. 

Character  of  the  Urine  in  Acute  Nephritis.— In  almost  every  severe 
nephritis  the  amount  of  urine  for  the  twenty-four  hours  is  more  or  less  dimin- 
ished. This  is  either  caused  directly  by  the  lessened  elimination  of  water  by  the 
kidneys,  or  by  the  plugging  of  many  uriniferous  tubules  by  casts,  desquamated 
epithelium,  etc.  The  amount  evacuated  daily  is  often  only  fifteen  or  twenty 
ounces  (400-700  c.  a),  but  it  sometimes  falls  to  a  much  lower  figure,  two  or  three 
ounces  (f00-50  c.  a),  and  there  may  finally  be  even  complete  anuria.  In  general, 
though  not  without  exceptions,  the  diminution  of  the  amount  of  urine  runs 
parallel  to  the  severity  of  the  anatomical  changes  in  the  kidney.  Improvement 
in  the  disease  is  very  often  first  seen  in  an  increase  of  the  amount  of  urine. 
If  there  was  a  previous  oedema,  and  this  is  absorbed,  the  daily  amount  of  urine 
of  ten  rises  during  convalescence  to  a  very  considerable  quantity,  eighty  to  a  hun- 
dred ounces  (2500-3000  c.  c). 

The  specific  gravity  of  the  urine  is  at  first  usually  increased,  since  the  urine  is 
poor  in  water,  but  comparatively  rich  in  solid  constituents,  especially  in  albumen 
(vide  infra).  Of  course  there  are  great  differences  here,  and  a  urine  secreted  in 
an  abnormally  small  amount  may  show  a  specific  gravity  of  only  1010  or  1015, 
while,  on  the  other  hand,  urines  with  a  specific  gravity  of  1020  to  1030,  or  even 
more,  have  been  observed.  If  during  convalescence  a  very  abundant,  watery 
urine  is  passed,  it  of  course  usually  has  a  low  specific  gravity,  1005  to  1008. 

In  many  cases,  but  of  course  not  in  all,  we  may  suspect  the  abnormal  character 
of  the  urine  from  its  appearance.     This  depends  chiefly  upon  an  admixture  of 


842  DISEASES  OF  THE  KIDNEYS. 

abnormal  morphological  constituents.  If  these  are  present  in  large  numbers,  as  is 
usually  the  case,  the  freshly  passed  urine  is  cloudy,  and  deposits  a  more  or  less 
abundant  floccular  sediment.  The  appearance  of  the  urine  is  most  altered  if 
blood  be  mixed  with  it  (hcemorrhagic  urine).  According  to  the  amount  of  blood, 
the  urine  is  a  light  or  dark  red,  or  even  a  dark  black-red,  and  often  has  a  greenish 
reflection  when  the  light  falls  on  it. 

The  microscopic  examination  of  the  sediment  gives  more  accurate  information 
upon  the  different  morphological  constituents.  We  can  not,  of  course,  enumerate 
all  the  possibilities  that  may  exist  in  these  cases  (see  page  826  et  seq.).  It  is 
generally  the  case  that  in  most  of  the  severe  forms  of  acute  nephritis  the  urine 
contains  many  casts  of  all  sorts,  usually  hyaline,  but  sometimes  partly  fatty  or 
waxy,  and  very  often  covered  with  red  or  white  blood-corpuscles,  epithelium, 
detritus,  etc.  The  different  cases  are  often  characterized  by  a  striking  predomi- 
nance of  some  one  constituent — epithelium,  white  blood-corpuscles,  or  red  blood- 
corpuscles — but  no  special  rules  in  regard  to  this  can  be  given.  We  have  spoken 
previously  (page  827)  of  the  special  conclusions  we  can  draw  from  the  different 
objects  found  in  the  sediment.  We  can  accordingly  distinguish  an  acute  haemor- 
rhagic,  or  non-basmorrhagic,  an  acute  desquamative,  and  a  fatty  degenerative 
nephritis,  but  we  must  always  bear  in  mind  that  all  these  forms  pass  into  one 
another  without  sharp  boundaries. 

The  chemical  examination  of  the  urine  gives,  as  the  most  important  and  con- 
stant result,  usually  a  considerable  amount  of  albumen.  Since  the  reaction  of  the 
urine  is  almost  invariably  acid,  the  albumen  is  immediately  precipitated  on  heating 
the  urine,  and  sinks  to  the  bottom  of  the  test-tube,  where  it  usually  takes  up  about 
one  half  or  three  fourths  of  the  volume  of  urine  used  for  the  heat-test.  More 
accurate  quantitative  determinations  of  albumen  give  most  frequently  in  acute 
nephritis  an  amount  of  albumen  of  from  three  tenths  to  one  per  cent. ;  higher 
percentages  are  rare.  The  daily  total  amount  of  albumen  eliminated  amounts  to 
about  one  or  two  drachms  (5-8  grammes),  or  sometimes  more,  but  the  daily  loss 
of  albumen  from  the  body  hardly  ever  exceeds  the  amount  of  five  drachms  (20 
grammes).  The  variation  in  the  amount  of  elimination  of  albumen  in  different 
cases  is  quite  noticeable. 

The  examination  of  the  other  solid  constituents,  which  is  not  generally  em- 
ployed in  practice,  usually  gives  a  diminished  secretion  of  urea,  phosphoric  acid, 
etc.,  corresponding  to  the  diminution  in  the  whole  amount  of  urine. 

The  other  Symptoms  of  Acute  Nephritis. — Local  symptoms  in  the  kidneys 
themselves  are  only  rarely  present.  There  is,  of  course,  a  certain  tenderness  in 
the  region  of  the  kidneys,  whicb,  however,  is  too  ambiguous  to  have  a  great  symp- 
tomatic importance.  It  is  more  frequently  the  case  that  the  abnormally  concen- 
trated urine  causes  the  patient  to  micturate  more  frequently  than  usual,  and  that 
micturition  itself  is  associated  with  a  disagreeable  burning — a  sort  of  vesical  tenes- 
mus. 

The  subsequent  symptoms  of  acute  nephritis,  which  appear  in  the  rest  of  the 
body,  and  among  which  dropsy  takes  the  first  place,  are  far  more  important  than 
the  local  symptoms.  Although  oedema  may  be  entirely  absent  in  acute  nephritis, 
it  is  present  in  most  severe  cases,  and  often  is  predominant  in  the  clinical  picture. 
We  must  always  be  prepared  for  its  appearance,  especially  when  the  amount  of 
urine  shows  a  considerable  diminution. 

The  oedema  is  usually  discovered  first  in  the  face,  which  has  a  bloated,  and 
often  a  pale  and  somewhat  shiny  appearance.  The  eyelids  are  usually  most 
swollen  at  first.  Beside  the  face,  the  ankles,  the  legs,  the  scrotum,  and  the  depend- 
ent parts  of  the  trunk  may  be  the  chief  seat  of  the  oedema,  the  severity  and  extent 
of  which  may  of  course  vary  greatly  in  different  cases.     If  a  high  degree  of  gen- 


ACUTE  NEPHRITIS.  843 

eral  dropsy  develops,  this  is  a  source  of  great  distress  to  the  patient.  The  move- 
ments of  the  body  are  much  restrained,  and  all  changes  of  position  are  difficult, 
associated  with  great  exertion,  and  painful.  In  the  severest  degrees  of  dropsy 
small  fissures  may  form  here  and  there  in  the  excessively  tense  skin,  from  which 
the  dropsical  fluid  oozes.  Such  little  wounds  are  sometimes  the  starting-point  for 
disagreeable  erysipelatous  inflammations,  etc. 

If  great  oedema  of  the  skin  is  present,  we  usually  find  at  the  same  time  a  more 
or  less  marked  dropsy  of  the  serous  cavities.  It  is  often  hard,  however,  to  mala; 
out  ascites  or  hydrothorax  on  physical  examination,  owing  to  the  oedema  of  the 
skin  that  is  present.  The  symptoms  mentioned  acquire  their  chief  clinical  signifi- 
cance from  the  difficulty  of  respiration  necessarily  associated  with  them,  since  the 
diaphragm  is  pressed  upward  by  ascites,  and  the  lungs  are  compressed  by  hydro- 
thorax.  If  a  hydrothorax  is  more  marked  on  the  left,  or  especially  if  hydroperi- 
cardium  sets  in,  the  activity  of  the  heart  is  materially  impaired. 

A  marked  oedema  of  the  mucous  membranes  develops  but  rarely;  in  a  few 
cases  we  have  seen  oedema  of  the  conjunctivae,  oedema  of  the  soft  palate,  and 
oedema  of  the  glottis.  Of  the  oedemas  of  internal  organs,  oedema  of  the  brain  has 
already  been  mentioned  as  a  possible  cause  of  severe  nervous  uraemic  symptoms. 
CEdema  of  the  lungs,  which  often  comes  on  toward  the  end  of  the  disease,  when 
it  terminates  unfavorably,  is  usually  not  to  be  regarded  as  a  part  of  the  general 
oedema,  but  as  a  result  of  the  final  cardiac  weakness. 

In  regard  to  the  other  symptoms  in  the  different  organs,  the  symptoms  on  the 
part  of  the  circulatory  apparatus  must  first  be  mentioned.  The  pulse  is  often 
abnormally  tense,  hard,  and  full  (see  page  835).  In  the  beginning  of  the  disease 
it  is  often  somewhat  slow ;  later  it  is  usually  accelerated.  A  beginning  cardiac 
hypertrophy  can  often  be  made  out  post  mortem,  and  sometimes  clinically,  in 
cases  which  have  lasted  a  somewhat  longer  time,  two  to  four  weeks.  It  seems 
to  develop  most  rapidly  in  children  who  were  previously  well  and  strong.  We 
pay  especial  regard  to  the  condition  of  the  apex-beat,  and  to  the  accentuation  of 
the  aortic  second  sound.  The  occasional  nose-bleeds  are  probably  connected  with 
the  increased  arterial  tension.  Pericarditis  is  seen  as  a  very  rare  complication — ■ 
a  complication  which  is  connected  with  the  general  fact  that  in  all  forms  of 
nephritis  the  different  internal  organs,  especially  the  serous  membranes,  have  a 
tendency  to  inflammation.  Whether  this  circumstance  is  connected  with  the 
retention  of  urinary  constituents,  as  has  been  repeatedly  imagined,  can  not  at 
present  be  decided  with  certainty. 

Of  the  symptoms  in  the  respiratory  apparatus,  we  have  mentioned  above  the 
dyspnoea  consequent  upon  the  dropsical  symptoms.  In  severe  cases  the  lungs 
themselves  are  often  drawn  into  sympathy,  since  a  diffuse  bronchitis  or  a  peculiar 
form  of  pneumonia  develops  in  them,  which  latter  stands  midway  between  a 
catarrhal  and  a  croupous  inflammation.  It  exhibits,  to  a  certain  degree,  a  form 
of  stiff  inflammatory  oedema,  and  occurs  in  just  the  same  way  in  the  chronic 
forms  of  nephritis  as  in  acute  nephritis.  When  it  involves  both  lungs  to  a  great 
extent,  it  may  be  the  immediate  cause  of  death.  The  development  of  a  pure  gen- 
eral pulmonary  oedema  is  almost  always  a  sign  of  beginning  weakness  of  the  left 
ventricle,  as  we  have  said  above. 

Vomiting  is  the  most  important  symptom  in  the  digestive  apparatus.  If  it 
appears  in  a  marked  degree,  it  may  almost  always  be  considered  as  a  urasmic 
symptom,  and  then  is  often  the  precursor  of  severe  nervous  symptoms.  The  appe- 
tite is  almost  always  diminished  in  acute  nephritis;  the  bowels  are  usually  consti- 
pated, but  there  may  be  quite  severe  diarrhoea  (see  page  882).  We  may  mention 
peritonitis,  which  is  sometimes  purulent,  as  a  very  rare  complication  {vide  supra). 

The  temperatui'e  is  markedly  influenced  by  acute  nephritis  only  in  those  cases 


844  DISEASES  OF  THE  KIDNEYS. 

where  the  disease  develops  in  previously  healthy  persons,  or  at  least  in  those  free 
from  fever.  Then  we  see  quite  frequently  a  moderate  fever,  with  an  irregular 
rise  of  temperature  of  about  100°  to  102°  (38°-39°  C).  It  is  quite  rare  that  an  appa- 
rently primary  acute  nephritis  begins  suddenly  with  a  chill  and  high  fever,  104° 
(40°  C).  The  condition  of  the  temperature  on  the  onset  of  urasniic  symptoms  has 
already  been  described  (page  833). 

The  state  of  the  general  nutrition  suffers  in  quite  a  noticeable  degree  in  most 
of  the  severe  cases  of  acute  nephritis.  The  emaciation  is  often  concealed  by  the 
oedema ;  but  the  anaemia  is  the  more  prominent,  and  often  lends  to  the  bloated  face 
a  peculiar  pallid  aspect. 

Uroamic  symptoms  may  come  on  at  any  time  in  the  course  of  acute  nephritis. 
We  are  often  prepared  for  the  onset  of  uraemia  by  a  previous  marked  decrease  in 
the  secretion  of  urine,  or  by  the  well-known  prodromal  symptoms,  but  in  other 
cases  it  begins  very  suddenly  with  severe  symptoms  of  eclampsia.  In  regard  to 
all  further  details  we  may  refer  to  what  was  said  on  page  829  et  seq. 

The  Course  and  Different  Forms  of  Acute  Nephritis. — The  whole  clin- 
ical picture  of  acute  nephritis  depends  very  materially  upon  the  form  of  its 
development.  If  an  acute  nephritis  comes  on  in  the  course  of  a  severe  infectious 
general  disease,  as  in  the  course  of  a  septic  affection,  of  ulcerative  endocarditis,  or 
of  severe  typhoid,  the  changes  in  the  urine  are  often  the  sole  factor  pointing  to 
the  occurrence  of  the  complication.  The  type  of  tbe  severe  febrile  general  disease 
is  in  no  way  materially  modified  by  the  added  renal  affection ;  oedema  and  uraemic 
symptoms  do  not  usually  appear,  often  because  the  primary  disease  soon  ends  in 
death. 

Also  when  nephritis  comes  on  in  previously  healthy  persons  or  in  chronic 
invalids,  the  tuberculous,  etc.,  in  many  cases  the  changes  in  the  urine  are  the 
chief  symptom,  while  the  other  general  and  secondary  symptoms  are  scarcely  evi- 
dent at  all,  or  at  least  only  in  a  very  slight  degree.  Such  mild  cases  are  associated 
only  with  more  or  less  general  dullness  and  loss  of  appetite.  CEdema  is  entirely 
absent,  or  present  only  to  a  very  slight  degree.  Of  course  such  cases  demand 
great  caution,  since  even  in  them  we  may  have  a  sudden  outbreak  of  severe 
uraemic  symptoms. 

The  fully  developed  type  of  severe  acute  nephritis  is  seen  especially  in  scar- 
latinous nephritis  (q.  v.),  which  comes  on  in  children  who  are  fully  convalescent 
or  apparently  wholly  well  ;  it  is  also  seen  in  many  cases  of  apparently  idiopathic 
nephritis,  or  nephritis  coming  on  after  exposure  to  cold,  etc.  In  these  cases  there 
is  often  the  development  of  a  general  dropsy,  secondary  pulmonary  affections, 
uraemic  symptoms,  the  symptoms  mentioned  in  the  circulatory  apparatus,  etc.  In 
these  cases,  too,  the  examination  of  the  urine  affords  the  only  certain  means  of 
judging  accurately  of  the  condition,  but  the  other  morbid  symptoms  which  appear 
early — oedema,  anaemia,  and  vomiting — may  direct  our  suspicions  to  the  develop- 
ing renal  affection. 

Scarcely  any  more  general  statements  can  be  made  as  to  the  wbole  course  and 
the  duration  of  acute  nephritis,  since  the  variations  in  this  respect  are  too  great. 
To  describe  here  in  particular  all  the  different  forms  of  nephritis  according  to  the 
aetiological  conditions  in  question  would  lead  us  too  far.  We  will  therefore  refer 
to  the  description  of  the  different  primary  diseases  in  which  the  characteristic 
marks  of  any  renal  complication  are  always  stated.  The  primary  nephritis  from 
exposure  to  cold  and  the  nephritis  of  pregnancy  still  demand  a  few  remarks. 

The  nephritis  from  exposure  TO  cold — primary  idiopathic  nephritis — usually 
comes  on  quite  speedily  after  the  exciting  cause.  The  first  symptoms  of  the  dis- 
ease are  sometimes  insignificant,  but  at  other  times  they  are  quite  severe — chills, 
fever,  renal  pain,  etc.     Sometimes  other  "  rheumatic  symptoms,"  like  angina  or 


ACUTE  NEPHRITIS.  845 

articular  pains,  are  also  present.  The  further  course  may  be  mild  or  severe.  In 
the  former  case  the  oedema  that  has  appeared  is  but  slight,  the  changes  in  the 
urine  (albuminuria,  haematuria,  etc.),  do  not  attain  a  very  high  degree,  and  after 
a  few  weeks  complete  recovery  ensues.  In  other  cases,  however,  the  type  of  a 
severe,  acute,  and  very  often  haemorrhagic  nephritis  develops,  with  great  general 
dropsy,  uraemia,  etc.,  which  in  three  or  four  weeks,  or  sooner,  may  lead  to  death  ; 
but  improvement  may  follow  in  spite  of  the  severest  symptoms.  Then  the  amount 
of  urine  gradually  increases,  and  the  abnormal  constituents  of  the  urine,  the 
oedema,  and  the  other  morbid  symptoms,  gradually  disappear.  Of  course,  it  is 
often  a  long  time  before  complete  recovery  ensues,  since,  even  when  the  patient 
feels  perfectly  well  subjectively,  the  urine  may  still  sometimes  contain  some  albu- 
men, a  few  casts,  or  a  few  red  blood-corpuscles.  We  must  also  bear  in  mind  the 
possibility  of  a  transition  from  acute  to  chronic  nephritis. 

The  nephritis  OF  pregnancy  usually  begins  gradually.  Frequent  micturition 
and  oedema  of  the  lower  extremities  make  their  appearance,  and  beside  these  there 
are  often  nausea  and  even  vomiting.  If  we  examine  the  urine,  we  usually 
find  it  quite  rich  in  albumen,  but  comparatively  poor  in  corporeal  elements.  The 
slight  sediment  consists  of  hyaline  casts,  a  few  white  blood-corpuscles,  and  some 
epithelium.     Only  rarely  does  the  urine  assume  a  haemorrhagic  character. 

The  condition  described  almost  always  lasts  to  the  end  of  pregnancy.  In  the 
cases  that  proceed  favorably  a  very  rapid  recovery  often  follows  after  the  birth 
of  the  child  ;  but  the  onset  of  eclampsia  gravidarum  is  to  be  dreaded  as  a  not 
infrequent  and  a  dangerous  complication.  This  is  to  be  regarded  as  entirely  anal- 
ogous to  uraemia.  It  begins  after  mild  prodromal  symptoms,  or  even  quite  sud- 
denly, with  violent  general  convulsions,  during  which  the  child  is  usually  born. 
A  more  or  less  persistent  coma  follows  the  convulsions.  The  convulsions  may  be 
very  frequently  repeated.  Death  ensues  in  about  one  third  of  the  cases ;  the  other 
cases  usually  recover,  only  rai'ely  passing  into  chronic  nephritis.  The  prognosis 
is  still  more  unfavorable  for  the  child  than  for  the  mother,  inasmuch  as  the  child 
dies  in  nearly  one  half  of  the  cases. 

The  anatomical  changes  in  the  nephritis  of  pregnancy  are  hardly  ever  very 
striking  to  the  eye.  The  kidneys  are  usually  pale  and  but  little  enlarged.  Under 
the  microscope  we  usually  find  a  slight  interstitial  oedema  and  degenerative 
changes  in  the  epithelium.  Only  rarely  are  more  marked  nephritic  appearances 
present. 

Diagnosis. — Acute  nephritis  can  be  overlooked  only  when  the  examination  of 
the  urine  is  neglected  or  can  not  be  carried  out.  The  latter  sometimes  happens, 
for  example,  when  the  patient  does  not  come  under  observation  until  after  the 
onset  of  severe  uraemic  symptoms.  Otherwise,  however,  the  changes  in  the  urine 
always  furnish  evidence  enough  to  recognize  the  existence  of  the  affection  of  the 
kidneys.  We  can,  of  course,  decide  that  the  nephritis  is  acute  only  by  considera- 
tion of  the  history,  the  astiological  conditions,  and  the  whole  course  of  the  dis- 
ease. We  must  also  bear  in  mind  the  possibility  that  there  may  be  an  acute  exa- 
cerbation in  a  chronic  nephritis  that  has  already  existed  for  a  long  time,  and  has 
been  perhaps  without  symptoms — acute  recurrent  haemorrhagic  nephritis. 

Prognosis. — The  prognosis  of  acute  nephritis  depends  in  many  cases  not  only 
upon  the  renal  affection,  but  also  upon  the  underlying  primary  disease.  We  can 
not  here  describe  in  detail  the  numerous  conditions  that  must  be  considered,  but 
they  are  to  be  found  in  the  appropi'iate  chapters. 

Many  cases  of  primary  nephritis  from  toxic  action,  or  exposure  to  cold,  and 
also  many  cases  of  secondary  nephritis  after  scarlet  fever,  in  pneumonia,  typhoid 
fever,  or  syphilis,  during  pregnancy,  etc.,  recover  perfectly  in  a  short  time  or 
after  several  weeks,  according  to  the  severity  of  the  individual  case.     On  the 


846  DISEASES  OF  THE  KIDNEYS. 

other  hand,  however,  it  must  be  said  that  every  nephritis  must  be  judged  with 
great  caution,  partly  because  it  may  be  the  starting-point  of  a  subsequent  chronic 
renal  disease,  and  partly  because  dangerous  sequelae  may  sometimes  develop  in 
cases  that  at  first  are  apparently  mild.  The  dangers  of  acute  nephritis  are 
chiefly,  first,  the  appearance  of  severe  general  dropsy,  especially  in  the  internal 
cavities  of  the  body.  Of  the  forms  of  dropsy  hydrothorax  is  the  most  dangerous, 
as  it  may  produce  suffocation  by  compression  of  the  lungs.  Second,  uraemia,  espe- 
cially in  its  severe  convulsive  forms,  with  high  temperature  and  finally  cardiac 
paralysis.  Tbird,  the  inflammation  of  internal  organs,  among  which  secondary 
pneumonia,  in  particular,  is  a  frequent  cause  of  death,  while  secondary  peri- 
carditis and  peritonitis,  as  we  have  said,  are  seen  in  but  very  few  cases.  We  must 
bear  in  mind,  however,  that  in  individuals  otherwise  healthy  the  severe  sequelae 
just  mentioned  may  also  be  recovered  from.  The  most  extreme  dropsy  may  be 
re-absorbed,  and  we  sometimes  see  recovery,  especially  in  children,  after  the 
severest  uraamic  symptoms. 

Treatment. — Since  we  may  omit  the  description  of  the  treatment  of  any  pri- 
mary disease,  we  have  here  to  speak  only  of  those  remedies  which  the  physician 
has  at  his  command  against  the  nephritis  itself  and  its  sequelae. 

Although  it  seems  alluring  to  try  to  exert  a  favorable  influence  upon  the 
nephritic  process  by  drugs  which,  like  the  injurious  substances,  also  reach  the 
kidneys  directly,  we  can  not  report  any  definite  practical  results  from  such  treat- 
ment. The  remedies  employed  with  this  object  in  view — tannin  in  one-  to  five- 
grain  powders  (grm.  0'05-0'2)  several  times  a  day,  and  the  drugs  containing 
tannin,  like  uva  ursi,  in  a  decoction  of  10  to  150,  and  also  nitric  acid,  tartar  emetic, 
etc. — prove,  on  sober  observation,  to  be  almost  wholly  useless.  We  may,  there- 
fore, try  them  only  when  there  are  no  more  pressing  indications  to  be  fulfilled. 
Fuchsine,  which  has  of  late  been  often  praised,  is  also  not  to  be  recommended. 

We  expect  as  little  result  at  present  from  "  external  antiphlogosis  "  as  from  the 
internal  remedies  mentioned — that  is,  from  local  blood-letting,  applications  of  ice 
to  the  region  of  the  kidneys,  etc.  Only  in  the  rare  cases  where  severe  pain  in  the 
region  of  the  kidneys  comes  on  at  the  beginning  of  nephritis,  in  an  otherwise 
robust  individual,  are  we  at  present  justified  in  trying  leeches  or  a  few  dry  cups. 
The  warm  baths,  to  be  described  more  fully  below,  have  perhaps  an  immediately 
favorable  action  on  the  process  in  the  kidneys,  since  they  produce  a  hyperaernia 
of  the  skin,  and  thus  lessen  the  flow  of  blood  to  the  kidneys. 

Although  we  must  accordingly  admit  that  there  is  scarcely  any  remedy  at  our 
service  which  has  a  direct  therapeutic  influence  upon  the  diseased  kidneys,  the 
treatment  of  nephritis  may  nevertheless  produce  very  significant  results,  since 
both  a  number  of  hygienic  measures  and  the  fulfillment  of  certain  symptomatic 
indications  are  of  the  greatest  importance. 

Among  the  general  hygienic  measures  we  must  mention  first  strict  confine- 
ment to  bed.  In  the  severe  cases  its  necessity  is  self-evident ;  but,  even  in  the 
milder  cases,  which  run  their  course  without  any  severe  subjective  symptoms, 
constant  rest  in  bed  is  necessary  throughout.  In  this  way  we  not  only  avoid  the 
unfavorable  action  of  cold  upon  the  external  skin,  but  the  activity  of  the  skin, 
which  must  act  vicariously  for  the  kidneys,  is  also  excited  by  the  uniform  warmth 
of  the  bed,  while  any  useless  muscular  exertion,  which  would  tax  the  heart's  capa- 
city for  work,  is  also  avoided  by  staying  in  bed.  In  general  it  is  advisable  to  cover 
the  patient  quite  warmly,  so  as  to  keep  him  in  a  constant  slight  perspiration. 

The  regulation  of  the  diet  is  very  important.  All  those  foods  and  drinks  which 
may  irritate  the  kidneys  are  to  be  strictly  avoided,  especially  spices,  very  sour 
substances,  strong  tea  and  coffee,  or  alcoholic  drinks.  Milk  has  for  a  long  time 
proved  itself  to  be  by  far  the  most  suitable  and  best  food.     This  has  won  for  itself 


ACUTE  NEPHRITIS.  S47 

the  reputation  of  a  remedy  in  renal  disease,  and  the  best  results  have  often  been 
seen  from  a  methodical  "milk-cure" — that  is,  from  feeding  the  patient  almost 
exclusively  with  milk.  The  great  aversion  of  some  patients  toward  milk,  how- 
ever, is  sometimes  an  obstacle  to  its  use.  We  may  often  be  aided,  then,  by  mak- 
ing the  milk  more  acceptable  to  the  patient  by  the  addition  of  a  little  coffee,  salt, 
a  little  cognac,  or  soda-water.  Among  other  foods  to  be  recommended  are 
buttermilk,  milk-gruel  with  rice  or  groats,  and  flour-gruel.  We  should  be  very 
cautious  about  giving  meat  as  long  as  there  are  severe  symptoms.  We  may  allow 
meat-broths,  with  eggs,  sooner.  For  drinks,  beside  milk,  we  may  give  water  and 
lemonade,  which  latter  is  especially  suitable.  Of  alcoholic  beverages,  a  little 
weak  red  wine  is  usually  the  only  thing  to  be  permitted.  Stronger  wines  are 
given  only  when  there  is  cardiac  weakness,  and  then  they  are  of  doubtful  benefit. 

The  chief  object  in  the  symptomatic  treatment  consists  in  preventing  the  inju- 
rious results  of  the  defective  elimination  of  the  water  and  the  solid  constituents 
of  the  urine  by  the  kidneys,  or  in  removing  these  results  if  they  have  already 
occurred.  This  purpose  can  be  attained  only  by  exciting,  as  far  as  possible,  the 
activity  of  other  organs  which  in  this  respect  may  act  vicariously  for  the  kidneys. 
The  skin  deserves  the  first  attention  here,  through  which,  by  means  of  the  sweat- 
glands,  large  amounts  of  water,  and  also,  to  a  certain  extent,  the  solid  constituents 
of  the  urine,  which  have  been  retained,  may  be  eliminated.  The  diaphoretic  treat- 
ment of  renal  diseases  has,  therefore,  been  generally  in  vogue  for  a  long  time.  If 
the  patient's  general  condition  permits,  we  always  begin  with  it  as  early  as  possi- 
ble, even  before  there  have  been  any  signs  of  oedema,  ursemic  symptoms,  etc.  Hot 
baths  from  95°  to  105°  (36°-40°  C.)  are  best.  The  patient  stays  about  half  an  hour 
or  an  hour  in  the  bath,  is  then  rapidly  dried  somewhat,  wrapped  up  in  bed  in  a 
previously  warmed  sheet,  and  then  is  well  covered  up  to  the  neck  with  blankets. 
In  order  to  make  the  procedure  somewhat  easier  for  the  patient,  it  is  a  good  plan 
to  cover  the  forehead  with  a  cold  compress,  always  to  wipe  the  sweat  carefully 
from  the  face,  and  frequently  to  give  him  a  little  swallow  of  fresh  cold  water. 
The  production  of  sweat  is,  of  course,  better  excited  during  the  pack  if  the  patient 
takes  some  hot  drink,  hot  milk  with  soda-water,  or  hot  elder-tea.  It  sometimes 
seems  to  aid  diaphoresis  if  an  internal  diaphoretic  be  given  at  the  same  time,  the 
best  being  five  to  ten  grains  of  Dover's  powder  (grm.  0'3-0-5),  or  three  or  four 
drachms  (grm.  10-15)  of  liquor  ammonii  acetatis  (Spiritus  Minderer?)  in  a  cup  of 
elder-tea.  We  have  also  found  a  good  rubbing  of  the  whole  body  with  dilute 
warm  French  brandy  of  service  before  the  pack.  The  pack  may  last  two  or  three 
hours. 

In  this  way  we  succeed  in  many  cases  in  causing  a  considerable  production  of 
sweat,  so  that  the  patient  loses  several  pounds  in  weight  at  each  pack,  and  an 
existing  dropsy  may  sometimes  be  made  to  disappear  completely  in  a  compara- 
tively short  time.  On  the  other  hand,  however,  we  can  not  deny  that  it  is  very 
hard  sometimes  to  make  patients  sweat,  even  when  there  is  oedema  of  the  skin, 
and  also  that  many  patients  do  not  bear  hot  baths  and  packs  at  all.  The  latter  is 
especially  true  if  the  patient  has  dyspnoea,  and  if  signs  of  cardiac  weakness  have 
already  set  in.  Then  we  have  to  be  very  cautious  about  using  sweating  as  a 
remedy.  Sometimes  we  can  bathe  the  patient,  but  we  have  to  omit  the  pack, 
while  in  other  cases  he  can  take  the  hot  pack  in  bed  ;  but  we  must  avoid  carry- 
ing him  to  the  bath  and  back.  We  also  have  to  get  along  with  hot  wet  packs,  if 
baths  can  not  be  used  for  extrinsic  reasons. 

Beside  hot  baths  and  packs,  one  diaphoretic  remedy  is  to  be  especially  consid- 
ered in  renal  disease,  and  that  is  the  hydrochlorate  of  pilocarpine,  derived  from  the 
jaborandi-leaves.  We  use  it  best  in  the  form  of  a  subcutaneous  injection,  of  one 
sixth  to  a  third  of  a  grain  in  one  dose  (grm.  0 '01-0 "02) ;  but  it  may  also  be  given 


848  DISEASES  OF  THE  KIDNEYS. 

internally  in  the  form  of  pills,  in  like  doses.  Its  action  consists  in  the  production 
of  a  copious  sweat,  and  also  usually  of  a  very  considerable  flow  of  saliva,  which  is 
often  very  disagreeable  to  the  patient.  In  general,  we  prefer  the  baths  to  pilo- 
carpine, and  we  try  the  latter  only  when  the  baths  are  contra-indicated  or  do  not 
exert  any  satisfactory  action.  The  diaphoretic  action  of  pilocarpine,  moreover,  is 
often  decidedly  less  in  dropsical  patients  with  kidney  disease  than  in  other  cases. 

Next  to  the  skin,  the  intestinal  mucous  membrane  is  the  organ  from  which  we 
may  soonest  expect  to  produce  a  vicarious  elimination  of  water,  and  also  of  urea, 
for  the  kidneys.  It  is  sometimes,  therefore,  of  distinct  service  to  prescribe  drastic 
cathartics  in  nephritis  with  a  diminished  secretion  of  urine,  especially  if  there  is 
a  tendency  to  constipation  beside  the  dropsy,  dyspnoea,  etc.  The  drastic  cathartics 
chiefly  used  are  infusion  of  senna,  decoction  of  colocynth,  3  or  6  to  150,  gamboge 
in  two-grain  powders  (grm.  0"1),  etc. 

Finally,  it  may  be  asked  whether  we  should  not  excite  the  secretory  function 
of  the  kidneys  themselves  by  the  exhibition  of  diuretics.  The  objection  is,  how- 
ever, that  all  diuretic  remedies  irritate  the  kidneys,  increase  the  flow  of  blood  to 
them,  and  therefore  can  act  only  injuriously  upon  the  nephritis.  We  must,  there- 
fore, be  very  cautious  in  using  diuretics.  Only  the  milder  remedies,  especially 
acetate  of  sodium,  may  sometimes  be  used  with  advantage,  especially  in  the  less 
acute  cases  or  during  the  period  of  convalescence.  The  diuretic  action  of  digitalis, 
which  is  very  important  under  some  circumstances,  will  be  mentioned  later. 

The  therapeutic  measures  so  far  spoken  of  correspond  to  the  task  of  prevent- 
ing as  far  as  possible  the  retention  of  urinary  constituents  in  the  body.  They 
are  also  very  much  employed  when  the  signs  of  this  retention  have  already 
appeared.  The  dropsy  especially  can  be  successfully  treated  only  by  methodical 
sweatings,  with  the  aid,  eventually,  of  drastic  and  diuretic  remedies.  When  urae- 
mia is  threatening,  and  often  even  when  it  has  broken  out,  we  may  try  to  produce 
an  elimination  of  the  injurious  products  of  tissue  metamorphosis  from  the  body  in 
the  well-known  ways  above  described,  by  sweating  or  drastic  purgatives.  Beside 
this,  the  uraemic  symptoms,  however,  often  demand  a  special  symptomatic  treat- 
ment. If  very  violent  and  frequent  uraemic  convulsions  appear,  we  consider  it 
advisable  to  try  to  suppress  the  attacks  by  chloroforming  the  patient.  At  any  rate, 
it  seems  to  us  to  be  better  to  use  chloroform  in  uraemia  than  to  give  narcotics 
internally,  because  with  this  we  can  watch  the  action  of  the  remedy  better,  espe- 
cially the  condition  of  the  pulse  and  respiration.  Chloroform  is  also  generally  used 
by  the  obstetricians  as  the  main  remedy  in  the  eclampsia  of  pregnancy.  If  the 
attacks  are  not  very  frequent,  but  if  there  is  marked  somnolence  or  coma,  tepid 
baths  with  cold  shower-baths  are  often  employed  with  distinct  advantage.  Cool 
baths  are  also  serviceable  where  there  is  a  great  increase  of  the  temperature.  If  we 
are  treating  a  robust  individual  with  a  full  pulse,  and  during  severe  uraemia  there 
is  a  decided  redness  or  cyanosis  of  the  face,  venesection  may  be  indicated.  This 
sometimes  has  a  striking  and  instant  effect,  as  has  lately  been  confirmed  by 
various  observers.  Great  attention  is  to  be  paid  to  the  condition  of  the  heart.  As 
soon  as  the  pulse  becomes  small  and  weak,  energetic  stimulants,  like  subcutaneous 
injections  of  camphor,  must  be  used.  If  the  signs  of  cardiac  weakness  appear 
before  the  beginning  of  severe  uraemic  symptoms,  digitalis  must  be  used  in  infusion 
or  powder.  Through  its  action  in  raising  the  blood-pressure — it  being  advisable 
under  some  circumstances  to  combine  with  it  acetate  of  potassium — a  greater 
diuresis  sometimes  comes  on,  and  with  it  a  disappearance  of  the  danger  from 
uraemia.  The  tinctura  nervina  Bestuscheflh  [nearly  equivalent  to  the  tincture  of 
the  chloride  of  iron,  U.  S.  P.]  may  also  be  sometimes  used  to  advantage  in  urae- 
mia. We  are  not  apt  to  interfere  with  uraemic  vomiting  or  uraemic  diarrhoea, 
because  these  symptoms,  as  we  have  said,  are  to  be  regarded  as  a  form  of  self-help 


SUBCHRONIC  AND  CHRONIC  FORMS  OF  NEPHRITIS.         849 

by  the  organism.  Only  when  these  symptoms  are  very  distressing  do  we  give 
cracked  ice,  morphine,  opium,  etc.  If  the  vomitus  contains  ammonia,  it  is  a  good 
plan  to  give  ten  or  fifteen  drops' of  dilute  hydrochloric  acid  in  water  several  times 
a  day. 

[A  method  of  treatment  of  uraimic  convulsions,  whether  post  partum  or  con- 
nected in  no  way  with  parturition,  which  gives  excellent  and  prompt  results,  is  the 
administration  of  pilocarpine  hypodermically — grain  J,  and  repeat  in  twenty 
minutes — followed  by  the  hot-air  bath,  to  maintain  the  action  of  the  skin  after 
it  has  once  been  started. 

Pilocarpine  sometimes  acts  as  a  decided  cardiac  depressant,  so  one  must  be 
ready  to  administer  stimulants — brandy  or  ether — under  the  skin  if,  as  is  apt  to  be 
the  case,  there  is  doubt  as  to  the  readiness  with  which  they  will  be  absorbed  from 
the  stomach  or  rectum.] 

In  severe  cases,  the  patient's  dyspnoea  often  demands  urgent  relief.  If  this  be 
caused,  or  at  least  increased,  by  hydrothorax,  and  we  do  not  succeed  in  removing 
the  hydrothorax  in  any  other  way,  it  is  necessary  to  evacuate  it  by  puncture.  In 
acute  nephritis,  indeed,  we  may  hope  by  this  means  sometimes  to  preserve  the 
patient's  life  until  improvement  sets  in.  Great  ascites  must  also  sometimes  be 
punctured.  Against  " renal  pneumonia"  our  remedies  are  powerless.  Tepid 
baths  and  shower-baths  sometimes  procure  relief.  In  "  uraeinic  asthma,"  morphine 
injections  may  act  beneficially.  If  pulmonary  oedema  ensues,  the  heart  again  is 
chiefly  to  be  considered.  We  may  try,  besides,  large  mustard  plasters,  baths,  and 
acetate  of  lead. 

We  accordingly  see  that  many  remedies  are  at  our  service  in  the  treatment  of 
nephritis,  the  choice  of  which  in  the  individual  case  must  be  committed  to  the 
personal  judgment  of  the  physician.  In  the  main,  we  should  always  begin  with 
the  necessary  hygienic  measures,  and,  if  possible,  with  a  methodical  diaphoretic 
treatment,  and  govern  ourselves  otherwise  by  any  symptomatic  indications. 
After  recovery  has  set  in,  great  caution  is  still  necessary  for  a  long  time.  The 
patient  must  guard  against  physical  over-exertion,  errors  in  diet,  and  exposure 
to  cold.  Preparations  of  iron  are  to  be  prescribed  when  there  is  a  subsequent 
anaemia. 

In  regard  to  the  influence  of  the  onset  of  an  acute  nephritis  on  the  treatment 
of  the  primary  disease,  we  may  yet  mention  that  cold  baths  are  in  general  not  to 
be  freely  used,  as  in  typhoid  fever  with  nephritis,  but  they  are  not  absolutely 
contra-indicated  if  they  are  otherwise  urgently  desirable.  We  may  mention  besides 
that  certain  internal  remedies,  especially  salicylic  acid,  must  be  used  only  with 
great  caution  when  there  is  nephritis.  In  the  eclampsia  of  lying-in  women  the 
induction  of  premature  labor  is  only  rarely  indicated,  since  the  child  is  usually 
born  during  the  paroxysms  without  interference. 


/ 

CHAPTER  III. 

THE   SUBOHRONIO  AND   CHRONIC  FORMS  OF  NEPHRITIS,  WITH  THE 
EXCEPTION  OF  THE   GENUINE   CONTRACTED  KIDNEY. 

("  Second  Stage  of  Br igMs  Disease."     Chronic  Parenchymatous  Nephritis,  Chronic  Hemorrhagic 
Nephritis,  Large  White  Kidney,  Seco?idary  Contracted  Kidney.) 

iEtiology. — While  the  acute  nephritis  described  in  the  preceding  chapter  runs 
its  course  in  several  days  or  weeks,  and  only  rarely  extends  over  some  months, 
we  will  now  speak  of  inflammatory  degenerative  affections  of  the  kidneys  which 
54 


S5Ü  DISEASES  OF  THE  KIDNEYS. 

last  at  least  several  months,  and  often  go  on  for  a  year  or  two.  The  term  "  sub- 
acute "  or  "  subchronic  "  is  chosen  for  the  cases  that  last  a  comparatively  short 
time.     As  we  must  once  more  repeat,  there  is  no  sharp  limit  in  this  respect. 

In  regard  to  the  aetiology  of  these  forms  of  nephritis,  they  do  arise  from  an 
acute  nephritis,  but  this  is  quite  rare.  Formerly  such  an  origin  was  erroneously 
regarded  as  the  rule,  and  this  is  the  reason  why  the  changes  in  the  kidney  in  these 
cases  were  described  as  the  ''second  stage  of  Bright's  disease"  (Frerichs).  The 
English  clinical  observers  Wilks  and  Johnson,  whom  Bartels  followed  in  Ger- 
many, first  pointed  out  the  fact  that  in  most  cases  the  disease  shows  a  chronic 
character  from  the  start,  and  that  we  can  only  exceptionally,  as  after  scarlet  fever, 
recognize  an  acute  "first  stage."  The  name  "chronic  parenchymatous  nephritis," 
since  frequently  used,  is  chosen  entirely  from  practical  reasons,  inasmuch  as  it 
briefly  states  the  distinction  from  the  genuine  contracted  kidney ;  but  it  is  incor- 
rect in  principle,  as  will  be  shown  from  the  description  of  the  anatomical  condi- 
tions later. 

If  we  look  for  the  aetiological  conditions  in  cases  that  have  a  chronic  course 
from  the  beginning,  we  can  often  discover  nothing  definite  at  all.  The  disease 
seems  to  have  developed  "  of  itself  "  in  previously  healthy  persons.  Most  probably 
we  have  here  some  toxic  or  infectious  agency  that  acts  on  the  kidneys,  whose 
detection,  however,  is  at  present  impossible.  In  malarial  regions  the  malarial 
poison  may  often  lead  to  chronic  nephritis.  It  is  also  attributed  to  syphilis  and 
tuberculosis,  but  the  cases  met  with  are  usually  combinations  of  these  diseases  with 
amyloid  kidney  {vide  infra).  Frequent  exposures  to  wet  and  cold,  damp  dwell- 
ings, etc.,  seem  sometimes  to  be  of  more  material  significance,  but  it  is,  of  course, 
hard  to  form  a  definite  opinion  on  this  point. 

Persons  in  middle  life  are  most  frequently  affected  by  the  disease,  and  men 
more  often  than  women.     In  children  and  old  people  the  disease  is  quite  rare. 

Pathological  Anatomy. — There  is  no  essential  distinction  between  the  ana- 
tomical lesions  of  the  kidney  in  acute  and  in  chronic  nephritis.  The  changes  that 
are  seen  in  both  are  essentially  the  same,  only  they  develop  and  extend  more 
slowly  in  the  chronic  forms ;  and  they  also,  during  their  longer  duration,  lead  to 
certain  sequelae  in  the  kidney,  which  can  not  develop  at  all  in  acute  nephritis, 
owing  in  part  to  the  lack  of  time.  Even  in  chronic  nephritis  the  individual  cases 
differ  from  one  another  in  many  respects.  First  this  and  then  that  histological 
process  is  especially  prominent,  and  thus  lends  certain  peculiarities  to  the  macro- 
scopic appearance  of  the  kidneys.  Certain  sequelae — like  contractions — have 
also  developed  but  little  in  many  cases  that  soon  end  fatally,  but  they  develop 
far  more  in  other  cases  of  longer  duration.  Hence  it  happens  that  we  can  quite 
well  regard  cei'tain  anatomical  forms  that  are  more  frequently  observed  as  types, 
although  we  must  never  lose  from  sight  the  principle,  to  be  firmly  held,  of  the 
pathological  unity  of  all  these  forms  and  types.  Then  we  shall  not  lose  the  clew 
to  the  understanding  of  the  morbid  process  if  the  individual  case  does  not  always 
harmonize  with  the  scheme  of  the  text-books. 

We  distinguish  the  three  following  chief  anatomical  types  of  subchronic  and 
chronic  nephritis : 

1.  Chronic  Hemorrhagic  Nephritis  in  the  form  of  the  Large  Eed  or  Varie- 
gated Kidney. — The  kidney  is  at  least  of  normal  size,  and  often  a  little  or  a  good 
deal  enlarged.  It  feels  firmer  than  normal ;  its  capsule  is  often  adherent  to  the 
surface  in  some  places.  The  surface  looks  either  uniformly  a  more  gray  red  or 
more  mottled,  while  dark-red  spots  alternate  with  lighter  gray  or  even  yellow 
spots.  The  red  spots  on  the  surface  can  not  be  wholly  wiped  off,  and  thus  prove 
to  be  haemorrhages.  The  gray  or  yellow  parts  correspond  to  the  anaemic  and  fatty 
degenerated  portions.     On  section,  the  cortical  substance  is  usually  broader,  its 


SUBCHRONIC  AND  CHRONIC  FORMS  OF  NEPHRITIS.         851 

normal  boundary  is  obliterated,  and  its  color  is  a  uniform  gray  red,  or  also  mottled 
and  striated. 

Under  the  microscope  we  find  in  part  the  same  changes  as  in  acute  nephritis — 
parenchymatous  and  fatty  degeneration  of  the  epithelium,  casts  or  haemorrhages 
in  the  uriniferous  tubules,  inflammatory  oedema  or  granular  infiltration  of  the  in 
terstitial  tissue,  the  capsules  of  the  glomeruli  sometimes  thickened,  the  epithelium 
of  the  glomeruli  sometimes  proliferated  or  desquamated,  etc.  The  special  char- 
acteristic of  this  chronic  form,  in  contrast  with  acute  nephritis,  is  that  in  many 
places  a  complete  destruction  of  the  uriniferous  tubules  has  occurred,  and  that 
a  genuine  interstitial  connective  tissue,  richer  or  already  poorer  in  cells,  has  taken 
their  place.  In  this  lies  the  anatomical  evidence  of  the  longer  duration  of  the  dis- 
ease, since  the  two  processes — both  the  complete  atrophy  of  the  epithelium,  and 
especially  the  secondary  proliferation  of  connective  tissue — of  course  need  a  certain 
time  for  their  development.  The  atrophy  and  the  proliferation  of  connective  tissue 
usually  predominate  in  some  parts,  while  in  others  nothing  but  fresher  inflam- 
matory and  degenerative  changes  are  perceived. 

2.  The  Inflammatory  Fatty  Kidney,  or  the  Large  White  Kidney  (yellow 
would  be  more  proper). — In  this  form  of  chronic  nephritis  the  kidney  is  usually 
enlarged,  or  at  least  of  normal  size.  Its  outer  surface  is  smooth  and  of  a  yellow 
or  an  alternating  yellow  and  gray-yellow  color  throughout.  The  broader  cortical 
substance  shows  a  yellow  and  usually  somewhat  mottled  appearance,  while  the 
pyramids  almost  always  appear  considerably  reddened.  Haemorrhages  are  also 
almost  always  present  in  this  form,  usually,  of  course,  in  smaller  numbers  than 
in  the  variegated  kidney,  but  they  are  sometimes  quite  abundant,  as  in  the  hsem- 
orrhagic  fatty  kidney. 

The  microscope  shows  the  great  affinity  between  this  form  of  nephritis  and  the 
preceding.  We  have  almost  precisely  the  same  changes,  and  we  always  have 
especially  a  partial  destruction  of  renal  tissue  with  a  subsequent  increase  of  inter- 
stitial connective  tissue.  The  macroscopic  appearance  of  the  kidney  is  due  to  the 
fact  that  it  is  anaemic,  and  that  the  fatty  degeneration  preponderates  in  the  epithe- 
lium. It  is  worthy  of  note  that  in  these  kidneys  marked  changes  in  the  glome- 
ruli are  usually  present. 

3.  The  Secondary  Contracted  Kidney.— While  in  the  two  forms  of  nephritis 
thus  far  described  the  outer  surface  of  the  kidney  is  still  smooth,  and  the  kidney, 
on  the  whole,  is  somewhat  enlarged,  we  have  to  do  here  with  kidneys  of  about 
normal  size,  on  whose  surface  there  are  granulations,  which  as  yet  are  slight,  but 
which  still  are  already  plain.  This  granulation  signifies  nothing  more  than  that 
the  destruction  of  the  renal  tissue  has  here  advanced  farther,  and  that  the  newly 
formed  connective  tissue  has  in  part  undergone  cicatricial  contraction.  These 
kidneys,  therefore,  represent  a  later  stage  of  the  two  forms  first-named.  They 
usually  come  under  observation  when  the  nephritis  has  lasted  about  a  year  and  a 
half  or  two  years,  or  even  somewhat  longer.  The  first  beginnings  of  granulation 
may,  of  course,  show  themselves  earlier,  while,  on  the  other  hand,  when  the 
process  lasts  a  longer  time,  a  completely  contracted  kidney  may  develop. 

The  color  of  these  kidneys  is  usually  reddish  or  mottled,  the  red  spots  corre- 
sponding to  the  sunken  atrophic  parts,  and  the  gray  or  yellowish  spots  to  the  ele- 
vated parts.  Yellow  kidneys,  however,  may  also  show  at  times  decided  granu- 
lations. Microscopically,  we  find  already  marked  atrophy  of  the  renal  paren- 
chyma, with  a  corresponding  increase  of  the  interstitial  connective  tissue. 

Formerly  these  kidneys  were  called  the  "  transition  between  the  second  and 
third  stages  of  Bright1  s  disease."  As  follows  from  the  above,  they  are  to  be 
regarded  only  as  a  more  advanced  form  of  chronic  nephritis.  Since  the  kidneys, 
in  spite  of  their  granulation,  have  on  the  whole  a  normal  size,  we  can  decide  from 


852  DISEASES  OF  THE  KIDNEYS. 

this,  and  from  the  clinical  course,  that  they  were  usually,  though  of  course  not 
always,  previously  enlarged.  Therefore  the  name  of  "  secondary  contracted  kid- 
ney "  is  quite  suitable,  in  opposition  to  the  genuine  contracted  kidney,  which 
represents  a  much  more  chronic  form  of  renal  atrophy. 

Of  other  pathological  lesions,  apart  from  the  changes  in  the  kidney,  we  will 
mention  here  only  the  hypertrophy  of  the  left  ventricle,  which  is  found  with  few 
exceptions  (vide  infra)  in  all  the  above-mentioned  forms  of  nephritis.  The 
chronic  parenchymatous  nephritis  without  cardiac  hypertrophy,  alleged  by 
Bartels  in  his  time,  does  not  exist.  Such  cases  were  probably  confused  with  amy- 
loid kidneys. 

Clinical  History. — Only  in  the  comparatively  rare  cases  when  the  renal  affec- 
tion begins  acutely,  do  the  symptoms  of  chronic  nephritis  follow  immediately  on 
the  first  acute  stage.  In  most  cases,  however,  the  disease  develops  slowly  and 
gradually  from  the  start,  as  we  have  said,  like  most  of  the  other  chronic  organic 
diseases,  so  that  it  is  usually  impossible  to  determine  accurately  the  moment 
when  the  disease  begins. 

The  first  signs  of  the  disease  consist  of  certain  general  symptoms,  pallor, 
dullness,  loss  of  appetite,  nausea  and  headache,  and  later  of  oedema.  The  latter 
is  often  the  first  symptom  which  sends  the  patient  to  the  physician,  since  in 
the  beginning  he  often  pays  little  attention  to  the  symptoms  first  named.  The 
oedema  usually  appears  first  in  the  ankles  and  legs,  more  rarely  at  an  early  period 
in  the  face.  It  often  disappears  at  first  after  a  night's  rest,  but  always  develops 
afresh  during  the  day,  gradually  increasing  in  intensity.  The  patient  himself 
now  sometimes  notices  a  change  in  the  urine,  either  an  abnormal  color  or  cloudi- 
ness or  a  diminished  amount.  The  accurate  examination  of  the  urine  by  the 
physician  first  establishes  the  diagnosis  with  certainty. 

In  regard  to  the  more  special  symptomatology  of  chronic  nephritis,  we  meet 
exactly  the  same  symptoms  as  have  been  described  in  the  preceding  chapter  on 
acute  nephritis.  The  characteristic  distinction  is  based  merely  upon  the  whole 
course  of  the  affection  and  the  order  of  development  of  the  different  symptoms, 
and  not  by  the  symptoms  themselves. 

The  urine  almost  always  is  diminished.  Of  course  the  figures  vary  quite 
considerably  both  in  different  cases  and  at  different  times  in  the  same  case.  The 
small  amount  of  urine,  ten  to  twenty-five  ounces  (300-700  c.c.)  a  day,  is  almost 
always  an  unfavorable  sign,  while  a  free  diuresis  signifies  an  improvement  of 
the  condition,  an  absorption  of  the  dropsy,  and  finally  a  passage  of  the  renal 
affection  into  a  still  more  chronic  condition,  the  secondary  contracted  kidney 
(vide  infra).  Under  such  circumstances  the  amount  of  urine  may  even  be  in- 
creased above  the  normal,  to  fifty  or  sixty  ounces  (1500  or  2000  c.  c.)  or  more. 

The  specific  gravity  of  the  urine  is  often  increased  to  about  1015-1025,  corre- 
sponding to  the  amount  of  albumen  and  of  other  solid  constituents.  It  is  of 
course  correspondingly  lower  when  there  is  a  more  abundant  elimination  of 
water  by  the  kidneys. 

The  amount  of  albumen  in  the  urine  is  quite  marked  in  all  severe  cases,  being 
one  third  to  three  fourths  of  its  volume.  It  amounts  to  about  1*5-3  per  cent,  by 
weight,  so  that  the  patient's  daily  loss  of  albumen  may  reach  half  an  ounce  to  an 
ounce  (15-30  grammes). 

The  examination  of  the  sediment,  which  is  usually  abundant,  is  of  the  greatest 
importance  for  the  accurate  determination  of  the  form  of  the  anatomical  changes 
in  the  kidneys.  Above  all,  the  question  arises  as  to  the  presence  or  absence  of  blood 
in  the  urine.  Every  abundant  hematuria  may  be  recognized  by  the  naked  eye 
from  the  color  of  the  urine.  The  detection  of  smaller  amounts  of  blood  can  be 
made  only  by  the  aid  of  the  microscope.     It  goes  without  saying  that  the  amount 


SUBCHRONIC  AND   CHRONIC  FORMS  OF  NEPHRITIS.        853 

of  blood  in  the  urine  varies  quite  considerably  in  the  different  cases,  and  in  tbe 
same  case  the  urine  often  contains  much  more  blood  during  certain  periods  in 
the  course  of  the  disease  than  at  other  times.  The  portions  of  urine  passed  at 
different  times  taken  separately  often  show  quite  marked  variation  in  this 
respect  ;  the  day's  urine  especially  usually  contains  more  blood  than  the  night's., 
From  the  detection  of  renal  haemorrhages,  of  course  in  connection  with  other 
symptoms,  we  can  always  make  with  certainty  the  diagnosis  of  a  "chronic 
haamorrhagic  "  nephritis. 

In  most  cases  casts  are  quite  abundant  in  the  sediment  of  the  urine,  but  of 
course  their  amount  and  variety  undergo  quite  great  variations  in  different  cases 
and  at  different  times  in  the  same  case.  They  are  the  direct  sign  of  the  presence 
of  an  inflammatory  exudative  process  in  the  kidneys,  although  the  deposits  on  the 
casts  are  more  important  for  the  diagnosis  of  the  special  form  of  renal  disease 
than  are  the  casts  themselves.  Those  formed  constituents  of  the  sediment  are  most 
characteristic  in  this  respect  which  point  directly  to  the  processes  of  fatty  degen- 
eration in  the  kidneys  :  the  fatty  granules  and  fatty  granular  cells,  free  or 
attached  to  the  casts.  The  number  of  these  elements  is  especially  great  in  the 
chronic  inflammatoiy  fatty  kidney,  the  "  large  white  kidney."  The  usually  clear, 
non-haemorrhagic  urine  may  in  some  cases  have  even  a  fatty  lustrous  surface. 
Renal  epithelium  is,  on  the  whole,  more  rarely  present  in  the  sediment  in  chronic 
nephritis  than  in  acute,  but  it  occurs  at  times  in  some  cases. 

Of  the  other  symptoms,  the  one  that  usually  most  strikes  the  eye  is  dropsy.  It 
usually  comes  on,  as  we  have  said,  in  the  beginning  of  the  disease,  and  slowly  or 
rapidly  reaches  a  great  extent  and  intensity.  A  medium  or  even  a  high  degree  of 
general  dropsy  may  often  persist  almost  unchanged  for  months.  In  other  cases 
it  shows  either  spontaneous  variations  or  variations  influenced  by  treatment ;  it 
decreases  for  a  time  only  to  increase  anew.  The  severer  and  more  acute  the 
case,  the  greater  in  general  is  the  dropsy.  In  the  more  chronic  cases,  in  sec- 
ondary contracted  kidney,  its  intensity  may  be  slight  for  a  time  or  even  perma- 
nently. The  dropsy  may  even  be  absent  in  some  cases,  as  we  learn  especially 
from  the  observations  reported  by  Wagner  under  the  name  of  "  chronic  hemor- 
rhagic Bright's  disease  without  oedema."  In  regard  to  the  different  localizations 
of  the  dropsy,  and  to  dropsy  of  the  internal  cavities,  hydrothorax,  ascites,  and 
hydropericardium,  and  their  results,  the  same  holds  true  as  was  described  in  the 
account  of  acute  nephritis. 

Of  the  internal  organs,  the  condition  of  the  heart  lays  claim  to  the  most  inter- 
est. In  all  cases  of  chronic  nephritis,  in  which  we  do  not  have  to  do  with  espe- 
cially weak  and  run-down  patients,  who  can  not  save  the  necessary  nutritive 
material  for  the  formation  of  a  cardiac  hypertrophy,  we  find  a  pronounced  and 
often  a  very  marked  hypertrophy  of  the  left  ventricle,  either  with  or  without  a 
co-existing  dilatation  of  its  cavity.  A  chronic  nephritis  without  cardiac  hyper- 
trophy, which  was  put  forward  by  Bartels  and  others  as  the  type  of  "  chronic 
parenchymatous  nephritis,"  does  not  exist,  as  we  have  said,  except  under  the 
above-mentioned  conditions.  The  detection  of  cardiac  hypertrophy  during  the 
patient's  life  is  sometimes  difficult,  especially  when  there  is  general  dropsy,  but 
the  diagnosis  can  usually  be  correctly  made  with  proper  attention  to  the  abnor- 
mally tense  radial  pulse,  the  accentuated,  valvular  aortic  second  sound,  and  the  dis- 
placement outward  of  the  apex -beat,  or  at  least  its  increased  strength.  We  often 
find  in  the  cadaver,  and  can  sometimes  make  out  during  life,  a  hypertrophy  of 
the  right  ventricle.  This  is  usually  a  sign  of  a  distm'bance  of  compensation — that 
is,  the  paralyzed  left  ventricle  can  no  longer  send  forward  in  a  sufficient  manner 
all  the  blood  coming  from  the  pulmonary  veins,  so  that  there  ensues  a  stasis  in 
the  pulmonary  circulation,  and  a  consequent  hypertrophy  of  the  right  ventricle. 


854  DISEASES  OF  THE  KIDNEYS, 

A  second  important  sequel  of  chronic  nephritis  consists  of  the  changes  in  the 
retina — albuminuric  retinitis.  Although  very  rare  in  acute  nephritis,  these  changes 
are  present  in  by  far  the  greater  majority  of  the  cases  of  this  class.  Sometimes 
the  patient's  subjective  visual  disturbance  (dimness  of  vision,  defects  in  the  field 
of  vision),  point  to  a  disease  of  the  retina,  but  the  existence  of  disease  can  be  estab- 
lished with  certainty  only  by  ophthalmoscopic  examination.  In  these  cases  we 
find  two  changes,  in  varying  numbers  and  combinations  :  first,  retinal  haemor- 
rhages ;  and,  second,  white  spots  and  streaks,  especially  in  the  vicinity  of  the  optic 
nerves.  The  origin  of  the  spots,  which  may  appear  and  disappear  again,  is  not 
yet  entirely  clear.  At  any  rate,  there  are  circumscribed  fatty  degenerations  of 
the  special  retinal  elements.  The  degree  of  amblyopia  depends,  of  course,  chiefly 
upon  the  localization  of  the  changes,  whether  in  the  macula  lutea,  or  other  parts. 

We  can  say  little  in  regard  to  the  other  symptoms,  since  they  agree  essentially 
with  those  of  acute  nephritis.  The  general  anaemia  is  very  pronounced  in  many 
cases,  but  it  is  less  marked  in  the  very  chronic  forms.  The  cerebral  symptoms, 
especially  the  headache  and  the  mild  vertigo,  may  depend  in  part  upon  the  cere- 
bral anaemia  ;  otherwise,  they  are  a  uraemic  symptom  {vide  infra).  Cerebral 
haemorrhages  have  been  observed  in  a  very  few  cases.  Haemorrhages  on  the 
inner  surface  of  the  dura  mater  are  more  frequent,  but  they  are  usually  without 
clinical  significance.  The  mouth,  larynx,  and  pharynx  usually  show  nothing 
particular,  except  accidentally  complicating  inflammations.  We  must,  however, 
remember  the  occasional  occurrence  of  a  very  distressing  or  even  dangerous 
oedema  of  the  soft  palate,  or  of  the  arytaeno-epiglottic  ligaments — oedema  of  the 
glottis.  Similar  forms  of  bronchitis  and  pneumonia,  as  in  acute  nephritis,  are 
found  in  the  bronchi  and  lungs.  Bronchitis  and  chronic  oedema  of  the  lungs  also 
make  their  appearance  in  the  more  advanced  stages  of  the  disease  as  a  result  of 
cardiac  insufficiency.  Finally,  we  must  remember  the  hindrance  to  respiration 
from  hydrothorax,  and  also  from  uraemic  dyspnoea.  The  changes  in  the  heart 
have  already  been  spoken  of.  Endocarditis  or  pericarditis  may  occur,  but  they 
are  very  rare. 

Loss  of  appetite  is  a  very  common  symptom  on  the  part  of  the  stomach.  Very 
persistent  vomiting  is  usually  to  be  regarded  as  a  chronic  uraemic  symptom.  The 
bowels,  as  a  rule,  are  constipated,  but  there  may  also  be  severe  diarrhoea,  as  in 
acute  nephritis.  In  severe  cases,  especially  in  the  last  stages  of  the  disease,  ulcer- 
ative and  dysenteric  processes  have  repeatedly  been  observed  in  the  large  intestine 
and  the  ileum.  Peritonitis  may  occur,  but  it  is  at  all  events  extremely  rare.  The 
liver  and  spleen  usually  show  no  peculiarities. 

Uraemic  symptoms,  both  of  the  milder  chronic  variety  and  also  in  their  severest 
acute  form,  may  come  on  at  any  time,  although  they  do  not  by  any  means 
attain  their  full  development  in  all  cases,  and  are  somewhat  rarer  than  in  genuine 
contracted  kidney. 

The  temperature  remains  normal,  as  a  rule,  as  long  as  it  is  not  influenced  by 
complicating  inflammations,  or  by  the  appearance  of  uraemia. 

Course,  Duration,  and  Termination  of  Chronic  Nephritis.— In  general,  the  whole 
course  of  chronic  nephritis  presents  quite  a  great  uniformity.  The  different  symp- 
toms may  show  certain  variations  within  long  periods,  but  the  patient  often  pre- 
sents almost  the  same  appearance  day  after  day  for  months.  The  duration  of  the 
disease  shows  all  the  transitions  from  three  to  six  months,  in  the  subacute  cases,  to 
two  or  three  years,  or  even  more,  in  the  very  chronic  cases.  The  cases  of  long 
duration  are  almost  all  cases  of  secondary  contracted  kidney.  They  sometimes 
show  in  their  clinical  relations  the  transition  from  the  enlarged  to  the  granular 
kidney,  since  the  picture  in  many  of  its  details  is  more  like  that  in  the  genuine 
contracted  kidney :  the  oedema  decreases,  disappears  completely,  or,  at  least,  con- 


SÜBCHRONIC  AND  CHRONIC  FORMS  OF  NEPHRITIS.  855 

tinues  in  a  lesser  degree;  the  amount  of  urine  becomes  more  abundant,  and  the 
specific  gravity  and  the  amount  of  albumen  become  correspondingly  less.  The 
condition  thus  lasts  for  a  long  time  until  it  grows  worse  again,  through  uraemia, 
or  disturbance  of  the  compensation  in  the  heart. 

The  final  termination  of  chronic  nephritis  is  in  most  cases  unfavorable.  In  the 
severe  forms  death  ensues  in  from  three  months  to  a  year,  either  in  consequence 
of  general  dropsy  or  from  uraemia,  from  complicating  inflammations,  etc.  The 
conditions  when  the  nephritis  goes  on  to  secondary  contraction  are  comparatively 
more  favorable,  inasmuch  as  the  patient  may  then  find  himself  in  a  tolerable  con- 
dition for  a  time  at  least.  Complete  recoveries  doubtless  occur  in  chronic  nephri- 
tis, but  they  are  rare.  An  apparent  recovery  may  be  simulated  by  the  appearance 
of  secondary  contraction.  Even  after  signal  improvement,  however,  relapses  are 
always  to  be  feared.  There  are  even  genuine  acute  attacks  in  the  course  of  chronic 
nephritis. 

Diagnosis. — On  careful  examination  of  the  urine  in  all  suspicious  cases  of 
oedema,  anaemia,  etc.,  the  diagnosis  of  chronic  nephritis  can  always  be  correctly 
made.  In  regard  to  the  more  exact  distinction  of  the  different  anatomical  forms, 
we  will  here  give  a  brief  schematic  glance  at  the  most  important  conditions : 

Chronic  Hcemorrhagic  Nephritis  (large  variegated  or  mottled  kidney). — Dura- 
tion from  six  to  eighteen  months.  Urine  often  haemorrhagic ;  usually  quite  rich 
in  red  blood-corpuscles  and  casts.  GCderna.  Cardiac  hypertrophy.  Retinal  changes. 
Quite  frequently  uraemia. 

Inflammatory  Fatty  Kidney  (large  white  kidney). — Duration  also  six  to  eighteen 
months,  but  usually  somewhat  shorter  than  in  the  preceding  form.  Urine  not  at 
all,  or  only  slightly,  haemorrhagic.  Frequently  many  white  blood-corpuscles,  and 
especially  signs  of  fatty  degeneration  in  the  kidneys,  fatty  granular  cells,  fat-drops 
in  the  urine,  etc.  Significant  amount  of  albumen  in  the  urine.  Marked  oedema. 
Cardiac  hypertrophy.     Very  often  retmal  changes.     Death  by  uraemia  frequent. 

Secondary  Contracted  Kidney. — Longer  duration  of  the  disease,  from  a  year  and 
a  half  to  three  years.  At  first  the  symptoms  of  the  preceding  forms ;  later,  urine 
more  abundant,  less  oedema,  etc.  Death  from  an  increase  of  the  dropsical  symp- 
toms due  to  cardiac  insufficiency,  uraemia,  etc. 

Treatment.— The  treatment  of  chronic  nephritis  corresponds  in  all  its  details 
so  closely  to  that  of  acute  nephritis  that  we  can  refer  almost  entirely  to  the  pre- 
ceding chapter. 

The  main  thing  here  is  also  regimen  and  symptomatic  treatment.  The  patient 
must  always  keep  himself  warm,  wear  flannels,  or  stay  in  bed.  Under  some  cir- 
cumstances climatic  cures,  like  Italy,  Egypt,  etc.,  are  indicated  in  the  more  chronic 
forms.     A  milk  diet  is  to  be  carried  out  as  far  as  possible. 

The  treatment  of  dropsy  follows  entirely  the  methods  previously  described,  and 
so  does  the  treatment  of  any  uraemic  symptoms. 

In  the  more  chronic  cases  with  great  anaemia  preparations  of  iron,  such  as 
iodide  of  iron,  are  often  to  be  used,  and  also  frequently  stomachics,  cathartics,  etc. 
The  condition  of  the  heart  always  deserves  careful  attention  (digitalis  !).  The  reti- 
nitis rarely  demands  a  special  treatment. 


856  DISEASES  OF  THE  KIDNEYS. 


CHAPTER  IV. 


CONTRACTED    KIDNEY. 

{Genuine    Contracted  Kidney.     Granular   Atrophy  of   the  Kidney.     Granular   Kidney.     Renal 
Sclerosis.     "  Third  Stage  of  BrighCs  Disease."     Chronic  Interstitial  Nephritis.) 

Definition  and  iEtiology.— The  genuine  contracted  kidney  is  the  result  of  an 
extremely  chronic  and  very  slowly  but  constantly  progressive  atrophy  of  the 
renal  tissue.  The  term  "chronic  nephritis"  is  also  used  for  contracted  kidney, 
but  the  special  inflammatory  processes  are  very  subordinate  here,  for  the  anatom- 
ical process  consists  essentially  in  nothing  but  a  simple  degenerative  atrophy  of 
the  renal  parenchyma,  and  in  a  corresponding  gradual  increase  of  the  interstitial 
connective  tissue.  From  a  general  pathological  point  of  view  the  process  is  to  be 
regarded  as  wholly  analogous  to  the  corresponding  changes  in  the  liver  in  cirrhosis 
of  that  organ,  in  the  spinal  cord  in  the  chronic  degenerations  of  the  different  sys- 
tems of  fibers,  etc.  In  all  these  cases  we  have  a  primary  destruction  of  the  special 
tissue-elements  as  a  result  of  some  deleterious  action,  and,  following  a  general 
pathological  law  (Weigert),  a  partial  replacement  of  the  parts  destroyed  by  a 
newly  formed  cicatricial  connective  tissue. 

In  the  "genuine"  contracted  kidney  the  atrophy  of  the  renal  parenchyma 
begins  in  a  previously  healthy  kidney.  Cell  after  cell  of  epithelium,  islet  after 
islet  of  tissue,  are  slowly  attacked,  while  other  parts  still  remain  intact.  It  was 
therefore  an  error  of  the  older  pathologists  to  regard  the  contracted  kidney  as  the 
"  third  stage  of  Bright's  disease,"  as  if  every  granular  kidney  were  first  found  in 
the  stage  of  acute  inflammation,  and  then  passed  into  the  stage  of  chronic  enlarge- 
ment, and  lastly  into  that  of  contraction.  This  theory,  of  course,  suits  certain 
cases  in  part,  for  chronic  nephritis  at  least  may  often  finally  pass  into  contraction, 
but  these  "  secondary  contracted  kidneys  "  (vide  Supra")  can  clinically,  and  almost 
always  anatomically,  be  differentiated  from  the  genuine  contracted  kidneys.  On 
careful  examination,  as  it  seems. to  us,  the  contracted  kidney  may  of  course  arise 
from  an  acute  nephritis  in  some  cases,  which  perhaps  are  not  very  rare ;  but  then 
the  process  hardly  ever  passes  through  the  three  stages  mentioned  above,  for  the 
acute  nephritis  apparently  recovers.  A  slight  remnant  of  it  is  left — a  little  fire,  as 
it  were,  glimmering  under  the  ashes ;  its  work  of  destruction  advances,  wholly  in 
secret,  and  perhaps  only  after  many  years  do  the  symptoms  of  a  pronounced  renal 
contraction  appear. 

If  we  inquire  into  the  causes  which  produce  the  atrophy  of  the  renal  tissue  in 
the  ordinary  cases  of  contracted  kidney,  which  are  chronic  from  the  first,  we  are 
very  often  unable  to  make  out  any  special  causes.  Of  course,  we  must  again  bear 
in  mind  first  the  two  great  groups  of  injurious  influences,  the  chemico-toxic  and 
the  organized  parasitic,  but  at  present  only  a  small  number  of  setiological  factors 
have  a  more  or  less  definite  significance. 

Experience  teaches  us  that  there  are  three  chemical  substances  to  be  mentioned 
which  may  favor  the  development  of  contracted  kidney:  alcohol,  lead,  and  uric 
acid.  Chronic  alcoholism  is  often  to  be  regarded  as  the  most  probable  cause  of 
renal  contraction,  especially  in  people  who  have  "  lived  well "  otherwise,  and  have 
become  corpulent.  This  is  the  explanation  of  the  combination  of  contracted 
kidney  and  cirrhosis  of  the  liver  repeatedly  observed.  The  connection  between 
contracted  kidney  and  chronic  lead-poisoning,  in  type-setters,  painters,  etc.,  is  also 
incontestable.  It  is  also  a  remarkable  circumstance,  and  one  not  yet  fully 
explained,  that  in  these  cases  we  very  often  see  at  the  same  time  a  genuine  gout 
(arthritis  uratica).     Gout,  however,  alone,  without  any  co-existing  chronic  lead- 


CONTRACTED  KIDNEY.  857 

poisoning,  often  leads  to  the  development  of  contracted  kidney,  "  gouty  kidney," 
in  which  we  probably  have  to  do  with  the  noxious  action  of  an  abnormal  amount 
of  uric  acid  on  the  renal  parenchyma. 

Infectious  influences  are,  probably,  first  to  be  considered  in  those  cases  where 
the  contracted  kidney  can  be  referred  to  a  former  infectious  nephritis 
scarlet  fever.  We  may  also  mention  here  the  appearance  of  contracted  kidney 
sometimes  observed  after  severe  acute  articular  rheumatism.  "We  may  perhaps 
imagine  a  similar  connection  in  the  cases  where  contracted  kidney  is  found  com- 
bined with  chronic  endocarditis  (valvular  heart  disease),  or  with  chronic  arthritis 
not  of  gouty  origin.  Of  the  chronic  infectious  diseases,  which  may  probably  some- 
times have  a  connection  with  the  origin  of  contracted  kidney,  we  may  mention 
malaria  and  syphilis.  The  latter  ought  especially  to  be  considered  more  than  it  is 
at  present,  because  we  may  have  either  an  immediate  action  of  the  syphilitic  poison, 
or  a  renal  atrophy  as  the  result  of  specific  disease  of  the  renal  arteries. 

We  must  here  spend  a  little  time  in  the  general  consideration  of  the  connec- 
tion between  renal  contraction  and  primary  disease  of  the  vessels,  which  has  been 
much  discussed.  It  is  true  that  we  often  find  general  arterio-sclerosis,  and  also 
atheroma,  especially  in  the  renal  arteries,  in  the  bodies  of  persons  who  have  died 
from  contracted  kidney,  but  this  frequent  coincidence  can  not  be  remarkable  in 
such  cases,  because  contracted  kidney  is  seen  chiefly  in  advanced  age,  and  in  those 
persons  in  whom  atheroma  of  the  arteries  is  also  a  very  common  symptom.  The 
theory  advanced  by  the  English  authors,  Grull  and  Sutton  and  others,  that  the  vas- 
cular disease,  "  arterio-capillary  fibrosis,"  always  represents  the  primary  process, 
to  which  the  renal  atrophy  is  only  secondary,  is,  however,  utterly  untenable.  We 
often  und  the  most  pronounced  contraction  of  the  kidneys  without  any  vascular 
changes  sufficient  to  explain  the  atrophy ;  and  where  the  latter  can  be  found  in 
the  small  renal  arteries,  we  usually  have  not  a  primary  but  a  secondary  process — 
namely,  the  well-known  obliterating  arteritis,  which  is  seen  in  almost  all  chronic 
inflammations  and  degenerative  atrophies  of  various  organs. 

Of  course,  it  can  not  be  denied  that  under  some  circumstances  primary  vascu- 
lar diseases  of  the  renal  arteries  may  lead  to  secondary  atrophy  in  circumscribed 
spots  by  checking  the  blood-supply  to  certain  parts  of  the  tissue — "  vascular  con- 
tracted kidney" — just  as  indurated  myocarditis  arises  after  primary  arterio-sclerosis 
of  the  coronary  arteries.  The  "  senile  kidney  " — that  is,  the  granular  kidney  of  old 
people — is  also  due  to  vascular  changes  like  atheroma,  as  are  also,  which  is  worthy 
of  special  note,  the  rare  cases  of  unilateral  contraction  of  the  kidney,  which  is 
observed  chiefly  in  syphilis. 

The  relation  of  contracted  kidney  to  amyloid  disease  of  the  kidney,  and  to 
chronic  diseases  of  the  urinary  passages,  especially  of  the  pelvis  of  the  kidney, 
will  be  spoken  of  later  in  the  appropriate  chapters. 

Pathological  Anatomy. — In  the  genuine  contraction  of  the  kidney,  both  kid- 
neys are  always  diminished  in  about  the  same  degree.  Their  size  is  sometimes 
reduced  to  one  half  or  even  one  third  of  the  normal,  so  that  it  is  almost  difficult  to 
find  the  little  kidney  in  the  very  abundant  and  thick  fatty  capsule  that  is  often 
present.  The  kidneys  feel  firm  and  dense,  and  show  on  their  surface  a  very  plain, 
coarse  or  fine,  uniform  or  irregular,  granulation.  On  pulling  off  the  somewhat 
thickened  fibrous  capsule,  these  granulations  become  more  prominent,  and  the  cap- 
sule usually  adheres  quite  firmly  to  the  depressed  portions.  The  raised  portions 
are  almost  always  darker  and  redder — that  is,  richer  in  blood — than  the  lighter 
and  grayer  depressions.  Whether  the  whole  kidney  appears  more  red  or  more 
white  depends  only  upon  the  amount  of  blood  in  the  organ,  and  there  is  no  reason 
for  separating  the  "  small  red  "  from  the  "  small  white  "  contracted  kidney. 

On  section  of  the  contracted  kidney,  we  find  the  cortex  much  smaller,  and  pale 


S58  DISEASES  OF  THE  KIDNEYS. 

atrophic  streaks  alternating  with  the  darker  portions.  The  pyramids  are  also 
somewhat  smaller,  and,  as  a  rule,  ai'e  darker  than  the  cortex.  In  the  pelvis  of 
the  kidney,  which  is  often  somewhat  dilated,  there  are  frequently  a  number  of 
uric-acid  concretions.  Striated  uric-acid  infarctions  in  the  pyramids  are  a  very 
chai'acteristic  mark  of  the  gouty  contracted  kidney.  The  microscope  shows  an 
advanced  destruction  of  the  renal  parenchyma,  which  is  replaced  by  a  cicatricial 
connective  tissue  which  is  still  granular  or  which  has  begun  to  be  poor  in  granules. 
We  can  always  make  out  signs  of  degeneration  and  atrophy  of  the  epithelium,  and 
the  formation  of  casts  in  the  uriniferous  tubules  which  still  remain,  but  which  are 
always  diseased.  Atrophy,  thickening  of  the  capsule,  etc.,  are  found  in  many  of 
the  glomeruli.  The  uriniferous  tubules  that  are  still  preserved  in  some  places  are 
often  in  part  dilated.  We  can  not  here  go  more  fully  into  the  manifold  histologi- 
cal details,  especially  the  formation  of  cysts,  the  changes  in  the  vessels  (vide  supra), 
the  deposition  of  lime-salts,  etc.     Hemorrhages  are  only  very  rarely  present. 

Thus  the  contracted  kidney  may  be  regarded  as  the  form  of  chronic  nephritis 
with  by  far  the  longest  course  (lasting  from  three  to  five  years,  and  even  much 
longer),  and  also  the  form  with  the  widest  extent.  Its  essential  nature  can  in  no 
way  be  con  toasted  with  "chronic  parenchymatous  nephritis"  as  a  "chronic  inter- 
stitial nephritis";  "for  we  always  find  interstitial  processes  in  the  former,  which 
have  reached  a  far  higher  degree  in  the  contracted  kidney  only  because  the  slow 
atrophy  of  tissue  is  compatible  with  a  much  longer  duration  of  life,  and  hence  can 
attain  a  much  greater  extent. 

The  anatomical  changes  in  the  other  organs  of  the  body  beside  the  kidneys 
will  be  spoken  of  in  connection  with  the  symptomatology  of  contracted  kidney. 

Clinical  Symptoms. — Except  in  the  comparatively  rare  cases  where  we  can 
refer  the  origin  of  a  contracted  kidney  to  a  previous  acute  or  chronic  nephritis, 
the  clinical  symptoms  of  contracted  kidney  develop  as  gradually  and  unnoticeably 
as  the  anatomical  process  itself.  There  is  no  doubt  but  that  a  contraction  of  the 
kidney  may  exist  for  years,  without  calling  the  patient's  attention  to  his  disease  by 
a  single  serious  subjective  symptom.  This  follows  in  part  from  the  chance  dis- 
coveries on  autopsy  of  a  contraction  of  the  kidney  in  people  who  have  lost  their 
lives  in  some  other  way,  but  especially  from  the  cases  where  the  severest  symp- 
toms, like  uraemia,  cerebral  haemorrhage,  etc.,  which  often  lead  immediately  to 
death,  suddenly  come  on  in  persons  previously  regarded  as  perfectly  healthy,  while 
the  autopsy  often  shows  quite  a  far  advanced  contraction  of  the  kidney  as  the 
special  cause  of  these  symptoms.  The  less  prominent  the  subjective  symptoms  of 
renal  contraction  are  in  the  earlier  stages  of  the  disease,  the  more  we  should  con- 
sider the  objective  changes,  which  in  fact  usually  permit  the  diagnosis  of  the  dis- 
ease quite  early  on  careful  examination  of  the  patient. 

The  condition  of  the  urine  is  most  important  in  this  respect.  As  soon  as 
changes  have  taken  place  in  the  epithelium  in  different  parts  of  the  kidneys,  the 
results  previously  spoken  of  must  make  themselves  manifest  in  the  secretion  of 
the  urine,  although  still  in  a  slight  degree,  and  the  diseased  patient  will  secrete  a 
urine  diminished  in  amount  and  in  solid  constituents,  but  containing  albumen. 
Since,  however,  many  normal  uriniferous  tubules  and  glomeruli  are  still  present, 
and  since  the  whole  process,  as  we  have  seen,  develops  only  very  slowly,  the  body 
gains  time  for  the  formation  of  one  of  those  judicious  compensatory  contrivances 
which  we  recognize  in  so  many  pathological  processes,  and  which  we  must  regard 
in  a  teleological  sense.  This  compensatory  process  consists  of  an  increase  in  the 
arterial  pressure,  corning  on  as  gradually  as  the  renal  contraction  itself,  and  con- 
stantly increasing,  and  of  a  hypertrophy  of  the  left  ventricle  dependent  upon  it. 
The  blood  therefore  courses  through  the  many  normal  glomeruli  of  the  contracting 
kidney  under  an  increased  pressure,  and  the  consequence  is  that  in  these  portions 


CONTRACTED  KIDNEY.  859 

the  secretion  of  the  urine,  especially  of  the  water,  is  much  more  abundant.  This 
is  the  reason  why,  as  a  rule,  in  contraction  of  the  kidney,  the  patient  passes  an 
abnormally  large  amount  of  urine,  which  is  more  watery,  and  therefore  lighter  and 
of  a  lower  specific  gravity,  and  which  contains  only  a  slight  amount  of  albumen 
coming  from  the  diseased  portions.  The  daily  amount  of  urine  is  often  seventy 
to  a  hundred  and  twenty  ounces  (2000-o500  c.  c.)  or  more  ;  the  urine  looks  light- 
yellow  and  clear,  contains  scarcely  any  morphological  constituents,  has  a  specific 
gravity  of  1010-1005  or  even  lower,  and  gives,  on  heating,  only  a  slight  precipitate 
of  albumen,  the  amount  excreted  in  the  twenty-four  hours  being  about  half  a 
drachm  to  a  drachm  (two  to  five  grammes).  On  careful  microscopic  examination 
of  the  urine,  we  usually  succeed  in  finding  a  few  hyaline  casts,  which  only  excep- 
tionally may  be  moi'e  abundant.  The  urine  also  frequently  contains  some  white, 
and  more  rarely  a  few  red  blood-corpuscles.  In  rare  but  definitely  attested  casus 
it  may  happen  that  for  a  time,  or  even  during  the  main  part  of  the  disease,  the 
urine  contains  no  albumen  at  all,  or  only  a  trace  of  it.  This  is  probably  explained 
by  the  fact  that  the  diseased  glomeruli  have  wholly  ceased  secreting,  and  that 
therefore  the  urine  is  secreted  only  by  the  healthy  portions  of  the  kidney. 

It  is  apparent  of  how  great  significance  this  abundant  secretion  of  water,  as  a 
result  of  the  abnormally  high  blood-pressure,  must  be  for  the  whole  morbid  pro- 
cess ;  for,  in  spite  of  the  renal  disease,  there  is  now  absolutely  no  retention  of 
water  in  the  body,  and  we  therefore  understand  why  there  is  no  oedema  in  con- 
tracted kidney,  even  after  a  course  of  years.  The  secretion  of  the  solid  con- 
stituents of  the  urine  is  not  quite  in  such  a  favorable  condition  as  the  secretion  of 
water.  It  is  self-evident  that  the  percentage  of  the  former  decreases  with  the 
increased  amount  of  urine,  but  the  whole  amount  of  urea,  uric  acid,  phosphoric 
acid,  etc.,  eliminated  is  also  at  times  somewhat  less  than  normal  in  relation  to  the 
food.  This  diminution,  however,  is  not  very  great,  as  long  as  the  work  of  the 
heart  is  sufficient,  and  at  certain  times,  especially  in  the  earlier  periods  of  the  dis- 
ease, it  may  certainly  be  entirely  absent.  We  accordingly  see  that  the  symptoms 
dependent  upon  an  accumulation  of  the  urinary  constituents  in  the  blood  do  not 
appear  at  all  for  a  long  time.  Thus  it  happens  that  the  patient  may  still  feel  per- 
fectly well  up  to  a  time  when  the  objective  examination  of  the  urine  discovers 
marked  pathological  changes.  Many  patients,  of  course,  notice  the  polyuria,  but 
often  no  further  attention  is  paid  to  it,  and  it  is  attributed  to  drinking  a  good  deal 
of  fluid.  The  patient  gets  accustomed  to  it,  even  if,  as  often  happens,  he  has  to 
pass  his  urine  much  more  frequently  than  formerly,  and  even  during  the  night. 

We  need  not  go  into  detail  here  in  regard  to  the  special  causes  of  cardiac 
hypertrophy  (compare  page  834).  It  was  with  regard  to  contracted  kidney  that 
Traube  advanced  his  mechanical  theory  of  cardiac  hypertrophy,  which,  however, 
brought  up  the  considerations  previously  mentioned,  and  therefore  was  properly 
replaced  by  the  chemical  theory,  which  was  also  very  applicable  to  this  form  of 
renal  disease.  In  its  clinical  relations  it  is  especially  important  that  the  cardiac 
hypertrophy  causes  no  subjective  symptoms  at  all,  as  long  as  the  heart  can  suffice 
for  the  work  put  upon  it  without  strain,  a  condition  which  is  perfectly  analogous 
to  that  of  any  fully  compensated  valvular  disease.  We  can  usually  recognise  the 
condition  correctly  only  by  a  careful  physical  examination  of  the  heart  and  the 
vascular  apparatus,  although  in  contracted  kidney  the  percussion  and  palpation  of 
the  heart  are  often  rendered  difficult  by  a  co-existing  pulmonary  emphysema. 
We  can  often  perceive,  however,  the  displacement  and  the  increased  strength  of  the 
apex-beat,  the  extension  of  the  cardiac  dullness  to  the  left,  and  almost  invariably 
the  abnormal  tension  of  the  radial  pulse,  and  the  accentuation  of  the  aortic  second 
sound.  In  the  later  stages  of  the  disease  a  hypertrophy  of  the  right  ventricle  is 
often  added  to  that  of  the  left  (compare  page  858).     Complete,  or  almost  complete, 


SCO  DISEASES  OF  THE  KIDNEYS. 

absence  of  the  cardiac  hypertrophy  is  observed,  as  we  have  said,  in  weak  and 
cachectic  patients. 

As  long-,  therefore,  as  the  high  arterial  pressure  kept  up  by  the  cardiac  hyper- 
trophy regulates  the  condition  of  the  renal  secretion  in  the  way  above  described, 
the  condition  of  the  patient  as  a  rule  shows  no  special  abnormality.  At  most  it 
happens  that  certain  cerebral  symptoms  now  appear,  especially  attacks  of  head- 
ache and  occasional  vertigo,  which  are  probably  to  be  referred  to  active  cerebral 
hyperemia.  Frequent  nose-bleed  is  also  sometimes  the  result  of  the  abnormally 
high  blood-pressure. 

The  picture  is  quite  different  as  soon  as  the  first  signs  of  a  beginning  cardiac 
insufficiency  appear.  Here,  as  in  most  diseases  of  the  heart,  the  disturbance  of 
compensation  does  not  usually  come  on  suddenly.  Its  results  begin  quite  gradu- 
ally, disappear  for  a  time,  to  come  on  afresh  and  to  increase  quite  slowly.  In  the 
first  place,  the  abatement  of  the  heart's  energy  usually  makes  itself  manifest  by 
symptoms  on  the  part  of  the  heart  itself,  and  of  the  lungs.  The  pulse  loses  in  ten- 
sion, and  becomes  smaller,  more  frequent,  and  sometimes  a  little  irregular  toward 
the  end  of  the  disease.  The  patient  begins  to  be  short  of  breath,  comparatively 
slight  physical  exertion  affects  him  more  than  formerly,  and  there  is  often  palpi- 
tation. Certain  anatomical  results  of  stasis  may  also  temporarily  or  permanently 
develop  in  the  lungs,  especially  a  mild  transitory  catarrh,  or  a  more  obstinate  and 
recurring  bronchitis.  In  the  more  advanced  stages  of  the  disease  the  dyspnoea 
often  comes  on  in  pronounced  paroxysms,  which  have  an  asthmatic  character. 
This  long-known  asthma  of  renal  disease,  often  termed,  without  reason,  "  uraemic 
asthma,"  does  not  always  have  the  same  origin.  It  usually  depends  distinctly 
upon  the  attacks  of  cardiac  weakness,  and  is,  accordingly,  a  genuine  cardiac  asthma, 
and  corresponds  precisely  to  angina  pectoris  in  its  different  symptoms  (see  page 
318) ;  but  in  other  cases  there  is  a  transudation  into  the  lungs  from  stasis,  coming 
on  as  a  result  of  the  cardiac  weakness,  so  that  the  dyspnoea  is  associated  with  the 
signs  of  an  acute  pulmonary  oedema,  and  is  sometimes  accompanied  by  a  copious 
expectoration  of  a  frothy,  serous,  and  often  somewhat  bloody  sputum.  This  is  the 
condition  which  may  pass  away  again  and  be  often  repeated,  which  was  formerly 
termed  humid  asthma.  In  the  last  stage  of  the  disease  the  dyspnoea  often  becomes 
continuous,  and  forms  the  patient's  chief  disturbance.  It  is  then  usually  due,  not 
merely  to  the  stasis  in  the  lungs,  but  often,  besides,  to  co-existing  lobular  pneu- 
monia (vide  infra),  to  hydrothorax,  etc. 

As  a  further  sequel  of  the  disturbance  of  compensation,  oedema  often  appears 
in  different  parts  of  the  body,  in  the  later  course  of  tbe  disease.  It  has,  indeed, 
been  repeatedly  observed  that  dropsy  may  be  entirely  absent  in  contracted  kidney ; 
but  this  is  the  case  only  when  death  ensues  from  some  intercurrent  attack  before 
the  pronounced  cardiac  insufficiency.  Otherwise  oedema  is  by  no  means  rare  in 
contracted  kidney.  It  usually  appears  first  in  the  ankles,  the  eyelids,  or  the  pre- 
puce, disappears  again  when  the  patient  is  in  a  quiet  condition,  and,  after  a  longer 
or  a  shorter  pause,  comes  on  anew,  until  finally,  in  the  last  period  of  the  disease,  a 
high  degree  of  general  dropsy  may  develop. 

Among  the  results  of  the  cardiac  insufficiency  on  the  internal  organs  we  must  first 
mention  the  cerebral  symptoms.  While  at  first,  as  we  have  said,  these  have  more  of 
an  active  hypersemic  character,  the  frequent  and  very  violent  headaches  that  come 
on  later,  in  so  far  as  they  are  not  of  a  uraemic  nature,  certainly  depend  mainly  upon 
the  passive  hyperaemia  of  stasis,  or  the  arterial  anaemia  of  the  brain.  The  pain  some- 
times shoots  into  the  back  of  the  neck,  and  sometimes  is  localized  chiefly  in  one  half 
of  the  head ;  it  is  often  associated  with  symptoms  of  vertigo,  with  a  gloomy  or  morose 
disposition,  with  troubled  sleep,  etc.  The  stasis  is  also  apparent  in  the  abdominal  or- 
gans.   Chronic  dyspeptic  disturbances  appear,  the  appetite  fails,  the  bowels  become 


CONTRACTED  KIDNEY.  861 

irregular,  and  we  can  even  make  out  a  moderate  enlargement  of  the  liver.  The  in- 
fluence which  the  altered  activity  of  the  heart  exerts  upon  the  function  of  the  kidneys 
themselves  is,  however,  particularly  important.  From  what  has  been  previously  s:iid 
of  the  dependence  of  the  secretion  of  urine  upon  the  arterial  pressure,  it  follows 
directly  that  any  compensatory  activity  of  the  still  normal  renal  territory  must  at 
once  experience  a  reduction,  as  soon  as  the  blood -pressure  can  no  longer  be  kept 
at  the  same  level.  Corresponding  to  this  we  sec,  in  fact,  that  the  secretion  of 
urine  also  usually  suffers  a  decline  at  the  same  time  with  the  other  symptoms  of 
stasis  already  mentioned.  The  amount  of  urine  is  less  abundant:  it  falls  to  forty 
or  fifty  ounces  (1500-1000  c.  c),  and  even  lower;  the  specific  gravity  rises,  rarely 
to  a  high  figure,  but  still  up  to  1010  or  1012,  or  over.  The  urine  often  retains 
its  clear  color  for  quite  a  long  time,  but  may  finally  more  and  more  resemble  the 
genuine  urine  of  stasis.  The  point,  however,  which  is  especially  to  be  considered, 
is  the  co-existing  and  increasing  retention  of  the  solid  constituents  of  the  urine  in 
the  blood,  and  the  consequent  allied  possibility  of  the  onset  of  uraemic  symptoms. 

It  must  be  stated  that,  in  contracted  kidney,  the  immediate  exciting  causes  of 
uraemia  are  not  always  clear.  Thus,  it  is  a  well-known  and  very  important  fact, 
clinically,  that  very  severe  and  often  fatal  uraemic  convulsions  may  sometimes 
attack  the  patient  quite  suddenly,  apparently  when  in  the  best  of  health.  Cases 
have  been  repeatedly  seen,  by  other  observers  and  by  ourselves,  where  the  daily 
amount  of  urine  has  shown  no  discoverable  diminution  in  the  days  preceding  the 
uraemia.  The  precise  explanation  of  these  cases  must  remain  undecided  ;  we  do 
not  know  whether  there  has  been  a  previous  retention  of  the  solid  constituents,  in 
spite  of  the  abundant  secretion  of  water,  or  whether  other  changes,  like  oedema  of 
the  brain,  are  to  be  considered.  It  is  certain,  however,  that  in  many  cases  at  least, 
the  onset  of  the  uraemia  is  connected  with  the  cessation  of  the  secretion  of  urine, 
produced  either  gradually  or  suddenly  by  the  cardiac  insufficiency.  In  the  former 
case  the  type  of  chronic  uraemia  (see  page  829)  develops  with  especial  frequency ; 
this  consists  of  headache,  vomiting,  diarrhoea,  severe  pruritus  of  the  skin,  etc.,  but 
these  symptoms  are,  of  course,  often  combined  with  the  immediate  symptoms  of 
stasis,  and  are  not  always  to  be  easily  and  distinctly  separated  from  them.  Such 
a  condition  of  chronic  uraemia,  in  patients  with  contracted  kidney,  often  presents 
a  very  mournful  picture,  since  the  unrestrainable  and  constantly  recurring  vomit- 
ing, the  headache,  and  the  general  mental  anxiety  may  last  for  weeks.  The 
severe  acute  uraemia  either  follows  the  preceding  chronic  uraemic  symptoms,  or 
comes  on  at  once  with  the  severest  symptoms,  general  and  often-recurring  con- 
vulsions, and  coma.  The  uraemia  may  pass  off  again,  even  in  contracted  kidney, 
but  quite  frequently  it  is  the  immediate  cause  of  death  (vide  infra). 

Beside  the  symptoms  so  far  described,  we  must  now  mention  a  set  of  anatom- 
ical complications  which  may  appear  in  the  course  of  contraction  of  the  kidney. 
From  its  diagnostic  and  clinical  importance  the  albuminuric  retinitis,  already 
known  to  us  from  the  preceding  chapter,  takes  the  first  place.  It  may  come  on 
at  any  time  in  the  course  of  the  disease  ;  but  it  often  develops  so  early  that  the 
patient,  up  to  this  time,  knows  nothing  at  all  of  his  other  disease.  He  merely 
consults  an  oculist,  who  often  first  recognizes,  from  the  ophthalmoscopic  picture 
(see  page  854),  the  special  seat  of  the  primary  disease.  Even  in  the  cases  where 
no  subjective  visual  disturbance  is  present,  the  retinal  examination  sometimes 
shows  a  positive  image.  In  general,  the  contracted  kidney  is  that  form  of  renal 
disease  in  which  retinal  changes  are  comparatively  the  most  frequent. 

Another  rarer  but  clinically  important  complication  consists  of  the  haemor- 
rhages of  internal  organs,  whose  cause  is  to  be  found  either  in  the  increased  arte- 
rial pressure,  or  in  an  abnormal  weakness  of  the  walls  of  the  vessels — arterio- 
sclerosis in  older  persons,  defective  nutrition  of  the  vascular  walls  in  young  and 


862  DISEASES  OF  THE  KIDNEYS. 

anaemic  patients.  Haemorrhages  into  the  brain  are  comparatively  the  most  fre- 
quent. They  cause  both  mild  and  severe  apoplectic  attacks,  which  pass  off  com- 
pletely or  leave  a  hemiplegia  behind,  and  sometimes  they  are  the  direct  cause  of 
death.  Beside  the  haemorrhages  into  the  brain  itself,  there  may  also  be  haemor- 
rhages on  the  inner  surface  of  the  dura  mater — haematoma.  Nose-bleed  is  also  of 
significance ;  in  many  patients  it  is  frequent  and  very  stubborn ;  we  have  ourselves 
seen  two  cases  where  the  fatal  termination  was  caused  directly  by  an  unrestrain- 
able  nose-bleed.'  Haemorrhages  into  the  other  organs  are  more  rare,  but  they 
have  also  been  observed  in  the  skin,  the  stomach,  the  intestines,  or  the  lungs.  In 
a  few  cases,  indeed,  a  sort  of  hemorrhagic  diathesis  seems  to  develop. 

Among  the  complicating  inflammations  of  internal  organs,  pneumonia  is  the 
most  frequent ;  it  appears  in  the  lobar  croupous  form  or  in  the  lobular  form  pecul- 
iar to  all  varieties  of  nephritis.  Inflammations  of  the  serous  membranes,  pleurisy, 
or  pericarditis,  occur,  but  they  are  rare.  The  catarrhal  inflammatory  affections — 
laryngitis,  bronchitis,  gastric  catarrh,  intestinal  catarrh — are  either  to  be  regarded 
as  catarrhs  from  stasis,  or  they  are  perhaps  connected  with  the  retention  of  the 
urinary  constituents  in  the  body.  We  must  also  refer  here  to  the  acute  exacerba- 
tions of  inflammation  in  the  kidneys  themselves  (acute  recurrent  nephritis),  which 
is,  of  course,  rare. 

Quite  great  variations  appear  in  regard  to  the  general  nutrition.  In  most  cases 
where  the  disease  develops  quite  gradually  in  persons  in  middle  or  advanced  life, 
the  general  nutrition  for  a  long  time  shows  no  striking  anomaly.  The  patient  is 
often  very  well  nourished,  and  even  corpulent,  at  the  period  when  the  first  cardiac 
symptoms  begin.  To  the  more  practiced  and  attentive  eye,  of  course,  he  shows 
a  certain  appearance  of  suffering,  which  later  becomes  more  pronounced.  He 
becomes  emaciated,  and  has  a  faded  and  often  somewhat  cyanotic  color  to  his 
skin.  Marked  anaemia  usually  develops  only  in  younger  patients,  who  then  show 
the  pallid  exterior  characteristic  of  so  many  patients  with  renal  disease. 

General  Course,  Duration,  and  Termination. — The  most  important  peculiarities 
in  the  course  of  renal  contraction  have  already  been  spoken  of  above.  We  have 
stated  that  the  disease  may  be  latent  for  a  long  time;  that  the  severest  symp- 
toms— like  uraemia  or  apoplexy — sometimes  come  on  suddenly  and  unexpectedly ; 
that  in  other  cases  the  disturbances  of  compensation  in  the  heart,  dyspnoea,  palpi- 
tation, or  slight  oedema,  are  the  first  symptoms ;  that,  under  some  circumstances, 
certain  complicating  conditions,  such  as  retinitis,  or  frequent  nose-bleed,  first 
direct  suspicion  to  a  renal  disease,  and  demand  an  examination  of  the  urine ;  while, 
finally,  in  a  last  class  of  cases,  only  general  disturbances,  loss  of  appetite,  pallor, 
general  physical  weakness,  and  similar  symptoms  induce  the  patient  to  consult  a 
physician.  It  is  usually  hard  to  decide  how  long  the  disease  has  lasted  before  a 
diagnosis  is  made.  Beside  any  mild  symptoms  we  must  especially  inquire  into 
the  existence  of  polyuria,  which  is  often  not  observed,  but  which  many  patients 
notice. 

The  further  course  may  also  vary  according  to  the  onset  of  complications,  the 
external  conditions  under  which  the  patient  lives,  etc.  In  general,  as  we  must 
repeatedly  emphasize,  almost  everything  depends  upon  the  heart's  capacity  for 
work  and  its  staying  qualities.  If  death  does  not  ensue  sooner  from  some  inter- 
current disease,  the  last  stage  of  the  disease  almost  always  presents  itself  under 
the  picture  of  cardiac  insufficiency  with  predominant  symptoms  of  dyspnoea  and 
general  dropsy. 

As  has  been  said,  we  usually  can  not  determine  with  any  accuracy  the  whole 
duration  of  the  disease.  It  may,  at  any  rate,  last  many  years,  probably  sometimes 
even  ten  years  or  more,  although  there  may  be  many  variations  in  its  course.  It 
is  not  impossible  that,  during  the  earlier  period  of  the  disease,  there  may  be  a  ces- 


CONTRACTED  KIDNEY.  863 

sation  in  the  process  of  renal  atrophy,  hut  it  is  hard  to  decide  with  certainly.  At 
all  events,  the  disease  must  generally  he  termed  completely  incurable,  although 
life  may  not  only  be  preserved  for  a  long-  time,  but  the  patient  may  even  exist 
without  much  discomfort.  We  need  not  refer  especially  here  to  the  different 
intercurrent  attacks,  the  possibility  of  which  must  always  be  kept  in  mind  in 
regard  to  prognosis. 

Diagnosis. — The  diagnosis  of  contracted  kidney  can  be  made  with  certainty 
only  by  examining  the  urine.  We  must,  therefore,  dwell  again  on  the  necessity 
of  making  this  examination  in  all  suspicious  cases,  because  only  in  this  way  can 
we  avoid  overlooking  the  condition.  The  suspicion  of  a  developing  renal  contrac- 
tion should  demand  an  examination  of  the  urine,  especially  in  all  cases  where  the 
patient  complains  of  frequent  headache,  of  congestive  conditions,  of  palpitation 
and  dyspnoea,  asthmatic  attacks,  disturbances  of  vision,  general  dullness,  and  dys- 
peptic symptoms,  without  finding  any  other  reason  for  these  symptoms.  The  poly- 
uria, the  clear  urine  of  low  specific  gravity,  containing  a  slight  amount  of  albu- 
men, in  connection  with  the  signs  in  the  circulatory  apparatus,  the  tense  pulse, 
and  the  hypertrophy  of  the  left  ventricle,  permit  us  to  recognize  the  disease  cor- 
rectly in  most  cases.  If  retinal  changes  are  present,  they  may  sometimes  be  of 
much  aid  in  confirming  the  diagnosis.  The  aetiological  conditions — lead,  gout, 
alcoholism,  etc. — of  course  also  merit  attention. 

The  diagnosis  presents  great  difficulty  in  the  quite  rare  cases  where  albuminuria 
is  absent.  In  these  cases  we  are  sometimes  able  to  reach  the  correct  interpretation 
of  the  morbid  condition  only  by  repeated  examinations  of  the  urine.  Otherwise 
we  can  scarcely  avoid  mistaking  it  for  chronic  affections  of  the  heart,  such  as 
myocarditis  or  idiopathic  hypertrophy. 

The  diagnosis  is  also  very  difficult  if  the  patient  does  not  come  under  observa- 
tion until  the  stage  of  fully  developed  disturbance  of  compensation.  The  charac- 
teristic features  of  the  urine  of  contracted  kidney  are  then  absent,  the  urine  is 
scantier,  darker,  richer  in  albumen,  and  it  is  often  scarcely  possible  to  decide 
whether  we  have  a  primary  renal  affection  with  secondary  cardiac  hypertrophy 
or  a  primary  heart  disease  with  a  secondary  congested  kidney.  If  general  arterio- 
sclerosis or  marked  pidmonary  emphysema  is  present  at  the  same  time,  the  judg- 
ment as  to  the  condition  is  still  more  difficult.  In  such  cases  a  correct  diagnosis 
is  possible  only  by  very  carefully  balancing  all  the  different  symptoms,  and  con- 
sidering the  whole  course  of  the  disease. 

Finally,  the  diagnosis  of  contracted  kidney  is  very  difficult  in  cases  where  the 
first  examination  of  the  patient  is  made  during  a  sudden  attack  of  uraemia  or  after 
an  apoplectic  seizure.  Here  the  albuminuria  is  the  symptom  which  points  most 
to  the  existence  of  a  renal  disease,  although,  in  spite  of  this  symptom,  the  judgment 
as  to  the  condition,  and  its  differentiation  from  other  acute  cerebral  affections, 
often  presents  great  difficulties. 

Treatment. — As  soon  as  the  diagnosis  of  renal  contraction  is  established,  the 
whole  hygienic  condition  of  the  patient  must  be  regulated  so  as  to  prevent  the 
advance  of  the  affection  in  every  possible  way.  In  this  respect  two  indications 
are  to  be  fulfilled,  to  guard  against  any  irritation  which  may  have  an  injurious 
action  on  the  kidneys,  and  to  relieve  the  work  of  the  heart  as  much  as  possible,  in 
order  to  keep  off  cardiac  insufficiency  as  long  as  we  can.  The  diet  must  be  care- 
fully regulated,  and  must  be  of  scant  measure  or  abundant  and  strengthening, 
according  to  the  patient's  physical  constitution.  In  these  cases,  too,  milk  is  the 
chief  food  to  be  considered.  Alcoholic  beverages  are  to  be  permitted  only  in  a 
moderate  degree.  All  physical  over- exertion  is  to  be  avoided,  although  moderate 
methodical  exercise  is  to  be  recommended  for  corpulent  patients.  We  should 
always  provide  for  regular  evacuation  of  the  bowels  by  appropriate  remedies. 


864  DISEASES  OF  THE  KIDNEYS. 

dietetic  prescriptions,  fruits,  bitter  waters,  etc.  The  general  condition  is  often 
materially  improved  by  proper  air  and  recreation,  and  in  this  way  the  use  of  a 
bath  may  be  of  service,  chosen  according  to  the  individual  conditions,  such  as  iron 
baths,  Marienbad,  Carlsbad,  Kissingen,  Ems,  or  Baden-Baden. 

If  disturbances  of  compensation  appear,  the  dietetic  regime  and  the  utmost 
bodily  rest  possible  are  still  more  strictly  to  be  advised,  and  a  symptomatic  treat- 
ment should  be  instituted  according  to  the  prevailing  symptoms.  First  of  all  we 
must  try  to  excite  the  heart's  energy  anew  by  the  exhibition  of  digitalis.  The 
details  of  treatment  here  are  almost  precisely  the  same  as  are  considered  in  the 
treatment  of  chronic  heart  disease  (q.  v.)  and  the  other  renal  affections.  [The 
nitrites,  especially  nitroglycerine,  are  of  gi'eat  service  in  some  cases  of  contracted 
kidney,  and  may  be  used  persistently  when  the  arterial  tension  is  unduly  high, 
and  the  compensatory  hypertrophy  of  the  left  ventricle  shows  signs  of  failing.  In 
these  cases  strophanthus,  which  is  said  not  to  increase  arterial  tension,  may  at 
times  be  substituted  for  digitalis  with  advantage.] 

At  present  it  is  impossible  to  influence  the  process  of  contraction  in  the  kidney 
favorably  by  the  direct  use  of  drugs.  The  iodine  preparations — iodide  of  potas- 
sium, and  in  anasmic  patients  iodide  of  iron — are  alone  recommended,  and  are 
worth  trying  in  this  respect. 

The  prophylaxis  of  renal  contraction  is  evident;  we  should  consider  as  far  as 
we  can  the  known  aetiological  conditions.  We  may  compare,  in  this  regard,  the 
chapter  on  gout. 

CHAPTER  V. 
AMYLOID  KIDNEY. 

JEtiology. — The  amyloid  kidney  is  invariably  a  part  of  the  more  or  less  extensive 
amyloid  degeneration  of  the  organs  in  the  rest  of  the  body.  In  its  clinical  rela- 
tions, however,  it  claims  the  most  interest  of  all  amyloid  diseases,  since  it  has  by 
far  the  greatest  significance  for  the  whole  clinical  picture  of  amyloid  degeneration. 

As  is  well  known,  we  understand  by  amyloid  degeneration  a  peculiar  change 
which,  under  certain  pathological  conditions,  is  observed  in  the  connective  tissue, 
and  especially  in  the  smaller  vessels.  The  walls  of  the  vessels  are  thicker,  they 
have  a  lustrous,  homogeneous  appearance,  and  they  show  peculiar  reactions  on 
treatment  with  certain  coloring  agents.  These  reactions  are  due  to  the  presence  of 
an  albuminoid  substance — amyloid — which  is  either  deposited  in  the  tissue  from 
the  blood,  or,  as  is  much  more  probable,  is  developed  in  that  place  and  spot  from 
the  albuminoid  substances  present.  In  marked  amyloid  degeneration  the  diseased 
organs  often  show  macroscopic  ally  an  altered,  "  bacon-like  "  appearance,  and  as- 
sume a  characteristic  red-brown  color  on  treating  the  affected  parts  with  Lugol's 
solution  of  iodine.  The  microscopic  examination  alone  affords  more  accurate  con- 
clusions as  to  the  presence  and  distribution  of  the  degeneration.  Here  we  make  use 
chiefly  of  staining  the  tissues  with  methyl-violet  or  gentian-violet.  The  amyloid 
portions  thus  take  on  a  very  characteristic  and  easily  defined  red  color.  In  this 
way  we  can  discover  that  the  amyloid  degeneration  begins  everywhere  in  the  walls 
of  the  small  vessels,  that  the  interparenchymatous  connective  tissue  may  also  be 
affected  later,  but  that  the  parenchymatous  cells  proper,  liver  cells,  renal  epithe- 
lium, etc.,  almost  always  remain  perfectly  free.  The  latter  often  show  atrophic 
and  fatty  degenerative  changes  (vide  infra),  but  never  amyloid  degeneration. 

Nothing  is  known  as  to  the  special  causes  which  effect  that  peculiar  metamor- 
phosis of  the  albumen  of  the  connective  substance  into  amyloid.  We  know  only 
that  there  are  a  number  of  primary  diseases  in  which  it  is  known  empirically  that 
amyloid  degeneration  quite  frequently  develops  as  a  secondary  condition  in  the 


AMYLOID  KIDNEY.  86S 

different  organs.  These  conditions  have  mainly  the  common  feature  that  they  go 
along  with  a  general  cachexia  and  weakness  of  the  body.  The  following  conditions 
(arranged  in  about  the  frequency  of  the  occurrence  of  amyloid  degeneration)  are 
the  special  ones  in  which  amyloid  degeneration  in  general,  and  therefore  amyloid 
kidney  in  particular,  are  chiefly  observed  : 

1.  Chronic  pulmonary  tuberculosis,  particularly  the  ordinary  ulcerative  phthisis, 
Tubercular  ulcers  of  the  intestines,  with  or  without  co-existing  marked  pulmonary 
tuberculosis,  may  also  lead  to  amyloid  disease. 

2.  Long-continued  chronic  suppuration  in  the  bones  or  soft  parts,  especially 
chronic  fungous  processes  with  fistulas  into  the  bones  or  joints,  empyema  with 
fistulas,  vertebral  caries,  etc. 

3.  Constitutional  syphilis,  chiefly  the  cases  with  ulcerative  and  usually  tertiary 
processes  in  the  bones  and  mucous  membranes. 

4.  Other  ulcerative  processes  or  processes  associated  with  chronic  suppuration  : 
saccular  bronchiectases,  chronic  intestinal  ulcers  (for  example,  of  dysenteric 
origin),  purulent  pyelo-cystitis,  vesico-vaginal  fistula,  ulcerated  new  growths,  like 
cancer,  etc. 

5.  In  rare  cases  amyloid  has  also  been  observed  in  other  chronic  diseases,  as  in 
malaria,  gout,  and  other  chronic  articular  affections.  In  the  medical  clinique  here 
at  Leipsic  we  once  saw  a  case  of  marked  amyloid  kidney  in  a  girl  of  twenty-one 
with  aortic  insufficiency. 

6.  Finally,  in  a  small  class  of  cases,  of  which  we  have  ourselves  seen  some 
examples,  no  discoverable  cause  at  all  may  be  found  at  the  autopsy  for  a  usually 
quite  extensive  amyloid  degeneration.  In  these  cases  there  accordingly  seems  to 
be  a  primary  amyloid  disease. 

Pathological  Anatomy. — Since  the  text-books  on  pathological  anatomy  have 
been  referred  to  in  regard  to  the  anatomical  conditions  of  amyloid  in  other  organs 
(compare  also  page  498),  we  must  here  describe  in  detail  only  the  pathological 
anatomy  of  amyloid  kidney. 

In  very  slight  and  not  extensive  amyloid  degeneration  in  the  kidneys  the  latter 
present  a  perfectly  normal  appearance  to  the  naked  eye.  Careful  microscopic 
examination  alone  shows  amyloid  degeneration  of  the  walls  of  different  vessels  in 
the  cortex,  and  especially  in  the  medullary  substance. 

The  commonest  and  most  characteristic  form  of  amyloid  kidney  is  the  so-called 
large  white  amyloid  kidney  (waxy  kidney,  lardaceous  kidney).  The  kidney  is 
usually  enlarged,  and  the  surface  is  smooth  and  of  a  grayish-white  or  yellowish 
color,  and  usually  somewhat  mottled.  On  section,  the  cortex  is  wider  and  also  of 
a  yellowish- white  color,  and  the  glomeruli  may  often  be  recognized  with  the  naked 
eye  as  dull,  lustrous,  translucent  points.  Haemorrhages  are  scarcely  ever  seen. 
The  medullary  substance  is  either  also  pale  or  darker.  In  many  cases  the  cortex 
may  also  have  a  darker  reddish  or  mottled  appearance,  which  is  due  merely  to  the 
greater  amount  of  blood  in  the  organ.  The  pale-yelloAV  color  is  due  either  to  the 
anaemia  or  to  the  fatty  degeneration,  while  the  amyloid  spots  show  a  more  trans- 
lucent character  with  a  bacon-like  luster. 

If  we  examine  the  kidney  microscopically,  we  find  first  the  amyloid  degenera- 
tion, which,  in  varying  extent  and  combination,  affects  most  frequently  the  glo- 
meruli and  also  the  capillaries  of  the  cortex,  the  vasa  recta,  and  sometimes  the 
membranae  propriae  of  the  uriniferous  tubules.  In  pure  amyloid  kidney  the  rest 
of  the  renal  tissue  is  normal,  but  in  many  cases  we  also  find  changes  in  the  epi- 
thelium, fatty  degeneration,  desquamation  and  disintegration,  and  also  not  infre- 
quently interstitial  cellular  infiltration. 

Thus  amyloid  degeneration  is  often  combined  with  degenerative  inflammatory 
changes  in  the  kidneys.  If  the  process  has  lasted  for  a  long  time,  it  leads,  as  in 
55 


866  DISEASES  OF  THE  KIDNEYS. 

ordinary  nephritis,  to  a  complete  atrophy  of  tissue  in  some  parts,  with  a  corre- 
sponding increase  of  connective  tissue.  Then  the  renal  tissue  sinks  in  at  the 
affected  parts,  and  there  is  a  decided  unevenness  to  the  surface  of  the  kidney. 
There  is  even  a  completely  developed  red  or  white  contracted  kidney,  in  which 
we  find  abundant  amyloid,  and  which  is,  therefore,  termed  amyloid  contracted 
kidney.  In  this  form  the  parenchymatous  and  interstitial  changes  correspond 
precisely  to  those  in  ordinary  contracted  kidney,  only  the  amyloid  degeneration 
is  added  to  them. 

At  present  differences  of  opinion  prevail  as  to  the  precise  connection  between 
amyloid  and  the  inflammatory  degenerative  processes  in  the  kidney.  Probably  we 
have  an  actual  combination  of  both  conditions,  sometimes  perhaps  even  co-effects 
of  tbe  same  cause.  For  since  genuine  nephritis,  as  well  as  amyloid  kidney,  occurs, 
as  we  have  seen,  in  syphilis,  tuberculosis,  and  other  diseases,  it  can  not  be  remark- 
able that  in  these  diseases  both  sequelae,  nephritis  and  amyloid,  develop  side  by 
side,  and  that  we  may,  therefore,  find  at  the  same  time,  beside  the  changes  of  an 
inflammatoiy  large  white  kidney,  of  a  secondary  contraction,  or  of  a  genuine  con- 
tracted kidney,  a  more  or  less  extensive  amyloid  degeneration  in  the  kidneys.  On 
the  other  hand,  it,  of  course,  can  not  be  questioned  that  the  disturbance  of  circula- 
tion, which  must  arise  in  consequence  of  a  marked  amyloid  of  the  vessels,  is  of 
influence  on  the  nutrition  of  the  renal  tissue,  and  that,  therefore,  many  changes  in 
it,  especially  fatty  degeneration  of  the  epithelium,  are,  under  some  circumstances, 
the  direct  result  of  the  amyloid  disease. 

Clinical  History.— rIf  we  consider  the  great  differences  which  the  distribution 
of  the  amyloid  in  the  kidneys  shows,  and  its  manifold  combinations  with  inflam- 
matory pi"ocesses,  it  is  clear  from  the  outset  that  we  can  not  set  up  a  uniform 
picture  of  the  symptoms  of  amyloid  disease  in  general.  To  this  we  must  add  that 
the  symptoms  of  amyloid  disease,  which  is  almost  always  a  secondary  condition, 
are  also  modified  in  various  ways  by  the  primary  disease. 

We  must  first  state  that  many  cases,  where  the  amyloid  in  the  kidneys  is  of 
comparatively  slight  extent,  can  not  be  recognized  by  any  clinical  symptom.  The 
albuminuria  in  particular  majT  be  entirely  absent,  as  has  been  repeatedly  proved 
(Litten  and  others),  which  is  perhaps  due  to  the  fact  that  in  such  cases  the  vasa 
recta  and  not  the  glomeruli  are  chiefly  affected  by  the  amyloid  degeneration. 

Except  in  these  cases,  however,  the  urine  secreted  from  the  amyloid  kidneys 
shows  marked  changes,  which,  of  course,  present  quite  great  variations  according 
to  the  form  of  the  individual  case.  The  amount  of  urine  is  most  frequently  about 
normal,  or  somewhat  diminished — in  some  cases  much  diminished — but  in  others  it 
is  decidedly  increased,  so  that  the  patient  may  pass  eighty  to  a  hundred  and  twenty 
ounces  (2500-3500  c.  c.)  in  the  twenty-four  hours.  We  quite  frequently  see  con- 
siderable variations  in  the  amount  of  the  urine  in  the  same  patient  at  different 
times.  All  these  differences  are  easily  explained  if  we  remember  how  many  cir- 
cumstances may  act  on  the  amount  of  urine — the  presence  or  absence  of  inflamma- 
tory changes  in  the  kidney,  the  presence  or  absence  of  cardiac  hypertrophy,  co-ex- 
isting perspiration,  diarrhoea,  cedema,  fever,  etc. 

The  color  of  the  urine  is  almost  always  light  yellow.  Only  exceptionally,  in 
amyloid  nephritis,  does  it  contain  an  abundant  sediment ;  usually  it  is  entirely,  or 
almost  entirely,  clear.  The  very  considerable  amount  of  albumen  in  the  urine, 
which  is  often  one  or  two  per  cent.,  is  also  characteristic  of  amyloid  kidney.  In 
many  cases,  of  course,  especially  in  amyloid  contracted  kidney,  the  amount  of  albu- 
men is  but  slight.  It  sometimes,  but  by  no  means  regularly,  happens  that  the 
urine  in  amyloid  kidney  contains  a  comparatively  large  amount  of  paraglobuline 
beside  the  ordinary  serum  albumen  (Senator). 

The  specific  gravity  of  the  urine  varies  very  much  according  to  the  amount 


AMYLOID  KIDNEY.  86? 

of  water  and  albumen  in  it.  It  may  be  increased  (1015-1020)  or  diminished 
(1010-1003). 

If  we  examine  the  urine  under  the  microscope,  we  usually  find  only  a  few  hya- 
line casts,  and  also  most  frequently  a  small  number  of  white  blood-corpuscles.  In 
the  combination  of  amyloid  with  more  marked  nephritic  changes  the  sediment  is 
more  abundant,  so  that  the  urine  is  cloudy.  The  microscope  then  shows  more 
numerous  hyaline  or  moderately  fatty  casts,  more  abundant  white  blood-corpus- 
cles, sometimes  a  little  renal  epithelium,  and  in  quite  rare  cases  even  red  blood- 
corpuscles.  Amyloid  reaction  occurs  in  the  casts,  but  it  is  very  rare,  and  therefore 
of  no  value  in  diagnosis. 

The  other  morbid  symptoms  which  are  observed  in  amyloid  kidney  depend 
either  upon  the  change  in  the  kidneys  themselves,  or  upon  co-existing  amyloid 
degeneration  in  other  organs;  or,  lastly,  upon  the  primaiy  disease.  The  symp- 
toms of  the  latter  are,  of  course,  extremely  varied,  but  in  many  cases  they  may  be 
entirely  subordinate. 

In  regard  to  the  directly  resulting  symptoms  of  amyloid  kidney,  their  occur- 
rence is  of  interest,  especially  in  comparison  with  the  analogous  conditions  in 
acute  nephritis.  Dropsy  of  a  moderate,  or  even  a  severe  degree,  is  often  present  in 
amyloid  kidney,  but  it  may  also  be  entirely  absent.  We  must  remember  that  an 
oedema  independent  of  a  renal  affection  may  be  produced  by  marantic  venous 
thrombosis.  Uraemic  symptoms  are  distinctly  rare  in  amyloid  kidney,  but  they 
are  sometimes  observed,  especially  in  their  milder  forms,  such  as  vomiting.  It  is  a 
very  important  point  that  a  hypertrophy  of  the  left  ventricle  is  absent  in  most 
cases  of  amyloid  kidney.  This  is  because  we  have  weak  and  cachectic  individuals, 
in  whom  a  cardiac  hypertrophy  can  not  develop  for  lack  of  an  excess  of  nutritive 
material.  Where  there  is  no  debility,  a  cardiac  hypertrophy  may  doubtless  develop, 
as  we  see  especially  in  amyloid  contracted  kidney.  At  the  autopsy  we  often  find 
the  heart,  of  course,  in  a  condition  of  brown  or  simple  atrophy. 

Albuminuric  retinitis  hardly  ever  appears  in  pure  amyloid  kidney.  In  the 
amyloid  contracted  kidney  it  has  sometimes  been  observed,  however,  in  cases 
where  there  has  probably  been  originally  a  pure  contracted  kidney,  with  amyloid 
coming  on  later.  The  secondary  inflammations  in  the  internal  organs,  such  as 
renal  pneumonia,  and  the  haemorrhages,  like  cerebral  haemorrhage,  are  also  rare. 

The  patient's  general  condition  is  also  dependent  in  part  upon  the  renal  disease, 
but  usually  upon  the  pi'imary  disease.  The  patient  with  amyloid  kidney  is  usu- 
ally correspondingly  cachectic,  and  shows  in  high  degree  a  pallid,  anaemic  color 
of  the  skin.  In  some  cases,  however,  such  as  syphilis,  bronchiectasis,  or  unilateral 
contraction  of  the  lung,  the  condition  of  the  nutrition  may  remain  tolerably  good 
for  a  long  time. 

The  symptoms  which  point  to  a  co-existing  amyloid  degeneration  in  other 
organs  beside  the  kidneys  are  of  great  diagnostic  significance.  The  symptoms  in 
the  liver  (enlargement,  abnormal  firmness,  and  a  hard,  sharp  lower  edge  to  the 
organ),  the  spleen  (enlargement. and  hardness),  and  intestines  (diarrhoea)  are  clin- 
ically important  in  this  respect.  The  explanation  of  the  diarrhoea  is,  of  course, 
usually  difficult,  since  it  may  often  depend  upon  tubercular  intestinal  ulcers  as  well 
as  upon  amyloid  of  the  intestines. 

We  can  scarcely  make  more  general  statements  in  regard  to  the  whole  course 
and  the  duration  of  amyloid  kidney,  since  the  form  of  the  primary  disease  is  to  be 
especially  considered  in  these  cases.  In  regard  to  the  time  that  it  takes  for  an 
amyloid  degeneration  to  develop  in  an  existing  primary  disease,  the  degeneration 
is  certainly  present  sometimes  after  a  few  months.  Of  course,  it  is  hardly  ever 
possible  to  determine  its  onset  accurately,  since  the  first  beginnings  of  amyloid 
degeneration  in  the  kidneys  do  not  usually  permit  themselves  to  be  recognized  at 


868  DISEASES  OF  THE  KIDNEYS. 

once  by  the  appearance  of  albuminuria  (vide  supra).  The  duration  of  amyloid 
kidney  varies  very  much  according1  to  the  severity  of  the  case ;  it  may  last  only 
a  few  weeks  or  months  until  death,  while  other  cases  have  certainly  lasted  for  a 
year,  especially  in  amyloid  contracted  kidney. 

The  prognosis  of  amyloid  kidney  is  in  most  cases  utterly  unfavorable,  which  is 
due  mainly  to  the  incurability  of  the  primary  disease ;  but  trustworthy  observers 
have  repeatedly  proved  that,  when  the  primary  disease  is  curable,  as  with  syphilis 
and  many  chronic  suppurations,  an  already  developed  amyloid  kidney  can  be 
completely  restored. 

The  diagnosis  of  amyloid  kidney  can  be  made  with  quite  great  certainty  when 
the  evident  signs  of  a  renal  affection  are  added  to  those  diseases  which  we  know 
empirically  often  give  rise  to  the  development  of  amyloid  degeneration.  Whether 
in  such  cases  we  have  a  pure  amyloid  or  a  pure  nephritis,  or  a  combination  of  the 
two,  can  be  decided  with  some  certainty  only  from  the  condition  of  the  urine :  a 
clear  urine,  containing  but  few  morphological  elements,  but  rich  in  albumen, 
points  to  amyloid,  while  a  large  number  of  casts  and  red  and  white  blood-corpus- 
cles in  the  urine,  point  to  the  presence  of  inflammatory  changes  in  the  kidney.  A 
very  characteristic  symptom  of  many  cases  of  amyloid  kidney,  and  one  that  is 
therefore  of  diagnostic  value,  is  the  rapid  and  frequent  change  in  the  amount  of 
the  urine  and  in  the  amount  of  albumen  in  it  (Wagner).  An  accurate  diagnosis 
of  the  anatomical  changes,  however,  is  hardly  ever  to  be  made  with  certainty,  and 
at  most  can  be  made  only  by  attention  to  the  whole  course  of  the  disease. 

A  very  material  support  for  the  diagnosis  of  amyloid  kidney,  and  therefore  one 
which  should  always  be  looked  for,  is  the  discovery  of  amyloid  in  other  organs. 
We  have  briefly  mentioned  above  the  most  important  symptoms  in  the  liver,  the 
spieen,  and  the  intestines  referable  to  this  point. 

Treatment. — Only  the  treatment  of  the  primary  disease  can,  of  course,  be  con- 
sidered, both  as  a  prophylactic  and  also  as  a  causal  indication.  In  many  surgical 
cases,  and  also  in  the  cases  of  amyloid  in  syphilis,  there  is  a  possibility  of  this  (as 
by  iodide  of  potassium)  ;  but  otherwise  we  try  to  improve  the  primary  disease  as 
far  as  is  possible. 

In  other  respects  the  treatment  is  purely  hygienic  and  symptomatic.  We  must 
try  to  strengthen  the  patient  as  much  as  possible  by  good  food  and  the  exhibition 
of  preparations  of  iron  and  quinine.  The  use  of  iodide  of  iron  is  to  be  recom- 
mended. In  a  symptomatic  point  of  view  the  same  remedies  are  used  as  in  other 
renal  diseases. 


CHAPTER  VI. 


PURULENT    NEPHRITIS    AND    PERINEPHRITIS. 

(Renal  Abscess.) 

^Etiology. — Although  in  the  forms  of  nephritis  so  far  described  the  occurrence 
of  interstitial  accumulations  of  granular  matter  has  been  repeatedly  mentioned, 
none  of  them  ever  come  to  genuine  suppuration — that  is,  to  a  purulent  liquefac- 
tion of  tissue,  a  true  abscess-formation.  The  origin  of  a  purulent  nephritis  is, 
rather,  always  associated  with  the  entrance  of  perfectly  definite  morbid  irritants 
into  the  kidneys.  These  are  invariably  organized  and  their  special  peculiarity  is 
to  excite  a  purulent  inflammation. 

There  are  two  chief  ways  through  which  the  morbid  irritants  may  reach  the 
kidneys — the  arterial  blood-current  and  the  urinary  passages.    The  first-mentioned 


PURULENT  NEPHRITIS  AND  PERINEPHRITIS.  869 

means  of  entrance  is  to  be  considered  in  all  the  cases  of  purulent  nephritis  which 
come  on  as  one  symptom  of  pyoemic  processes  and  certain  forms  of  ulcerative 
endocarditis  (see  page  112  on  the  point).  Far  more  rarely  purulent  nephritis 
develops  in  this  way  as  a  complication  in  other  diseases,  such  as  dysentery.  Puru- 
lent nephritis  also  occurs  in  actinomycosis  (Israel). 

The  excitants  of  inflammation  take  the  second  path  in  those  cases  where  a 
purulent  nephritis  follows  an  inflammation  of  the  lower  urinary  passages,  the 
pelvis  of  the  kidney,  the  bladder,  etc.  Here  the  bacteria,  which  almost  always 
enter  directly  into  the  urinary  passages  (the  urethra  and  bladder)  from  without, 
pass  gradually  upward  from  the  bladder  through  the  ureters  to  the  pelvis  of  the 
kidney,  from  this  they  enter  the  apertures  of  the  collecting  tubes  and  the  urinif- 
erous  tubules  of  the  kidney,  everywhere  exciting  a  purulent  inflammation.  We 
therefore  term  these  forms  of  purulent  nephritis— with  regard  to  their  origin- 
purulent  pyelo-nephritis. 

We  must  remark  in  conclusion  that  a  purulent  nephritis  may  arise  in  direct 
wounds  of  the  kidney  from  infection  of  the  wound;  this  is  usually  associated 
with  a  perinephritic  suppuration  {vide  infra). 

Pathology.— Purulent  nephritis  shows  quite  characteristic  peculiarities  and 
differences  according  to  its  mode  of  origin.     (We  omit  traumatic  abscesses  here.) 

The  renal  abscesses  in  pyaemia  and  analogous  diseases  are  usually  focal  suppu- 
rations, which  only  exceptionally  attain  a  great  extent,  but  which  are  usually  to  be 
recognized  with  the  naked  eye  as  numerous  little  yellowish  dots  or  lines,  scattered 
over  the  whole  kidney,  about  half  a  millimetre  or  a  millimetre  in  diameter.  On 
microscopic  examination,  these  nodules  prove  to  be  genuine  little  abscesses,  in 
whose  territory  the  renal  tissue  proper  is  completely  destroyed.  In  the  middle 
of  them  we  often  find  the  originating  colony  of  micrococci,  the  "micrococci 
embolus,"  seated  in  a  central  vessel.  The  conditions  are  still  plainer  if  we  exam- 
ine the  earlier  stage  of  the  process.  We  find  vessels  (the  loops  of  the  glomeruli, 
or  the  encircling  capillaries),  which  are  completely  plugged  with  micrococci,  and 
in  whose  vicinity  the  renal  tissue  is  still  perfectly  normal.  We  further  see  analo- 
gous spots  where  the  renal  tissue  is  already  necrosed  in  the  vicinity  of  the  colony 
of  micrococci,  and  is  infiltrated  with  emigrated  cells.  These  nodules  show,  finally, 
a  continuous  transition  to  the  completed  abscess,  which  is  often  surrounded  by  a 
hyperaemic  or  even  a  haemorrhagic  areola. 

In  purulent  pyelo-nephritis  the  renal  abscesses  appear  somewhat  different. 
The  abscesses  also  have  a  characteristic  striated  appearance,  corresponding  to  the 
distribution  of  the  inflammation  along  the  straight  tubules.  They  often  extend 
from  the  point  of  the  renal  papilla  through  the  cortex  to  the  surface  of  the  organ, 
so  that  from  the  outside  we  see  the  abscesses,  appearing  through  as  yellowish 
points.  The  broader  abscesses  arise  from  the  confluence  of  neighboring  striae. 
The  microscope  shows  that  the  purulent  inflammation  arises  from  the  vessels  of 
the  interstitial  tissue,  in  whose  territory  the  uriniferous  tubules  are  of  course 
destroyed.  The  clusters  of  micrococci  form  the  most  interesting  feature.  These 
settle  originally  in  the  uriniferous  tubules  and  are  the  special  cause  of  the  necrosis 
of  epithelium  and  the  inflammation.  Pyelo-nephritis,  indeed,  was  one  of  the  first 
diseases  for  which  Klebs  discovered  a  bacterial  origin. 

Clinical  Symptoms. — We  can  speak  very  briefly  here  in  regard  to  the  clinical 
symptoms  of  purulent  nephritis,  since  they  can  never  be  sharply  separated  from 
the  symptoms  of  the  primary  disease.  The  pyaemic  renal  abscesses,  and  the 
abscesses  in  ulcerative  endocarditis,  hardly  ever  cause  special  clinical  symptoms, 
so  that  their  presence  is  first  recognized  on  the  autopsy-table.  Since  the  abscesses 
do  not  usually  communicate  with  the  uriniferous  tubules,  there  is  usually  not  even 
a  large  amount  of  pus  in  the  urine. 


870  DISEASES  OF  THE  KIDNEYS. 

The  clinical  symptoms  of  pyelo-nephritis  also  depend  less  upon  the  nephritic 
ahscesses  than  upon  the  previous  and  accompanying  pyelitis  and  cystitis.  We 
will  therefore  return  to  renal  abscesses  in  the  description  of  these  diseases. 

Perinephritic  (Paranephritic)  Abscess. 

Perinephritic  abscess  is  the  name  given  to  suppurations  in  the  vicinity  of  the 
kidney,  especially  in  its  fatty  capsule  or  in  the  peri-renal  connective  tissue.  Apart 
from  auy  traumatic  origin  for  such  abscesses,  they  develop  most  frequently  as  a 
result  of  purulent  nephritis  or  purulent  pyelitis.  The  escape  of  pus,  which  involves 
the  surrounding  tissue  in  the  inflammation,  may  come  from  the  ureter  or  pelvis  of 
the  kidney,  or  from  the  kidney.  The  special  form  of  primary  disease  differs  very 
much;  it  may  be  either  simple  purulent  pyelitis,  or  pyelitis  from  renal  calculi,  or 
sometimes  tubercular  processes  and  new  growths  tbat  finally  suppurate,  such  as 
cancer,  or  echinococci.  The  peri-renal  suppuration  may  also  take  its  start  from  the 
other  organs  in  the  neighborhood.  Thus  cases  have  been  seen  in  which  the  peri- 
nephritis followed  a  perityphlitic  abscess,  a  hepatic  abscess,  or  a  psoas  abscess  after 
vertebral  disease.     Perinephritic  suppuration  may  also  be  due  to  actinomycosis. 

In  many  cases  of  this  sort  the  accumulation  of  pus  is  so  considerable  that  there 
is  a  protrusion  in  the  lumbar  region  exactly  like  a  tumor.  This  is  at  first  only 
obscure ;  but  later  the  skin  becomes  cedematous  there,  it  constantly  protrudes  more 
and  more,  it  assumes  an  inflammatory  hypera^mic  redness,  until  finally  a  definite 
fluctuation  shows  the  advance  of  the  abscess  up  to  the  skin.  In  other  cases  the 
inflammatory  swelling  extends  forward  into  the  iliac  fossa;  then  there  is  also 
abnormal  resistance  and  dullness  above  Poupart's  ligament.  The  swelling  may 
also  extend  upward  toward  the  diaphragm,  so  that  the  diaphragm  is  crowded 
upward,  giving  rise  to  marked  dyspnoea.  The  relations  of  the  swelling  to  the 
descending  colon  are  sometimes  the  same  as  in  new  growths  of  the  kidney  (com- 
pare Chapter  VIII). 

Beside  the  swelling,  there  is  almost  invariably  a  very  great  pain  in  the 
affected  region,  either  spontaneous  or  on  pressure.  If  the  swelling  presses  on  the 
large  nerve-trunks  in  the  vicinity,  it  produces  severe  shooting  pains  in  the  leg  of 
the  same  side,  and  sometimes  a  numb  feeling  and  paresis.  The  leg  is  then  often 
kept  in  a  position  similar  to  that  in  coxitis. 

The  condition  is  almost  always  associated  with  fever,  which  shows  the  charac- 
teristic remitting  or  intermitting  type  of  most  suppurative  fevers,  and  may  be 
interrupted  by  occasional  chills  with  a  marked  rise  of  temperature.  The  patient 
becomes  very  much  debilitated  and  emaciated  by  the  fever  and  the  pain,  and  he 
may  finally  fall  into  a  sad  general  condition.  The  urine  contains  pus  only  when 
the  abscess  communicates  in  some  way  with  the  urinary  passages. 

Recovery  can  take  place  only  when  the  abscess  is  evacuated  through  some 
external  channel.  Except  for  operative  procedures,  the  spontaneous  escape  of  pus 
through  the  skin  is  the  most  favorable;  this  most  frequently  takes  place  in  the 
lumbar  region,  or  more  rarely,  like  a  psoas  abscess,  under  Poupart's  ligament. 
Sometimes  persistent  fistulse  are  left  after  such  a  rupture.  The  rupture  of  the 
abscess  into  the  intestine  (the  colon)  has  also  been  observed,  with  an  evacuation 
of  pus  by  the  bowels,  and  also  ruptures  into  the  bladder,  the  pleural  cavity,  and 
the  peritoneum.  We  need  not  here  discuss  in  detail  under  what  circumstances 
death  may  ensue ;  it  comes  on,  in  many  cases,  after  the  disease  has  lasted  a  con- 
siderable time. 

The  diagnosis  is  based  chiefly  lipon  the  swelling,  the  tenderness,  the  fever,  and 
a  consideration  of  the  aetiological  factors.  The  disease  may  be  confused  with 
hydro-nephrosis,  psoas  abscess,  or  solid  renal  tumors.  The  result  of  an  explora- 
tory puncture  is  sometimes  decisive  in  such  cases. 


DISTURBANCES  OF  CIRCULATION  IN  THE  KIDNEYS.         S71 

The  only  treatment,  apart  from  the  fulfillment  of  any  symptomatic  indications, 
is  surgical,  and  consists,  if  possible,  in  opening  and  draining  the  abscess.  The 
success  depends  chiefly  upon  the  patient's  general  condition,  and  the  form  of  the 
primary  disease.     The  details  are  to  be  found  in  the  text-books  of  surgery. 


CHAPTER  VII. 
DISTURBANCES   OF   CIRCULATION   IN   THE   KIDNEYS. 

1.  The  Congested  Kidney. — Although  local  impediments  to  the  flow  of  venous 
blood  from  the  kidneys,  as  from  thrombosis  of  the  renal  veins,  hardly  ever  attain 
a  clinical  significance,  the  participation  of  the  kidneys  in  a  general  venous  stasis, 
as  it  is  chiefly  seen  in  heart  disease  (compare  page  300),  pulmonary  emphysema, 
etc.,  is  of  great  diagnostic  importance,  since  we  possess  in  the  condition  of  the 
urine  quite  an  accurate  measure  of  the  intensity  as  well  as  of  the  increase  and 
decrease  of  the  stasis. 

The  congested  kidney  is  easily  recognized  anatomically.  The  organ  is  often 
somewhat  enlarged,  it  feels  firmer  than  normal,  and  shows,  both  on  its  surface 
and  on  section,  a  dark,  bluish-red  color — "  cyanotic  induration."  The  medullary 
substance  is  usually  darker  than  the  cortex.  Under  the  microscope  we  see  con- 
siderable dilatation  and  a  tense  fullness  of  the  veins  and  capillaries.  The  paren- 
chyma is  normal,  but  in  more  advanced  cases  it  may  show  a  beginning  fatty 
degeneration  of  the  epithelium,  which  is  a  result  of  the  defective  arterial  blood- 
supply.     Interstitial  changes  are  usually  absent. 

The  clinical  symptoms  of  congested  kidney  concern  only  the  changes  in  the 
urine.  The  amount  of  urine  diminishes,  corresponding  to  the  diminution  of  the 
arterial  pressure  and  the  diminished  rapidity  of  the  blood-current.  Only  twenty 
or  twenty-five  ounces  (800-500  c.  a),  or  less,  are  secreted  daily.  The  urine  is  also 
more  concentrated  and  darker  than  normal,  and  often  has  an  abundant  sediment 
of  uric  acid  or  urates.  If  nutritive  disturbances  have  begun  in  the  epithelium  of 
the  glomeruli  as  a  result  of  stasis,  the  urine  is  also  albuminous,  but  the  amount  of 
albumen  in  pure  congested  kidney  is  always  slight — about  one  tenth  to  one  sixth 
of  the  volume.  The  urine  often  contains,  besides,  a  few  hyaline  casts,  and  a  few 
white  and  red  blood-corpuscles,  the  latter  pointing  to  little  congestive  hemor- 
rhages. 

If  the  changes  mentioned  come  on  as  one  symptom  of  a  general  venous  stasis, 
and  are,  accordingly,  often  associated  with  cyanosis,  and  dropsy,  the  diagnosis  of 
congested  kidney  can  be  made  with  certainty.  If  we  succeed  in  restoring  the  cir- 
culation by  appropriate  remedies,  such  as  digitalis,  the  urine  at  once  becomes  more 
abundant  and  clearer  and  its  albumen  disappears.  Otherwise  the  symptoms  of 
the  urine  of  passive  congestion  last  until  the  patient's  death. 

2.  Embolic  Infarction  in  the  Kidneys.— Since  the  renal  infarction,  although  it 
has  great  pathological  interest,  is  hardly  ever  of  clinical  significance,  we  will  limit 
ourselves  here  to  a  brief  description  of  the  most  essential  points. 

If  one  of  the  smaller  renal  arteries  is  plugged  by  an  embolus  in  heart  disease, 
the  affected  portion  of  the  organ  cut  off  from  the  circulation  must  perish,  since 
all  the  renal  arteries  are  terminal  arteries.  The  epithelium  undergoes  the  well- 
known  changes  of  coagulation  necrosis,  disappearance  of  the  nuclei  of  the  cells, 
and  disintegration,  and  the  tissue  becomes  entirely  or  in  part  a  hemorrhagic 
infarction  (compare  page  300).  In  this  way  arise  the  characteristic  wedge- 
shaped,  red,  hemorrhagic  infarctions  in  the  kidney,  or  far  more  frequently  the 


S72  DISEASES  OF  THE  KIDNEYS. 

yellowish-gray,  anaemic  infarctions,  often  surrounded  by  a  hemorrhagic  areola, 
the  base  of  which  is  at  the  surface  of  the  kidney ;  the  base  may  reach  a  width  of 
half  a  centimetre  to  a  centimetre  or  more,  while  its  apex  extends  a  varying  dis- 
tance into  the  cortex,  or  even  into  the  medullary  substance.  Later  on  the  gradu- 
ally disintegrated  tissue  of  the  infarction  is  absorbed,  round  cells  emigrate  from 
without  into  the  region  destroyed,  and  a  shrunken  connective-tissue  cicatrix  grad- 
ually develops  in  .place  of  the  former  infarction.  Many  kidneys  may  have  such  a 
granular  surface  from  numerous  infai'ction  cicatrices  that  they  may  be  appro- 
priately termed  "  embolic  contracted  kidneys." 

The  anatomical  processes  just  briefly  described  cause  in  most  cases  no  special 
clinical  symptoms  at  all.  Only  in  a  few  cases  does  a  slight  amount  of  blood  in 
the  urine  seem  to  depend  on  the  development  of  a  hsemorrhagic  infarction  in  the 
Iddneys,  so  that  when  a  cause  for  embolic  processes,  like  heart  disease,  is  present, 
we  may  sometimes  entertain  the  suspicion  of  the  development  of  a  renal  infarction 
during  life.  In  a  few  cases  the  development  of  a  large  renal  infarction  may  be 
accompanied  by  a  sudden  severe  pain  in  the  renal  region. 

The  embolic  processes  in  the  kidney  never  demand  special  treatment. 


CHAPTER  VIII. 
NEW   GROWTHS  IN  THE  KIDNEYS. 

Of  the  primary  forms  of  tumor  occurring  in  the  kidney,  two  especially  claim 
our  interest :  cancer  of  the  kidney  and  congenital  sarcoma.  The  latter  is  of  great 
importance  in  regard  to  the  general  theory  of  tumors,  since  it  points  definitely  to 
the  development  of  the  new  growth  from  scattered  portions  of  embryonic  tissue. 
Striped  muscular  fibers  have  been  repeatedly  found  in  tumors  consisting  otherwise 
of  round  or  spindle  cells,  from  which  the  name  of  "  rhabdomyoma  "  has  been 
chosen  for  these  tumors.  Since  there  are  no  muscular  fibers  in  the  kidney  itself, 
their  occurrence  in  the  tumors  points  undeniably  to  disturbances  of  development. 
This  theory  obtains  a  further  interesting  confirmation  from  our  own  observation 
of  the  development  of  left-sided,  and,  probably,  congenital  renal  sarcoma  in  two 
brothers.  Both  children  died  when  between  two  and  three  years  of  age,  and  the 
autopsy  gave  almost  precisely  the  same  lesion  in  both :  numerous  metastases  in 
the  liver  and  lungs,  beside  a  new  growth  almost  as  large  as  a  child's  head  in  place 
of  the  left  kidney. 

Renal  cancer  is  also  remarkably  frequent,  comparatively  speaking,  in  children 
under  four  years  of  age,  and  about  equally  common  in  the  two  sexes,  although,  of 
course,  we  find  renal  cancer  in  persons  of  more  advanced  years.  Usually  only 
one  kidney  is  affected,  chiefly  the  left,  as  it  seems,  but  the  new  growth  has  some- 
times been  found  in  both  kidneys.  In  its  character,  renal  cancer  belongs  either  to 
the  denser  or  to  the  softer,  medullary  form.  It  may  permeate  the  whole  kidney 
and  change  it  to  a  large  tumor,  weighing  fifteen  or  twenty  pounds  (five  or  ten 
kilogrammes).  Softening  and  haemorrhage  very  often  take  place  within  the 
tumor.  The  proliferation  has  been  repeatedly  observed  to  extend  to  the  neighbor- 
ing parts,  especially  the  pelvis  of  the  kidney,  and  metastases  also  form  in  other 
organs,  as  in  the  liver  or  the  lungs. 

The  clinical  symptoms  of  renal  tumor  are  entirely  absent,  or  of  a  very  indefi- 
nite nature,  in  the  first  period  of  the  disease.  Dull  pain  in  the  renal  region  is 
repeatedly  given  as  the  first  symptom,  but,  of  course,  this  is  hardly  ever  of  definite 
significance.     The  diagnosis  almost  always  first  takes  a  definite  direction  by  the 


NEW  GROWTHS  IN  THE  KIDNEYS.  873 

appearance  of  a  palpable  tumor.  This  develops  in  the  lumbar  and  lower  lateral 
abdominal  region,  constantly  extending  from  this  point  upward  and  inward.  As 
stated  above,  both  carcinoma  and  sarcoma  of  the  kidney  may  cause  enormous 
tumors,  especially  in  children,  which  may  make  the  whole  abdomen  protrude  to 
a  marked  degree.  The  tumor  feels  dense,  and  either  smooth  or  rough,  and  it 
does  not  move  with  the  respiration.  The  relation  of  the  tumor  to  the  descend- 
ing colon  in  left-sided  renal  tumors  is  not  unimportant  in  diagnosis.  Since  the 
latter  is  pressed  forward  by  the  growth  of  the  tumor,  and  thus  gets  into  a  position 
between  the  new  growth  and  the  anterior  abdominal  wall,  we  can  often  succeed  in 
making  out  by  percussion,  and  sometimes  even  by  palpation,  that  the  affected  por- 
tion of  intestine,  and  sometimes  even  a  loop  of  small  intestine  besides,  is  drawn 
forward  over  the  tumor;  the  percussion  may  vary  as  the  large  intestine  is  empty 
or  full.  In  right-sicled  renal  tumors  analogous  conditions  may  also  be  present, 
but  they  are  rarer.     The  liver  is  then  sometimes  pushed  to  the  left. 

In  many  cases  of  renal  tumor  the  urine  shows  no  abnormal  conditions  at  all, 
since  its  secretion  is  performed  compensatorily  by  the  other  healthy  kidney.  In 
carcinoma  of  the  kidney  it  sometimes  presents,  however,  one  valuable  sign  for 
diagnosis — namely,  an  admixture  of  blood.  This  hasmaturia  often  comes  on  very 
early,  even  before  there  is  any  tumor  to  be  felt.  It  is  repeated  either  frequently 
or  only  rarely  in  different  cases,  and  sometimes  it  is  entirely  absent.  The  haem- 
orrhage is  associated  with  colicky  pains  only  when  large  clots  have  to  pass  through 
the  urinary  passages.  It  is  a  remarkable  fact  that  in  a  few  cases  the  blood,  as  it 
seems,  may  come  from  stasis  in  the  healthy  kidney,  which  is  very  hyperaemic. 
Sometimes,  but  very  rarely,  small  particles  and  shreds  of  tissue  from  the  disin- 
tegrated new  growth  may  be  found  in  the  urine. 

The  general  symptoms  are  often  very  late  at  first,  especially  in  children ;  but 
finally  a  general  condition  of  marasmus  almost  always  develops.  A  constant  and 
great  frequency  of  the  pulse  is  often  striking.  We  must  also  mention  the  peculiar 
symptoms  several  times  observed,  that  in  girls  with  congenital  renal  tumors  there 
is  an  abnormally  early  development  of  the  pubic  and  axillary  hair,  and  sometimes 
a  peculiar  pigmentation  of  the  skin  (Kühn).  We  need  not  mention  in  detail  the 
symptoms  of  compression  of  neighboring  organs  by  the  tumor,  which  may  develop 
in  different  ways. 

The  diagnosis  of  renal  tumor  may  be  made  with  quite  great  certainty  in  many 
cases.  The  position  of  the  tumor,  its  immobility,  its  relation  to  the  large  intestine, 
and,  especially,  our  general  experience  as  to  the  occurrence  of  renal  tumors  in 
children,  lead  us  at  once  to  think  of  the  correct  diagnosis.  In  older  people  renal 
haemorrhages,  which  are  otherwise  inexplicable,  must  direct  our  suspicions  toward 
the  possibility  of  a  renal  cancer.  Renal  tumors  may,  of  course,  often  be  mistaken 
for  retroperitoneal  glandular  tumors,  ovarian  tumors,  large  psoas  abscesses,  or 
splenic  tumors.  The  differential  diagnosis  must  accordingly  be  carefully  con- 
sidered in  every  case. 

The  prognosis  is,  of  course,  always  unfavorable.  The  disease  sometimes  lasts 
only  a  few  months,  sometimes  a  year  or  two,  rarely  longer. 

The  treatment  must  in  most  cases  be  purely  symptomatic.  The  only  expecta- 
tion of  success  lies  in  the  operative  removal  of  the  new  growth,  the  details  of 
which  are  to  be  found  in  the  later  writings  on  renal  surgery. 


874:  DISEASES  OF  THE  KIDNEYS. 


CHAPTER  IX. 

PARASITES   OF   THE   KIDNEYS  AND   OF   THE   URINARY   PASSAGES. 

CHYLURIA. 

Echinococcus  of  the  Kidney.* — Echinococcus  cysts  have  been  repeatedly  found 
in  the  kidney,  although  much  more  rarely  than  in  the  liver.  Usually  only  one 
kidney  is  affected,  and  the  parasite  is  generally  situated  in  the  renal  substance 
itself,  only  exceptionally  between  it  and  the  capsule  of  the  kidney.  The  size  of 
the  echinococcus  cysts  may  be  very  considerable,  the  diameter  reaching  to  twenty 
centimetres  or  more. 

Clinical  symptoms  usually  first  appear  when  the  tumor  can  be  felt  through  the 
abdominal  walls.  Subjective  symptoms  may  even  then  be  entirely  wanting.  Pain 
on  pressure  develops  gradually  later.  The  tumor  usually  has  an  approximately 
globular  shape.  Its  relations  to  the  neighboring  organs,  especially  to  the  colon, 
are  the  same  as  we  have  learned  to  recognize  in  the  preceding  chapter,  in  the 
description  of  cancer  of  the  kidney.  The  feeling  of  the  so-called  "  hydatid  thrill," 
from  a  sudden  impulse  on  the  tumor  with  the  palm  of  the  hand  against  it  on 
palpation,  is  characteristic  of  echinococcus,  but,  unfortunately,  it  is  but  seldom 
manifest. 

It  happens  rather  frequently  that  the  sac  of  the  echinococcus  bursts  into  the 
pelvis  of  the  kidney.  Then  single  echinococcus  cysts,  or  at  least  bits  of  membrane, 
hooks,  etc.,  are  passed  with  the  urine,  usually  with  severe  colicky  pains,  which  are 
exactly  like  the  renal  colic  from  the  passage  of  a  calculus.  Such  attacks  may  be 
often  repeated,  and  may  form  a  very  severe  type  of  disease  by  obstructing  the 
urinary  passages — the  bladder  and  urethra.  In  such  cases  the  symptoms  of  a  sec- 
ondary pyelitis  and  cystitis  are  often  added. 

Perforations  in  other  directions  are  much  rarer.  The  rupture  of  a  renal  echi- 
nococcus into  the  lungs  has  sometimes  been  observed,  the  patient  coughing  up 
echinococcus  cysts. 

Sometimes,  especially  after  injuries,  the  sac  of  the  echinococcus  inflames,  sup- 
purates, and  thus  leads  to  a  general  pyasmic  condition. 

The  diagnosis  of  renal  echinococcus  is  possible  only  when  a  tumor  can  be  made 
out  belonging  to  the  kidney,  and  when  portions  of  echinococcus  are  passed  with 
the  urine,  or  through  an  exploratory  puncture.  They  are  most  frequently  con- 
founded with  hydronephrosis  {vide  infra),  and,  in  women,  with  ovarian  tumors. 

The  prognosis  is  not  wholly  unfavorable.  Permanent  recoveiy  has  been 
repeatedly  observed,  especially  after  the  rupture,  or  single  or  repeated  evacuations 
of  the  sac  of  the  echinococcus;  but,  of  course,  echinococcus  of  the  kidney  may 
also  be  attended  with  numerous  dangers,  such  as  suppuration  of  the  sac.  The 
whole  course  of  the  disease  is  always  very  tedious. 

A  radical  treatment  is  possible  only  by  surgical  means.  Symptomatically,  ice 
and  local  blood-letting  are  used  when  there  are  symptoms  of  local  inflammation ; 
and  morphine,  warm  baths,  and  sometimes  mechanical  aids,  like  the  catheter,  when 
there  are  symptoms  of  colic. 

2.  Distoma  Haematobium  (see  Fig.  113)  is  a  parasite,  occurring  frequently  in 
Egypt  and  Abyssinia;  it  is  one  of  the  fluke-worms  (hematodes),  and  has  its  seat 
in  the  branches  of  the  portal  vein,  the  splenic  vein,  the  vesical  plexus,  etc:,  and 
is  nourished  by  the  blood.  Its  eggs  are  often  deposited  in  great  numbers  in  the 
mucous  membrane  of  the  pelvis  of  the  kidney,  the  ureters,  and  the  bladder,  and 

*  In  regard  to  the  general  natural  history  of  the  echinococcus,  compare  page  494. 


PAEASITES  OF  THE  KIDNEYS  AND  UKINARY  PASSAGES.     875 

there  cause  very  intense  inflammation,  ulceration  with  subsequent  stricture,  deposit 
of  concretions,  etc.  Many  cases  of  the  so-called  tropical  hematuria  are  caused  by 
the  distoma.  The  diagnosis  of  the  disease  can  be  made  with  certainty  by  finding 
the  eggs  in  the  urine. 


Fig.  113.— Distoma  haematobium  (from  Leuckart).  a.  Male  and  female,  the  latter  in  the  canalis  gynee- 
cophorus  of  the  former.  Ten  diameters,  b.  Egg  with  a  terminal  spine,  c.  Egg  with  a  lateral  spine. 
150  diameters. 


3.  Strongylus  or  Eustrongylus  Gigas  (palisade  worm)  is  a  parasite  occurring 
in  the  pelvis  of  the  kidney  in  many  animals — the  clog,  the  wolf,  the  marten,  and 
very  rarely  in  man.  In  size  and  color  it  is  not  unlike  an  ordinary  earth-worm. 
It  may  produce  symptoms  of  severe  pyelitis,  with  haemorrhages,  and  colicky 
pains. 

4.  Filaria  Sanguinis  Chyluria.—  The  blood  filaria  of  man,  belonging  to  the 
round-worms,  has  obtained  a  special  clinical  interest,  since  it  is  recognized,  from 
the  investigations  of  Wucherer  in  Bahia  in  1868,  and  of  Lewis  in  the  East  Indies 
in  1870,  as  the  cause  of  the  tropical  chyluria  and  some  allied  diseases,  such  as 
lymph  scrotum,  elephantiasis  Arabum,  and  chylous  ascites. 

The  full-grown  filaria,  " filaria  Bancrofti"  a  very  thin  worm,  about  three  or 
four  inches  long,  has  been  found  only  a  few  times  in  man.  Its  seat  is  in  the 
larger  lymphatics,  where  it  gives  rise  to  chronic  stasis  of  the  lymph  with  its  conse- 
quences— chronic  hyperplasia  of  the  connective  tissue,  etc.  In  the  affection  which 
here  especially  interests  us,  chyluria,  the  parasites  are  probably  situated  in  the 
main  branches  of  tbe  thoracic  duct — at  any  rate,  in  such  a  place  that  a  stasis  of 
the  lymph  ensues  in  the  lymphatics  of  the  bladder,  or  perhaps,  in  some  cases,  of 
the  pelvis  of  the  kidney  and  the  other  urinary  passages.  If  the  distended  lymph- 
sac  ruptures,  the  lymph  or  chyle  is  poured  out  into  the  ui'inary  passages  and  is 
evacuated  with  the  urine.  Since  this  process  may  be  often  repeated,  the  inter- 
mittent course  of  chyluria  is  thus  explained.  The  individual  attacks  of  the  disease 
may  come  on  during  years  at  intervals  of  weeks  or  months.  They  are  often  asso- 
ciated with  pain  and  febrile  symptoms. 

The  condition  of  the  urine,  which  in  many  cases  may  look  almost  exactly  like 
milk,  is  most  characteristic.  A  creamy  layer  of  fat  forms  upon  the  surface.  If  we 
shake  the  urine  with  ether,  the  greater  part  of  the  fat  can  be  removed,  and  the 
urine  rendered  clear.  The  fat  in  the  urine  may  amount  to  two  or  three  per  cent. 
The  chyluria  is  often  associated  with  a  hematuria  coming  from  the  ruptured 
veins.  The  urine  then  looks  bloody  red,  and  shows  under  the  microscope  many 
red  blood-corpuscles  beside  the  fat-drops.     Large  clots  often  form  in  the  urine. 

The  embryos  of  filaria,  found  in  the  urine  in  very  many  cases,  although  not  in 
all,  form  the  most  important  diagnostic  feature  in  the  urine.  These  (see  Pig.  114) 
are  objects  two  to  three  tenths  of  a  millimetre  long,  with  a  diameter  about  equal 
to  that  of  a  red  blood-corpuscle.  They  are  usually  imbedded  in  a  very  delicate 
sheath,  which  often  projects  at  the  end  of  the  animal,  and  show  a  constant,  vigor- 


876 


DISEASES  OF  THE  KIDNEYS. 


ously  vibrating  motion. 


Fig.  114.— (From  Scheube.)    Embryos  of 
ülaria. 


They  have  also  been  found  in  the  blood  of  the  patient, 
as  well  as  in  the  urine,  and,  strange  to  say, 
especially  during  the  night. 

The  course  of  the  filaria  disease  may 
vary  considerably.  Many  patients  reach 
an  advanced  age ;  in  others,  severe  general 
symptoms,  like  anaemia  and  emaciation, 
finally  come  on.  The  different  forms  in 
which  the  disease  occurs  —  chyluria,  ele- 
phantiasis, etc. — are  combined  in  manifold 
ways. 

The  region  of  the  geographical  distribu- 
tion of  the  disease  lies  almost  wholly  in 
hot  countries.  It  has  so  far  been  most  fre- 
quently observed  in  Brazil,  the  Antilles, 
the  East  Indies,  China,  Japan,  Egypt,  Cape 
Colony,  and  Australia.  Nothing  definite 
is  yet  known  of  the  precise  mode  of  inva- 
sion of  the  parasites.  According  to  Man- 
son's  investigations,  mosquitoes  play  an  im- 
portant part  here. 

In  regard  to  treatment,  apart  from  any 
surgical  interference,  we  may  try  picro- 
nitrate  of  potassium,  three  to  ten  grains 
(grm.  O'^O'ö),  in  pills  or  capsules,  several 
times  a  day  (Scheube). 


CHAPTER    X. 
MOVABLE   KIDNEY   (FLOATING  KIDNEY,  REN  MOBILIS). 

iEtiology.— Although  under  normal  conditions  the  kidney  is  fixed  firmly  in  its 
position  by  its  fatty  capsule,  over  which  the  peritoneum  is  tightly  drawn,  and  by 
the  diaphragm,  there  is  not  infrequently  a  pathological  condition,  in  which  the 
kidney  shows  quite  a  high  degree  of  displacement  and  mobility.  The  causes  of 
this  anomaly  are  not  always  quite  clear,  and  there  are  probably  different  factors 
which  may  give  rise  to  movable  kidney. 

First,  perhaps,  a  congenital  predisposition  is  often  to  be  considered ;  this  may 
be  based  chiefly  upon  an  abnormally  loose  character  of  the  tissue  surrounding  the 
kidney,  and  also  upon  an  abnormal  length  of  the  renal  artery ;  but  in  later  life 
it  is  chiefly  the  factors  that  lead  to  a  marked  distention  and  laxity  of  the  abdomi- 
nal cavity,  which  further  the  development  of  a  movable  kidney.  Frequent 
pregnancies  are  especially  unfavorable  in  this  respect,  which  explains  the  fact 
that  floating  kidney  is  very  much  commoner  in  women  than  in  men.  Severe 
and  persistent  bodily  labor  may  also  give  rise  to  floating  kidney ;  in  some  cases, 
too,  injuries  which  affect  the  abdomen,  and  especially  the  region  of  the  kidney, 
also  play  a  part.  Too  tight  lacing,  and  the  wearing  of  corsets,  have  been  repeatedly 
accused  of  gradually  causing  a  mobility  of  the  kidney.  Finally,  a  loss  in  the 
general  nutrition,  by  which  the  fatty  capsule  of  the  kidney  undergoes  a  reduc- 
tion, sometimes  seems  to  favor  the  occurrence  of  movable  kidney. 

We  have  just  mentioned  the  frequent  occurrence  of  floating  kidney  in  women 


MOVABLE  KIDNEY.  877 

but  some  cases  have  also  been  observed  in  men,  and  even  in  children.  It  is  remark- 
able that  the  right  kidney  shows  the  anomaly  in  question  much  oftencr  than  the 
left,  which  is  possibly  connected  with  the  fact  that  the  right  kidney  may  be  more 
easily  displaced  by  the  respiratory  movements  of  the  liver.  Litten  has  lately 
pointed  out  that  we  often  find  the  right  kidney  dislocated  upward  in  simple  gas- 
trectasia,  arising  from  immoderate  distention  of  the  stomach,  relaxation  of  the 
muscular  coat  of  the  stomach  as  a  result  of  chronic  gastric  catarrh,  etc.  In  sucli 
cases  the  distended  stomach  and  sometimes  the  duodenum  push  up  the  liver,  and 
with  it  the  right  kidney.  Movable  kidney  can  be  confirmed  in  the  cadaver  only 
when  the  kidney  is  found  in  an  abnormal  position — for  instance,  in  front  of  the; 
vertebral  column. 

Clinical  Symptoms  are  not  necessarily  present  in  every  case  of  movable  kidney. 
If  we  examine  old  women  with  special  regard  to  this  point,  we  not  very  rarely 
find  movable  kidneys  without  any  symptoms  caused  by  them.  In  other  cases, 
however,  the  floating  kidney  gives  rise  to  a  whole  set  of  symptoms  which  are 
inexplicable  except  by  the  discovery  of  their  cause.  Drawing  and  pressing  pains 
in  the  abdomen  are  the  most  frequent ;  these  may  shoot  into  the  epigastrium  or 
into  the  sacral  and  lumbar  region,  and  may  sometimes  assume  almost  a  colicky 
character.  They  are  also  frequently  associated  with  nausea  and  even  vomiting. 
All  these  disagreeable  sensations  usually  increase  still  more  as  the  patient  moves, 
in  walking  or  riding,  while  they  are  slightest  or  even  disappear  entirely  when  the 
patient  lies  down. 

In  many  cases  of  floating  kidney  more  severe  attacks  come  on  periodically, 
often  at  the  time  of  the  menses;  they  have  been  termed  by  Dietl  "  incarceration 
symptoms."  They  consist  of  the  sudden  onset  of  pain,  chills  which  may  increase 
almost  to  a  rigor,  vomiting,  and  symptoms  of  general  collapse.  Diuresis  is  usu- 
ally diminished  during  this  period,  and  increases  only  when  the  attack  ceases— that 
is,  three  or  four  days  later.  The  special  cause  of  these  symptoms  is  to  be  found 
partly  in  circumscribed  inflammatory  changes  in  the  vicinity  of  the  kidney,  but 
chiefly  in  a  sudden  urinary  stasis  from  bending  or  twisting  the  ureter.  There 
then  arises  an  acute  hydronephrosis  whose  attendant  symptoms  disappear  when 
micturition  has  again  become  possible.  In  some  cases  floating  kidney  seems  to 
cause  persistent  hydronephrosis,  with  secondary  pyelitis. 

We  find  quite  frequently  in  women  with  floating  kidney  a  line  of  general 
nervous  "hysterical"  symptoms— headache,  backache,  mental  irritability,  parass- 
thesiae,  etc.  It  is  often  hard  to  decide  whether  these  symptoms  are  due  to  floating 
kidney  or  are  only  co-ordinate  with  it.  They  often  arise,  at  any  rate,  only  as  a 
result  of  the  mental  condition,  for  the  mere  idea  of  possessing  a  "  floating  kid- 
ney "  may  be  enough  in  nervously  disposed  women  to  provoke  a  host  of  subjec- 
tive sensations.  Hence  we  must  be  cautious  in  informing  the  patient  of  the  diag- 
nosis. 

Movable  kidney  also  seems  able  sometimes  to  produce  certain  resultant  condi- 
tions by  pressure  on  neighboring  organs.  Thus  Bartels  has  claimed  that  many 
cases  of  dilatation  of  the  stomach  are  due  to  a  compression  of  the  descending 
part  of  the  duodenum  by  the  movable  kidney.  In  an  analogous  way,  jaundice 
may  arise  from  pressure  on  the  gall-ducts,  constipation  from  pressure  on  the  colon, 
cedema  of  the  legs  from  pressure  on  the  inferior  vena  cava,  and  finally  it  has  been 
stated  that  floating  kidney  in  women  may  be  the  cause  of  abortion.  All  these 
accidents,  at  any  rate,  are  only  rarely  to  be  considered. 

The  diagnosis  of  floating  kidney  can  be  made  only  by  its  objective  discovery. 
It  is  rather  a  theoretical  assumption,  which  is  only  rarely  of  value  in  practice, 
that,  we  can  recognize  the  displacement  of  the  kidney  from  its  normal  position, 
by  the  sinking  in  of  the  affected  lumbar  region  (almost  always  the  right),  and 


878  DISEASES  OF  THE  KIDNEYS. 

by  the  abnormal  clearness  of  the  percussion-note  there.  The  only  certain  proof 
is  feeling  the  kidney  as  a  movable  tumor  of  the  proper  size  and  shape  beneath 
the  edge  of  the  right  ribs  or  toward  the  umbilicus  or  the  inguinal  region.  Occa- 
sionally we  can  succeed  in  feeling  the  pulsation  of  the  renal  artery.  Palpation 
of  the  movable  kidney,  however,  is  not  always  equally  easy,  and  generally 
demands  a  certain  amount  of  practice.  Bimanual  palpation  and  counterpressure 
in  the  lumbar  region  with  the  left  hand  is  very  advisable.  If  we  can  reach  the 
kidney  with  the  fingers,  we  can  push  it  about  and  often  bring  it  back  into  its 
proper  place. 

In  general,  the  diagnosis  is  not  very  difficult  in  patients  whose  abdominal  walls 
are  lax,  if  the  attention  be  directed  to  the  possibility  of  floating  kidney.  Of  course 
a  positive  result  is  alone  decisive,  while  a  negative  result,  or  finding  it  only  once, 
proves  nothing.  In  many  cases,  of  course,  floating  kidney  is  confused  with  other 
sorts  of  tumors,  with  pedunculated  ovarian  cysts,  faecal  tumors,  enlargements  of 
the  gall-bladder,  or  echinococci. 

The  prognosis  is  so  far  favorable  that  the  patient's  life  is  never  threatened  by 
an  uncomplicated  floating  kidney.  The  symptoms,  are  of  course,  very  obstinate, 
and  may  resist  any  therapeutic  attempts  for  years.  In  advanced  age  they  often 
cease  of  themselves. 

Treatment. — If  there  are  severe  disturbances  or  "  incarceration  symptoms  "  on 
the  part  of  a  floating  kidney,  a  quiet  dorsal  decubitus  is  to  be  prescribed;  and 
if  the  kidney  does  not  return  to  its  proper  place  of  itself,  we  should  try  artificial 
reposition,  which  can  be  performed  in  many  cases,  and  which  is  then  attended 
with  success.  If  we  can  not  relieve  the  symptoms  in  this  way.  prolonged  warm 
baths,  warm  poultices,  and  opium  must  be  used  as  indicated.  Various  bandages 
provided  with  pads  and  supports  are  recommended  to  guard  against  a  new  dis- 
placement of  the  kidney ;  these,  of  course,  sometimes  do  good  service,  but  they  are 
often  useless.  At  all  events,  they  should  be  tried.  The  hope  of  "  removing  the 
laxity  of  tissue"  by  a  "tonic  treatment,"  iron  preparations,  cold  rubbing,  etc., 
must  be  illusory;  nevertheless,  these  remedies  are  very  much  recommended  in 
practice,  since  they  often  act  very  favorably,  especially  on  the  general  nervous 
symptoms,  as  mental  remedies.  Certain  general  hygienic  measures,  especially  the 
avoidance  of  any  great  bodily  movements,  and  care  for  easy  dejections,  are  also 
of  service. 

In  cases  with  very  severe,  distressing  symptoms,  surgeons  who  are  fond  of 
operations  have  repeatedly  stitched  the  kidney  to  the  parietes,  sometimes  with 
success,  sometimes,  too,  without  the  desired  result.  At  any  rate,  the  indication 
for  operation  is  furnished  only  when  the  symptoms  are  very  marked,  and  when 
all  other  remedies  have  been  unsuccessful. 


APPENDIX. 

THE   DISEASES   OF  THE   SUPRA-RENAL   CAPSULES  AND  ADDISON'S 
DISEASE  (BRONZED  SKIN). 

In  the  year  1855  the  English  physician  Addison  published  for  the  first  time  a 
list  of  cases  in  which,  besides  the  symptoms  of  a  general  bodily  weakness  and 
anaemia,  a  peculiar  dark  pigmentation  of  the  skin  had  gradually  developed. 
Since  disease  of  the  supra-renal  capsule  was  found  at  the  autopsy  in  all  cases, 
Addison  concluded  that  this  was  the  immediate  cause  of  the  bronze  coloring  of 
the  skin.  Observations  similar  to  Addison's  were  soon  made  in  greater  numbers, 
so  that  the  fact  itself  can  not  be  doubted;  but  even  at  present  nothing  definite  is 
known  as  to  the  special  cause  of  the  disease  or  the  theory  of  this  remarkable  con- 


ADDISON'S  DISEASE.  879 

nection  between  disease  of  the  supra-renal  capsules  and  pigmentation  of  the 
skin. 

Attempts  have  been  made  in  different  quarters  to  obtain  an  explanation  from 
experiments  on  animals;  but  up  to  the  present  time  these  attempts  have  remained 
quite  fruitless,  and  even  lately  Nothnagel,  in  spite  of  having  destroyed  both  supra- 
renal capsules  in  a  large  number  of  rabbits,  has  not  succeeded  a  single  time  with 
certainty  in  provoking  the  symptoms  of  the  disease  artificially.  The  anatomical 
lesions  in  man  are  up  to  the  present  time  not  calculated  to  add  clearness  to  the 
case,  since  they  seem  to  contradict  one  another  in  various  points.  In  the  first 
place,  some  observations  must  be  mentioned  in  which  the  supra-renal  capsules 
were  found  perfectly  normal  in  spite  of  an  existing  pigmentation  of  the  skin. 
Such  cases,  however,  prove  little,  since  it  of  course  can  not  be  put  in  question  that 
a  staining  of  the  skin  may  sometimes  develop  from  some  other  reason  besides 
disease  of  the  supra-renal  capsules.  On  the  other  hand,  it  has  been  asserted  that 
extensive  changes  are  sometimes  found  in  the  supra-renal  capsules  on  autopsy 
without  the  existence  of  the  symptoms  of  bronzed  skin  during  the  patient's  life; 
but  these  cases  are  also  open  to  the  objection  that  the  disease  has  perhaps  not  been 
extensive  and  intense  enough  to  cause  the  bronze  coloring  of  the  skin.  The  con- 
tradictions just  mentioned,  however,  have  led  to  many  other  attempts  at  an 
explanation  of  Addison's  disease,  of  which  one  especially  deserves  considera- 
tion. According  to  this,  the  symptoms  met  with  are  produced  not  by  the  disease 
of  the  supra-renal  capsules  themselves  but  by  the  invasion  of  the  solar  plexus  and 
the  semilunar  ganglia  of  the  sympathetic  by  the  morbid  process  (Eisel,  Burger, 
and  others).  According  to  this  theory,  the  symptoms  of  Addison's  disease  may 
arise  when  the  aforesaid  nervous  parts  are  diseased  independently,  or  by  the 
extension  of  a  pathological  process  from  some  other  neighboring  organ.  A  num- 
ber of  anatomical  lesions  are  cited  to  favor  this  view,  but  it  is  not  certainly 
proven,  and  the  internal  connection  between  the  symptoms  is  by  no  means  clear 
by  this  hypothesis. 

Pathological  Anatomy  and  JEtiology  of  Addison's  Disease.— Addison  himself 
has  pointed  with  emphasis  to  the  fact  that  the  special  form  of  disease  in  the  supra- 
renal capsules  is  by  no  means  always  the  same.  At  any  rate,  the  disease  named 
from  him  is  not  to  be  regarded  as  a  definite  anatomical  affection,  but  rather  as  a 
particular  group  of  symptoms.  By  far  the  most  frequently  it  is  tuberculosis 
of  the  supra-renal  capsules  which  lies  at  the  bottom  of  Addison's  disease.  The 
capsules  then  are  either  enlarged  and  studded  with  caseous  tubercular  new 
growths,  or  they  are  in  part  cicatricially  contracted.  Other  tubercular  affections 
are  almost  always  present  in  the  body  at  the  same  time,  especially  caseation  of 
the  mesenteric  lymph-glands  and  pulmonary  tuberculosis.  Other  morbid  pro- 
cesses besides  tuberculosis  may  also  be  found  in  the  supra-renal  capsules:  simple 
chronic  inflammations,  enlargement  of  the  organ  (which  Virchow  has  called 
"  struma  of  the  supra-renal  capsules  "  ),  haemorrhages,  new  growths  such  as  cancer, 
and  even  echinococci.  It  is  self-evident,  from  what  has  been  said  above,  that  in 
every  case  we  must  consider  some  implication  of  the  neighboring  sympathetic 
ganglia,  by  compression,  cicatricial  contraction,  or  chronic  inflammation.  Both 
supra-renal  capsules  are  almost  always  diseased  at  the  same  time,  rarely  only  one 
is  affected.  • 

Of  the  lesions  in  other  organs  we  must  also  mention  that  Peyer's  patches  and 
the  solitary  follicles  of  the  intestine  are  as  a  rule  swollen.  The  spleen  is  some- 
what enlarged  in  some  cases,  but  not  in  others.  There  is  no  striking  pigmenta- 
tion of  the  internal  organs.  The  changes  in  the  skin  and  in  certain  mucous 
membranes  will  be  mentioned  below. 

Considering  the  variety  of  the  anatomical  causes  there  can  be  no  question  of  a 


880  DISEASES  OF  THE  KIDNEYS. 

uniform  aetiology  of  the  disease.  Among  the  causal  factors,  those  most  frequently 
reported  are  defective  nutrition,  care  and  anxiety,  and  finally  traumatic  action  on 
the  abdomen.  The  majority  of  cases  are  met  with  in  the  male  sex  and  in  middle 
life.  Addison's  disease,  however,  must  be  regarded  as  a  rare  affection,  of  which 
but  few  cases  are  observed  even  in  the  larger  cliniques. 

Symptomatology. — The  purest  type  of  Addison's  disease  appears  in  those  cases 
where  the  symptoms  are  apparently  primary  in  their  development,  and  do  not 
come  on  in  the  course  of  some  other  disease,  such  as  phthisis  or  cancer. 

The  first  symptoms  of  the  disease  are  usually  of  a  general  nature,  and  are 
referable  to  a  gradually  increasing  anaemia  and  to  general  weakness  and  phys- 
ical lassitude.  The  anaemia  shows  itself  objectively  through  the  pallor  of  the  skin 
and  the  diminution  in  the  number  of  red  blood-corpuscles,  but  without  other 
definite  anomalies  of  the  blood  that  can  be  made  out.  A  number  of  symptoms 
appear  besides,  which  are  due  secondarily  to  the  anaemia,  especially  to  the  anaemia 
of  the  brain.  Among  them  are  mental  lassitude  and  loss  of  energy,  frequent 
headaches,  attacks  of  vertigo  and  faintness,  and  tinnitus  aurium.  The  patient's 
general  nutrition  often  suffers  very  considerably ;  but  it  must  be  added  that  in 
Addison's  disease,  as  in  other  anaemias,  the  fatty  layer,  especially  over  the  abdomen, 
often  remains  remarkably  well  developed. 

Besides  the  anaemic  symptoms,  there  frequently  are  disturbances  of  the  stomach. 
The  appetite  is  poor,  and  there  is  very  often  vomiting.  The  latter  may  sometimes 
be  almost  unrestrainable,  and  then  it  is  one  of  the  most  distressing  symptoms  of  the 
disease.  It  is  usually  due  not  to  an  anatomical  change  in  the  stomach,  but  prob- 
ably to  the  anaemia  of  the  brain,  or  to  other  nervous  influences.  Cardialgic 
symptoms  are  also  frequent.  The  bowels  are  sluggish  as  a  rule,  but  there  is  some- 
times diarrhoea.  We  sometimes  hear  functional  murmurs  in  the  heart,  but  as  a 
rule  its  sounds  are  low  and  pure.  The  pulse  is  usually  moderately  accelerated. 
The  liver  and  spleen  present  no  constant  changes.  Albuminuria  is  only  excep- 
tionally found,  and  is  due  to  complications,  such  as  amyloid  kidney. 

The  special  characteristic  symptom,  which  alone  renders  the  diagnosis  possible, 
is  the  gradual  onset  of  a  peculiar  pigmentation  of  the  skin.  This  usually  shows 
itself  first  in  the  face  and  on  the  backs  of  the  hands,  and  also  in  those  parts  which 
normally  present  a  greater  pigmentation  (the  areola  of  the  nipples,  the  axillae, 
and  the  genitals),  or  which  are  exposed  to  greater  pressure  by  the  clothing,  as 
the  hips  and  shoulders.  It  is  especially  noteworthy  that  dark  pigmented  spots 
usually  develop  on  the  mucous  membrane  of  the  lips  and  mouth.  The  intensity 
of  the  coloring  differs  in  different  cases.  It  usually  increases  as  the  general  con- 
dition grows  worse.  In  the  most  intense  cases  the  whole  skin  may  become  dai'k 
brown  or  black,  like  that  of  a  mulatto  or  negro.  Sometimes,  however,  the  pig- 
mentation remains  limited  to  separate  large  or  small  spots,  and  in  other  parts 
of  the  skin  there  may  then  be  even  a  marked  loss  of  pigment.  The  nails  and 
the  scler-a  always  remain  white,  and  frequently  the  palms  of  the  hands  and  the 
soles  of  the  feet  also.  The  pigmentation  of  the  skin  usually  increases  during  the 
whole  disease ;  only  exceptionally  does  the  skin  become  light  again  in  the  later 
stages. 

The  special  cause  of  the  accumulation  of  pigment  in  the  skin  is  wholly  un- 
known. We  find  on  microscopic  examination  of  the  skin  that  the  pigment  lies  not 
only  in  the  cells  of  the  rete  Malpighii,  but  also  in  the  corium,  especially  along  its 
blood-vessels.  It  is  probably  formed  from  the  blood-pigment,  and  is  carried  by 
wandering  cells  from  the  cutis  into  the  epithelial  layers  of  the  skin  (Demieville, 
Nothnagel). 

The  course  of  Addison's  disease  is  almost  always  chronic,  and  may  last  for 
years,  but  cases  have  been  described  with  a  more  acute  course.     The  disease  some- 


INFLAMMATION  OF  THE  PELVIS  OF  THE  KIDNEY.  881 

times  begins  with  violent  initial  febrile  symptoms,  vomiting  and  diarrhoea.  The 
disease  then  has  a  comparatively  rapid  termination  after  a  few  months,  or  a  second 
chronic  stage  may  follow  the  first  acute  one. 

The  final  termination  of  Addison's  disease  is  always  unfavorable.  Temporary 
remissions  are  often  observed,  but  the  disease  always  becomes  worse  again  after 
them.  Death  usually  ensues  gradually  amid  the  signs  of  increasing  general 
ursemia  and  weakness.  In  some  cases  severe  nervous  symptoms  also  come  on 
toward  the  end  of  the  disease— coma,  delirium,  or  epileptiform  attacks.  Such 
conditions,  which,  according  to  Jaksch,  may  depend  upon  acetonuria,  may  some- 
times develop  quite  rapidly  and  unexpectedly. 

Treatment. — There  can  be  no  question  of  a  specific  treatment  of  Addison's  dis- 
ease, especially  considering  the  differences  in  the  primary  diseases  and  in  the  com- 
plications. Tonic  remedies,  strengthening  diet,  iron,  quinine,  and  arsenic,  are  most 
indicated,  although  iodide  and  toomide  of  potassium,  electricity,  etc.,  have  been 
tried  by  some  physicians.  Otherwise  the  treatment  is  purely  symptomatic;  the 
vomiting,  diarrhoea,  and  nervous  attacks  demand  special  measures.  We  know  by 
experience  that  great  caution  is  to  be  used  in  prescribing  cathartics,  since  patients 
have  repeatedly  been  observed  to  grow  considerably  worse  after  them. 


SECTION  II. 
Diseases  of  the  Pelvis  of  the  Kidney  and  of  the  Bladder. 

CHAPTER  I. 
INFLAMMATION   OF  THE   PELVIS   OF  THE   KIDNEY.     PYELITIS. 

iEtiology. — Isolated  primary  pyelitis  hardly  ever  occurs  as  an  independent  dis- 
ease. Pyelitis  is  rather  in  most  cases  either  a  complication  or  a  result  of  other 
diseases,  and  in  such  cases  often  claims  but  little  clinical  interest. 

We  sometimes  find  a  rather  moderate  pyelitis  in  the  bodies  of  persons 
who  have  died  of  severe  general  infectious  diseases,  typhoid  fever,  smallpox 
diphtheria,  or  pyaemia.  The  affection  depends,  in  all  probability,  upon  the  elimin- 
ation by  the  kidneys  of  substances  that  excite  inflammation,  and  is  thus  to  be 
regarded  as  analogous  to  the  renal  changes  which  often  coexist.  Toxic  sub- 
stances, such  as  cantharides  and  copaiba,  which  pass  through  the  kidneys,  may 
also  cause  pyelitis  as  well  as  other  disturbances. 

Pyelitis  very  often  arises  from  a  direct  extension  of  inflammation  from  the 
neighboring  organs.  In  many  cases  of  acute  and  chronic  nephritis  the  pelvis  of 
the  kidney  takes  part  in  the  inflammation  to  a  greater  or  less  degree;  but  an 
ascending  extension  of  the  inflammation  from  primary  diseases  of  the  urethra  or 
bladder  is  still  more  common.  Any  urethritis  or  cystitis  may,  if  it  lasts  long, 
advance  upward  to  the  ureters  and  the  pelvis  of  the  kidney,  so  that  in  severe  cases 
we  often  find  an  inflammation  of  the  whole  urinary  tract,  a  pyelo-cystitis,  and 
even  a  "  ureteritis."  We  have  already  stated  (compare  page  868)  that  the  inflam- 
mation may  extend  still  farther  to  the  kidneys  themselves,  and  this  exten- 
sion will  be  repeatedly  spoken  of. 

Another  frequent  cause  of  pyelitis  is  the  presence  of  foreign  bodies  in  the 
pelvis  of  the  kidney,  which  act  as  direct  mechanical  irritants.  Among  these  are, 
56 


882  DISEASES  OF  THE  KIDNEYS. 

in  the  first  place,  renal  calculi  (vide  infra  ),  and  also  retained  coagula,  parasites 
(see  page  874),  etc.  The  pyelitis  arising  as  a  result  of  retention  of  urine  in  the 
pelvis  of  the  kidney  {vide  infra,  hydronephrosis),  does  not  belong  here  directly, 
since  it  first  develops  from  a  decomposition  of  the  urine. 

Whether  there  is  a  primary  independent  pyelitis,  arising  in  ways  other  than 
those  so  far  mentioned,  is  doubtful,  as  we  have  said.  The  occurrence  of  a  primary 
pyelitis  after  exposure  to  cold  especially  lacks  confirmation.  The  pyelitis  coming 
on  in  women  in  childbed,  or  following  different  sorts  of  diseases  of  the  sexual 
organs,  may  in  all  cases  be  referred  to  an  infection  of  the  pelvic  mucous  mem- 
brane from  the  bladder  or  from  the  kidneys. 

Pathological  Anatomy. — In  simple  catarrhal  inflammation  the  mucous  mem- 
brane of  the  pelvis  of  the  kidney  is  reddened,  swollen,  and  covered  with  an  abun- 
dant secretion,  which  contains  varying  amounts  of  pus-corpuscles  and  epithelium. 
In  severer  inflammations  we  often  find  quite  numerous  little  haemorrhages  in  the 
mucous  membrane,  and  sometimes  little  gray  nodules,  which  correspond  to  the 
swollen  lymph-follicles. 

In  severe  cases,  which  are  seen  almost  solely  as  a  complication  of  a  more 
extensive  affection  of  the  urinary  passages,  such  as  pyelocystitis,  we  have  a  puru- 
lent, ulcerative  inflammation,  which  may  even  assume  a  diphtheritic  character. 
In  these  cases  the  kidneys  are  almost  always  coincidently  involved — pyelo- 
nephritis. If  the  nephritic  abscesses  break  into  the  pelvis  of  the  kidney,  there 
arises  an  ulcerative  destruction  of  the  renal  tissue,  so  that  the  pelvis  of  the  kidney 
is  filled  with  pus  and  bounded  by  extensive  ulcers,  which  often  penetrate  deeply 
into  the  substance  of  the  kidney — pyonephrosis.  The  usually  striated,  pyelo- 
nephritic  abscesses  reaching  to  the  surface  of  the  kidney  have  already  been 
described  in  the  previous  section  (see  page  869),  where  their  bacterial  origin  has 
also  been  mentioned. 

The  condition  differs  when  the  kidney  is  involved,  as  in  many  cases  of  chronic 
pyelitis.  This  appears  most  frequently  as  a  result  of  retention  of  urine,  and  hence 
it  is  usually  associated  with  a  dilatation  of  the  pelvis  of  the  kidney.  In  these  cases 
we  sometimes  find  pronounced  processes  of  contraction  in  the  kidneys — that  is,  a 
partial  atrophy  of  the  renal  tissue,  increase  of  the  interstitial  connective  tissue, 
and  evident  cicatricial  depressions  on  the  surface — in  a  word,  a  secondary  con- 
tracted kidney,  arising  as  a  result  of  pyelitis,  which  differs  from  genuine  contrac- 
tion of  the  kidney  only  in  its  aetiology. 

Clinical  Symptoms. — Since  in  most  cases  pyelitis  develops  only  as  one  symptom 
of  a  more  extensive  morbid  process,  its  clinical  symptoms  are  usually  but  slightly 
prominent  in  the  whole  course  of  the  disease.  In  what  follows,  therefore,  we  can 
not  give  any  complete  description  of  the  clinical  course  of  pyelitis,  but  we  must 
mention  only  those  symptoms  from  which,  when  there  is  an  affection  of  the  uri- 
nary passages,  we  can  conclude  that  the  pelvis  of  the  kidney  takes  part  in  the 
morbid  process. 

The  most  essential  sign  which  the  urine  presents  in  all  inflammatory  affections 
of  the  urinary  passages,  the  presence  of  mucus  and  pus,  will  be  described  more  fully 
in  the  chapter  on  cystitis  (vide  infra).  In  pyelitis,  also,  the  muco-purulent  secretion 
of  the  pelvic  mucous  membrane  must  mix  with  the  urine,  and  in  every  severe 
purulent  inflammation  the  amount  of  pus  in  the  urine  must  be  quite  considerable. 
We  can  never  decide  with  certainty,  from  the  mere  presence  of  pus  in  the  urine, 
as  to  the  place  where  the  pus  mixes  with  the  urine,  whether  in  the  pelvis  of 
the  kidney  or  in  the  bladder,  or  even  in  the  urethra.  Only  when  the  urine  con- 
tains other  characteristic  morphological  elements  besides  the  pus-corpuscles  can 
we  decide  upon  the  portion  of  the  urinary  tract  which  must  be  especially  affected. 
Among  these  morphological  constituents  is,  first  of  all,  the  epithelium,  which  in  the 


INFLAMMATION  OF  THE  PELVIS  OF  THE  KIDNEY.  883 

pelvis  of  the  kidney  shows  in  part  another  shape  than  in  the  bladder.  If  we  find 
in  the  urine,  then,  the  triangular,  long  caudate  pelvic  epithelium  (see  Fig.  115), 
with  its  cells  sometimes  laid  over  one  another  in  the  form  of  tiles,  we  may  assume 
that  the  pelvis  of  the  kidney  is  involved  in  the  inflammation.  Of  course,  the  re- 
verse of  this  law  does  not  obtain;  for,  even  in  severe  purulent  pyelitis  and  pyelo- 
nephritis, we  often  fail  entirely  to  find  the  caudate  epithelium  in  the  urine.  We 
must  also  add  that  similar  forms  of  epithelium  are  also  found  in  the  bladder,  so 
that  great  caution  is  always  to  be  enjoined  in 
estimating  the  diagnostic  value  of  the  epithe- 
lium found.  Blood  is  only  rarely  found  in  the 
urine  in  simple  pyelitis,  but  it  is  common  in 
pyelitis  calculosa  (see  the  following  chapter). 
The  reaction  of  the  urine  in  pyelitis  is  usually 
acid,  but  it  is  not  correct  to  assume  that  there 
is  in  this  a  comprehensive  mark  of  distinction 
between   pyelitis  and  cystitis,  in  which  the  Fig.  H5.— Pelvic  epithelium, 

urine  is  often  alkaline. 

Another  symptom  to  be  referred  directly  to  the  pyelitis,  is  the  local  pain  in 
the  region  of  the  kidney,  which  sometimes  passes  from  this  point  down  along  the 
ureters  to  the  bladder.  This  symptom  has  not,  therefore,  a  great  diagnostic  value, 
because  only  its  presence  is  in  favor  of  pyelitis,  while  its  absence  proves  nothing 
against  the  existence  of  the  disease. 

All  the  other  symptoms  may  be  directly  dependent  upon  the  pyelitis,  but  they 
may  usually  be  referred  in  great  degree  to  the  other  co-existing  affections.  First 
among  these  is  fever,  which  either  shows  an  irregularly  remitting  course,  or 
appears  in  single  high  elevations  of  temperature,  usually  associated  with  rigors. 
The  fever,  however,  seldom  shows  this  latter  pyaemic  character  except  in  the 
severe  purulent  forms,  where  we  usually  also  have  the  formation  of  renal  ab- 
scesses— tbat  is,  a  pyelo-nephritis.  Besides  the  fever  there  are  often  in  severe  cases, 
general  nervous  symptoms,  such  as  headache,  delirium,  and  sopor,  which  are  to  be 
referred  partly  to  the  general  pyaemic  infection  of  the  body  and  partly,  perhaps,  to 
the  absorption  of  ammonia  from  the  urine  decomposing  in  the  blood — the  "  am- 
moniasmia  "  of  Treitz  and  Jaksch. 

The  whole  course  of  pyelitis  differs  so  much  according  to  the  primary  disease 
present  that  nothing  of  general  application  can  be  said  about  it.  The  milder 
forms,  which  often  pass  off  rapidly,  are  found  most  commonly  in  childbed,  and 
sometimes  in  acute  infectious  diseases,  poisonings,  and  as  a  result  of  mild  cystitis. 
The  severe  forms  occur  chiefly  as  cysto-pyelitis  and  pyelo-nephritis,  as  a  result  of 
strictures  of  the  urinary  tract  (vide  infra),  of  severe  cystitis  in  diseases  of  the 
spinal  cord,  and  in  other  severe  diseases  of  the  kidney  and  of  the  pelvis  of  the  kid- 
ney, such  as  new  growths,  and  parasites.  They  usually  form  then  a  very  tedious 
and  often  incurable  affection,  which  lasts  until  the  patient's  death. 

The  signs  of  pyelitis  which  are  important  in  diagnosis  have  already  been  men- 
tioned above.  The  main  point  is  always  to  pay  careful  attention  to  the  aetiology 
of  the  case,  and,  next  to  that,  to  the  changes  in  the  urine.  If  the  whole  condition 
points  to  a  severe  affection  of  the  urinary  tract,  we  can  often  decide  correctly  on 
a  pyelitis  or  a  pyelo-nephritis  without  the  presence  of  direct  signs  of  these  diseases, 
because  we  know  by  experience  that  such  an  extension  of  the  affection  is  the  rule 
in  all  severe  and  long-continued  cases. 

The  implication  of  the  kidneys  is  sometimes  shown  directly  by  the  presence  of 
casts  in  the  urine  in  addition  to  the  pus-corpuscles.  In  the  cases  above  mentioned, 
where  a  chronic  cysto-pyelitis  is  complicated  with  a  contracted  kidney,  the  condi- 
tion of  the  urine  is  the  same  in  many  respects  as  in  genuine  contracted  kidney. 


884  DISEASES  OF  THE  KIDNEYS. 

It  is  abundant,  usually  has  a  low  specific  gravity,  and  contains,  besides  the  pus- 
corpuscles,  a  few  short  hyaline  casts. 

Treatment. — The  treatment  of  pyelitis  coincides  mainly  with  the  treatment  of 
the  primary  disease,  and  therefore  it  needs  no  detailed  description  here.  Ordi- 
narily only  the  accompanying  cystitis  (vide  infra)  is  accessible  to  a  direct  local 
treatment,  and  here  an  important  prophylactic  factor  is  discovered,  since  by  a 
timely  treatment  of  the  cystitis  we  can  certainly  hinder  the  advance  of  the  inflam- 
mation to  the  pelvis  of  the  kidney. 

Among  the  internal  remedies  to  which  we  ascribe  a  favorable  influence  on  the 
mucous  membrane  of  the  urinary  tract,  and  which  are  therefore  used  in  like 
manner  both  in  pyelitis  and  in  cystitis,  we  may  mention  the  astringents,  tannin, 
alum,  and  acetate  of  lead.  Balsams,  such  as  copaiba,  are  sometimes  prescribed, 
and  also  antiseptic  substances,  such  as  salicylic  acid  and  chlorate  of  potassium. 
The  details  in  regard  to  all  these  remedies  will  be  found  in  the  treatment  of 
cystitis.  The  copious  ingestion  of  fluids  sometimes  acts  favorably,  especially  the 
use  of  certain  mineral  waters,  among  which  the  waters  of  Carlsbad,  Vichy,  Ems 
Neuenahr,  and  Wildungen  have  obtained  the  most  reputation.  A  methodical 
milk  cure  is  also  greatly  to  be  recommended,  especially  when  there  are  symptoms 
of  irritation,  such  as  pain  on  micturition. 

Local  applications  to  the  region  of  the  kidneys,  warm  poultices,  or  exception- 
ally local  bloodletting,  are  indicated  only  when  there  is  severe  pain,  where,  of 
course,  narcotics  must  also  be  used  under  some  circumstances.  In  this  respect 
warm  baths  also  do  good  service  at  times. 


CHAPTER  II. 

NBPHROLITHI A  SIS. 

(Renal  Calculus.     Renal  Gravel.     Pyelitis  Calculosa.) 

Occurrence,  Chemical  Composition,  and  JEtiology  of  Renal  Concretions.— The 

precipitated  concretions  of  the  urinary  constituents  which  form  in  the  pelvis  of 
the  kidney,  and  which,  under  some  circumstances,  may  be  passed  from  it  with  the 
urine,  are  designated,  according  to  their  size  and  nature,  as  renal  sand,  a  fine, 
pulverized  precipitate;  renal  gravel,  gravel-like,  granular  concretions  about  the 
size  of  the  ordinary  coarse  grains  of  sand,  which  can  usually  pass  through  the 
ureters  without  special  difficulty;  or  renal  calculi,  the  larger  concretions.  The 
latter  are  about  the  size  of  a  pea  or  beau,  but  larger  stones  are  occasionally  seen 
which  may  even  resemble  actual  casts  of  the  pelvis  of  the  kidney.  We  usually 
find  a  calculus  only  in  one  kidney,  although  both  kidneys  may  be  affected. 

In  regard  to  the  chemical  nature  of  renal  concretions,  they  consist  most  fre- 
quently of  uric  acid.  They  then  have  a  brown-red  or  blackish  color,  and  have  a 
crystalline  breakage,  which  in  large  stones  is  usually  plainly  laminated ;  and,  on 
the  whole,  a  smooth  although  irregularly-shaped  surface.  More  rarely  the  renal 
concretions  consist  of  calcic  oxalate.  The  oxalate  calculi  are  extremely  hard, 
have  a  dark-brown  color  and  a  rough  surface,  often  furnished  with  many 
prickles,  from  which  reason  they  are  often  called  "mulberry  calculi."  Their 
breakage  sometimes  has  a  radiated  but  never  a  laminated  arrangement.  Stones 
are  also  frequently  seen,  which  consist  of  alternating  layers  of  uric  acid  and  calcic 
oxalate,  or  which  have  a  nucleus  of  uric  acid  and  a  coating  of  calcic  oxalate.  The 
phosphatic  calculi  are  another  variety  of  renal  concretions.    We  only  very  rarely 


NEPHROLITHIASIS.  885 

have  to  do,  however,  with  stones  which  consist  exclusively  of  ba!-;ic  calcic  phos- 
phate or  amrnonio-magnesic  phosphate,  but  we  usually  have  secondary  deposits  of 
layers  of  phosphate  which  are  precipitated  on  uric  acid  or  mulberry  calculi  in 
urine  which  has  become  alkaline.  The  phosphatic  calculi  have  a  grayish-white 
color,  and  are  comparatively  soft.  The  largest  examples  of  them  are  found,  not 
in  the  pelvis  of  the  kidney,  but  in  the  bladder.  The  cystine  and  xanthine  calculi 
are  the  rarest  of  all. 

But  little  is  definitely  known  as  to  the  exact  causes  for  the  origin  of  all  these 
concretions.  We  must  suppose  for  the  deposition  of  uric  acid  an  abnormally 
great  acidity  of  the  urine,  but  we  are  not  in  a  position  to  state  by  what  circum- 
stances (the  patient's  food  and  manner  of  life,  acid  fermentation  of  the  urine 
within  the  urinary  tract?)  this  may  be  provoked.  It  is  a  very  probable  theory 
that  some  solid  body  usually  affords  the  nucleus  and  the  first  cause  for  the 
formation  of  at  least  the  larger  stones,  among  these  bodies  being  mucous 
coagula,  shreds  of  epithelium,  and  perhaps  bacteria.  The  oxalate,  cystine,  and 
xanthine  calculi  are  also  deposited  from  acid  urine,  but  scarcely  anything  is 
known  as  to  the  precise  conditions  to  be  here  considered.  We  can  point  only  to 
the  fact  that  with  the  close  chemical  alliance  between  uric  acid  and  oxalic  acid 
the  origin  of  the  latter  from  uric  acid  seems  possible,  and  the  frequent  co-existence 
of  the  two  substances  in  the  calculi  therefore  seems  plausible.  We  have  already 
indicated  above  that  the  cause  of  the  deposition  of  phosphatic  concretions  can  be 
found  only  in  the  existence  of  an  alkaline  reaction  in  the  urine. 

In  regard  to  the  predisposing  causes  of  calculus  formation  we  must  mention, 
first  of  all,  that  they  are  often  found  in  children,  and  next  in  frequency  in 
advanced  life.  Men  show  a  greater  disposition  to  renal  calculi  than  women. 
Heredity  also  seems  to  play  a  certain  part,  since  the  disease  has  been  repeatedly 
observed  in  different  members  of  the  same  family.  The  many  relations  which 
have  been  imagined  between  the  formation  of  calculi  and  certain  conditions  in 
the  manner  of  life  and  in  the  food  taken,  all  lack  accurate  foundation.  In  regard 
to  this  the  chief  blame  is  laid  upon  an  excessive  meat-diet,  drinking  copiously  of 
new  sour  wines,  and  drinking  water  containing  lime.  In  regard  to  the  occur- 
rence of  uric-acid  concretions  in  gouty  patients,  compare  the  chapter  on  arthritis 
uratica. 

The  Anatomical  Changes  caused  by  Renal  Calculi.— The  most  frequent  change 
which  the  presence  of  concretions  in  the  pelvis  of  the  kidney  excites  is  pyelitis. 
This  may  exhibit  all  degrees,  from  a  simple  catarrhal  inflammation  to  a  diph- 
theritic or  severe  purulent  inflammation  of  the  pelvic  mucous  membrane.  As  a 
result  of  the  mechanical  irritation,  there  are  quite  frequently  large  or  small 
haemorrhages. 

If  a  severe  purulent  pyelitis  has  developed,  this  may  bring  with  it  all  the 
sequelae  with  which  we  have  previously  become  acquainted.  In  severe  cases  the 
process  may  involve  the  kidneys,  and  there  arises  a  pyelo-nephritis,  with  a  puru- 
lent breaking  down  of  the  renal  tissue,  and,  under  some  circumstances,  even  a 
perinephritis,  with  extensive  suppuration  into  the  vicinity  of  the  kidney,  and  with 
occasionally  perforation  into  the  neighboring  organs.  If  the  renal  calculi  have 
previously  passed  outward,  they  are  not  found  at  the  autopsy,  although  they  form 
the  special  starting  point  of  the  disease.  Sometimes,  however,  the  pus-cavity  is 
entirely  filled  with  calculi. 

A  second  important  sequel  of  a  renal  calculus  which  sometimes  develops  is 
hydronephrosis  {vide  infra).  It  arises  when  a  large  stone  blocks  the  passage  from 
the  pelvis  of  the  kidney  into  the  ureter,  or  when  a  smaller  stone  remains  fast 
in  the  ureter  and  completely  shuts  off  the  passage  of  the  urine.  In  the  latter  case 
there  may  also  arise  a  pressure  necrosis  and  perforation  of  the  ureter.     It  goes 


886  DISEASES  OF  THE  KIDNEYS. 

without  saying  that  inflammation  and  hydronephrosis  or  pyonephrosis  may  he 
combined  with  each  other. 

Clinical  Symptoms. — If  there  is  merely  the  formation  of  renal  sand  or  renal 
gravel  in  the  urinary  tract,  this  condition  is  sometimes  associated  with  no  symp- 
toms at  all.  The  little  granules  are  washed  away  by  the  urine  and  evacuated, 
and  at  most  they  may  give  rise  to  slight  pain  in  the  region  of  the  kidney. 
Larger  stones,  however,  may  sometimes  he  wholly,  or  almost  wholly,  without 
symptoms,  if  from  their  position  and  their  smooth  surface  they  can  cause  no 
special  bad  results. 

The  characteristic  clinical  symptoms  of  nephrolithiasis  do  not  appear  until  the 
results  of  mechanical  irritation  of  the  pelvis  of  the  kidney  arise,  or  until  there  is 
an  incarceration  of  a  calculus  in  the  ureter.  It  is  the  latter  circumstance  which, 
after  the  analogy  of  gall-stones,  causes  the  most  important  symptom  in  the  diag- 
nosis of  renal  calculi — the  pains,  the  so-called  renal  colic.  Such  an  attack  of  colic 
sometimes  comes  on  quite  suddenly  and  unexpectedly;  in  other  cases  it  is  pro- 
duced by  some  exciting  cause — jumping,  running,  walking,  or  riding.  The  pain 
often  attains  an  uncommonly  severe  intensity;  it  shoots  from  the  lumhar  region 
along  the  course  of  the  ureters,  but  sometimes  extends  still  farther,  to  the  testicles, 
the  thighs,  or  the  back.  In  severe  attacks  there  may  he  a  general  state  of  collapse 
with  a  small  rapid  pulse,  cold  sweat,  and  attacks  of  fainting.  The  temperature 
may  be  somewhat  raised.  "We  often  see  nausea  and  repeated  vomiting.  The 
urine  is  sometimes  entirely  normal,  inasmuch  as  it  comes  exclusively  from  the 
other  free  kidney ;  but  oliguria,  or  even  complete  anuria,  with  its  consequences, 
invariably  sets  in  if  both  ureters  be  stopped.  Even  when  one  kidney  remains 
normal,  the  evacuation  of  urine  may  be  inhibited  hy  a  reflex  spasm  of  the  Mad- 
der. Sometimes  the  urine  passed  contains  pus  and  blood.  The  duration  of  renal 
colic  depends  upon  the  duration  of  the  incarceration ;  it  may  last  for  a  few  hours 
or  several  days.  The  attack  often  ends  with  the  passage  of  the  stone  outward  into 
the  bladder. 

The  other  symptoms  occurring  in  nephrolithiasis  refer  mainly  to  the  results  of 
the  mechanical  irritation  of  the  pelvis  of  the  kidney.  The  urine  then  shows  an 
admixture  of  pus,  and  contains  pelvic  epithelium  and  often  blood.  The  frequent 
appearance  of  blood  in  the  urine,  which  usually  has  its  cause  in  purely  mechanical 
lesions  of  the  mucous  membrane,  is  a  characteristic  symptom  of  pyelitis  calculosa. 
If  we  find,  as  sometimes  happens,  the  urine  at  many  times  perfectly  clear  and 
normal,  but  at  other  times  containing  pus,  we  may  suspect  an  occasional  blocking 
of  the  ureter  coming  from  the  diseased  kidney  hy  a  renal  calculus. 

The  symptoms  are  much  more  severe  if  the  trouble  goes  on  to  a  severe  purulent 
pyelitis  and  pyelonephritis.  We  need  not  describe  the  details  again  here — the 
pain,  fever,  swelling,  and  perforation  internally  or  externally — since  they  agree 
completely  with  what  has  been  said  before  (see  the  previous  chapter  and  Chapter 
VI  in  the  previous  section).  A  special  chapter  is  devoted  below  to  the  symptoma- 
tology of  hydronephrosis. 

The  whole  course  of  nephrolithiasis  is,  as  a  rule,  very  tedious.  Since  the  dis- 
position to  the  formation  of  calculi  usually  persists,  and  since  also  the  sequelae 
which  have  once  developed  may  last  for  a  long  time,  a  very  chronic  state  often 
develops,  which,  in  varying  ways  and  with  manifold  exacerbations  and  remis- 
sions, is  composed  of  attacks  of  colic,  haemorrhages,  and  symptoms  of  pyelo- 
cystitis. 

In  many  cases,  of  course,  complete  recovery  may  finally  ensue.  The  calculi 
present  are  passed,  new  ones  are  not  formed,  the  pyelitis  that  has  arisen  disappears, 
and,  of  course,  all  the  morbid  symptoms  cease ;  hut,  on  the  other  hand,  nephro- 
lithiasis has  also  a  number  of  dangers  in  itself,  which  threaten  life  very  seriously. 


NEPHROLITHIASIS.  88Y 

These  are,  besides  the  rare  occurrence  of  uraemia,  first  of  all  the  development  of 
pyelo-nephritis  and  of  still  more  extensive  suppurations,  with  a  general  decline  in 
strength,  pyaemic  states,  etc.  There  is  also  a  possible  danger  in  such  chronic  sup- 
purations that  there  may  be  the  appearance  of  a  general  amyloid  degeneration  of 
the  internal  organs. 

Among  the  complications  occurring  in  other  organs,  only  one  circumstance 
has  especial  interest:  that  gall-stones  and  renal  calculi  are  found  quite  fre- 
quently in  the  same  individual.  We,  of  course,  can  not  well  speak  of  a  compli- 
cation with  vesical  calculi,  since  a  great  part  at  least  of  the  vesical  calculi  are 
originally  formed  in  the  pelvis  of  the  kidney,  and  undergo  merely  a  further 
growth  in  the  bladder. 

Diagnosis. — The  diagnosis  is  made  perfectly  certain  only  by  finding  the  special 
corpora  delicti  in  the  urine.  For  this  purpose  the  urine  must  always  be  examined 
as  soon  as  possible  after  its  passage,  and  it  is  best  to  pour  it  through  a  fine  sieve. 
In  many  cases,  however,  we  can  diagnosticate  nephrolithiasis  quite  certainly,  with- 
out the  direct  evidence  of  concretions,  from  the  characteristic  symptoms,  espe- 
cially from  the  periodical  renal  haemorrhages  and  from  the  attacks  of  colic.  Of 
course  it  may  be  confused  with  renal  cancer,  parasites  of  the  kidney  such  as  echino- 
cocci,  and  similar  affections,  but  this  does  not  happen  very  often,  because  renal 
calculus  is  a  far  commoner  affection  than  the  diseases  just  mentioned.  Finally, 
we  must  state  that  these  diseases  may  comparatively  often  be  combined  with 
n  ephrolithiasis. 

Treatment. — Since  the  uric-acid  concretions  are  by  far  the  commonest,  the 
methods  of  treatment  most  in  use  for  nephrolithiasis  refer  first  to  these ;  but  they 
are  to  be  used  in  like  manner  in  the  allied  oxalate  calculi. 

If  the  tendency  to  the  formation  of  urinary  gravel  be  confirmed  in  a  patient,  or 
if  the  severer  symptoms  of  nephrolithiasis  have  already  appeared,  we  must  first 
give  a  number  of  general  dietetic  directions,  which  check  the  formation  of  uric 
acid  in  general,  and  aid  the  solubility  of  the  uric  acid  already  formed  as  far  as 
possible.  Without  entering  too  much  on  theoretical  reasoning,  we  will  give  in 
what  follows  the  measures  which  have  been  proven  practically  and  quite  gener- 
ally acknowledged.  In  the  first  place,  the  patient  must  avoid  any  immoderate 
indulgence  in  food  in  general,  and  particularly  too  great  indulgence  in  meat. 
We  should  recommend  for  him  a  diet  mainly,  though  not  exclusively,  vegetable, 
with  a  moderate  supply  of  meat;  milk  is  also  a  proper  food.  Alcoholic  beverages 
should  be  taken  only  in  slight  amount,  and  acid  foods  and  drinks,  except  lemon- 
ade, should  not  be  taken  at  all.  It  is  a  good  plan  to  control  the  supply  of  food  by 
weighing  the  patient  regularly,  in  order  to  avoid  any  further  addition  to  the 
weight  in  all  persons  in  a  state  of  normal  nutrition,  and  to  obtain  a  loss  of  weight 
in  the  corpulent.  We  should  also  aid  the  using  up  of  tissue  by  regular  physical 
exercise  and  muscular  work,  gymnastics,  sawing  wood,  or  gardening;  and,  finally, 
the  urine  must  be  diluted  by  an  abundant  supply  of  fluid,  and  its  soluble  power  be 
thus  increased. 

This  latter  indication  will  usually  correspond  at  the  same  time  with  those 
which  diminish  the  acid  reaction  of  the  urine  by  a  supply  of  alkalies  and  thus 
hinder  the  deposition  of  ui'ic  acid  as  far  as  possible.  From  this  comes  the  very 
extensive  use  of  the  alkaline  mineral  waters  in  nephrolithiasis.  The  simplest  plan 
is  to  dissolve  some  alkaline  salt  in  a  large  amount  of  plain  water,  soda  water,  or 
lemonade,  and  let  the  patient  drink  it.  Among  these  salts  we  may  mention  sodic 
phosphate,  one  to  four  drachms  (grm.  5-15)  a  day,  or  better,  sodic  carbonate,  one  to 
two  drachms  (grm.  5-10),  or  carbonate  of  lithium,  which  has  lately  been  especially 
recommended,  two  to  five  grains  (grm.  0"l-0'3)  several  times  a  day.  Of  course, 
the  special  mineral  waters  enjoy  a  greater  reputation ;  these  may  be  used  in  con- 


888  DISEASES  OF  THE  KIDNEYS. 

fornaity  with  the  treatment  at  home,  or  especially  at  the  appropriate  springs.  The 
following  springs  enjoy  the  greatest  reputation  in  this  respect :  Carlsbad,  Vichy, 
Salzbrunn,  Fachinger,  Tarasp,  Neuenahr,  Ems,  and  Wildungen. 

The  symptomatic  treatment  is  also  very  important.  In  so  far  as  this  relates  to 
the  accompanying  pelvic  and  vesical  catarrh,  we  may  refer  to  the  appropriate 
chapters  in  tbis  book,  while  the  surgical  methods  of  treatment  in  the  severer 
sequelae — hydronephrosis,  pyonephrosis,  or  perinephritic  abscess — are  to  be  found 
in  the  special  treatises.  Against  renal  haemorrhages  some  internal  remedies,  such 
as  ergotine  or  tannin,  have  been  recommended,  but  their  action  is  quite  doubtful. 
The  treatment  of  the  attacks  of  colic  is  of  greater  practical  significance.  The 
chief  remedies  are  the  narcotics,  opium,  and  morphine,  internally,  or,  with  very 
severe  pain,  better  subcutaneously.  Warm  baths,  warm  poultices,  or  narcotic  em- 
brocations, such  as  chloroform  liniment,  also  frequently  give  relief.  Local  blood- 
letting is  only  rarely  indicated.  An  abundant  supply  of  fluid  is  always  advisable, 
in  order  to  aid  the  washing  out  of  the  incarcerated  stone  by  an  increased  secretion 
of  urine. 

As  we  have  stated,  what  has  thus  far  been  said  obtains  chiefly  in  the  treatment 
of  uric-acid  and  oxalic-acid  calculi.  We  know  no  special  prescriptions  to  be  con- 
sidered for  the  occasional  cystine  calculi.  When  there  are  phosphatic  calculi, 
however,  which  can  be  deposited  only  from  alkaline  urine,  the  use  of  acids  has 
been  recommended,  especially  of  lactic  acid,  seven  to  fifteen  grains  (grm.  0'5-l), 
internally  in  an  aqueous  solution.  The  main  thing,  of  course,  is  always  the  treat- 
ment of  the  catarrh  of  the  urinary  tract,  which  usually  lies  at  the  bottom  of  the 
calculus  formation. 


CHAPTER  III. 
TUBERCULOSIS   OF  THE   GENITO -URINARY  APPARATUS. 

iEtiology  and  Pathological  Anatomy. — It  does  not  seem  remarkable  that,  with 
the  presence  of  many  tubercular  processes  in  the  body,  tubercle  bacilli  should  quite 
easily  reach  the  kidneys  by  way  of  the  blood-current,  and  there  give  rise  to  an 
eruption  of  tubercle.  Accordingly,  we  quite  frequently  find  a  few  or  many  mili- 
ary tubercles  in  the  kidneys  in  acute  miliary  tuberculosis,  in  pulmonaiy  tubercu- 
losis, etc.,  which  are  distributed  over  the  whole  kidney,  or  sometimes  only  in  the 
territory  of  one  arterial  branch. 

WhUe  miliary  tuberculosis  of  the  kidney,  however,  is  without  any  clinical  sig- 
nificance, there  is  also  an  extensive  local  tuberculosis  of  the  kidney,  as  well  as  of 
the  urinary  tract  and  the  sexual  organs.  Such  affections  sometimes  occur  as  a 
result  of  pronounced  pre-existing  tuberculosis  of  other  organs,  especially  the 
lungs,  or  they  arise  as  an  apparently  independent  disease,  which  is  termed  genito- 
urinary tuberculosis.  In  such  cases  the  infection  with  the  tubercular  poison  often 
seems  to  take  place  by  means  of  the  blood  from  some  previously  existing — perhaps 
concealed — tubercular  foci  in  the  body,  such  as  glands,  tubercular  bone  or  joint 
disease,  etc.  In  other  cases,  the  tubercle  bacilli  perhaps  enter  the  urinary  tract 
from  without,  but  the  point  of  the  first  anatomical  lesion  need  not,  apparently, 
always  be  the  same.  The  kidneys  often  seem  to  be  first  diseased,  in  other  cases 
the  bladder,  and  quite  frequently,  as  it  seems,  the  prostate,  and  sometimes  perhaps 
the  vesiculee  seminales  or  the  testicles.  From  the  organ  first  affected  the  process 
then  extends  continuously  or  by  leaps  to  the  neighboring  parts.  If  the  cases  come 
to  autopsy,  the  tuberculosis  is  often  so  extensive  that  we  can  no  longer  make  out 


TUBERCULOSIS  OF  THE  GENITO-URINARY  APPARATUS.      889 

wich  certainty  the  place  where  it  first  began.  In  women  the  urinary  apparatus  is 
only  very  rarely  affected  by  tuberculosis,  while  uterine  and  ovarian  tuberculosis 
represents  a  localization  of  the  tubercular  poison  of  clinical  importance  (compare 
the  chapter  on  tuberculosis  of  the  lungs). 

In  the  kidneys  the  tubercular  infiltration  develops  either  chiefly  from  the  pel- 
vis of  the  kidney  or  in  the  renal  substance  itself.  Yellow  cheesy  nodules  arise, 
which  finally  break  down  and  thus  lead  to  an  actual  "nephro-phthisis."  If 
the  disease  arise  from  the  pelvis,  the  infiltrated  renal  papilla)  are  usually  first 
affected,  from  which  the  whole  pelvis  of  the  kidney  is  changed  into  an  ulcerating 
surface  covered  with  necrotic  tissue  and  cheesy  detritus.  In  very  advanced  cases 
almost  the  whole  kidney  is  destroyed.  The  process  is  usually  bilateral,  but  it  is 
often  more  advanced  on  one  side  than  on  the  other. 

If  the  process  invade  the  ureters,  their  walls  are  also  infiltrated  with  tubercular 
deposits,  and  hence  they  are  thickened,  while  the  mucous  membrane  is  often 
changed  in  great  part  to  a  necrotic  ulcerating  surface.  Precisely  analogous  con- 
ditions are  found  in  the  bladder,  and  in  some  cases  even  in  the  uretlna;  while 
in  the  prostate,  the  vesiculae  seminales,  and  the  testicles  there  is  more  frequently 
the  formation  of  cheesy  tubercular  nodules,  and  more  rarely  disintegration  and 
perforation. 

Clinical  Symptoms. — The  picture  of  genito-urinary  tuberculosis  corresponds  in 
most  of  its  details  completely  to  that  of  a  severe  chronic  pyelo-cystitis.  The  occa- 
sional local  symptoms  are  pain  in  the  region  of  the  kidneys  and  bladder.  This 
may  sometimes  assume  great  severity,  like  colic,  if  the  ureter  become  plugged  by 
a  broken-down,  crumbling  mass;  yet  in  other  cases  the  pain  is  but  slight  during 
the  whole  disease. 

The  urine  shows  the  most  important  changes.  It  almost  invariably  contains 
an  abundant  sediment,  consisting  of  pus-corpuscles  and  detritus.  Its  amount 
usually  remains  normal  for  a  long  time;  its  reaction  is  faintly  acid,  but  in  severe 
cases  it  may  become  alkaline  through  complication  with  an  alkaline  fermentation 
of  the  urine.  The  discovery  of  shreds  of  tissue  in  the  urine,  elastic  fibers  and 
connective  tissue,  is  sometimes  possible,  and  is  of  diagnostic  value  because  it  is 
direct  evidence  of  an  ulcerative  process.  The  discovery  of  tubercle  bacilli  in  the 
purulent  urinary  sediment  (Rosenstein  and  others)  is,  however,  far  more  impor- 
tant. This  is  performed  by  the  same  method  as  in  the  sputum;  it  succeeds  in 
almost  all  cases,  and  is  an  infallible  and  absolutely  decisive  sign  in  diagnosis. 
Admixtures  of  blood  in  the  urine  are  also  seen  in  genito-urinary  tuberculosis,  but 
they  may  often  be  entirely  absent.  In  one  of  our  cases  a  slight  hEematuria  was 
the  first  symptom  which  called  the  patient's  attention  to  the  trouble  with  the 
bladder. 

The  local  objective  examination  of  the  kidneys  usually  gives  a  negative  result. 
Only  in  a  few  cases  have  we  been  able  to  feel  the  diseased  kidney  as  a  tumor 
through  the  abdominal  walls.  This  is  usually  due  less  to  the  tubercular  infiltration 
of  the  kidney  itself  than  to  the  dilatation  of  the  pelvis  of  the  kidney  from  hydro- 
nephrosis. We  can  sometimes  feel  the  thickened  walls  of  the  bladder.  The  local 
examination  of  the  prostate  and  the  testicles  is  far  more  important  in  diagnosis. 
Especially  in  the  latter  we  often  feel  the  hardening  corresponding  to  the  tuber- 
cular infiltration,  and  manifesting  itself  chiefly  in  the  epididymis,  while  the 
hardening  and  enlargement  of  the  prostate  can  usually  be  easily  detected  by 
rectal  palpation. 

Among  the  general  symptoms  we  must  mention,  first  of  all,  fever,  which  is 
only  exceptionally  absent,  and  usually,  in  the  severe  cases,  shows  a  pronounced 
remitting,  hectic  character.  The  other  general  symptoms  are  the  same  as  in  most 
of  the  other  tubercular  diseases — anaemia,  emaciation,  loss  of  appetite,  increasing 


890  DISEASES  OF  THE  KIDNEYS. 

bodily  weakness,  etc.  We  have  a  special  sign  in  the  occasional  co-existence  of 
other  tubercular  diseases  in  the  body,  the  lungs,  the  intestines,  the  bones,  etc., 
but  these  may  also  be  wholly  absent,  so  that  we  have  to  do  with  a  purely  local 
genito-urinary  tuberculosis. 

The  course  of  the  disease  is  steadily  progressive.  Recovery  does  not  occur,  at 
least  not  in  any  cases  where  the  disease  has  attained  any  extent.  The  disease 
lasts  from  a  few  months  to  a  year  or  two,  but  sometimes  much  longer.  The  fatal 
termination  usually  ensues  from  the  increasing  general  weakness,  more  rarely 
under  the  symptoms  of  ammoniaemia,  or  sometimes  from  a  miliary  tuberculosis 
or  some  other  tubercular  disease,  such  as  pulmonary  tuberculosis,  tubercular 
meningitis,  etc. 

Diagnosis. — The  diagnosis  of  genito-urinary  tuberculosis  is  now  usually  no 
longer  difficult  in  fully  developed  cases,  since  it  can  be  made  with  complete  cer- 
tainty by  the  discovery  of  the  tubercle  bacilli  joined  to  the  presence  of  pus  in  the 
urine.  Of  course  this  gives  no  information  as  to  the  more  special  extent  of  the 
process.  In  order  to  judge  of  this,  we  must  add  the  local  symptoms  and  the  phys- 
ical examination  of  the  different  organs.  We  are  aided  in  the  confirmation  of 
our  first  suspicion  of  a  tubercular  disease  chiefly  by  the  consideration  of  the  gen- 
eral condition  and  the  habit  of  the  patient,  the  discovery  of  a  hereditary  taint,  or 
at  least  the  approximate  possibility  Of  tubercular  infection,  and  also  the  discovery 
of  other  tubercular  affections,  especially  in  the  testicles,  the  hectic  fever,  and  the 
tedious  course,  upon  which  nothing  has  a  favorable  influence.  At  any  rate  we 
must  make  it  a  rule,  in  every  case  of  persistent  pyuria  which  can  not  be  otherwise 
explained,  to  examine  the  purulent  sediment  for  tubercle  bacilli.  We  may  then 
often  be  able  to  recognize  with  certainty  the  milder  and  incipient  cases  of  this  not 
very  rare  affection. 

Treatment. — Since  we  do  not  know  at  present  any  efficient  remedy  to  combat 
the  tubercular  process,  the  treatment  has  merely  the  task  of  improving  the  patient's 
general  condition  as  far  as  possible,  and  also  of  undertaking  a  local  symptomatic 
treatment  in  the  same  way  as  in  ordinary  pyelitis  and  cystitis  (q.  v.).  Of  internal 
remedies  we  have  most  frequently  used  chlorate  of  potassium  and  turpentine,  and 
have  sometimes  seen  good  results,  especially  from  the  latter.  The  internal 
exhibition  of  creosote  sometimes  seems  to  us  to  act  well.  In  vesical  tuberculosis 
it  is  well  to  wash  out  the  bladder.  As  an  operative  procedure  we  may  remove 
tubercular  testicles  and  epididymes,  but  we  must  remember  that  in  such  cases 
there  is  usually  co-existing  disease  of  other  parts  of  the  genito-urinary  apparatus, 
such  as  the  prostate,  etc. 


CHAPTER  IV. 

HYDRONEPHROSIS. 

(Dilatation  of  the  Pelvis  of  the  Kidney.) 

JEtiology. — If  a  contraction  arises  in  any  part  of  the  urinary  tract  and  checks 
the  flow  of  urine,  there  is  a  stasis  of  the  urine  in  the  portion  behind  the  stenosis, 
which  gradually  leads  to  a  constantly  increasing  dilatation  of  the  tract  as  a  result 
of  the  pressure  of  the  retained  fluid.  If  the  obstacle  be  situated  in  a  ureter,  the 
pelvis  of  the  kidney,  as  well  as  the  part  of  the  ureter,  dilates,  and  there  arises  a 
so-called  hydronephrosis.  If,  however,  the  obstacle  have  its  seat  in  the  urethra, 
the  bladder  and  both  ureters  gradually  dilate,  and  there  finally  arises  a  bilateral 
hydronephrosis. 


HYDRONEPHROSIS.  891 

A  closure  of  the  ureter  arises  most  frequently  in  adults  from  impacted  renal 
calculi,  and  also  from  new  growths  in  the  vicinity,  in  the  uterus  or  ovaries,  which 
compress  the  ureter  from  without.  So  great  a  pressure  may  also  be  exerted  on 
the  ureters  by  the  gravid  uterus  as  to  be  followed  by  a  hydronephrosis,  which 
is  usually  bilateral.  Cicatricial  strictures,  valve- formations  and  bends,  also  are 
found  in  the  ureter,  and  form  an  obstacle  to  the  flow  of  urine.  Finally,  in  can- 
cer of  the  bladder  the  lower  opening  of  the  ureter  may  be  contracted  or  entire!} 
closed. 

Constrictions  of  the  urethra,  which  finally  lead  to  a  bilateral  hydronephrosis, 
arise  most  frequently  from  strictures  as  a  result  of  gonorrhoea,  and  also  from 
enlargements  of  the  prostate.  In  a  rare  cases  a  phimosis  may  even  form  the 
obstacle. 

In  general,  it  is  evident  that  gradual  constrictions  of  the  urinary  tract  and  peri- 
odic obstructions,  as  from  calculi,  interrupted  by  free  intervals,  lead  to  more 
marked  degrees  of  hydronephrosis  than  rapid  and  complete  obstructions.  Under 
the  first-named  circumstances  the  renal  secretion  persists  much  longer  and  is  more 
abundant  than  in  the  latter  case,  when  it  usually  soon  ceases.  Nevertheless,  even 
then  there  still  follows  a  further  slow  distention  of  the  pelvis  of  the  kidney,  since 
its  mucous  membrane  continues  to  secrete. 

It  is  worthy  of  note  that  hydronephrosis  may  also  be  congenital,  and  then  it  is 
usually  due  to  congenital  defects  of  development  in  the  ureters  or  other  urinary 
passages.  In  later  life  hydronephrosis  is  in  general  more  frequently  observed  in 
women  than  in  men. 

Pathological  Anatomy. — The  pathological  anatomy  of  hydronephrosis  is  on 
the  whole  very  simple.  We  have  a  dilatation  of  the  pelvis  of  the  lddney,  which 
is  associated  with  a  pressure  atrophy  of  the  renal  tissue.  The  papillae  are  flattened, 
the  uriniferous  tubules  and  the  glomeruli  are  gradually  more  and  more  obliterated, 
and  finally  the  whole  kidney  may  be  changed  to  a  connective-tissue  sac  filled 
with  fluid.  The  size  of  such  a  hydronephrotic  sac  may  sometimes  be  so  large  as  to 
contain  ten  or  twenty  quarts  (litres)  of  fluid.  The  latter  consists,  of  course,  at  first 
of  urine,  but  the  farther  the  atrophy  of  the  kidney  advances,  the  more  it  contains 
merely  the  secretion  of  the  mucous  membrane.  Inflammatory  conditions  are 
found  in  hydronephrosis  only  when  they  have  existed  previously,  as  in  pyelitis 
calculosa,  or  when  excitants  of  inflammation  in  addition  have  reached  the  pelvis 
of  the  kidney. 

Clinical  Symptoms. — Since  the  whole  type  of  the  disease  is,  of  course,  depend- 
ent in  many  respects  upon  the  nature  of  the  primary  disease,  we  have  here  to 
describe  only  those  symptoms  which  point  particularly  to  the  development  of 
hydronephrosis.  Such  a  condition  often  causes  no  special  clinical  symptoms  at 
all,  so  that  we  can  at  most  suspect  its  existence  from  the  presence  of  an  setiological 
cause. 

The  appearance  of  a  visible  and  palpable  tumor  is  the  first  definite  point  in  the 
diagnosis  of  hydronephrosis.  This  first  shows  itself  in  the  region  of  the  affected 
kidney,  but  then  it  gradually  enlarges  toward  the  hypochondrium  and  the  median 
line  of  the  body,  and  it  may  finally  show  very  considerable  dimensions.  The  tumor 
is  not  movable  on  respiration.  Its  resistance  is  usually  quite  considerable,  but 
sometimes  a  marked  feeling  of  fluctuation  may  be  present.  On  percussion,  the 
tumor  gives  a  dull  note,  from  which  the  tympanitic  note  of  the  colon  in  front  of 
the  tumor  is  sometimes  distinct  (see  page  873).  It  is  an  important  diagnostic  sign 
if  the  tumor  show  variations  in  its  size  at  times,  since  it  decreases  in  size  with  a 
co-existing  increase  in  diuresis,  and  increases  again  when  the  amount  of  urine 
becomes  smaller. 

In  doubtful  cases  an  exploratory  puncture  of  the  tumor  may  also  be  of  signifi- 


892  DISEASES  OF  THE  KIDNEYS. 

cance  in  diagnosis.  It  of  course  favors  the  existence  of  hydronephrosis  if  urinary 
constituents,  especially  urea,  can  be  found  in  the  fluid  evacuated ;  but  if  the  hydro- 
nephrosis be  of  long  standing,  its  contents,  as  we  have  said,  will  be  simply  sero- 
mucous,  and  then  chemical  examination  gives  no  definite  data  for  distinguishing 
hydronephrosis  from  ovarian  tumors,  or  other  cystic  tumors  of  the  kidney.  In 
regard  to  the  procedui'e  first  devised  by  Simon,  which  is  also  important  in  regard 
to  palliative  therapeutics — namely,  catheterization  of  the  ureter  in  women  after 
having  previously  dilated  the  urethra  artificially,  and  in  this  way  confirming  the 
diagnosis — the  details  may  be  found  in  the  special  works  on  surgery. 

The  secretion  of  urine  in  unilateral  hydronephrosis  may  be  completely  normal 
if  the  other  healthy  kidney  act  vicariously.  In  stricture  of  the  urethra,  and  also 
in  bilateral  constrictions  of  the  ureters,  however,  there  is,  of  course,  an  obstacle  for 
the  passage  of  urine,  so  that  the  amount  of  urine  may  be  abnormally  small.  There 
may  be  at  times  complete  anuria,  and  even  urcemic  symptoms.  The  composition 
of  the  urine  depends  entirely  upon  the  form  of  the  primary  disease.  If  only  the 
healthy  kidney  secrete,  the  urine  passed  is  normal.  If  there  be  at  the  same  time 
pyelitis  or  cystitis,  the  urine  may  contain  pus  or  blood.  If  the  urine  can  also 
come  from  the  diseased  kidney  at  one  time  and  not  at  another,  the  urine  also 
exhibits  a  vai'ying  composition,  as  we  have  said  before  (page  886). 

In  many  cases  of  hydronephrosis  quite  severe  local  symptoms  are  present; 
there  are  frequently  severe  pains  in  the  tumor,  which  shoot  chiefly  toward  the 
thigh.  Of  course,  these  local  symptoms  are  sometimes  only  slight.  In  regard  to 
the  symptoms  on  the  part  of  other  organs,  gastric  disturbances  appear  to  be  of 
.  the  most  frequent  occurrence ;  among  them  are  nausea,  loss  of  appetite,  vomiting, 
and  eructations.  In  some  cases  the  bowels  are  constipated,  in  others  there  is 
obstinate  diarrhoea. 

The  whole  course  of  the  disease  is  always  chronic.  There  are  often  variations 
in  its  course,  but  no  general  statements  can  be  given,  because  the  conditions  vary 
in  the  different  cases  according  to  the  form  of  the  primary  disease.  Most  cases 
of  hydronephrosis  end  fatally,  either  in  consequence  of  the  primary  disease  or 
in  consequence  of  secondary  pyelo-nephritic  or  perinephritic  inflammations,  of 
ursemia,  etc.  Eecovery  takes  place  in  rare  cases,  especially  if  one  kidney  be  per- 
fectly normal,  and  there  be  no  incurable  primary  disease.  Eecovery  may  ensue 
spontaneously  from  perforation  or  obliteration,  or  it  may  be  brought  about  arti- 
ficially from  operative  procedures. 

In  the  diagnosis  of  hydronephrosis,  the  points  especially  to  be  considered  have 
already  been  mentioned.  The  diagnosis  is  usually  not  easy,  especially  if  the  setio- 
logical  factors  be  unknown ;  and  the  disease  is  often  confused  with  other  renal 
tumors  and  echinococci  of  the  kidneys,  with  ovarian  tumors,  and  even  with  splenic 
and  hepatic  tumors. 

Treatment.— Except  for  the  symptomatic  ti'eatment  of  the  pain  and  any  accom- 
panying pyelo-cystitis,  an  efficient  treatment  of  hydronephrosis  can  be  attempted 
only  by  sui'gical  means.  Puncture,  incision,  extirpation  of  the  kidney,  and  the 
establishment  of  a  renal  fistula,  are  the  methods  of  operation  most  in  use— the 
details  of  which  are  to  be  found  in  the  special  surgical  treatises. 


CYSTITIS.  893 

CHAPTER  V. 

CYSTITIS. 

(  Vesical  Catarrh,.) 

iEtiology. — In  most  cases  of  vesical  catarrh  the  agents  of  inflammation  reach 
the  bladder  from  without  through  the  urethra.  The  most  unequivocal  experiment 
in  this  regard  is,  unfortunately,  often  made  by  the  physician  himself,  when  he 
excites  a  cystitis  by  the  use  of  an  insufficiently  purified  and  disinfected  catheter 
or  bougie.  The  development  of  the  vesical  catarrh  is  generally  aided  in  such  cases 
by  the  fact  that  there  is  usually  a  defective  evacuation  of  urine,  from  stricture  of 
the  urethra  or  paralysis  of  the  detrusor,  and  that  there  is  at  the  same  time  reten- 
tion of  urine,  in  which  the  bacteria  can  develop  undisturbed.  The  agents  of 
inflammation  may  also  enter  from  the  urethra  into  the  bladder  in  incontinence 
of  urine.  On  account  of  the  imperfect  closure  of  the  sphincter,  a  stagnating 
column  of  urine,  directly  connected  with  the  contents  of  the  bladder,  forms  in  the 
urethra,  and  to  this  column  the  air  and  the  bacteria  that  excite  decomposition  of 
the  urine  have  direct  access.  In  this  way  many  cases  of  cystitis  arise  in  patients 
with  nervous  disease  who  have  paralysis  of  the  bladder,  and  also  many  of  the  fre- 
quent cases  of  cystitis  arise  in  this  way  in  persons  who  are  severely  ill  and  stupid 
from  some  other  disease,  such  as  typhoid  fever. 

Cystitis  often  follows  diseases  of  the  neighboring  urinary  tract.  Gonorrhoeal 
urethritis  is  the  most  common,  and  this  invades  the  bladder  directly  and  leads  to 
a  gonorrhoeal  cystitis.  In  women,  the  agents  of  inflammation  may  quite  easily 
enter  the  bladder  from  the  vagina  through  the  short  female  urethra.  Thus  arise 
especially  the  frequent  cases  of  cystitis  in  childbed.  In  some  cases  communica- 
tions may  develop  between  the  bladder  and  certain  neighboring  organs  as  in 
vesico-rectal  or  vesico-vaginal  fistulse,  by  which  again  access  to  the  bladder  is  open 
to  the  agents  of  inflammation. 

Another  group  of  cases  is  due  to  the  presence  of  foreign  bodies,  which  irritate  the 
vesical  mucous  membrane  mechanically.  Among  these  is,  first  of  all,  the  cystitis 
which  so  often  accompanies  stone  in  the  bladder.  It  must  be  stated,  however  that 
many  cases  of  the  vesical  catarrh  which  here  exists  are  not  directly  dependent 
upon  the  calculi,  but  are  first  excited  by  examination  with  catheters  and  sounds. 

In  distinction  from  the  methods  of  the  origin  of  cystitis  so  far  described,  the 
production  of  inflammation  by  way  of  the  blood-supply  is  much  rarer.  Certain 
chemical  substances,  already  mentioned  (page  837),  which  are  eliminated  by  the 
kidneys  and  provoke  an  inflammation  of  the  urinary  tract,  are  the  most  important 
in  this  respect.  Cantharides  shows  the  most  intense  action  of  this  sort,  and  it  may 
cause  an  actual  croupous  cystitis.  Slight  irritative  states  of  the  bladder  also  fre- 
quently appear  after  taking  certain  foods  and  drinks,  as  after  drinking  new  beer. 
Infectious  substances  only  rarely  come  under  consideration  in  this  regard.  Most 
of  the  cases  of  cystitis  in  severe  acute  infectious  diseases  are  secondary  complica- 
tions (vide  supra).  It  can  not  be  doubted  that  in  some  cases  an  apparently  idio- 
pathic primary  cystitis  appears  after  exposure  to  cold,  but  it  is  very  rare.  In  such 
cases  we  usually  have  to  do  with  acute  exacerbations  of  an  old  chronic  cystitis— 
for  example,  of  gonorrhoeal  origin. 

It  has  been  stated  in  the  previous  chapters  how  frequently  cystitis  is  only  one 
symptom  of  a  more  extensive  disease  of  the  urinary  tract.  As  cystitis  may  further 
invade  the  pelvis  of  the  kidney  through  the  ureters,  so,  on  the  other  hand,  any 
pyelitis  of  primary  origin  may  extend  downward  and  involve  the  bladder. 

Pathological  Anatomy.— The  pathological  anatomy  of  cystitis  presents  the 
same  conditions  as  the  inflammation  of  any  other  mucous  membrane.     In  simple 


S94  DISEASES  OF  THE  KIDNEYS. 

catarrhal  cystitis  the  mucous  membrane  is  swollen  and  covered  with  pus,  and  is 
often  studded  with  haemorrhages.  In  old  chronic  cystitis  the  mucous  membrane 
often  takes  on  a  slaty,  grayish-black  color  as  a  result  of  the  haemorrhages.  The 
severer  forms  of  cystitis,  such  as  are  often  observed  in  diseases  of  the  spinal  cord, 
are  termed  vesical  diphtheria.  These  cases  come  to  a  necrotic  destruction  of  the 
superficial  layers  of  the  mucous  membrane,  ulcerations,  etc.  In  such  severe  cases 
submucous  and  pericystitic  abscesses  sometimes  develop,  which  may  perforate  into 
the  surrounding  parts  in  various  ways.  The  incrustation  of  the  mucous  mem- 
brane -with  urinary  salts,  especially  with  ammonio-magnesic  phosphate,  is  also 
frequently  found  in  chronic  cystitis,  and  is  wortby  of  mention. 

Clinical  Symptoms. — The  local  symptoms  in  the  bladder  are  sometimes  quite 
severe  in  cystitis,  but  in  other  cases  they  are  only  slight.  In  general,  they  show 
a  greater  intensity  in  acute  cases  than  in  chronic  cystitis.  The  pain  in  the  region 
of  the  bladder  is  rarely  entirely  continuous;  it  usually  comes  on  only  on  micturi- 
tion, but  it  is  often  very  distressing  then,  and  shoots  to  the  opening  of  the  urethra. 
Since  the  inflamed  vesical  mucous  membrane  shows  an  increased  irritability,  and 
since  the  morbidly  altered  urine  (vide  infra)  also  exerts  an  abnormal  irritation 
on  the  mucous  membrane,  there  is  very  often  an  increased  desire  to  micturate. 
The  patient  has  to  empty  the  bladder  much  offener  than  normal,  and  in  severe 
cases  there  is  an  almost  constant,  painful  ''  vesical  tenesmus,"  from  which,  at  any 
attempt  to  micturate,  only  a  very  small  amount  of  urine  is  passed,  with  severe 
burning.  As  a  result  of  the  increased  irritability  of  the  vesical  mucous  membrane, 
there  sometimes  comes  on  a  very  troublesome  reflex  spasm  of  the  sphincter,  by 
which  the  symptoms  are  increased. 

Only,  the  character  of  the  urine  is  decisive  in  the  diagnosis.  This  is  secreted  in 
a  perfectly  normal  amount  and  character,  in  case  there  is  no  complication  on  the 
part  of  the  kidneys;  but  in  the  bladder  it  is  mixed  with  the  products  of  the  dis- 
eased mucous  membrane,  and  it  is  here  exposed  to  the  action  of  the  bacteria  in  a 
way  that  will  presently  be  described.  The  abnormal  admixtures  in  the  urine  con- 
sist chiefly  of  pus-corpuscles  and  bladder  epithelium,  and  sometimes  of  some  of 
the  mucus  produced  by  the  mucous  membrane.  The  specific  action  of  the  bacteria, 
which  have  reached  the  bladder  from  without,  consists  of  the  so-called  alkaline 
fermentation  of  the  urine — that  is,  in  the  fermentative  change  of  urea  into  car- 
bonate of  ammonia.  This  process  is  associated  entirely  with  the  presence  of  cer- 
tain micro-organisms,  the  " micrococci  ureae"  and  the  retention  of  urine  as  such 
never  leads  to  an  alkaline  fermentation.  As  Lepine  and  Eoux  have  shown,  we 
can  produce  a  veiy  severe  cystitis,  and  even  nephritis,  by  injecting  very  small 
amounts  of  a  pure  culture  of  micrococcus  ureae  (Cohn)  into  the  bladder  of  a 
guinea-pig.  The  stagnation  is  only  a  factor,  which  greatly  aids  the  whole  process 
since  the  activity  of  the  bacteria,  as  we  have  said,  can  develop  much  better  here 
than  if  the  bladder  were  to  a  certain  degree  constantly  purified  and  washed  out 
by  the  urine  'that  is  always  coming  afresh.  As  soon  as  a  part  of  the  urea  is 
changed  to  carbonate  of  ammonia,  the  acid  reaction  of  the  urine  must  be  less. 
The  urine  has  a  faintly  acid  or  neutral  reaction,  and  sometimes  it  is  even  already 
decidedly  alkaline  when  passed.  The  latter,  however,  is  only  rarely  the  case,  but 
it  is  often  simulated  by  the  fact  that  the  urine  is  not  examined  until  it  has  stood 
for  some  time.  Since  during  this  time  the  alkaline  fermentation  which  has  once 
begun  makes  rapid  progress,  the  cystitic  urine  that  has  stood  is  very  often  alkaline. 
Many  crystals  of  ammonio-magnesic  phosphate  and  urate  of  ammonia  then  form 
in  it;  the  former  are  easily  recognized  by  their  "coffin-lid  shape,"  and  the  latter 
by  their  "  thorn-apple  shape  "  (see  Fig.  116) . 

If  we  then  briefly  put  together  what  has  been  said,  the  urine  is  passed  in  about 
the  normal  amount  in  cystitis.     It  usually  looks  clear,  and  has  an  abundant  sedi- 


CYSTITIS. 


895 


Fig.  116. —Crystals  of  triple  phosphate  and  am 
monic  urate.     (From  Funke.) 


ment,  which  can  often  be  recognized  as  purulent  with  the  naked  eye,  and  in 
which,  microscopically,  we  can  find  pus-corpuscles,  often  bladder  epithelium,  and 
constantly  innumerable  bacteria — usually  short  rods  in  vigorous  motion.  The 
alkaline  fermentation  may  usually  be  recognized  by  the  strong  ammoniacal  odor, 

and  also,  as  we  have  said,  by  the  reaction 
of  the  urine.  In  the  severe  diphtheritic 
forms  of  cystitis  we  find  entire  shreds  of 
necrotic  tissue  in  the  urine.  If  there  are 
haemorrhages  in  the  bladder,  the  urine 
often  contains  red  blood-corpuscles  and 
sometimes  even  large  blood-clots.  The 
mucus  in  the  urine  appears  in  milder  cases 
as  a  cloudy  opacity — "nubecula."  The 
viscid  masses  which  can  be  drawn  out  into 
threads,  and  which  are  usually  abundant 
in  the  urine  in  severe  cystitis,  are  not  the 
special  product  of  the  mucous  membrane, 
mucine,  but  they  arise  from  the  pus-cor- 
puscles and  the  epithelium  dissolved  in 
the  alkaline  urine,  and  hence  give  the 
reactions  for  albumen.  It  goes  without 
saying  (compare  page  824)  that  every 
cystitic  urine  is  albuminous  from  its  mix- 
ture with  pus-serum.  The  presence  of  slimy  threads  in  the  urine — the  so-called 
"clap-threads"  (Tripperfäden) — is  characteristic  of  gonorrhceal  cystitis. 

There  can  be  no  doubt  that  the  decomposing  alkaline  urine  acts  as  a  chemical 
excitant  of  inflammation  on  the  vesical  mucous  membrane.  Hence  cystitis  often 
arises  perhaps  in  this  way,  that  the  bacteria  which  have  entered  the  bladder  first 
excite  only  an  alkaline  fermentation,  and  that  then  the  mucous  membrane  is 
affected  by  the  irritation  of  the  ammonia  salts  that  are  formed.  It  is,  however, 
at  present  hard  to  decide,  and  it  is  also  without  special  practical  interest,  whether 
the  bacteria  as  such  can  not  directly  excite  inflammation. 

The  other  morbid  symptoms  associated  with  cystitis  usually  depend  only  in 
part  upon  the  disease  itself  and  in  part  upon  some  existing  primary  disease.  The 
most  important  symptom  is  the  fever,  which  is  often  to  be  referred  directly  to  the 
cystitis.  In  severer  cases  it  may  be  very  intense,  and  often  assumes  a  pyaemic 
intermittent  character,  especially  if  there  have  arisen  pericystitic  suppurations  or 
if  the  cystitis  has  extended  to  the  pelvis  of  the  kidney  and  the  kidneys  (see  page 
881).  An  acute  cystitis  may  also  begin  with  a  chill  and  high  fever.  If  the  escape 
of  the  purulent  urine,  however,  always  remains  undisturbed,  the  fever  may  be 
entirely  absent  in  spite  of  the  existence  of  cystitis. 

Sometimes  in  severe  cystitis  with  a  marked  alkaline  fermentation  certain  nerv- 
ous symptoms  appear,  such  as  headache,  vertigo,  stupor,  and  nausea.  The  idea  has 
been  advanced  that  in  these  cases  we  have  to  do  with  an  auto-intoxication  of  the 
body,  since  ammonia  and  perhaps  other  products  of  decomposition,  like  sulphu- 
retted hydrogen  (?),  are  absorbed  from  the  bladder  into  the  blood  (ammonia3mia), 
and  in  this  way  excite  the  symptoms  of  poisoning  mentioned. 

According  to  the  course  of  the  disease  we  distinguish  an  acute  and  a  chronic 
cystitis.  The  former,  which  may  come  on,  for  example,  after  catheterization,  in 
gonorrhoea,  etc.,  often  passes  off  favorably  after  a  few  days.  The  amount  of 
mucus  and  pus  in  the  urine  remains  slight.  Chronic  cystitis  is  observed  especially 
as  a  complication  in  other  diseases  of  the  urinary  tract,  like  stricture,  in  chronic 
diseases  of  the  spinal  cord  with  paralysis  of  the  bladder,  etc.     It  is  very  ofteu 


896  DISEASES  OF  THE  KIDNEYS. 

incurable  because  the  primary  disease  is  incapable  of  improvement  and  the  cause 
of  the  disease  therefore  persists.  The  longer  a  cystitis  lasts,  the  nearer  is  the 
possibility  of  the  development  of  more  severe  and  dangerous  complications,  espe- 
cially the  development  of  a  pyelo-nephritis,  and  the  formation  of  pericystitic  sup- 
purations. In  this  way  cystitis,  especially  in  chronic  nervous  diseases,  may  become 
the  immediate  cause  of  death. 

Treatment. — The  dangers  last  mentioned  must  urgently  impress  upon  us  the 
prophylaxis  of  cystitis.  Fortunately,  a  good  deal  can  be  done  in  this  respect,  in 
the  first  place,  by  the  avoidance  of  all  unnecessary  use  of  bougies  and  catheters, 
by  the  greatest  care  for  cleanliness  in  tbe  use  of  all  instruments  of  this  sort,  and 
by  the  timely  treatment  of  all  those  conditions  which  may  lead  to  cystitis. 

The  treatment  of  cystitis  is,  in  the  milder  and  acute  cases,  hygienic  and  medi- 
cinal, but  in  the  severer  cases  only  a  careful  local  treatment  can  be  useful. 

In  any  severe,  and  especially  in  any  acute  cystitis,  the  greatest  bodily  rest  (if 
possible  rest  in  bed)  is  urgently  desirable,  since  otherwise  an  increase  of  the  symp- 
toms and  a  prolongation  of  the  course  of  the  disease  is  the  almost  inevitable 
result.  The  diet  must  be  mild  and  unirritating.  Spiced  food  and  alcoholic  drinks 
are  to  be  avoided,  but  we  should  recommend  an  abundant  supply  of  fluid,  by 
which  the  urine  is  diluted  and  the  bladder  washed  out.  We  have  the  patient 
drink  plenty  of  ordinary  water,  tea,  or  a  suitable  mineral-water,  like  Wildunger, 
Selters,  or  Fachinger.  A  diet  mainly  of  milk  is  very  good;  by  it  the  cystitic 
symptoms  often  very  rapidly  cease. 

Among  internal  remedies  those  are  to  be  considered  which  are  eliminated  with 
the  urine,  and  are  thus  able  to  act  on  the  diseased  mucous  membrane,  or  directly 
upon  the  agents  of  inflammation.  One  of  the  most  efficient  drugs,  which  never 
does  harm  with  necessary  caution,  is  chlorate  of  potassium,  of  whose  favorable 
influence  on  vesical  catarrh  we  have  often  convinced  ourselves.  It  is  prescribed 
in  an  aqueous  solution,  forty  to  seventy-five  grains  a  day  (grm.  3-5),  and 
should  never  be  taken  on  an  empty  stomach.  Salicylic  acid  is  sometimes  used 
with  good  results  in  doses  of  half  a  drachm  to  a  drachm  (grm.  2-4)  a  day  in 
ten-grain  (grm.  0"5)  capsules.  The  two  remedies  mentioned  have  largely  replaced 
tannin,  which  was  formerly  in  great  favor.  At  present  a  decoction  of  uva  ursi  is 
still  more  frequently  prescribed,  10  or  15  to  150,  whose  active  principle,  arbutine, 
in  doses  of  forty-five  to  sixty  grains  a  day  (grm.  3-4)  in  an  aqueous  solution, 
seems  worthy  of  further  trial  (Lewin  and  others).  In  more  advanced  stages  of 
vesical  catarrh,  if  the  initial  symptoms  of  irritation  have  ceased,  the  resinous 
drugs  are  to  be  used,  of  which  oil  of  turpentine  and  balsam  of  copaiba  especially 
sometimes  show  a  very  good  action.     Both  are  best  given  in  gelatine  capsules. 

If  there  are  severe  local  symptoms,  we  prescribe  warm  compresses  and  poul- 
tices to  the  region  of  the  bladder.  In  robust  persons  with  acute  cystitis,  local 
blood-letting,  three  to  six  leeches  to  the  perineum,  sometimes  has  a  decidedly 
favorable  symptomatic  action  in  such  a  case.  In  other  respects  narcotics,  especially 
.  subcutaneous  injections  of  morphine,  are  the  best  remedy  where  there  is  severe 
pain  and  tenesmus.  Camphor,  extract  of  belladonna,  etc.,  are  much  more  uncer- 
tain in  their  action.  The  frequent  use  of  protracted  warm  baths  may,  however, 
be  greatly  recommended. 

In  chronic  cystitis  all  the  remedies  previously  mentioned  are  also  to  be  con- 
sidered ;  but  they  are  usually  not  sufficient  alone,  and  at  any  rate  they  are  far  less 
effective  than  a  methodical  local  treatment.  This  consists  in  washing  out  the 
bladder  regularly  every  day  by  the  aid  of  an  elastic  catheter,  to  which  a  T-tube  is 
fastened  by  means  of  rubber  tubing,  one  arm  being  connected  with  an  irrigator 
and  the  other  with  the  escape-tube.  We  thus  let  a  moderate  amount  of  fluid, 
eight  or  ten  ounces  (200-300  c.  c),  run  into  the  bladder  and  run  out  again,  fre- 


NEW  GROWTHS  IN  THE  BLADDER  897 

quently  repeating  the  process,  until  it  comes  away  perfectly  clear.  For  this  pur- 
pose we  use  either  pure  warm  water,  or,  better,  a  dilute  solution  of  plumbic 
acetate  (1  to  1000),  permanganate  of  potassium  (1  to  1000),  boric  and  salicylic  water, 
and  the  like.  By  such  a  treatment  many  cases  of  chronic  vesical  catarrh  may 
recover,  and  others  may  at  least  be  kept  constantly  in  check. 

Attention  to  the  causal  indication  is  sometimes  very  important  also  in  chronic 
vesical  catarrh — for  example,  the  treatment  of  any  strictures,  the  removal  of  cal- 
culi, or  the  improvement  of  paralytic  states  of  the  bladder. 

In  pericystitic  suppuration  surgical  treatment  is  only  rarely  possible.  We 
must,  therefore,  confine  ourselves  to  purely  symptomatic  procedures. 


CHAPTER  VI. 
NEW   GROWTHS  IN   THE   BLADDER. 

Primary  new  growths  in  the  bladder  are  quite  rare.  The  commonest  is  the 
so-called  villous  cancer  (which  is  properly  a  papillary  fibroma),  which  may  attain 
the  size  of  a  walnut,  and  is  usually  situated  in  the  lower  portion  of  the  bladder 
near  the  entrance  of  the  urethra.  Since  the  tumor  is  usually  very  vascular,  there 
are  often  haemorrhages  into  the  bladder,  and  repeated  haematuria  is  therefore  one 
of  the  commonest  symptoms  of  vesical  papilloma.  In  this  affection  the  blood- 
clots  often  assume  a  peculiar  long,  worm-like  shape,  from  their  passage  through  the 
urethra.  Severe  symptoms  on  micturition  sometimes  appear,  since  portions  of 
the  tumor  may  lie  in  front  of  the  opening  of  the  urethra.  A  definite  diagnosis  of 
a  villous  tumor  is  possible  only  when  single  portions  of  the  tumor  are  thrown  off, 
and  are  found  in  the  urine  passed.  Examination  of  the  bladder  by  the  catheter 
may  also  give  information  as  to  the  presence  and  seat  of  the  tumor. 

Primary  carcinoma  of  the  bladder  is  rare.  It  is  usually  spread  diffusely  over 
the  wall  of  the  bladder,  and  leads  to  so  considerable  a  thickening  of  it  that  we  can 
often  feel  the  bladder  from  without  through  the  abdominal  walls.  Otherwise  the 
symptoms  are  the  same  as  in  severe  chronic  cystitis.  The  urine  contains  much 
pus,  and  is  sometimes  bloody.  The  general  cancerous  cachexia  developed  rather 
late  in  the  cases  which  we  have  seen,  of  which  one  was  in  a  man  still  quite  young. 
The  diagnosis  is  not  always  easy.  Except  from  attention  to  the  general  course  of 
the  disease  and  any  vesical  tumor  that  may  be  felt,  it  must  aim  to  be  based  chiefly 
upon  the  discovery  of  particles  of  cancer  in  the  urine. 

A  secondary  invasion  of  the  bladder  by  carcinomatous  new  growths  from  the 
uterus,  rectum,  and  vagina  is  quite  frequently  observed. 

The  treatment  can  usually  be  only  symptomatic,  since  surgical  procedures  are 
possible  only  in  rare  cases. 


57 


898  DISEASES  OF  THE  KIDNEYS. 


CHAPTEE  VII. 

ENURESIS   NOCTURNA. 

{Nocturnal  incontinence  of  Urine.) 

Enuresis  nocturna  is  a  nervous  affection  of  the  bladder  by  no  means  rare  in 
children  of  both  sexes,  and  therefore  quite  important  in  its  practical  relations. 
Of  course,  in  small  children  there  is  no  sharp  boundary  to  be  drawn  between 
normal  and  pathological  conditions ;  but  it  is  decidedly  pathological  if  larger  chil- 
dren, from  four  to  ten  years  of  age  and  even  older,  pass  their  urine  in  bed  more 
or  less  frequently  during  sleep,  in  spite  of  ■well-developed  reasoning  powers  and 
professedly  the  best  intentions.  This  anomaly  may  extend  to  the  years  of  puberty 
and  even  beyond  it,  and  then  it  frequently  produces  a  very  depressing  mental 
affection  for  the  patient.  Special  causes  for  it  are  not  to  be  discovered  in  most 
cases.  We  are  compelled  to  assume  either  an  abnormal  weakness  of  the  sphincter, 
which  is  probably  sometimes  congenital,  or  an  abnormal  irritability  of  the  detru- 
sor. At  any  rate,  in  wetting  the  bed  at  night  the  process  of  micturition  comes  on 
in  a  purely  reflex  way,  but  it  is  often  accompanied  by  certain  ideas  in  dreams 
referable  to  micturition.  It  does  not  hold  in  all  cases  that  the  sleep  is  especially 
deep.  Many  patients,  of  course,  first  notice  the  trouble  in  the  morning,  but  others 
almost  always  wake  directly  after.  The  involuntary  micturition  usually  occurs 
in  the  first  hours  after  going  to  sleep,  but  sometimes  it  is  later,  and  even  first 
toward  morning.  By  day  micturition  is  often  perfectly  normal  ;  but  in  many 
cases  there  is  even  then  a  noticeable  weakness  of  the  bladder,  so  that  the  child  has 
to  make  water  offener  than  usual,  and  sometimes  wets  its  clothes  even  by  day. 

Although,  as  we  have  said,  we  can  usually  find  no  special  cause  for  the  trouble, 
still,  in  some  cases,  certain  morbid  changes  in  the  urinary  organs  may  give  rise  to 
the  incontinence.  We  should,  therefore,  in  every  case  at  least  think  of  the  pos- 
sibility of  stone  in  the  bladder,  of  congenital  phimosis  and  adhesions  of  the  pre- 
puce to  the  glans  penis,  of  ascarides,  and  of  inflammatory  conditions,  and  make  a 
special  examination  of  these  points.  We  must  also  bear  in  mind  polyuria  caused 
by  diabetes  or  renal  disease,  and  finally,  of  course,  in  the  diagnosis  of  a  purely 
nervous  nocturnal  incontinence  of  urine,  we  must  exclude  the  existence  of  any 
actual  anatomical  spinal  affection. 

In  all  the  cases  just  mentioned,  the  treatment  must  of  course  refer  first  to  the 
primary  disease  ;  but  in  the  ordinary  nocturnal  incontinence  the  treatment  must 
first  take  into  consideration  the  prevention  of  the  appearance  of  nocturnal  mic- 
turition as  far  as  possible.  The  child  must  take  only  a  very  little  fluid  in  the 
evening,  and  he  should  be  made  to  empty  his  bladder  immediately  before  going 
to  sleep,  and  once  again  later.  He  should  not  be  covered  up  too  warmly,  and,  if 
possible,  he  should  not  lie  on  his  back  during  sleep.  Tying  a  brush  to  the  back  is 
therefore  a  well-known  domestic  remedy.  A  somewhat  strict  mental  treatment  is 
often  effective,  since  thus  the  attention  to  the  process  is  increased,  although  uncon- 
sciously, and  the  child  often  learns  to  wake  up  at  the  right  time.  The  use  of  the 
rod  is  of  course  on  the  whole  only  rarely  admissible.  On  the  contrary,  we  often 
have  to  protect  the  child  against  unreasoning  parents. 

Internal  remedies,  especially  belladonna  and  tincture  of  nux  vomica,  which 
were  formerly  recommended,  rarely  avail.  Iron  preparations  are  indicated  only 
in  anaemic  children.  Electrical  treatment,  however,  is  often,  if  not  always,  very 
effective.  We  put  the  broad  anode  over  the  lumbar  cord,  and  the  smaller 
kathode  over  the  region  of  the  bladder  or  on  the  perineum,  and  let  quite  a  strong 
constant  current  pass  through  for  two  or  three  minutes.     Then  we  pass  the  wire 


ENURESIS  NOCTURNA.  899 

end  of  a  conducting  cord,  which  we  make  the  kathode,  into  the  mouth  of  the 
urethra  for  one  or  two  centimetres,  and  let  quite  a  strong  and  somewhat  painful 
faradic  current  act  for  one  or  two  minutes  (Seeligmüller).  The  sittings  must  at 
first  be  repeated  daily.  It  is  also  a  very  good  plan  to  let  the  whole  body  be  well 
rubbed  with  cold  water  before  going  to  sleep. 

The  prognosis  of  these  forms  of  incontinence,  which  have  no  organic  disease 
at  the  bottom  of  them,  is  almost  always  favorable,  since  in  the  worst  case  the 
anomalous  condition  usually  disappears  gradually  of  itself  with  increasing  years. 

[Belladonna,  strychnia  or  nux  vomica,  or  a  combination  of  the  two,  are  often 
of  unquestionable  service.  If  the  enuresis  is  only  nocturnal,  belladonna  alone 
may  be  used,  either  in  a  single  dose  at  bedtime  or  three  times  a  day.  If  the 
enuresis  is  diurnal  also,  the  two  drugs  should  be  combined  and  given  three  or 
four  times  a  day.] 


DISEASES   OF   THE  ORGANS  OF  LOCOMOTION. 


CHAPTER  I. 
ACUTE   ARTICULAR   RHEUMATISM. 

./Etiology. — Acute  articular  rheumatism  is  an  infectious  disease.  This  is  shown 
by  all  the  clinical  and  anatomical  peculiarities  of  the  disease ;  and,  although  the 
specific  organic  pathogenetic  poison  can  not  yet  he  demonstrated,  still  this  view  of 
the  disease,  which  was  first  brought  forward  by  Hüter,  is  the  only  one  which  ena- 
bles us  properly  to  understand  its  symptoms  and  course. 

Like  many  other  infectious  diseases,  acute  articular  rheumatism  is  often  indis- 
putably endemic  and  epidemic.  According  to  Hirsch,  the  disease  is  most  preva- 
lent in  the  temperate  zones,  being  much  rarer  in  cold  and  tropical  latitudes ;  but 
even  in  Europe  it  is  by  no  means  uniform  in  its  frequency,  and  certain  districts  of 
England,  Belgium,  and  Russia  are  said  to  be  almost  exempt  from  it.  It  is  also 
possible  to  observe  epidemic  influences  with  regard  to  the  frequency  of  its  appear- 
ance, as  already  intimated.  Here  in  Leipsic,  where  articular  rheumatism  is  one 
of  the  most  frequent  of  acute  diseases,  we  have  observed  for  years  that  at  certain 
times  there  are  only  a  few  cases,  while  at  others  there  is  a  striking  increase  in 
their  number.  Usually  attacks  are  most  prevalent  in  the  winter  and  spring 
months,  but  again  it  is  sometimes  in  summer  that  the  disease  is  especially 
common. 

Among  the  exciting  causes  of  the  disease,  taking  cold  is  always  mentioned  as 
of  first  importance ;  and  in  fact  it  can  not  be  denied  that  the  influence  of  cold  does 
often  seem  to  contribute  to  the  occurrence  of  the  disease. 

This  result,  however,  seldom  follows  a  single  severe  exposure,  but  it  rather 
follows  persistent  causes,  and  in  particular  the  long-continued  influence  of  wet 
and  cold,  as  in  certain  occupations— for  example,  washing  and  scrubbing,  or  inhab- 
iting unhealthy  damp  dwellings,  and  the  like.  This  explains  why  those  who  follow 
certain  callings  are  especially  subject  to  articular  rheumatism ;  thus  servant-girls 
and  coachmen  are  frequently  victims  to  the  disease.  And  yet  it  is  possible  to 
regard  all  these  injurious  influences  as  being  merely  indirect  causes,  inasmuch  as 
they  favor  the  development  or  action  of  the  specific  micro-organisms ;  and,  further- 
moi*e,  it  is  by  no  means  exceptional  to  see  a  case  of  articular  rheumatism  where 
no  histoiw  pf  exposure  to  cold  can  be  obtained. 

Sex  exerts  no  special  influence  upon  the  frequency  of  the  disease.  As  to  age, 
acute  articular  rheumatism  is  most  frequent  in  young  adults  between  fifteen  and 
thirty-five  years  of  age.  In  later  life,  and  particularly  in  old  age,  it  is  much 
rarer.  In  children  six  years  old  or  more  the  disease  is  not  especially  infrequent, 
but  in  younger  chikhen  it  occurs  only  exceptionally.  We  may  be  permitted  to 
mention  a  single  interesting  case  which  we  met  with  here  in  Leipsic,  where  a 
child  who  died  when  only  a  few  days  old,  and  whose  mother  at  the  time  of  its 


ACUTE  AETICÜLAR  RHEUMATISM.  <>0l 

birth  was  suffering1  from,  a  severe  attack  of  acute  articular  rheumatism,  was  found 
to  have  multiple  purulent  arthritis. 

Much  has  been  said  with  regard  to  the  relations  of  acute  articular  rheumatism 
to  other  acute  diseases.  We  must,  therefore,  call  particular  attention  to  the  fact 
that  the  joint  diseases,  whether  simple  or  multiple,  which  occur  after  scarlet  fever, 
gonorrhoea,  or  in  connection  with  puerperal  and  septic  diseases,  us  well  us  recent 
cases  of  secondary  syphilis,  have  nothing  to  do  with  genuine  acute  rheumatism. 
In  cases  of  this  sort  the  trouble  in  the  joints  is  merely  a  special  localization  of  the 
general  disease;  and,  indeed,  the  circumstance  that  the  joints  are  a  favorite  point 
of  attack  for  infectious  diseases  may  be  brought  forward  as  another  proof  that 
acute  articular  rheumatism  is  of  infectious  origin.  There  is,  however,  a  single 
affection,  namely,  chronic  endocarditis,  about  which  the  facts  are  different.  This 
disease  is  serologically  identical  with  acute  endocarditis,  and  therefore  with  acute 
rheumatism  (vide  infra).  At  least  this  is  true  in  many  cases,  although  probably 
not  in  all.  It  may  be  regarded  as  a  proof  of  this  connection  between  the  two  dis- 
eases that  patients  with  chronic  cardiac  disease  are  especially  liable  to  attacks  of 
acute  articular  rheumatism.  Here,  therefore,  we  have  a  genuine  articular  rheu- 
matism as  a  symptom  of  more  general  disease.  It  may  be  regarded  in  some  sense 
as  a  fresh  acute  exacerbation  of  this  disease,  localized  mainly  in  the  joints. 

A  very  noteworthy  fact  is  that  acute  articular  rheumatism  can  not  be  num- 
bered among  those  infectious  diseases  which  usually  occur  but  once  in  the  same 
individual.  This  disease,  on  the  contrary,  resembles  pneumonia  and  erysipelas,  in 
that  it  is  very  apt  to  occur  repeatedly  in  the  same  person.  Acute  rheumatism, 
therefore,  even  when  it  ends  favorably  and  leaves  behind  it  no  evident  lesions, 
seems  to  render  the  patient  more  liable  to  the  disease  than  he  was  before. 

Symptomatology. — The  chief  symptom  of  acute  articular  rheumatism  is  an  acute 
febrile  synovitis,  which  almost  always  affects  several  joints.  The  synovitis  is 
associated  with  the  usual  local  phenomena  of  swelling  and  tenderness  in  the  parts 
affected.  Often  this  articular  affection  is  the  first  symptom,  and,  indeed,  it  may 
be  the  only  symptom  of  the  disease.  It  is,  however,  by  no  means  exceptional  for 
the  arthritic  trouble  to  be  preceded  by  certain  prodromal  or  initiatory  symptoms, 
as  is  true  of  other  infectious  diseases.  These  prodromata  consist  either  of  a  slight 
general  malaise,  or  of  certain  local  symptoms.  It  is  not  rare  to  have  sore  throat, 
or,  as  we  have  repeatedly  had  opportunity  to  observe,  laryngitis.  These  pre- 
monitory symptoms  are,  however,  generally  insignificant,  and  may,  as  we  have 
said,  be  entirely  absent. 

The  articular  disturbance  is  almost  always  very  rapid  in  its  development. 
Some  of  the  larger  joints  are  usually  first  affected,  and  perhaps  those  of  the  lower 
extremities  somewhat  offener  than  those  of  the  upper.  It  is  extremely  exceptional 
for  all  the  joints  that  are  affected  to  be  attacked  at  one  and  the  same  time.  It  is 
somewhat  characteristic  of  acute  articular  rheumatism  that  it  "  jumps  from  one 
joint  to  another."  To-day  this  joint  will  be  affected  and  to-morrow  that,  while  the 
joint  first  attacked  may  still  remain  diseased  or  undergo  rapid  recovery.  Thus, 
there  may  be  either  a  few  joints  affected  or  many,  in  varying  sequence,  and  they 
may  sometimes  be  affected  rapidly  and  at  other  times  more  slowly.  In  many 
of  the  milder  cases  the  disease  is  an  extremely  temporary  one,  while  in  others  it 
may  attach  itself  most  persistently  to  some  one  or  more  joints. 

There  is  usually  fever  in  addition  to  the  arthritis ;  but  it  is  not  usually  very 
high,  seldom  exceeding  103°  (39*5°  C).  The  fever,  on  the  whole,  corresponds  with 
the  arthritic  phenomena,  and  does  not  present  a  curve  which  is  at  all  typical,  but 
one  which  is  irregularly  remittent.  We  have  scarcely  ever  seen  the  disease  begin 
with  an  initial  rigor,  nor  are  the  so-called  "  genei'al  febrile  symptoms  "  of  headache, 
stupor,  and  subjective  feeling  of  heat  as  a  rule  at  all  marked  in  acute  rheumatism. 


902  DISEASES  OF  THE  ORGANS  OF  LOCOMOTION. 

This  indicates  that  the  constitutional  infection  does  not  as  a  rule  attain  great 
severity.  The  skin  is  noticeably  inclined  to  perspiration,  but  the  perspiration  is 
not  at  all  a  result  of  any  sudden  fall  in  temperature  such  as  is  seen  in  other  dis- 
eases. 

The  course  of  the  disease  is  marked  by  alternate  ameliorations  and  aggrava- 
tions of  the.  local  symptoms  and  of  the  fever,  and  lasts,  particularly  if  it  is  not 
treated,  one  or  more  weeks,  or  a  still  longer  period.  Then,  as  a  rule,  the  symp- 
toms gradually  abate  and  convalescence  begins ;  but  it  generally  is  tedious  and 
frequently  interrupted  by  relapses.  In  other  cases,  however,  the  disease  contrasts 
strongly  with  this  simple  course,  for  articular  rheumatism  is  notoriously  subject 
to  numerous  complications  and  peculiarities  in  its  course.  The  protean  character 
of  the  disease  will  be  evident  upon  a  perusal  of  the  following  description  of  the 
symptoms  referable  to  the  different  organs  of  the  body. 

Symptoms  referable  to  the  Different  Organs,  and  Peculiarities  in  the  Course  of 
the  Disease.  1.  Joints  and  Sheaths  of  the  Tendons. — The  favorable  termination 
of  most  cases  of  acute  articular  rheumatism  prevents  us  from  often  examining  the 
anatomical  changes  in  the  affected  joints;  but  there  can  be  no  doubt  that  in  most 
instances  the  trouble  is  merely  a  simple  serous  synovitis — that  is,  an  inflammation 
of  the  synovial  membrane,  with  an  exudation  into  the  cavity  of  the  joint  composed 
mainly  of  serum  with  but  little  admixture  of  fibrine  and  pus.  The  synovial  mem- 
brane itself,  in  the  cases  which  do  come  to  autopsy,  is  usually  very  little  affected. 
It  is  somewhat  injected,  opaque,  and  thickened.  Necrosis  of  the  cartilages  is  seen 
only  in  severe  cases,  or  in  those  which  have  lasted  a  rather  long  while.  From  a 
clinical  standpoint,  the  articular  disturbance  is  noticeable  chiefly  for  the  pain 
which  it  causes  the  patient  upon  every  movement  of  the  joint  and  any  pressure 
upon  it.  The  painfulness  is  often  in  striking  contrast  with  the  slight  apparent 
change  in  the  structure  of  the  joint,  for  a  joint  which  is  extremely  sensitive  may 
appear  to  be  scarcely  at  all  diseased.  Usually,  however,  the  joints  exhibit  the 
signs  of  synovitis.  The  effusion  into  the  joint  produces  an  evident  swelling, 
which  can  be  seen  particularly  well  in  the  knees,  but  also  in  the  joints  of  the 
ankle,  wrist,  shoulder,  and  elbow,  and  sometimes  even  in  the  smaller  joints  of  the 
fingers  and  toes,  particularly  the  great  toe.  It  is  rather  exceptional  to  detect  swell- 
ing of  the  hip-joint.  It  should  be  remembered,  however,  that  the  swelling  in  the 
region  of  the  joint,  particularly  the  ankle  or  wrist,  is  often  less  the  result  of  a 
synovial  effusion  than  of  an  inflammatory  periarticular  oedema.  This  oedema, 
for  example,  may  extend  over  almost  the  whole  posterior  surface  of  the  hand. 
The  joints  are  by  no  means  invariably  the  only  parts  attacked.  Not  infrequently 
there  are  analogous  inflammatory  changes  visible  in  the  sheaths  of  the  tendons, 
the  bursse,  and  perhaps,  in  many  cases,  even  the  fascias  and  muscles.  The  skin 
over  the  affected  joints  often  has  an  inflammatory  blush,  which  is  usually  pale 
red  and  spotted,  and  can  be  best  seen  at  the  ankle,  knee,  and  wrist.  It  has  been 
maintained  that  the  cutaneous  sensibility  is  diminished  over  the  joints  affected, 
but  we  regard  this  as  a  mistake. 

As  might  be  expected,  the  number  of  joints  attacked  and  the  sequence  in  which 
they  are  attacked  differ  greatly  in  different  cases ;  but  almost  invariably  a  number 
of  joints  suffer,  so  that  any  monarticular  arthritis  should  not  be  regarded  as  rheu- 
matic except  after  careful  deliberation  (vide  infra,  diagnosis).  It  should  be  said 
that,  in  mild  cases,  there  may  be  only  two  or  three  joints  affected,  these  being 
usually  some  of  the  larger  joints  of  the  extremities ;  and  of  these,  one  may  be  so 
much  worse  than  the  others  that  their  participation  in  the  trouble  can  be  ascer- 
tained only  by  careful  questioning  and  examination.  In  severe  cases,  on  the  other 
hand,  the  number  of  joints  attacked  is  often  very  great.  Such  patients  become 
extremely  helpless,  because  any  movement  is  possible,  if  at  all,  only  under  the 


ACUTE  ARTICULAR  RHEUMATISM.  903 

penalty  of  very  severe  suffering.  The  patient  usually  lies  with  hended  knees  and 
feet  curved  so  as  to  be  concave  on  the  plantar  surface,  and  screams  with  pain  at 
any  attempt  to  change  his  position.  The  joints  of  the  trunk  sometimes  participate 
in  the  disease,  but  hardly  ever  except  in  the  severe  cases.  The  articulations  of  the 
vertebrae,  the  ster no-clavicular  joint,  the  articulation  of  the  lower  jaw,  and  the 
symphysis  pubis,  are  particularly  apt  to  be  affected.  The  fugitive  character  of 
the  arthritis  has  been  spoken  of  as  characteristic  of  acute  articular  rheumatism, 
and,  indeed,  it  is  not  infrequently  the  case  that  comparatively  large  swellings  of 
the  joints  soon  abate  and  yield  to  new  disturbances  in  other  joints ;  but,  on  the 
other  hand,  the  disease  may  persist  very  obstinately  in  a  single  joint.  In  this  case 
one  joint,  or  rarely  several,  are  attacked  with  marked  severity,  either  from  the 
start  or  subsequently  to  milder  affections  of  other  joints,  and  often  remain  for 
weeks  swollen  or  painful  long  after  all  other  symptoms  have  vanished. 

2.  Cardiac  Symptoms.  — The  condition  of  the  heart  in  acute  articular  rheuma- 
tism is  next  in  importance  to  that  of  the  joints.  The  physician  should  therefore, 
in  every  case,  even  the  mildest,  maintain  a  continuous  watch  over  this  organ.  In 
1336  Bouillaud  made  careful  auscultatory  investigations  in  this  disease,  and  was 
thus  the  first  to  discover  that  the  course  of  acute  articular  rheumatism  is,  with 
noticeable  frequency,  accompanied  by  endocarditis,  and  sometimes  even  by  peri- 
carditis. Complications  of  this  sort  may  occur  in  any  case,  whether  mild  or  severe, 
or  may  be  absent  in  any  case,  even  the  worst.  They  may  develop  at  the  beginning 
or  later  on  in  the  course  of  the  disease.  Their  development  is  often  unattended 
by  any  subjective  symptoms,  so  that  they  can  be  recognized  only  by  careful  phys- 
ical examination.  In  many  cases,  however,  the  onset  of  cardiac  disease  is  marked 
by  a  fresh  exacerbation  of  the  fever,  or  possibly  by  palpitation,  or  by  painful  sen- 
sations in  the  prsecordia,  or  by  dyspnoea. 

We  will  consider  first  rheumatic  endocarditis.  This  is  almost  always  the  benign 
verrucous  variety  (see  page  278). 

It  is  far  more  prone  to  attack  the  mitral  than  the  aortic  valves,  and  is  accord- 
ingly usually  betrayed  by  a  blowing  systolic  murmur  at  the  heart's  apex.  Uncer- 
tainty may  be  cast  upon  the  diagnosis  by  the  fact  that  functional  murmurs  are 
not  very  infrequent  at  the  apex  of  the  heart  in  cases  of  acute  articular  rheuma- 
tism. "We  once  observed  a  case  of  "  hyperpyretic  rheumatism  "  (vide  infra)  where 
there  was  an  evident  murmur  of  this  sort  during  life,  and  yet  at  the  autopsy  we 
were  able  to  assure  ourselves  of  the  complete  integrity  of  the  cardiac  valves. 
Even  an  expert  may  for  a  time  be  in  doubt  as  to  the  significance  of  many  cardiac 
murmurs,  and  this  explains  in  part  the  conflicting  statements  as  to  the  frequency 
of  cardiac  complications  in  acute  rheumatism.  In  general,  one  may  say  that  such 
complications  occur  in  25  to  33  per  cent,  of  the  cases.  The  ultimate  results  of  this 
endocarditis  we  do  not  need  to  describe  over  again  in  this  connection  (see  the  chap- 
ters on  acute  and  chronic  endocarditis) .  Complete  recovery  is  possible.  Often,  how- 
ever, the  lesion  gives  rise  to  a  chronic  endocarditis — that  is,  to  a  cardiac  valvular 
disease,  which  lasts  through  life. 

The  close  connection  between  endocarditis  and  the  arthritis  must  formerly 
have  seemed  very  puzzling,  despite  the  many  hypotheses  made  to  explain  it.  If, 
however,  we  regard  acute  articular  rheumatism  as  an  infectious  disease,  this 
obscurity  vanishes.  Acute  articular  rheumatism  is  plainly  not  a  merely  local 
disease,  but  the  result  of  a  general  infection.  The  specific  pathogenetic  matter  is 
not  only  present  in  the  joints  affected,  but  it  also  circulates  in  the  blood.  It  is  there- 
fore easy  to  understand  why  the  valves  of  the  heart  should  be  attacked  by  it.  as  is 
the  case  in  so  many  infectious  diseases  (see  page  276).  Often  the  specific  properties 
of  the  micro-organisms  in  question  produce  a  typical  endocarditis.  The  endocar- 
ditis, therefore,  is  not  strictly  a  "  complication,"  but  a  symptom  of  the  disease. 


904  DISEASES  OF  THE  ORGANS  OF  LOCOMOTION. 

Rheumatic  pericarditis  is  not  infrequent,  although  less  common  than  endocar- 
ditis. The  only  certain  way  to  recognize  it  is  by  a  characteristic  friction-sound  ; 
and  even  when  this  is  heard  there  may  be  a  doubt  as  to  its  significance,  inasmuch 
as  functional  murmurs  are  not  infrequently  heard  at  the  base  of  the  heart.  The 
pericarditis  is  of  a  sero-fibrinous  nature.  Sometimes  it  is  of  slight  severity  ;  but  it 
may  be  extremely  severe,  with  a  large  effusion  and  the  most  urgent  dyspnoea 
(see  page  323).  In. rare  instances  this  pericarditis  proves  fatal.  Usually,  however, 
recovery  ensues,  although  in  severe  cases  there  may  be  obliteration  of  the  peri- 
cardial sac,  with  the  consequences  described  on  page  326. 

With  regard  to  the  origin  of  the  pericarditis,  it  may  be  said  that  it  would  not 
be  impossible  for  the  pericardium  to  be  directly  infected  by  the  blood.  We  have 
reason,  however,  to  believe  that  in  most  cases  the  infection  proceeds  from  the 
endocardium,  and  probably  in  the  great  majority  of  cases  from  the  aortic  valves 
(see  page  298).  It  is  not  always  possible  to  prove  that  an  endocarditis  precedes  the 
pericarditis,  but  yet  this  does  not  overthrow  the  opinion  we  have  expressed,  inas- 
much as  many  cases  of  acute  endocarditis  do  not  betray  themselves  by  any  audi- 
ble murmurs. 

We  should  also  mention  that  there  may  be  functional  cardiac  derangement 
without  any  grave  anatomical  lesion.  We  have  already  spoken  of  the  functional 
murmurs.  There  may  also  be  a  rai)id  and  irregular  pulse,  and,  in  rare  instances, 
attacks  of  angina  pectoris  of  apparently  purely  nervous  origin. 

3.  Serous  and  Mucous  Membranes. — The  pleura  and  peritoneum,  as  well 
as  the  pericardium,  may  be  affected  in  articular  rheumatism ;  so  that  it  was  for- 
merly often  maintained  that  acute  articular  rheumatism  is  a  disease  of  the  serous 
membranes  of  the  body  in  general,  inclusive  of  the  joints.  Rheumatic  pleurisy  is 
much  rarer  than  either  endocarditis  or  pericarditis;  and  rheumatic  peritonitis  is 
rarer  still.  The  pleurisy,  at  least  in  most  instances,  is  propagated  directly  from 
an  inflamed  pericardium;  and  in  the  same  way  the  peritoneum  may  become 
infected  from  the  pleura  by  way  of  the  diaphragm.  Few  of  these  severe  cases,  pre- 
senting a  simultaneous  inflammation  of  several  serous  membranes,  occur,  now 
that  the  salicylic-acid  treatment  has  been  introduced.  We  do  not  say  that  it  is 
absolutely  impossible  for  a  pleurisy  or  a  peritonitis  to  occur  in  rheumatism  with- 
out inflammation  in  any  other  serous  cavity,  but  such  an  occurrence  is  extremely 
rare. 

The  mucous  membranes  are  seldom  greatly  affected  in  acute  articular  rheuma- 
tism. As  has  already  been  stated,  a  catarrh  of  the  pharynx  or  larynx  sometimes 
occurs  in  the  beginning  of  the  disease.  Bronchitis  is  often  spoken  of  by  the  older 
authors ;  but  it  is  probably  in  many  cases  not  due  directly  to  the  rheumatism,  but 
it  is  a  complication,  just  as  in  any  disease  attended  by  great  prostration.  The 
stomach  and  intestinal  canal  are  seldom  especially  affected. 

4.  Skin. — Cutaneous  phenomena  are  not  infrequent  in  the  course  of  acute 
articular  rheumatism.  A  prominent  symptom  of  the  disease  is  the  tendency  to 
profuse  perspiration.  The  perspiration  often  has  a  strongly  acid  odor  and  reac- 
tion. Many  patients  exhibit  an  abundant  crop  of  sudamina,  the  back  in  particu- 
lar being  sometimes  entirely  covered.  Sometimes  there  are  other  cutaneous 
eruptions.  In  a  whole  series  of  cases  we  observed  erythema  nodosum.  This 
affected  the  lower  extremities  more  than  the  upper.  Urticaria  is  not  very  infre- 
quent, while  herpes  labialis  has  been  very  rare  in  our  experience.  It  is  well 
known  that  arthritic  affections  and  the  so-called  "  hemorrhagic  diseases  "  are  in 
many  ways  related  to  each  other ;  and  it  is  therefore  an  interesting  fact  that 
extensive  hemorrhagic  disturbance  of  the  skin  also  occurs  in  connection  with 
acute  articular  rheumatism,  as  we  have  repeatedly  had  opportunity  to  observe. 
We  have  seen  several  cases  of  hemorrhagic  urticaria :  wheals  appear  upon  the 


ACUTE  ARTICULAR  RHEUMATISM.  905 

skia,  and  a  haemorrhage  takes  place  into  their  centers  and  spreads  gradually. 
There  may  also  be  simple  cutaneous  ecchymoses.  These  may  in  severe  cases  be 
merely  one  symptom  of  a  general  haemorrhagic  diathesis,  with  haemorrhages 
from  mucous  membranes.  The  occurrence  of  these  symptoms  again  points  most 
clearly  to  the  infectious  character  of  acute  articular  rheumatism. 

5.  The  Muscles  and  Nervous  System.— The  condition  of  the  muscles  is  very 
important  in  many  cases  of  acute  polyarthritis.  They  are  often  quite  painful  on 
pressure,  and  apparently  somewhat  swollen  about  a  joint  that  has  been  long 
affected.  The  muscular  atrophies  and  muscular  paralyses  that  often  remain  after 
the  arthritis  is  well  are  especially  important. 

According  to  a  general  law,  there  are  certain  definite  trophic  relations  between 
a  joint  and  the  muscles  belonging  to  it,  whereby  almost  every  severe  and  persistent 
disease  of  the  joint  is  necessarily  followed  by  an  atrophy  of  the  affected  muscles. 
The  extensors  of  the  joint  are  often  most  affected  by  this  atrophy.  This  atrophy 
has  long  been  recognized,  and  was  formerly  regarded,  particularly  by  surgeons,  as 
merely  the  result  of  inactivity  of  the  muscles — "atrophy  from  disuse";  but  this 
view  is  certainly  erroneous.  We  do  not  know  its  precise  cause,  but  it  is  without 
doubt  the  result  of  the  disease  of  the  joint,  and  may  therefore  be  termed  "  muscu- 
lar atrophy  of  arthritic  origin."  If  an  attack  of  acute  articular  rheumatism 
affects  any  one  joint  for  a  long  period  there  is  a  secondary  atrophy  of  the  corre- 
sponding muscles.  This  is  seen  most  often,  and  in  its  most  typical  form,  where 
there  is  obstinate  trouble  in  the  shoulder- joint,  the  deltoid  becoming  extremely 
atrophied.  This  atrophy  of  the  muscles  may  contribute  largely  to  the  sum-total 
of  functional  derangement.  We  have  repeatedly  seen  cases  where  the  patient 
could  hardly  lift  his  arm  at  all,  although  the  inflammation  of  the  shoulder-joint 
had  passed  away,  and  that  without  leaving  any  anchylosis.  It  is  therefore  en- 
tirely justifiable  to  speak  of  a  rheumatic  paralysis.  We  have  seen  similar  muscu- 
lar paralyses  after  acute  articular  rheumatism  in  the  rest  of  the  muscles  of  the 
upper  arm,  also  in  the  quadriceps  extensor,  and  once  in  the  serratus  magnus.  The 
explanation  given  by  Charcot,  that  the  cause  of  the  atrophy  is  a  "  reflex  "  implica- 
tion of  the  trophic  centers  in  the  cord  which  starts  from  the  joint,  seems  to  us 
hardly  satisfactory.  There  are  probably  local  disturbances  of  nutrition,  and 
sometimes  apparently  a  direct  extension  of  the  inflammatory  process  from  the 
joint  to  the  neighboring  muscles.  It  is  noteworthy  that  the  atrophied  muscles 
respond  promptly  to  the  faradic  current,  and  never  exhibit  the  reaction  of  degen- 
eration. 

Chorea  (vide  supra,  page  780)  may  be  a  sequel  of  acute  articular  rheumatism, 
and  it  is  one  of  the  nervous  symptoms  which  may  arise  in  connection  with  it. 
This  complication  is  seen  most  frequently  in  children.  Endocarditis  may  accom- 
pany it,  but  it  does  not  always  do  so. 

There  are  certain  peculiar  cases  of  acute  articular  rheumatism  which  excite  the 
greatest  interest.  In  these,  very  severe  cerebral  symptoms  are  developed,  often 
most  acutely.  They  are  therefore  called  "  cerebral  rheumatism  " ;  or,  as  they  are 
almost  always  characterized  by  an  extraordinarily  high  temperature,  another  name 
is  "hyperpyretic  articular  rheumatism."  In  these  cases  the  disease  may  exhibit 
severe  nervous  symptoms  from  the  start,  particularly  delirium ;  or  it  may  at  first 
run  an  apparently  favorable  course,  and  not  change  for  the  worse  until  after  sev- 
eral days,  or  even  at  a  later  pei'iod.  The  change  may  be  quite  abrupt.  The  tem- 
perature rises  to  104°  or  106°  (40°-41°  C).  There  are  great  uneasiness,  delirium, 
and  sometimes  also  signs  of  motor  irritation,  such  as  general  convulsions,  or  tonic 
spasm  of  the  extremities,  or  trismus.  The  face  grows  pale  and  cyanotic,  the  pulse 
small  and  extremely  rapid.  With  slight  interruptions,  the  temperature  continues 
to  rise,  and  attains  107'5°  to  109-5°  (42°-43°  C).     This  great  rise  is  most  apt  to 


906  DISEASES  OF  THE  OEGANS  OF  LOCOMOTION. 

occur  just  before  death,  arid  there  may  be  a  still  further  increase  of  temperature 
after  death  occurs.  As  has  been  implied,  the  termination  is  usually  unfavorable. 
It  is  only  in  exceptional  cases  that  recovery  takes  place. 

It  has  been  stated  that  cerebral  rheumatism  attacks  mainly  hard  drinkers  and 
other  individuals  whose  nervous  system  has  been  previously  impaired ;  but  our 
own  experience  does  not  confirm  this  view.  No  case  is  absolutely  secure  from  the 
occurrence  of  hyperpyrexia ;  but  it  is  a  very  rare  phenomenon,  occurring  perhaps 
once  in  several  hundred  cases.  On  post-mortem  examination,  the  brain  seldom 
shows  any  change  in  these  cases  of  cerebral  rheumatism.  We  are  therefore 
obliged  to  regard  the  condition  as  the  result  of  an  unusually  severe  infection, 
affecting  chiefly  the  intellectual,  motor,  and  thermal  centers.  Cases  have  also 
been  reported  where  there  have  been  actual  anatomical  lesions  of  the  brain — in 
particular,  purulent  meningitis.  Probably,  however,  most  of  these  cases  were 
falsely  diagnosticated,  the  observer  having  confounded  articular  rheumatism  with 
epidemic  meningitis,  pyaemia,  and  similar  diseases.  Of  course,  if  there  be  endocar- 
ditis, cerebral  embolism  is  possible.  Mental  derangements  deserve  a  brief  men- 
tion. They  rarely  occur  during  the  coui^se  of  the  disease,  but  are  somewhat  more 
frequent  after  it  has  terminated.  We  may  have  either  melancholia  attended  with 
marked  excitement  or  anxiety,  or  a  more  general  insanity.  The  prognosis  is  usu- 
ally favorable. 

6.  Other  Viscera. — Other  parts  of  the  body  than  the  heart,  the  serous  mem- 
branes, and  the  brain,  are  seldom  much  affected  in  articular  rheumatism.  Lobar 
pneumonia  occurs  only  in  especially  severe  cases,  but  in  such  it  may  attain  quite  a 
considerable  development  and  occasion  great  dyspnoea.  It  usually  requires  quite 
a  long  while  to  recover  from  it.  Lobular  inhalation-pneumonia  may  also  occur 
in  severe  cases.  Acute  nephritis  has  certainly  sometimes  occurred,  but  it  is  ex- 
tremely rare.  The  spleen  may  be  somewhat  swollen,  but  it  is  not  the  rule  to  find 
a  splenic  tumor,  such  as  is  present  in  other  acute  infectious  diseases. 

7.  General  Symptoms. — In  many  cases  the  general  condition  of  the  patient  is 
but  little  affected,  but  in  others  the  disease  seems  to  exert  a  peculiar  influence 
upon  the  constitution.  This  may  show  itself  in  a  striking  anaemia;  and  we  have 
observed  this  repeatedly  where  there  was  no  cardiac  complication.  Another 
much  more  dangerous  but  extremely  rare  complication  has  already  been  briefly 
referred  to,  namely,  the  occurrence  of  a  general  haemorrhagic  diathesis.  This  is 
almost  always  associated  with  high  fever  and  great  prostration,  and  is  usually 
fatal. 

Course,  Duration,  and  Prognosis. — Acute  articular  rheumatism  may  be  described 
as  generally  a  benign  disease,  for  it  usually  terminates  in  recovery.  It  is  only  in  a 
very  few  cases  that  an  unfavorable  termination  takes  place  immediately,  whether 
as  the  result  of  pericarditis  or  other  severe  cardiac  complication,  or  from  hyper- 
pyrexia, or  the  development  of  a  general  haemorrhagic  diathesis.  The  entire  dura- 
tion of  the  disease  varies  greatly  according  to  its  severity.  There  are  mild  cases, 
which  terminate  in  a  few  days;  and,  on  the  other  hand,  the  disease  may  be  very 
tedious,  lasting  for  weeks  and  months,  and  finally  merging  into  chronic  articular 
rheumatism.  Quite  often  the  violent  symptoms  experienced  at  first  disappear 
quite  rapidly,  but  only  to  be  replaced  by  such  milder  ones  as  pain  and  stiffness  of 
the  joints — these  latter  persisting  for  a  long  while.  It  is  a  general  rule,  that  the 
severity  and  persistency  of  the  case  correspond  with  the  number  of  joints  affected ; 
but  to  this  rule  there  are  numerous  exceptions.  The  disease  may  persist  with 
great  obstinacy  in  a  single  joint.  It  need  hardly  be  said  that  the  duration  of  the 
disease  is  greatly  modified  by  the  occurrence  of  complications,  cardiac  or  other- 
wise, and  such  sequelae  as  muscular  atrophy,  anchylosis  of  the  joints,  or  chorea. 
The  most  important  of  all  sequelae  is  cardiac  disease,  and  this  must  always  be 


ACUTE  ARTICULAR  RHEUMATISM.  907 

considered  in  giving  a  prognosis ;  for,  although,  the  disease  as  such  does  in  most 
instances  terminate  in  recovery,  yet  too  often  it  gives  rise  to  a  tedious  and  usually 
incurable  disease  of  the  heart.  It  is,  however,  true  that  complete  recovery  from 
the  acute  endocarditis  seen  in  articular  rheumatism  is  possible,  but  in  a  large 
majority  of  cases  recovery  is  not  complete,  and  the  acute  passes  into  a  chronic 
endocai'ditis.  In  these  cases  the  cardiac  symptoms  may  be  developed  directly,  so 
that  the  patient  at  once  begins  to  complain  of  palpitation  and  shortness  of  breath  ; 
or  he  may  seem  to  regain  his  health  completely,  and  a  murmur  which  the  physi- 
cian alone  can  detect  may  be  the  only  sign  of  the  incurable  injury  which  the  body 
has  suffered.  The  patient  may  feel  perfectly  well  for  years  after,  and  then  at  last 
begin  to  suffer  from  the  failure  of  compensation  (see  page  283  et  seq.). 

Diagnosis. — Most  cases  of  articular  rheumatism  can  be  easily  recognized,  for 
the  acute  occtirrence  of  pain  and  swelling  in  several  joints  is  sufficiently  charac- 
teristic of  the  disease.  It  should  nevertheless  be  borne  in  mind  that  articular 
swelling  may  also  take  place  in  the  course  of  other  diseases,  and  that  mistakes 
in  diagnosis  are  by  no  means  impossible.  Where  there  are  grave  constitutional 
symptoms  with  fever  from  the  start,  we  should  not  forget  the  possibility  of 
pyaemia,  or  of  acute  osteomyelitis,  since  these  affections  occasionally  give  rise  to 
the  swelling  of  several  joints.  In  such  cases,  however,  careful  attention  to  the 
further  course  of  the  disease  will  generally  enable  us  to  see  that  we  can  not  be 
dealing  with  a  simple  acute  articular  rheumatism.  Again,  after  childbirth  there 
may  be  swelling  of  the  joints,  of  septic  origin,  and  therefore  entirely  independent 
of  any  genuine  rheumatic  infection. 

If  a  single  joint  be  attacked,  the  diagnosis  of  articular  rheumatism  must  be 
made  with  extreme  caution.  These  monarticular  inflammations  often  prove  to  be 
something  entirely  different,  namely,  fungous  disease  of  the  joint,  or  an  osteo- 
myelitis. The  arthritis  which  follows  gonorrhoea  is  also  sometimes  monarticular 
(affecting  especially  the  knee-joint),  or  at  any  rate  it  is  confined  to  the  lower 
extremities;  and,  in  conclusion,  it  should  be  stated  that  it  is  not  very  rare  to 
observe  pain  and  swelling  in  various  muscles  and  joints  at  the  commencement  of 
the  secondary  stage  of  syphilis,  simulating  an  acute  articular  rheumatism. 

Sometimes  the  diagnosis  is  doubtful  in  those  cases  which  present  cutaneous 
ecchymoses  (purpura  and  peliosis)  and  erythema  nodosum,  because  we  may  be 
unable  to  determine  which  should  be  regarded  as  the  primary  symptoms  and 
which  the  secondary ;  but  in  these  cases,  after  all,  it  is  often  merely  a  question  of 
nomenclature,  and  the  best  way  is  to  follow  the  rule  that  the  greater  should  include 
the  less. 

Genuine  gout  (q.  v.)  can  usually  be  readily  diagnosticated  from  articular  rheu- 
matism by  its  localization  in  the  toe,  and  by  the  gastric  and  other  symptoms 
which  attend  it. 

Finally,  we  must  mention  that  acute  multiple  neuritis  (q.  v.),  beginning  with 
fever  and  severe  pain  in  the  extremities,  may  sometimes,  if  we  are  not  sufficiently 
careful,  be  mistaken  for  polyarthritis. 

Treatment. — Acute  articular  rheumatism  is  one  of  the  few  diseases  for  which 
we  possess  an  undoubtedly  specific  and  universally  accepted  remedy.  Kolbe  sug- 
gested its  use,  and  since  1876  it  has  been  largely  employed  upon  the  recommenda- 
tion of  Strieker,  Buss,  and  others,  for  articular  rheumatism.  This  remedy  is  sali- 
cylic acid.  Although  this  medicine  does  not  in  all  cases  produce  its  surprisingly 
favorable  results  with  equal  rapidity  and  completeness,  yet  it  almost  invariably 
does  produce  a  decided  and  beneficial  effect  upon  the  disease.  We  might  even 
say  that  this  influence  is  so  constant  that  where  salicylic  acid  proves  entirely 
inefficient  in  a  fresh  case,  such  failure  throws  doubt  upon  the  correctness  of  the 
diagnosis.    Thus,  where  there  is  monarticular  arthritis  dependent  upon  some  local 


908  DISEASES  OF  THE  OEGANS  OF  LOCOMOTION. 

cause,  the  remedy  has  hardly  any  beneficial  influence.  The  same  is  true  with 
regard  to  affections  of  the  joints  connected  with  gonorrhoea,  pyaemia,  and  similar 
troubles.  In  genuine  acute  articular  rheumatism,  on  the  other  hand,  the  salicylic- 
acid  treatment  is  so  superior  to  any  other  that  it  is  the  first  duty  of  the  physician 
in  every  case  to  give  this  remedy  a  fair  trial. 

There  are  but  two  preparations  of  salicylic  acid  used  in  rheumatism— the  pure 
acid  and  its  sodium  salt,  salicylate  of  sodium.  Each  of  these  two  remedies  has  its 
peculiar  advantages,  but  the  specific  influence  of  each  is  about  the  same.  Sali 
cylic  acid  should  never  be  prescribed  in  solution,  but  always  in  capsules,  usually 
containing  ten  grains  (grm.  0-50).  In  this  way  the  salicylic  acid  can  be  taken  by 
almost  any  patient  quite  easily,  especially  if  a  little  water  or  milk  be  drunk  after 
each  dose.  Adults  should  receive  ten  grains  every  hour  until  about  one  or  two 
drachms  (grm.  5-8)  have  been  administered.  Usually  there  will  by  this  time  be 
a  very  decided  abatement  of  the  articular  pain  and  swelling,  while  on  the  other 
hand  there  will  also  usually  be  such  toxic  "  salicylic  symptoms  "  (vide  infra)  as 
to  forbid  its  further  use.  The  salicylate  of  sodium  is  best  exhibited  in  single  large 
doses  of  a  drachm  to  a  drachm  and  a  half  (grm.  4-6),  each  dose  being  given  with 
about  an  ounce  (grm.  20-30)  of  peppermint  water.  The  quite  disagreeable  taste  of 
the  medicine  is  only  exaggerated  by  the  addition  of  such  things  as  syrup  or  fluid 
extract  of  licorice,  added  for  the  sake  of  elegance;  but  the  simple  solution  in  pep- 
permint water  is  quite  well  taken,  at  least  by  most  patients.  It  is  a  very  good  plan 
to  give  salicylate  of  sodium  in  a  glass  of  Hungarian  wine,  or  in  strong  black  coffee 
without  sugar.  The  advantage  of  the  salicylate  over  the  pure  acid  consists  in  its 
being  possible  to  give  a  larger  dose  at  one  time,  so  that  it  need  not  be  taken  more 
than  two  or  three  times  a  day.  In  general,  the  amount  given  in  twenty-four 
hours  should  not  exceed  two  and  a  half  drachms  (grm.  10) ;  one  and  a  half  to  two 
drachms  (grm.  6-8)  may  suffice.  For  children  the  dose  is,  of  course,  smaller,  say 
five  grains  of  salicylic  acid  (grm.  0-30),  or  half  a  drachm  to  a  drachm  (grm.  2-4) 
of  the  sodium  salt. 

Which  of  these  two  preparations  shall  be  employed  is,  as  has  been  stated,  of 
little  consequence.  We  ourselves  usually  prescribe,  at  first,  capsules  of  salicylic 
acid  to  be  taken  hourly,  as  being  most  agreeable  to  the  patient;  but  if  our  first 
visit  be  made  in  the  evening,  we  prescribe  a  single  large  dose  of  a  drachm  to  a 
drachm  and  a  half  (grm.  4-6)  of  salicylate  of  sodium,  so  that  the  patient  may  not 
be  disturbed  every  hour  through  the  night  in  order  to  take  medicine.  It  is  often 
possible  to  give  the  two  remedies  in  alternation.  This  is  a  good  way  later  on  in 
the  disease,  when  the  patient  has  already  acquired  a  distaste  for  the  medicine. 
In  such  cases  also  it  may  be  desirable  to  give  the  salicylate  of  sodium  as  an 
enema.  About  two  and  a  half  drachms  should  be  given,  in  two  ounces  of  water 
(grm.  10  and  60).  There  is  no  doubt  that  the  specific  effects  can  be  obtained  in 
this  manner. 

The  benign  influence  of  this  remedy  upon  the  disease  is  apparent  in  many 
fresh  cases  as  early  as  ten  to  eighteen  hours  after  treatment  begins ;  and  it  is  often 
astonishing  to  see  how  soon  a  patient,  who  before  lay  helpless  and  complaining, 
becomes  free  from  pain  and  able  to  move  his  limbs.  It  must  be  confessed,  how- 
ever, that,  apart  from  its  taste,  salicylic  acid  may  produce  disagreeable  incidental 
effects.  In  the  first  place,  there  may  be  nausea  with  epigastric  distress,  and  even 
vomiting.  Tinnitus  auriuxn  may  be  exceedingly  troublesome,  and  may  be  at- 
tended with  marked  vertigo.  In  somewhat  rarer  instances  the  mind  is  especially 
affected.  Young  girls  in  particular  are  often  peculiarly  excited ;  but  the  frame 
of  mind  is,  however,  in  general  a  cheerful  one.  After  large  doses  there  may  be 
an  actual  "salicylic  delirium."  It  should  also  be  said  that  respiration  may  be 
affected,  becoming  very  deep  and  rapid  (salicylic  dyspnoea).     All  these  incidental 


ACUTE  ARTICULAR  RHEUMATISM.  909 

effects,  and  particularly  the  nausea  and  ringing- in  the  ears,  render  difficult  the 
employment  of  the  remedy  in  those  large  doses  which  alone  are  of  any  benefit. 
This  is  the  more  unfortunate,  as  it  is  often  very  desirable  to  employ  salicylic  arid 
persistently. 

Although  it  is  not  exceptional  to  have  the  symptoms  almost  entirely  vanish 
at  the  end  of  one  or  two  days,  yet  it  is  only  in  the  minority  of  cases  that  the 
entire  process  ends  with  this  release  from  pain.  There  is  very  often,  sooner  or 
later,,  a  relapse,  with  fresh  pain  or  even  fresh  swelling  in  one  or  more  joints.  It 
has  been  recommended  to  continue  the  salicylic  acid  in  smaller  doses  for  son  if, 
time,  in  order  to  avert  such  relapses;  but  of  late  we  have  abandoned  this  method, 
for  the  reason  that  these  small  doses  do  not  prevent  the  return  of  the  disorder,  but 
are  calculated  to  give  the  patient  a  strong  dislike  to  the  remedy,  and  lessen  his 
confidence  in  it.  We  therefore  recommend  to  stop  the  medicine  entirely  as  soon 
as  the  pain  ceases,  and  to  guard  the  patient  as  much  as  possible  from  relapses  by 
preventing  his  catching  cold  (vide  infra).  If  there  be  fresh  pain,  we  should  at 
once  resume  the  acid  or  its  salt  in  large  doses,  and  thus  we  will  very  frequently 
be  able  to  cut  short  the  relapse  at  once. 

[One  other  salicylic  compound  deserves  mention — the  oil  of  wintergreen  ;  this 
has  been  used  largely  by  Kinnicutt,  who  finds  it  efficacious,  easy  to  take,  and  not 
likely  to  produce  the  unpleasant  symptoms  which  sometimes  follow  the  com- 
pounds in  more  general  use.  It  is  given  in  doses  of  HI  x-xv  every  two  hours, 
either  in  milk,  on  sugar,  or  in  capsules. 

The  salicylic  treatment  markedly  diminishes  the  pain  and  fever,  shortens  the 
time  spent  in  bed  by  four  oil  five  days,  does  not  shorten  the  time  spent  in  hospital, 
and  seems  to  have  little  or  no  influence  on  the  cardiac  complications.  The  full 
alkaline  treatment  does  not  curtail  the  pain  and  fever  in  the  same  degree,  but 
does  seem  to  afford  some  protection  against  the  heart  affection,  and  to  shorten  the 
stay  in  hospital  several  days. 

A  combination  of  the  salicylic  and  alkaline  treatments  seems  therefore  rational, 
and  it  has  been  adopted  by  the  editor  for  some  years.  Citrate  of  potash  is  given  in 
sufficient  doses  to  produce  and  maintain  alkalinity  of  the  urine.  The  salicylic 
compound  is  given  at  first  in  full  doses,  wdiich  are  diminished  in  size  and  frequency 
with  the  control  of  the  articular  symptoms,  but  are  not  omitted  entirely  until 
recovery  is  practically  complete.  The  editor  is  inclined  to  believe  that  relapse  is 
less  common  if  the  system  be  kept  somewhat  under  the  influence  of  the  drug. 
Salicin  is  often  perfectly  well  borne  when  the  sodium  salt  causes  gastric  irritability, 
and  the  oil  of  wintergreen  is  another  form  which  has  advantages  in'some  cases.] 

Despite  the  admirable  qualities  of  salicylic  acid,  it  must  be  confessed  that  we 
can  not  always  bring  about  a  rapid  and  complete  cure  of  the  disease  by  this  rem- 
edy. There  are  cases  where,  although  at  first  evident  improvement  follows  its 
use,  relapses  continually  recur,  or  the  disease  fastens  itself  obstinately  in  single 
joints.  In  such,  the  continued  use  of  salicylic  acid  proves  almost  unavailing,  and 
indeed  the  patient  can  hardly  be  persuaded  to  take  it.  In  these  cases,  and  also 
when  the  salicylic  preparations  are  ill  borne  or  cause  unpleasant  attendant  symp- 
toms, antipyrine  is  the  best  substitute.  Many  physicians  therefore  often  prescribe 
it  from  the  first  in  place  of  salicylic  acid,  although  we  think  the  action  of  the 
latter  upon  acute  articular  rheumatism  is  greater  than  that  of  antipyrine.  "We 
should  give  antipyrine  in  doses  of  fifteen  grains  (grm.  1)  several  times  a  day  in 
water  or  wine.  Its  attendant  symptoms  (sweating,  nausea,  and  sometimes  an 
eruption  like  measles)  are  usually  without  special  significance,  and  its  influence  on 
the  articular  pains  is  often  so  favorable  that  the  remedy  is  of  much  value  in  the 
treatment  of  protracted  rheumatism.  Antifebrine,  in  doses  of  four  to  seven  grains 
(grm.  0"25-0'50),  seems  also  to  have  a  certain  favorable  action  in  joint  affections, 


910  DISEASES  OF  THE  ORGANS  OF  LOCOMOTION. 

but  it  is  distinctly  inferior  to  antipyrine.  Salili  has  recommended  salol  (salicylic 
acid,  phenyl  ether),  which  deserves  more  confidence;  it  is  given  in  fifteen-grain 
(grm.  1)  powders  several  times  a  day  (five  to  eight  powders  a  day).  We  are 
often  compelled,  especially  in  articular  rheumatism  which  has  frequent  relapses, 
to  try  in  turn  the  different  remedies  mentioned. 

There  are  still  other  internal  remedies  which  should  he  tried,  but  their  effects 
are  rarely  satisfactory.  Most  important  among  these  are  iodide  of  potassium 
and  the  preparations  of  Colchicum  (tincture  of  Colchicum,  twenty-five  to  forty 
drops  several  times  a  day).  Numerous  other  remedies  have  been  recommended, 
and  they  were  formerly  largely  employed,  hut  at  present  they  are  almost  aban- 
doned. Among  these  are  large  doses  of  the  alkalies  (such  as  bicarbonate  of 
soda),  trimethylamine,  veratrine,  and  quinine.  Local  treatment  of  the  diseased 
joints  is  far  more  important  and  effective  in  such  cases.  Properly  executed 
massage  deserves  special  mention,  as  its  effects  are  often  very  brilliant.  Elec- 
tricity also  may  have  a  beneficial  effect,  particularly  the  galvanic  current.  We 
would  caution  against  the  too  early  use  of  warm  baths,  as  these  of  tea  aggravate 
the  pain  instead  of  mitigating  it.  Steam  baths  are  sometimes  very  beneficial, 
but  they  may  also  do  harm,  and  they  should  therefore  be  given  only  when  the 
acute  inflammatory  symptoms  have  entirely  vanished,  leaving  behind  only  stiff- 
ness and  tenderness  in  the  joints. 

The  application  of  an  ice-bag  in  genuine  articular  rheumatism  is  seldom  neces- 
sary, but  it  may  sometimes  be  desirable  where  there  are  violent  and  obstinate  symp- 
toms of  acute  inflammation.  Warm,  moist  applications  are  useless,  if  not  harmful, 
in  acute  cases.  In  the  advanced  stages  of  subacute  cases  a  wet  pack  may  afford 
some  relief.  Painting  the  skin  over  the  joints  with  tincture  of  iodine  produces  no 
effect  in  acute  cases,  and  even  in  the  chronic  ones  it  is  probably  mainly  a  sub- 
jective remedy.  Some  observers  report  that  injections  of  carbolic  acid  beneath  the 
skin  of  the  affected  joints  greatly  relieve  the  pain.  A  Pravaz's  syringeful  (thir- 
teen minims)  of  a  one-per-cent.  solution  may  be  injected  one  to  three  times  a 
day.  We  have  had  no  personal  experience  with  this  remedy.  In  all  severe  cases 
careful  attention  should  be  given  from  the  start  to  maintaining  a  correct  position 
of  the  diseased  joints,  because  of  the  possibility  of  anchylosis.  Before  salicylic 
acid  was  intooduced,  "  the  treatment  of  articular  rheumatism  with  splints  "  was 
largely  and  very  advantageously  employed.  The  use  of  salicylic  acid  has  greatly 
diminished  the  necessity  of  such  procedure,  but  even  now  it  is  sometimes  required. 
It  is  often  possible  to  give  the  patient  great  relief  by  applying  a  suitable  paste- 
board or  wooden  splint  to  an  affected  extremity. 

General  hygienic  and  dietetic  treatment  should  not  be  undervalued.  An 
equable  temperature  should  be  caref ully  maintained  in  the  sick-room,  inasmuch 
as  cold,  or  draughts,  or  moisture  have  very  often  been  found  to  exert  an  evil 
influence  upon  the  disease  and  excite  fresh  pain.  The  patient  should  therefore 
be  kept  warm,  and  it  is  sometimes  advantageous  to  wrap  up  the  affected  joints  in 
cotton  batting.  It  is  of  great  importance  that  even  in  the  mildest  cases  the  patient 
should  be  strictly  confined  to  bed,  and  he  should  by  no  means  get  up  too  soon. 
If  possible,  we  keep  our  own  patients  in  bed  for  a  week  after  the  pain  has  ceased. 
Getting  up  too  early  will  very  often  bring  on  a  relapse.  With  regard  to  diet, 
milk  is  the  best  food.  We  may  also  allow  soup,  eggs,  and  a  little  meat.  •  In 
France,  great  weight  is  laid  upon  an  exclusive  milk  diet ;  but  this  would  seem  to 
us  an  extreme  view. 

We  do  not  need  to  speak  at  length  about  the  treatment  of  the  complications 
and  sequela?,  since  we  should  merely  repeat  what  has  already  been  said  in  the 
appropriate  chapters  of  this  work.  There  has  been  much  said  on  both  sides  as  to 
the  influence  of  salicylic  acid  in  preventing  complications,  particularly  cardiac 


CHRONIC  RHEUMATISM  AND  ARTHRITIS  DEFORMANS.        !)H 

complications.  This  much  is  certain,  that  cardiac  complications  are  not  abso- 
lutely prevented  by  the  salicylic  treatment,  and  that  they  too  frequently  occur 
while  it  is  being  employed;  but  we  do  believe  that  this  treatment  decidedly 
shortens  the  course  of  the  disease  as  a  whole,  in  many  instances,  and  thus  lessens 
the  liability  to  endocarditis.  If,  however,  a  cardiac  complication  have  made  its 
appearance,  salicylic  acid  does  not  apparently  exert  any  appreciable  influence 
upon  it.  Another  important  question  is  in  regard  to  the  efficiency  of  salicylic 
acid  in  the  graver  forms  of  articular  rheumatism,  particularly  in  cerebral  rheu- 
matism. It  may  be  stated,  in  the  first  place,  that  in  Leipsic  cerebral  rheuma- 
tism has  apparently  become  much  less  frequent  since  the  salicylic  treatment 
was  introduced.  At  any  rate,  not  a  single  case  of  hyperpyrexia  occurred  in 
the  clinique  in  that  city  out  of  many  hundred  cases  treated,  where  the  salicylic 
acid  was  properly  employed  from  the  first.  We  had  an  opportunity  to  observe 
a  case  in  which  hyperpyretic  symptoms  had  already  appeared  when  we  first  saw 
it,  and  which  had  not  been  treated  with  salicylic  acid.  Here  large  doses  of  that 
remedy  produced  no  effect.  We  should  nevertheless  be  inclined  to  employ  it, 
first  of  all,  in  such  cases;  and  the  energetic  use  of  cool  baths  would  probably  be 
the  most  speedy  way  of  modifying  the  dangerously  high  temperature.  Stimu- 
lants, in  particular  camphor,  are  also  required  in  these  severe  cases. 

In  the  severe  hemorrhagic  varieties  of  rheumatism  we  should  also  give  sali- 
cylic acid  a  trial.  The  milder  hemorrhagic  cases  (hemorrhagic  urticaria)  do  well 
under  ordinary  methods  of  treatment. 

If  the  acute  affection  merge  into  a  chronic  condition  of  stiffness  and  swelling 
of  certain  joints,  such  as  the  wrist  or  shoulder,  we  must  employ  the  same  remedies 
as  in  chronic  articular  rheumatism.  Massage  furnishes  the  best  results.  Warm 
baths  may  also  be  ordered  in  such  cases  (see  the  following  chapter).  The  patient 
might  be  sent  to  Teplitz  or  Wiesbaden.  The  subsequent  muscular  atrophies  and 
paralyses  recover  most  rapidly  under  electricity. 

Prophylaxis  requires,  first  of  all,  that  one  should  avoid  cold  or  wet,  and  other 
"  rheumatogenous  influences."  Persons  who  have  already  had  one  attack  of 
articular  rheumatism  must  be  especially  careful,  inasmuch  as  they  are  more  than 
ever  liable  to  the  disease,  as  has  already  been  said.  It  is  not  inconsistent,  how- 
ever, with  the  exercise  of  due  caution,  to  endeavor  to  lessen  the  sensitiveness  of 
the  skin  by  such  procedures  as  cold  sponging,  followed  by  friction. 


CHAPTER  II. 


CHRONIC   ARTICULAR   RHEUMATISM    (CHRONIC   POLYARTHRITIS) 
AND  ARTHRITIS   DEFORMANS. 

iEtiology. — The  two  diseases  known  as  "chronic  articular  rheumatism"  and 
"arthritis  deformans"  are  considered  together  here,  because  it  is  impossible  to 
draw  a  sharp  distinction  between  them.  It  is,  indeed,  not  unlikely  that  the  above 
names  are  sometimes  applied  to  diseases  which  differ  essentially  from  each  other; 
but  as  we  do  not  yet  understand  the  nature  or  the  etiology  of  many  chronic 
diseases  of  the  joints,  we  must  provisionally  be  guided  by  the  external  changes 
they  produce.  We  shall  therefore  embrace  all  chronic  inflammatory  processes 
affecting  the  joints  under  the  name  of  chronic  arthritis.  Traumatic  arthritis  it  is 
not  intended  to  include,  much  less  those  chronic  affections  of  the  joints  which  are 
evidently  of  tubercular  origin,  and  which  have  ordinarily  been  termed  fungous 
arthritis.    These  belong  to  the  domain  of  surgery.    We  would  also  exclude  chronic 


912  DISEASES  OF  THE  ORGANS  OF  LOCOMOTION. 

syphilitic  diseases  of  the  joints,  about  which,  indeed,  there  is  still  less  known  than 
about  the  tubercular  affections ;  besides,  they  are  rare.  Chronic  articular  affections 
from  gonorrhoea  are  probably  more  frequent. 

The  aetiology  of  those  cases  of  chronic  arthritis  where  the  disease  is  a  direct 
sequel  of  acute  articular  rheumatism  is  evident  enough.  It  is  hardly  possible  to 
doubt  that  the  same  specific  poison  which  excited  the  acute  arthritis  maintains 
possession  of  the  joints,  and  produces  the  chronic  inflammatory  changes.  Cases 
of  this  sort  especially  deserve  the  name  of  chronic  articular  rheumatism.  They 
are  not  very  infrequent,  and  may  be  of  slight  or  great  severity.  The  worst  cases 
pi'oduce  macroscopic  changes  which  fully  justify  the  other  appellation  of  arthritis 
deformans. 

It  is  also  possible  that  many  cases  which  are  chronic  from  the  start  have  the 
same  aetiological  origin — that  is,  are  due  to  the  same  pathogenic  agents.  This 
might  be  inferred  from  analogy  with  numerous  other  diseases,  and  it  is  rendered 
still  more  probable  by  the  fact  that  the  same  exciting  causes  which  promote  acute 
articular  rheumatism  often  play  a  conspicuous  part  in  chronic  arthritis.  Such 
causes  are  exposure  to  cold  and  wet,  and  working  in  cold  or  draughty  places,  or 
dwelling  in  newly  built  and  damp  houses.  This  explains  why  those  who  follow 
certain  callings — for  instance,  washerwomen — are  more  apt  to  suffer  from  the 
disease  than  others,  and  why  arthritis  deformans  has,  with  some  justice,  been  called 
a  disease  of  the  poor,  in  contrast  with  the  gout  of  the  wealthy.  Many  of  the  laity, 
and  even  some  physicians,  believe  that  gout  and  arthritis  deformans  are  in  some 
way  related,  but  this  view  is  erroneous. 

It  is  very  questionable  whether  all  cases  of  chronic  multiple  arthritis  are  refer- 
able to  the  causes  already  enumerated.  Such  other  influences,  however,  as  are 
concerned  in  its  production  are  not  at  all  understood.  Various  authorities  have 
maintained  that  arthritis  deformans  is  the  result  of  a  primary  disease  of  the  nerv- 
ous centers,  and  in  particular  of  the  spinal  cord.  We  regard  this  statement  as 
entirely  unwarranted.  It  originated  at  a  time  when  there  was  a  tendency  to 
ascribe  all  sorts  of  ills  to  disease  of  the  "  trophic  centers,"  but  there  is  no  doubt 
that  this  tendency  was  carried  very  much  too  far.  We  may  state  in  this  connec- 
tion that  a  careful  microscopic  examination  of  the  spinal  cord  in  one  case  of  very 
severe  arthritis  deformans  yielded  an  entirely  negative  result. 

[Some  striking  cases  are  reported  by  Blake,  which  go  to  show  that  the  arthritic 
changes  may  set  up  chronic,  though  slight,  suppuration,  in  analogy,  perhaps, 
with  the  synovitis  of  gonorrhoea.  Careful  examination  should  consequently  be 
made  of  all  the  mucous  membranes,  especially  in  cases  which  seem  to  have  no 
connection  with  true  rheumatism.] 

Predisposing  Influences.— Chronic  arthritis  is  mainly  a  disease  of  advanced 
years.  Certain  monarticular  varieties,  about  whose  aetiology,  it  must  be  confessed, 
we  know  little  as  yet,  have  been  termed  arthritis  senilis— in  particular  the  malum 
coxgr  senile.  Even  the  common  and,  in  a  certain  sense,  typical  form  of  arthritis 
deformans  {vide  infra)  is  not  apt  to  occur  in  people  under  thirty-five  years  of  age. 
This  rule,  however,  has  exceptions,  and  we  have  ourselves  seen  a  few  perfectly 
characteristic  cases  of  arthritis  deformans  in  children  between  ten  and  fifteen 
years  of  age.  Women  are  much  offener  attacked  than  men.  It  is  often  said  that 
trouble,  anxiety,  and  other  emotional  influences  favor  the  outbreak  of  the  disease; 
but  the  proof  of  this  is  lacking.     The  disease  does  not  often  seem  to  be  hereditary. 

Pathology. — The  process  is  described  as  simple  chronic  arthritis  so  long  as  it  is 
confined  mainly  to  the  synovial  membrane  of  the  joint  and  the  periarticular  con- 
nective tissue.  These  parts  often  undergo  decided  inflammatory  thickening;  the 
synovial  membrane  becomes  cloudy ;  and  the  amount  of  synovial  fluid  is  more  or 
less  increased— that  is,  we  have  chronic  dropsy  of  the  joint.     Sometimes  different 


CHRONIC  RHEUMATISM  AND  ARTHRITIS  DEFORMANS.       913 

parts  of  the  synovial  membrane  are  connected  by  adhesions,  which  considerably 
interfere  with  the  movements  of  the  joint.  There  may  even  be  complete  anchy- 
losis :  for  example,  in  the  shoulder  or  knee. 

Chronic  synovitis  may  pass  imperceptibly  into  arthritis  deformans.  In  this, 
not  only  the  capsules  of  the  joint,  but  the  articular  cartilages  and  the  articular 
extremities  of  the  bones,  are  so  much  affected  as  to  produce  the  most  striking 
deformity.  These  changes  almost  always  originate  in  the  articular  cartilages. 
The  cartilage  is  roughened  and  worn  away;  its  free  borders  and  surfaces  undergo 
proliferation  and  then  disintegration,  or  become  polished  on  the  surface,  while 
deeper  in  the  newly  formed  layers  of  cartilage  undergo  ossification.  The  under- 
lying bone  undergoes  inflammation  and  degeneration.  Sometimes,  also,  the 
periosteum  near  the  joints  undergoes  ossific  periostitis.  On  microscopic  examina- 
tion, we  find  fibrous  disintegration  of  the  matrix  of  the  cartilage,  and  prolifera- 
tion and  subdivision  of  the  cartilage-cells,  at  the  same  time  that  there  is  destruc- 
tion of  the  newly  formed  cells  by  simple  or  fatty  degeneration.  Analogous 
processes  of  proliferation  and  destruction  also  affect  the  bony  structures.  The 
synovial  membrane  is  invariably  affected  in  cases  of  any  severity.  Usually  the 
most  striking  change  is  a  great  proliferation  of  the  joint  villi,  which  may  cover 
the  walls  of  the  cavity  like  great  fringes. 

Of  course  the  normal  structure  of  the  joint  is  at  last  completely  destroyed  by 
these  various  pi'ocesses.  The  articular  extremities  of  the  bones  waste  away  more 
and  more,  and  take  new  relative  positions,  as  the  parts  which  impinge  upon  each 
other  are  worn  away.  Externally,  the  joint  usually  becomes  larger  and  larger ; 
and  this  is  the  more  evident  because  the  surrounding  muscles  undergo  great 
atrophy.  Often  there  is  no  synovial  fluid  whatever  {arthritis  sicca),  but  some- 
times there  is  a  considerable  effusion — for  instance,  in  the  knee-joint. 

Clinical  History. — The  symptoms  of  chronic  arthritis  are  usually  quite  simple 
and  uniform.  They  are  almost  exclusively  referable  to  the  local  disturbances 
and  their  results. 

Except  in  the  cases  which  are  preceded  by  acute  articular  rheumatism,  the  dis- 
ease usually  begins  quite  gradually  and  insidiously.  The  first  subjective  symp- 
toms are  stiffness  and  pain  in  the  joints,  the  latter  being  aggravated  by  pressure 
or  movement.  The  stiffness  is  most  noticeable  when  the  joint  has  remained  quiet 
for  some  time  previous,  and  is  therefore  ordinarily  greatest  on  waking  up  in  the 
morning.  The  pain  often  shoots  from  the  joints  upward  and  downward,  and  is 
of  a  burning  character,  or  less  often  neuralgic.  Even  in  advanced  cases  the  pain 
usually  occurs  only  when  the  affected  joints  are  moved,  although  then  it  may  be 
very  severe.  When  the  body  is  entirely  at  rest  there  is  little  or  no  pain.  Motion 
is  impaired  very  early.  This  is  due  at  first  to  the  pain,  and  to  a  certain  reflex  in- 
hibition and  ataxia  of  the  muscles ;  to  which  are  later  added  the  purely  mechanical 
hindrances  and  the  ever-increasing  atrophy  of  the  muscles. 

The  objective  changes  in  the  affected  joints  begin  to  appear  soon  after  the 
symptoms  just  mentioned,  at  least  in  cases  of  any  severity.  The  joints  seem 
enlarged  and  thickened.  If  we  attempt  to  move  them,  we  not  only  cause  pain 
and  meet  with  mechanical  obstruction,  but  we  may  hear  and  feel  the  cracking  and 
grating  produced  by  the  rubbing  of  the  denuded  and  uneven  surfaces  upon  each 
other.  This  is  often  noticed  by  the  patient  himself.  As  the  disease  gradually 
progresses,  there  are  usually  developed  certain  characteristic  deformities,  which 
are  apt  to  be  most  strikingly  exhibited  in  the  hands  (see  Fig.  117).  The  meta- 
carpophalangeal joints  are  thickened  and  swollen,  and  are  made  all  the  more 
prominent  because  the  interossei  upon  the  back  of  the  hand  are  atrophied.  The 
bases  of  the  first  phalanges  are  directed  obliquely  toward  one  side,  so  that  the  fin- 
gers assume  more  and  more  the  appearance  of  subluxation.  They  are  bent  over 
58 


914 


DISEASES  OF  THE  ORGANS  OF  LOCOMOTION. 


toward  the  back  of  the  hand,  and  are  also  displaced  toward  the  ulnar  side,  so  that 
they  often  actually  come  to  rest  one  upon  the  other.  The  palm  of  the  hand  is  fre- 
quently deeply  hollowed  out.  Often  the 
4  phalangeal  joints  are  also  distorted,  so 

H  that,  for  example,  there  will  be  an  ob- 

tuse angle  on  the  dorsal  surface  of  the 
fingers  between  the  first  and  second 
phalanx,  while  the  terminal  phalanx  is 
apt  to  be  flexed,  although  the  second 
phalanx  preserves  a  position  of  exten- 
sion. Despite  these  changes,  many  pa- 
tients, if  only  the  thumb  remains  toler- 
ably movable,  are  able  to  use  their 
hands  for  quite  delicate  work,  although 
at  the  expense  of  much  time  and  effort. 
The  feet  exhibit  analogous  deformities, 
but  seldom  to  the  same  extent  as  the 
hands.  The  knees  and  elbows  are  like- 
wise enlarged.  At  the  hip-joint,  sub- 
luxation is  not  infrequent,  the  head  of 
the  femur  slipping  upward.  The  mo- 
tion of  the  shoulder-joint,  and  as  a  con- 
sequence the  use  of  the  arms,  is  gradu- 
ally more  and  more  impaired.  If  the 
joints  of  the  lower  extremities  are 
affected,  of  course  it  becomes  painful 
and  difficult  either  to  get  up  or  to  walk. 
It  may  finally  be  necessary  for  the  pa- 
tient to  have  the  help  of  some  other 
person,  or  of  crutches. 

There  are  monarticular  and  polyar- 
ticular forms  of  the  disease — the  name  indicating  that  one  or  several  joints  are 
affected.  The  monarticular  form  is  usually  regarded  as  a  surgical  trouble,  and 
is  most  often  located  in  the  hip-joint  (malum  coxce  senile),  or  more  rarely  in  the 
knee-  and  shoulder-joints.  The  polyarticular  form  is  the  characteristic  one.  In 
most  of  the  typical  cases  it  begins  in  the  small  joints  of  the  hand  and  fingers.  At 
a  later  period  the  larger  joints  are  also  invaded,  one  after  the  other,  the  invasion 
taking  place  symmetrically  on  both  sides  of  the  body,  although  the  disturbance  is 
not  infrequently  greater  on  one  side  than  on  the  other.  In  severe  cases  the  joints 
of  the  spinal  column  are  also  involved.  This  impairs  particularly  the  movement  of 
the  head.  The  articulation  of  the  lower  jaw  is  usually  very  little  affected,  if  at  all. 
In- less  frequent  instances  the  arthritis  is  confined  principally  to  the  lower 
extremities,  while  the  upper  escape  intact  for  a  long  while,  or  even  permanently. 
It  is  very  possible  that  such  cases  often  have  a  different  aetiology  from  ordinary 
arthritis  deformans ;  and  the  same  is  true  of  the  cases  which  are  confined  mainly 
to  the  vertebral  column,  and  are  termed  spondylitis  deformans.  A  remarkable 
and,  as  it  seems  to  us,  unique  disorder  may  be  mentioned  in  passing.  It  leads 
very  gradually  and  painlessly  to  a  complete  anchylosis  of  the  entire  spinal  column 
and  the  hip-joints,  so  that  head,  trunk,  and  thighs  are  firmly  united  and  com- 
pletely stiffened,  while  all  the  other  joints  retain  their  normal  mobility.  It  need 
scarcely  be  said  that  this  necessarily  causes  a  peculiar  modification  of  the  carriage 
and  gait  of  the  sufferer.  We  have  ourselves  seen  two  cases  of  this  peculiar  affec 
tion  which  resembled  each  other  very  closely. 


Fig.  117.— Appearance  of  the  hand  in  a  case  of  pro- 
tracted arthritis  deformans. 


CHRONIC  RHEUMATISM  AND   ARTHRITIS  DEFORMANS.       915 

There  is  hardly  any  affection  of  parts  of  the  body  other  than  the  joints  in 
arthritis  deformans.  The  muscles  should  be  excepted,  for  they  always  undergo 
that  muscular  atrophy  which  we  have  already  described  (vide  page  905)  as  the 
result  of  joint  disease.  This  atrophy  is  most  marked  in  the  interossei,  the  shoulder 
muscles,  and  in  the  muscles  of  the  calf  and  thigh.  Sometimes  the  skin  over  the 
wrist  and  other  affected  joints  appears  peculiarly  wrinkled  and  flabby.  The  inter- 
nal organs  almost  always  perform  their  functions  in  a  perfectly  normal  manner. 
Appetite  and  digestion  remain  good,  although  there  is  often  some  tendency  to 
constipation.  Rarely  there  is  valvular  disease  of  the  heart,  but  usually  only  in 
such  cases  as  originate  in  an  acute  articular  rheumatism.  Once  in  a  while  it  is 
seen  in  cases  chronic  from  the  start.  This  last  fact  is  not  without  interest  from 
an  serological  point  of  view.  Sometimes  there  are  certain  nervous  symptoms 
to  be  observed,  such  as  headache,  congestion,  or  mental  depression,  but  these  are 
probably  not  the  direct  result  of  the  disease,  but  arise  indirectly  in  a  way  to  be 
easily  imagined. 

General  Course  of  the  Disease. — Arthritis  deformans  is  an  extremely  chronic 
trouble.  It  may  last  even  ten  or  twenty  years,  or  more.  Sometimes  there  is  an 
apparent  arrest  of  the  process  extending  over  months,  or  even  longer.  Sometimes 
the  progress  of  the  disease  is  marked  by  remissions  and  exacerbations,  affecting 
either  the  general  or  the  local  manifestations.  In  general,  however,  the  disease 
continually  advances. 

The  prognosis  is  therefore  unfavorable.  Recovery,  if  it  ever  occurs,  is  extremely 
rare,  and  is  possible  only  in  the  early  stages.  For  the  encouragement  of  the 
patient,  it  may  be  said  that  under  proper  care  and  treatment  the  disease  often  runs 
so  gradual  a  course  that  the  general  condition  remains  at  least  bearable  for  a  very 
long  while,  although  there  may  be  considerable  local  disturbance.  The  disease  is 
not  directly  dangerous  to  life.  The  eventual  fatal  termination  ensues  either  from 
general  debility,  or  because  of  some  intercurrent  disease. 

The  prognosis  is  somewhat  more  favorable  in  the  milder  cases  of  "chronic 
articular  rheumatism,"  where  the  anatomical  changes  are  less  severe,  and  are 
completely  limited  to  the  synovial  membrane.  Even  here,  however,  recovery  is 
by  no  means  frequent,  and  it  is  always  to  be  feared  that  grave  deformities  of  the 
joints  will  gradually  be  developed. 

Treatment.— With  regard  to  regimen,  it  is  requisite  in  the  first  place  to  avoid 
all  unfavorable  external  influences.  If  possible,  the  dwelling  should  be  dry  and 
warm ;  and  it  may  often  seem  advisable  to  make  a  change  of  climate.  The  patient 
must  dress  warmly,  without,  however,  undermining  his  powers  of  resistance  too 
much,  as  he  will  be  in  danger  of  doing.     The  diet  must  be  abundant  and  nutritious. 

Internal  remedies  may  be  tried,  with  the  hope  of  modifying  the  disease,  but  our 
chief  reliance  must  be  upon  local  treatment  of  the  joints.  Among  internal  reme- 
dies, the  most  important  are  iodine  and  arsenic.  Iodine  may  be  given  in  the  form 
of  tincture  (a  few  drops  in  mucilage  several  times  a  day),  or  a  better  form  is  in 
combination  with  potassium.  As  yet,  we  ourselves  have  not  seen  any  great  benefit 
from  iodine,  but  we  have  in  repeated  instances  witnessed  a  quite  striking  result  from 
the  use  of  arsenic.  It  is  best  administered  in  pills  containing  one  thirtieth  to  one 
fifteenth  of  a  grain  (grm.  0-002-0-004)  of  arsenious  acid,  one  pill  two  or  three  times 
a  day.  If  this  remedy  prove  beneficial,  it  must  be  continued  for  at  least  months, 
perhaps  with  occasional  brief  intermissions.  Salicylic  acid  and  antipyrine  have 
no  permanent  effect,  and  are  useful  only  when  there  is  an  acute  exacerbation  of 
the  disease.  The  preparations  of  Colchicum  may  be  tried,  but  they  will  seldom  be 
found  efficient.  Iron,  quinine,  and  cod-liver  oil  are  sometimes  indicated  by  the 
general  condition. 

First  among  local  methods  of  treatment  comes  massage,  although  the  good  it 


916  DISEASES  OF  THE  ORGANS  OF  LOCOMOTION. 

accomplishes  is,  of  course,  apt  to  be  evanescent.  It  will,  however,  do  much  to 
hasten  the  absorption  of  inflammatory  exudations,  and  also  to  loosen  up  the 
joints,  invigorate  the  muscles,  and  improve  the  general  health.  The  Swedish 
movement  cure  will  be  found  of  great  benefit  in  all  cases  if  begun  early  and 
methodically  persevered  in.  It  preserves  the  mobility  of  the  joints  as  long  as 
anything  can.  Electricity  also  has  a  palliative  influence.  The  galvanic  cur- 
rent is  applied  to  the  affected  joints,  and  the  faradic  current  to  the  atrophied 
muscles. 

Baths  are  universally  employed  in  chronic  arthritis.  Their  value  should  not  be 
overestimated,  but  it  is,  notwithstanding,  undeniable  in  many  cases.  Simple  warm 
baths,  or  salt  baths  (two  to  ten  pounds  of  salt  for  each  bath),  are  practicable  in 
almost  any  household.  As  health-resorts  in  arthritis  deformans,  experience  shows 
the  following  to  be  most  desirable:  The  different  warm  baths,  such  as  Teplitz, 
Wildbad,  Ragatz,  and  Baden  in  Switzerland;  the  warm  chloride-of-sodium  baths 
in  Wiesbaden;  the  acidulated  baths  of  Oeynhausen  and  Nauheim;  and  the  mud 
baths  of  Elster,  Marienbad,  Franzensbad,  and  Schmiedeberg.  Steam  baths  are 
admissible  only  in  the  early  stages  of  the  disease,  and  for  patients  whose  general 
condition  is  still  vigorous.     Even  then  they  should  be  employed  cautiously. 

[The  mineral  springs  within  the  limits  of  our  own  country  chiefly  to  be  recom- 
mended are  Sharon  and  Richfield,  in  New  York  State,  the  Sulphur  Springs  of 
Virginia,  and  the  Hot  Springs  of  Arkansas.  At  the  two  former,  particularly, 
there  is  every  provision  for  comfort  as  well  as  for  the  use  of  the  waters.] 

We  have  repeatedly  seen  quite  excellent  results  follow  the  employment  of  hot 
sand-baths.  These  also  can  be  easily  used  at  home,  particularly  if  applied  merely 
to  the  hands  or  feet.  They  are  employed  more  elaborately  in  Köstritz  and  Blase- 
witz.  These  hot  sand-baths  seem  to  do  good,  not  only  from  the  temperature, 
but  also  from  the  uniform  and  persistent  compression  which  they  exert. 

Stimulating  or  narcotic  remedies  may  be  rubbed  into  the  joints,  but  they  are 
beneficial  only  because  of  the  massage  which  accompanies  their  employment.  In 
practice  it  is  not  always  possible  to  omit  their  use.  The  application  of  tincture  of 
iodine  is  usually  entirely  without  effect.  As  to  morphine  and  other  narcotics,  the 
disease  is  so  chronic  that  it  is  desirable  to  employ  them  as  little  as  possible.  A 
considerable  number  of  those  who  suffer  from  chronic  arthritis  become  opium- 
eaters. 

We  may  say,  therefore,  that  the  use  of  the  various  remedies  which  have  been 
suggested  will  enable  us  to  oppose  some  obstacles  to  the  progress  of  the  dis- 
ease. Persistent  treatment  will,  in  many  cases,  be  rewarded  by  at  least  tempo- 
rary improvement. 


CHAPTER  III. 

ACUTE   AND   CHRONIC   MUSCULAR  RHEUMATISM. 

(Myositis,  or  Myalgia,  Eheurnatica.) 

Definition  and  iEtiology. — Certain  acute  affections  may  originate  primarily  in 
the  muscles.  These  are  to  all  appearance  inflammatory  in  their  character,  and  not 
infrequently  result  from  taking  cold,  or  other  causes  similar  to  those  which  pro- 
duce acute  articular  rheumatism.  These  affections  are  classed  as  "acute  muscu- 
lar rheumatism,"  or  rheumatic  myositis.  It  is  possible  that  this  disease  is  also  an 
infectious  one,  but  the  question  remains  entirely  undecided.  The  analogy  which 
this  trouble  bears  to  acute  articular  rheumatism  is  not  complete.     It  is  seldom 


ACUTE  AND   CHRONIC  MUSCULAR  RHEUMATISM.  917 

that  the  two  processes  are  seen  in  combination;  and,  furthermore,  acute  myositis 
is  not  "  polymuscular,"  but  is  usually  confined  to  one  muscle,  or  to  a  single  group 
of  muscles;  and  it  is  never  followed  by  acute  endocarditis.  Tbe  two  diseases, 
therefore,  are  alike  only  in  certain  symptoms  (pain  and  impairment  of  motion), 
and  in  the  fact  that  they  are  often,  although  not  always,  ascribable  to  wet  or 
cold,  and  the  like.  There  are  many  cases  where  pain  suddenly  occurs  in  the  mus- 
cles ("myalgia")  without  any  attendant  objective  change.  These  cases  can  not 
be  called  genuine  acute  myositis.  Indeed,  it  is  sometimes  diffcult  to  know  how 
to  regard  them.  In  practice  they  are  often  termed  muscular  rheumatism,  espe- 
cially when  they  are  referable  to  exposure;  and  it  is  possible  that  many  such 
cases  are  really  a  very  mild  form  of  the  genuine  inflammatory  disease.  On  the 
other  hand,  however,  there  must  often  be  some  different  process  going  on.  Tbus, 
traumatic  pain  in  the  muscles  is  the  result  of  some  excessive  strain,  and  in  many 
instances  is  apparently  due  to  laceration  of  some  of  the  muscular  fibers.  This  is 
generally  occasioned  by  too  violent  muscular  exertion.  Any  physician  who  sees 
many  patients  from  the  laboring  classes  meets  with  an  abundance  of  cases  of  this 
sort.* 

The  limitations  of  acute  muscular  rheumatism  are  obscure;  but  still  more  so 
are  those  of  "chronic  muscular  rheumatism."  This  disease  is  also  a  frequent  one, 
and  only  imperfectly  understood.  It  does  not  bear  a  close  analogy  to  chronic 
articular  rheumatism,  except  in  this  point,  that  chronic  muscular  rheumatism 
seems  to  be  quite  often  occasioned  by  meteorological  influences.  While  the  ana- 
tomical changes  in  chronic  articular  rheumatism  are  almost  always  striking, 
similar  lesions  are  very  exceptional  in  chronic  muscular  rheumatism.  On  the 
contrary,  the  name  is  usually  applied  to  cases  where  there  is  pain  in  various  mus- 
cles all  over  the  body,  but  where  there  is  no  discoverable  objective  disturbance. 
Older  authorities  used  to  speak  of  "rheumatic  induration"  of  the  muscles,  but 
this  or  any  other  actual  anatomical  change  is  very  exceptional. 

These  facts  justify  a  doubt  as  to  whether  all  cases  of  chronic  muscular  rheu- 
matism actually  deserve  their  name.  It  is  certainly  quite  appropriate  in  those  not 
infrequent  cases  which  are  due  to  "  rheumatogenous  influences,"  and  which  are  so 
evidently  aggravated  upon  every  exposure  to  cold,  or  every  period  of  bad  weather, 
that  the  patient  often  asserts  that  he  carries  in  his  legs  the  best  of  thermometers. 
Such  is  the  "  old  rheumatism  "  of  those  who  have  passed  a  large  part  of  their  lives 
in  the  open  air,  regardless  of  wind  or  weather.  There  are  other  cases,  the  charac- 
ter of  which  is  different.  In  them  the  muscular  pain  is  associated  with  a  general 
neurasthenic  condition,  or  with  corpulence  (when  it  is,  perhaps,  the  result  of  cir- 
culatory disturbance),  or  possibly  with  chronic  poisoning.  An  important  instance 
is  the  "  rheumatic  pain  "  sometimes  complained  of  by  topers,  which  we  are  inclined 
to  ascribe  not  to  changes  in  the  muscles  but  to  nutritive  disturbances  of  the  nerves. 
For  these  and  similar  disorders  there  are  no  special  names,  and  the  practicing  phy- 
sician often  terms  them  all  "muscular  rheumatism,"  a  diagnosis  with  which  the 
patient  is  usually  quite  contented. 

Clinical  History. — Genuine  acute  muscular  rheumatism  is  usually,  as  has  been 
said,  limited  to  some  one  definite  group  of  muscles.  The  affected  muscles  often 
seem  somewhat  swollen  and  infiltrated,  are  very  sensitive  to  pressure,  and,  if  not 
quite  useless,  are  nearly  so,  greatly  impairing  the  motion  of  the  corresponding 
member  of  the  body.  All  these  symptoms  are  best  illustrated  in  acute  myositis  of 
the  deltoid  (omalgia).     The  whole  shoulder  is  swollen,  the  muscle  is  very  painful, 

*  Some  time  ago  I  saw  an  organ-player  who  had  to  work  the  pedals  for  many  hours  a  day ;  he  had 
an  extremely  painful  affection  of  the  lower  extremities  associated  with  swelling,  which  could  be  re- 
garded only  as  an  acute  myositis. 


918  DISEASES  OF  THE  ORGANS  OF  LOCOMOTION. 

and  the  upper  arm  is  almost  incapable  of  voluntary  motion,  although,  if  caution 
be  exercised,  passive  movement  can  be  made  without  causing  any  pain. 

The  various  forms  of  acute  muscular  rheumatism  have  received  names  descrip- 
tive of  the  locality  of  the  affection.     We  have : 

1.  Omalgia,  as  already  mentioned. 

2.  Acute  rheumatic  myositis  of  the  cervical  muscles,  myalgia  cervicalis,  or 
rheumatic  torticollis.  Here  the  muscles  of  the  back  of  the  neck  and  throat  are 
very  painful.  The  head  is  usually  held  to  one  side,  and,  in  severe  cases,  is  almost 
perfectly  immovable. 

3.  Lumbago,  or  myalgia  lumbalis.  This  is  the  most  frequent  form  of  acute 
muscular  rheumatism.  The  common  people  in  Germany  have  termed  it  "  witch's 
shot"  (Hexenschuss),  on  account  of  its  sudden  onset.  The  entire  lumbar  region 
is  very  sensitive ;  and  any  motion  of  the  trunk,  such  as  stooping  or  turning,  is 
extremely  difficult  and  painful.  The  disease  is  more  frequent  in  men  than  in 
women.  Certain  persons  seem  to  be  especially  predisposed  to  it.  It  should  also 
be  stated  that  lumbago  is  not  always  of  a  rheumatic  character,  but  of  traumatic 
origin,  as  from  lifting  a  heavy  weight,  or  from  sudden  stooping.  [It  is  very  com- 
mon in  the  traumatic  neuroses,  where  it  was  once  regarded  as  indicative  of  spinal 
injury.— K.] 

4.  Rheumatism  of  the  thoracic  muscles,  and  particularly  of  the  intercostals. 
This  may  cause  great  discomfort,  as  it  renders  breathing,  coughing,  and  sneezing 
very  painful.  It  is  comparatively  rare ;  and  caution  should  be  exercised  in  diag- 
nosticating it  to  avoid  confusion  with  pleurisy  and  periostitis  of  the  ribs.  Very 
often,  also,  thoracic  disturbance  is  regarded  as  rheumatic  when  it  is  really  trau- 
matic, being  the  result  of  stretching  or  laceration  of  the  fibers  of  the  pectoral  or 
other  muscles. 

5  Rheumatism  of  the  head  also,  probably,  belongs  in  this  category,  although 
the  affection  is  seldom  confined  to  the  muscles  of  the  scalp,  but  involves  also  the 
fasciae,  and  may  even  be  almost  confined  to  them.  It  is  not  infrequently  excited 
by  exposure  to  cold.  The  pain  is  quite  violent,  and  greatly  increased  by  any 
movement  of  the  scalp.  Of  course,  the  diagnosis  requires  the  previous  exclusion 
of  the  various  forms  of  headache  described  on  pages  530  and  591. 

The  duration  of  acute  muscular  rheumatism  is  brief.  Usually  the  pain  abates 
in  a  few  days ;  but  a  tendency  to  relapse  persists  for  some  time.  In  chronic  mus- 
cular rheumatism  there  are  usually  no  objective  changes  to  be  detected.  The  pain 
is  seldom  located  permanently  in  any  one  place,  but  it  is  felt  first  here  and  then 
there.  It  is  usually  increased  during  bad  weather,  and  is  less  severe  when  the 
weather  is  warm.  The  pains  are  often  described  as  "wandering."  Motion  is. sel- 
dom much  impaired.  Sometimes,  however,  there  may  be  a  certain  stiffness  of  the 
muscles,  most  marked  after  a  period  of  rest. 

The  diagnosis  of  chronic  muscular  rheumatism  rests,  therefore,  mainly  upon 
the  rational  signs.  Hence  it  is  often  impossible  to  avoid  the  suspicion  of  malin- 
gering, particularly  where  certain  applicants  for  hospital  care  are  concerned.  We 
should  not,  however,  be  too  uncharitable,  since  without  doubt  there  are  cases 
where  quite  severe  pain  is  felt,  now  in  one  set  of  muscles  and  now  in  another, 
without  any  anatomical  basis  for  such  pain  being  discoverable.  Nor  should  we 
ever  forget  that  other  diseases  may  have  pain  for  their  first  symptom.  It  is  not 
at  all  exceptional  for  the  lancinating  pains  of  locomotor  ataxia  to  be  for  a  long 
time  regarded  as  "lumbago."  Lumbago  may  be  confounded  with  insidiously 
developing  diseases  of  the  vertebrae,  or  with  various  hypogastric  disorders  (par- 
ticularly in  women).  We  should  therefore  never  omit  to  make  a  careful  phys- 
ical examination. 

Treatment. — Acute   muscular  rheumatism  has   this   in   common   with  acute 


ACUTE  POLYMYOSITIS.  919 

articular  rheumatism,  that  it  is  usually  very  favorably  affected  by  salicylic  acid. 
In  cases  of  genuine  acute  rheumatic  myositis  the  employment  of  this  remedy  in 
the  manner  already  described,  for  twelve  to  twenty-four  hours,  will  often  give 
surprising  relief.  We  also  see  good  results  from  antipyrine.  Local  treatment  of 
the  affected  muscles  may  also  be  followed  by  great  and  speedy  improvement. 
Massage  is  particularly  valuable.  It  is  not  infrequently  the  case  that  a  single 
properly  conducted  massage  will  cause  a  violent  lumbago  or  omalgia  to  disappear 
almost  completely,  and  like  favorable  results  are  witnessed  where  there  is  trau- 
matic pain  of  the  muscles.  Most  of  the  external  applications  which  are  so  fre- 
quently prescribed  for  rheumatism — such  as  spirits  of  camphor  or  chloroform  lini- 
ment— accomplish  less  through  the  cutaneous  irritation  they  produce  than  by  the 
massage  incident  to  their  employment.  Next  in  value  comes  electricity.  Both 
the  constant  and  the  faradic  current  may  be  employed.  Simple  counterirritation 
by  means  of  mustard  poultices  or  hot  compresses  will  often  prove  palliative,  but 
it  is  less  effective  than  the  remedies  previously  mentioned.  Great  benefit  often 
follows  excessive  perspiration.  The  best  means  to  this  end  is  a  steam  bath.  This 
is  so  favorite  a  remedy  that  patients  often  take  it  of  their  own  accord. 

In  chronic  muscular  rheumatism  the  benefit  of  salicylic  acid  and  antipyrine  is 
merely  temporary,  and  therefore  is  to  be  sought,  if  at  all,  only  when  there  is  an 
acute  exacerbation.  Massage  and  electricity  are  more  effective,  and,  if  persevered 
in  for  some  time,  will  often  accomplish  good  results  even  in  obstinate  cases. 
Treatment  by  baths  is  frequently  prescribed  with  advantage.  Steam  baths  are 
often  beneficial,  but  their  use  requires  great  caution  where  the  patient  is  corpulent 
and  has  a  tendency  to  congestion  or  cardiac  failure.  There  is  also  value  in  mud 
baths,  pine-needle  baths,  and  in  the  baths  given  at  Teplitz,  Wiesbaden,  and  other 
places. 

In  many  cases  of  chronic  muscular  rheumatism  constitutional  treatment  is  of 
great  importance.  Particularly  where  the  patient  is  overfed,  and  intemperate  in 
the  use  of  alcohol,  much  benefit  will  often  be  accomplished  by  a  proper  regulation 
of  the  ingesta  and  the  prescription  of  a  sufficient  amount  of  muscular  exercise. 
Such  patients  may  also  be  helped  by  a  cautiously  conducted  cold-water  treatment. 

[In  acute  cases  with  localized  pain  I  have  found  a  thick  flaxseed  poultice, 
applied  as  hot  as  it  can  be  borne,  renewed  once  or  twice,  and  followed  by  the 
application  of  a  thick  layer  of  cotton,  useful. 

A  dry  cup  or  two  is  also  often  productive  of  great  relief.  In  chronic  cases, 
plasters  and  the  iodide  of  potash  are  often  of  benefit. 

Muscular  rheumatism  is  a  common  and  often  very  troublesome  affection  in 
those  whose  occupation  calls  for  decided  muscular  exertion.  A  muscle  is  strained, 
pain  settles  in  and  is  apt  to  recur  in  the  part;  and,  while  the  general  health  is  suf- 
ficiently good,  the  man  is  compelled  to  remain  idle.  Quack  advertisements  dwell 
so  much  upon  pain  in  the  back  as  a  symptom  of  Bright's  disease,  that  we  are  fre- 
quently consulted  by  those  who,  suffering  from  muscular  pain  and  soreness,  think 
themselves  the  subjects  of  serious  disease  of  the  kidneys.] 

APPENDIX. 

ACUTE  POLYMYOSITIS. 

From  some  very  recent  observations  (E.  Wagner,  Unverricht,  and  others)  we 
have  obtained  knowledge  of  a  disease  which  consists  essentially  of  an  acute  inflam- 
mation of  most,  or  even  of  all,  the  muscles  of  the  body.  The  disease  occurs  chiefly 
in  young  or  middle-aged  persons.  Without  special  cause  they  begin  to  have 
pains  in  the  arms,  legs,  and  trunk,  which  more  or  less  rapidly  result  in  a  consid- 


920  DISEASES  OF  THE  ORGANS  OF  LOCOMOTION. 

erable  disturbance  of  motion.  The  general  disturbance  is  at  first  slight,  but  it  in- 
creases later,  especially  if,  as  usually  happens,  there  be  fever.  A  marked  cedem- 
atous  swelling  is  soon  very  noticeable;  it  is  irrst  seen  on  the  extensor  side  of  the 
extremities,  and  later  in  the  face  and  trunk.  The  oedema  is  stiff  and  painful,  and 
it  may  be  very  considerable.  As  soon  as  the  muscles  of  deglutition  and  respiration 
are  affected  the  whole  condition  becomes  distinctly  worse.  It  becomes  harder 
and  harder  to  take  food,  and  there  is  severe  dyspnoea.  Bronchitis  and  lobular 
pneumonia  soon  develop,  which  become  the  more  distressing,  since  expectoration 
is  more  and  more  impaired,  and  finally  becomes  impossible.  The  spleen  as  a  rule 
seems  swollen.     There  is  usually  a  marked  tendency  to  sweating. 

In  the  cases  thus  far  published  death  always  ensues  after  a  few  weeks,  with 
symptoms  of  extreme  dyspnoea  and  cyanosis.  We  do  not  yet  know  certainly 
whether  there  are  also  milder  cases  which  recover. 

In  the  cases  observed  thus  far  there  was  on  examination  a  true  acute  inflam- 
mation of  the  muscles.  Not  only  do  the  muscular  fibers  show  all  forms  of  degen- 
eration and  destruction,  but  also  in  the  interstitial  connective  tissue  we  find  true 
inflammatory  foci  (accumulation  of  nuclei  about  the  vessels,  etc.).  In  a  case 
which  we  recently  examined  these  changes  were  apparently  to  be  found  in  all  the 
muscles,  even  in  the  tongue,  the  ocular  muscles,  etc.  In  genuine  polymyositis  the 
peripheral  nerves  are  found  to  be  perfectly  normal,  but  it  is,  of  course,  possible  that 
on  future  investigation  relations  may  be  established  between  polymyositis  and 
multiple  neuritis  {vide  supra). 

The  diagnosis  of  polymyositis  will  probably  soon  be  comparatively  easy,  when 
the  disease  becomes  better  known.  The  distinction  from  trichinosis  must  be  the 
most  difficult;  here  we  must  first  of  all  consider  the  aetiology.  Polymyositis  is  to 
be  distinguished  by  the  pronounced  oedema  from  multiple  neuritis,  which  in  other 
respects  closely  resembles  it. 

Experience  is  still  limited  in  regard  to  the  treatment  of  the  disease.  We 
would  first  recommend  the  exhibition  of  salicylic  preparations,  antipyrine,  and 
similar  remedies.  Toward  the  close  of  the  disease  narcotics  usually  become  un- 
avoidable. 


CHAPTER  IV. 

RACHITIS. 

(Richcts.) 


iEtiology. — The  first  accurate  description  and  the  now  universal  name  of 
"rachitis"  (from  ß&xis,  the  spinal  column)  is  to  be  ascribed  to  the  Englishman 
Glisson,  who  published  a  comprehensive  monograph  upon  this  disease  in  1650.  It 
was  his  opinion  that  it  first  appeared  in  England  in  the  beginning  of  the  seven- 
teenth century;  and  for  this  reason  rachitis  is  still  often  called  by  Germans  "the 
English  disease." 

Although  the  clinical  and  anatomical  phenomena  of  rachitis  have  been  often 
and  accurately  investigated  since  that  time,  its  true  cause  still  remains  entirely 
unknown.  It  is  certain  only  that  its  development  is  promoted  by  all  unfavorable 
external  circumstances  affecting  the  nourish  me  at  and  health  of  the  child.  It  is 
therefore  more  frequent  among  the  poor  than  the  wealthy,  in  the  clamp  and 
crowded  quarters  of  large  cities  than  in  the  country,  and  among  artificially  fed, 
and  therefore  weakly  and  anaemic  children,  than  such  as  receive  the  mother's 
milk.     Nevertheless,  the  essential  cause  of  the  disease  is  not  to  be  sought  among 


RACHITIS.  921 

these  various  influences,  for  rickets  undoubtedly  does  occur,  although  rarely,  in 
children  whose  circumstances  seem  in  every  respect  most  favorable. 

Guerin,  Friedleben,  E.  Voit,  Wagner,  Baginsky,  and  many  others  have  made 
very  exhaustive  experimental  researches  with  regard  to  the  development  of 
rachitis.  It  has  been  found  possible  to  produce  certain  changes  in  the  bones  of 
growing  animals  by  giving  them  as  little  lime  as  possible  in  their  ingest  a,  or  by 
administering  very  large  amounts  of  lactic  acid,  with  the  purpose  of  dissolving 
the  calcium  salts,  or  by  giving  small  quantities  of  phosphorus.  The  changes  thus 
caused  have  been,  with  more  or  less  correctness,  regarded  as  analogous  to  those 
of  rachitis.  These  investigations  are  of  great  interest  with  regard  to  the  physiol- 
ogy of  bony  structures  in  general,  but  in  our  opinion  they  throw  little  light  upon 
the  clinical  question  which  here  concerns  us.  It  is  indeed  natural  enough  to  sup- 
pose that  rachitis  in  childhood  may  be  due  to  an  insufficient  proportion  of  lime  in 
the  food;  or  to  a  defective  absorption  of  the  lime-salts,  on  account  of  intestinal 
catarrh;  or  to  an  abnormally  abundant  production  of  lactic  acid,  or  even  of  car- 
bonic acid,  which  may  dissolve  the  lime-salts  in  the  system ;  but  every  one  of 
these  theories  is  contradicted  by  the  facts  of  experience ;  for  it  is  wholly  improper 
to  assume  that  the  food  of  children  with  rachitis  contains  less  lime  than  the  food 
of  healthy  children,  and  the  hypothesis  of  a  mere  poverty  in  lime  of  the  bony  tis- 
sues is  by  no  means  adequate  to  explain  the  whole  complicated  rachitic  process. 
In  our  opinion  everything  seems  to  indicate  that  some  special,  specific,  aetiological 
factor  is  requisite  for  the  development  of  rachitis.  This  factor,  however,  is  as  yet 
entirely  unknown  to  us.  The  thought  had  occurred  to  many  that  the  disease 
bears  some  relation  to  congenital  syphilis;  but  this  assumption  has  long  since 
been  proven  to  be  entirely  without  foundation.  It  is  also  claimed  that  heredity 
plays  an  important  part  in  rachitis.  The  proof  of  this  is  lacking.  It  is,  however 
noteworthy  that  quite  often  several  children  of  the  same  family  are  attacked  by 
the  disease. 

Rickets  is  most  common  in  children  of  two  or  three  years  old.  According  to 
Kassowitz,  the  disease  usually  begins  in  the  first  months  of  life,  while  the  severe 
symptoms,  of  course,  appear  only  at  the  age  of  two  or  three  years.  Congenital 
rachitic  changes  (foetal  rachitis)  have  been  repeatedly  observed,  but  the  cases  of 
so-called  rachitis  tarda,  where  the  disease  is  said  to  develop  in  children  of  eight 
or  ten  years  of  age  and  over,  are  at  least  extremely  rare. 

Sex  exercises  no  great  influence  upon  the  occurrence  of  the  disease. 

Pathology. — Rachitis  consists  in  a  peculiar  disturbance  of  the  processes  con- 
nected with  the  growth  of  the  bones.  As  a  result  of  an  increased  absorption  of  the 
already  formed  bony  tissue,  and  especially  as  a  result  of  an  insufficient  or  an 
almost  wholly  deficient  deposition  of  lime-salts,  the  bones  become  or  remain 
abnormally  flexible  and  soft,  so  that  they  can  easily  be  cut  with  a  knife. 

Upon  minute  examination,  we  find  both  the  periosteum  and  the  marrow  much 
reddened  and  congested.  If  we  try  to  detach  the  thickened  periosteum  from  the 
bone,  not  infrequently  a  few  bits  of  bone  adhere  to  the  membrane.  The  most 
striking  changes,  however,  are  exposed  upon  making  a  longitudinal  section  of  the 
bone.  They  are  located  at  the  base  of  the  epiphyses,  because  here  is  the  place 
where  the  normal,  and  therefore  the  abnormal,  processes  of  ossification  are  most 
active.  Under  normal  circumstances,  the  epiphyseal  cartilage  of  the  bones  in  child- 
hood is  separated  from  the  main  shaft  by  two  narrow  layers :  first,  an  outer  one, 
nearest  the  epiphyseal  cartilage,  of  a  bluish  color,  and  one  or  two  millimetres  thick; 
this  is  the  proliferative  layer,  or  hyperplastic  zone,  where  the  cartilage-cells 
become  divided  and  arrange  themselves  in  rows.  Secondly,  an  inner,  dull  yellow 
layer,  only  about  half  a  millimetre  thick,  known  as  the  ossiflc  layer,  or  zone 
of  calcification,  in  which  the  real  process  of  ossification  takes  place.     That  is, 


922  DISEASES  OF  THE  ORGANS  OF  LOCOMOTION. 

blood-vessels  grow  into  it,  osteoblasts  develop,  lime  is  deposited,  and  medullary 
spaces  are  hollowed  out.  In  healthy  bone  these  two  layers  are  parallel  to  each 
other,  and  are  limited  by  perfectly  straight  lines.  In  rachitic  bone,  on  the  other 
hand,  they  are  both  much  enlarged,  and  their  naturally  sharp  boundaries  are 
replaced  by  an  irregular  serrated  edge,  so  that  the  two  zones  encroach  mutually 
upon  each  other.  These  changes  affect  both  layers,  but  are  most  marked  in  the 
proliferative  layer.  Upon  microscopical  examination,  the  details  of  which  can 
not  be  given  here,  we  can  see  most  plainly  the  complete  confusion,  if  we  may  be 
permitted  to  use  the  expression,  into  which  the  growth  of  the  bone  has  fallen. 
The  proliferation  of  the  cartilage-cells  has  increased  beyond  all  bounds,  and  the 
scanty  matrix  of  the  cartilage  displays  a  fibrous  character.  In  the  bony  layer  are 
saen  irregularly  scattered  foci,  which  are  already  undergoing  incomplete  calcifica- 
tion, or  marrow  formation,  breaking  down  the  cartilage.  The  latter  is  due  to  an 
invasion  of  the  vessels,  which  are  always  affected  in  an  active  new  growth,  pierce 
the  cartilage  like  lacunar  spaces,  and  are  surrounded  by  a  so-called  osteoid  tissue. 

The  periosteum  presents  analogous  changes.  The  innermost  osteoblastic  layer 
of  the  periosteum  is  thickened ;  but  the  newly  formed  tissue  does  not  become  com- 
pletely calcified,  but  remains  in  large  part  soft  and  spongy.  Finally  an  increased 
absorption  of  bone  takes  place  inside  the  bones.  The  bony  partitions  disappear, 
and  the  cortical  layer  of  bone  often  becomes  much  smaller. 

These  various  processes  furnish  a  direct  explanation  of  the  macroscopic  changes 
presented  by  rachitic  bones.  The  proliferative  process  causes  marked  swelling  of 
the  epiphyses  of  the  long  bones,  and  thickening  of  the  flat  bones  of  the  skull. 
The  abnormal  softness  of  the  bones  is  due  to  the  increased  absorption  of  bone, 
their  insufficient  calcification,  and  it  in  turn  causes  various  deformities,  which 
are,  for  the  most  part,  very  characteristic  {vide  infra).  If  recovery  takes  place, 
the  whole  bone  becomes  firm  at  last,  but  often  remains  permanently  deformed. 

The  deficient  development  of  rachitic  bones  can  also  be  recognized  upon  chem- 
ical examination.  While  normal  bones  in  a  dry  state  contain  about  sixty-three 
to  sixty-five  per  cent,  of  lime,  rachitic  bones  have  only  about  twenty  to  thirty  per 
cent. 

Clinical  History. — Rachitis  often  begins  so  insidiously  that  it  can  hardly  be 
detected.  Attention  is  not  called  to  the  disease  until  the  deformity  of  the  bones 
becomes  very  obvious,  or  it  is  noticed  that  the  child  does  not  learn  to  walk  as 
early  as  other  children,  or,  having  already  learned,  is  no  longer  able  to  do  so. 
At  last  the  anxiety  of  the  parents  is  excited;  and,  on  seeking  medical  advice,  they 
find  their  fears  only  too  well  grounded. 

In  other  cases,  certain  prodromata  precede  the  development  of  the  character- 
istic changes  in  the  bones,  which  are  especially  mentioned  by  Oppenheimer. 
There  is  often  a  peculiar  form  of  diarrhoea,  which  is  said  to  occur  only  in  the  first 
half  of  the  day,  being  entirely  absent  at  other  times.  The  discharges  are  scanty 
and  almost  colorless.  Not  infrequently  the  diarrhoea  is  attended  by  fever,  and  it 
is  said  that  the  spleen  is  almost  invariably  swollen.  The  children  are  pale,  but 
not  emaciated.  The  first  characteristic  changes  in  the  cartilages  of  the  ribs  and 
elsewhere  are  said  to  appear  within  two  or  three  weeks  of  these  first  symptoms. 
In  other  cases,  Oppenheimer  observed  that  the  development  of  rachitis  was  pre- 
ceded by  attacks  of  screaming  at  night,  likewise  associated  with  intermittent 
elevations  of  temperature  and  splenic  tumor ;  or,  again,  there  were  simple  febrile 
attacks  at  night,  which  passed  away  in  the  morning  with  profuse  perspiration. 

These  facts  indicate  that  the  entire  organism  is  considerably  affected  by  rachitis. 
It  would  seem  reasonable  to  suppose  that  the  disorder  is  caused  by  some  specific 
infection.  That  this  infection  is  malarial,  as  Oppenheimer  thought,  is  more  than 
improbable. 


RACHITIS.  933 

The  diagnosis  of  rachitis  can  not  be  definitely  established  until  the  character- 
istic changes  in  the  bones  have  been  developed.  These  anomalies  vary,  of  course, 
in  their  severity  and  extent  in  different  cases.  We  append  a  list  of  the  most 
important: 

The  head  is  often  noticeable  for  its  great  size  and  somewhat  square  shape;  the 
fontanelles  remain  open  until  the  second  or  third  year  of  life;  their  edges  seem 
soft  and  yielding;  the  thinness  and  softness  of  the  occiput  is  sometimes  very 
striking,  so  that  it  can  be  pressed  in  like  parchment.  This  phenomenon  (the 
craniotabes  of  Elsässer)  appears  to  be  due  to  the  pressure  exerted  upon  the  occiput 
when  the  child  is  lying  on  its  back.  There  is  often  a  peculiar  change  in  the  shape 
of  the  jaws,  particularly  of  the  lower  jaw.  This  is  not  rounded,  but  angular, 
being  sharply  bent  in  the  neighborhood  of  the  canine  teeth ;  so  that  the  incisors 
stand  in  a  perfectly  straight  line,  besides  being  somewhat  inclined  inward.  Fleisch - 
mann  was  the  first  to  describe  this  condition,  and  referred  it  to  the  action  of  the 
mylohyoid  and  masseter  muscles  upon  the  soft  bone.  Dentition  in  rachitic  chil- 
dren is  usually  tardy  and  tedious. 

The  thorax  presents,  even  in  the  mildest  cases,  very  characteristic  and  notice- 
able changes.  There  is  a  swelling  at  the  junction  of  the  cartilages  with  the  ribs> 
which  can  be  felt  and  seen  through  the  skin,  and  produces  what  is  called  the 
"rosary  of  rickets."  In  severe  cases  the  lateral  portions  of  the  thorax  are  often 
drawn  inward,  particularly  at  the  parts  which  correspond  with  the  insertion  of 
the  diaphragm.  This  change  is  due  mainly  to  the  action  of  the  diaphragm  during 
inspiration  upon  the  abnormally  soft  and  therefore  yielding  ribs.  The  changes 
are  greatest  when  the  respiratory  efforts,  and  particularly  abdominal  respiration, 
are  exaggerated  because  of  bronchitis,  pneumonia,  or  some  other  disease  of  the 
air-passages.  In  such  cases  the  entrance  of  air  into  the  lungs  is  impeded,  so  that 
it  is  possible  that  the  external  atmospheric  pressure  also  contributes  to  produce 
the  deformity  of  the  thorax.  Deep  hollows  may  finally  be  developed  on  each  side 
of  the  chest,  while  the  sternum  becomes  unusually  prominent,  giving  the  whole 
chest  that  shape  which  has  been  termed  pigeon-breast,  or  pectus  carinatum. 
When  once  this  deformity  has  been  developed,  of  course  it  in  turn  contributes  to 
render  respiration  difficult. 

The  clavicles  are  sometimes  distorted,  and  may  even  be  partially  fractured 
(vide  infra).  The  spinal  column  is  usually  unaffected  if  the  child  remains  quiet 
in  bed;  but  if  it  sits  up,  or  is  carried  about,  or  tries  to  walk,  the  traction  and 
pressure  thus  exerted  often  produce  curvature  of  the  spinal  column  (rachitic  scoli- 
osis and  kyphosis).  These  deformities  may  become  extreme.  Changes  in  the 
bones  of  the  pelvis  are  of  no  special  clinical  importance  at  this  period  of  the 
patient's  life ;  but  in  later  life  the  consequent  shortening  of  the  antero-posterior 
diameter  of  the  pelvis  may,  as  is  well  known,  prove  a  great  obstacle  to  childbirth. 

The  extremities  not  only  present  swelling  of  the  epiphyses,  but  are  liable  to 
curvature.  This  latter  change  is  most  mai'ked  in  the  lower  limbs,  inasmuch  as 
they  have  to  support  the  weight  of  the  body.  The  swelling  is  especially  well 
developed  at  the  lower  ends  of  the  bones  of  the  forearm  and  of  the  tibia  and  fibula. 
The  curvature  is  almost  invariably  greatest,  and  therefore  most  easily  recognized, 
in  the  tibia,  which  becomes  convex  outward,  giving  the  rachitic  child  its  "  bow- 
legs." Similar  curvature  of  the  femur  is  less  often  seen,  although  it  may  be 
obvious  enough  in  severe  cases.  The  same  is  true  of  the  humerus.  The  deformity 
of  the  lower  limbs  causes  that  waddling  gait  which  can  be  so  often  seen  on  the 
streets  of  any  large  city.  Sometimes  the  limbs  present  a  sharp  bend,  the  result  of 
partial  fracture.  These  "  green-stick  fractures  of  rachitis  "  are  invariably  referable 
to  some  slight  traumatism,  and  are  most  often  seen  in  the  lower  third  of  the  tibia, 
although  sometimes  visible  in  the  clavicles,  ribs,  and  bones  of  the  lower  arm.    The 


924  DISEASES  OF  THE  ORGANS  OF  LOCOMOTION. 

iuf  raction  usually  takes  place  upon  one — generally  the  concave — side,  so  that  it 
is  often  compared  to  the  partial  fracture  of  a  quill  or  an  osier  rod. 

Symptoms  in  Other  Parts  of  the  Body. — Apart  from  the  changes  in  the  bones, 
a  rachitic  child  may  seem  to  be  perfectly  well.  Even  the  general  nutrition  may 
be  unimpaired.  As  a  rule,  bowever,  rickets  is  associated  with  anaemia  and 
impaired  nutrition.  The  cbild  seems  pale,  thin,  and  feeble,  and  may  present 
swollen  lymph-glands  and  other  "  scrofulous  "  symptoms.  Sometimes  there  is  a 
tendency  to  profuse  perspiration,  especially  from  the  scalp.  Very  frequently  there 
is  chronic  intestinal  catarrh,  and  sometimes  tbere  is  chronic  bronchitis  or  lobular 
pneumonia.  The  liver  and  spleen  are  often,  but  not  invariably,  enlarged.  It 
shoidd  also  be  stated  that  spasm  of  the  glottis  and  convulsions  are  frequently 
observed  in  rachitic  children.  Possibly  they  are  due  to  the  effect  of  the  disease 
upon  the  skull. 

Tbe  fasces  and  urine  have  been  repeatedly  subjected  to  careful  chemical  exam- 
ination, in  the  hope  of  gaining  some  information  as  to  tbe  pathogenesis  of  the  dis- 
ease. The  results  have  thus  far  been  rather  contradictory.  Much  emphasis  has 
been  laid  upon  the  fact  that  the  faeces  contain  a  comparatively  large  amount  of 
lime.  This  has  been  ascribed  to  a  deficient  absorption  of  the  lime-salts  from  the 
intestinal  canal.  The  amount  of  lime  in  the  urine,  on  the  other  hand,  seems  to 
be  diminished  rather  than  increased. 

The  disease  almost  invariably  runs  a  chronic  course.  Usually  months,  or  even 
years,  pass  before  the  process  ends.  Its  termination  is  to  be  recognized  by  closure 
of  the  fontanelies,  increase  in  the  length  of  the  bones,  and,  above  all,  by  the  fact 
that  the  patient  becomes  stronger  and  makes  attempts  to  walk.  Unfortunately, 
many  results  of  the  disease  persist  through  life.  The  legs  are  crooked,  the  thorax 
deformed,  the  spinal  column  curved,  and  the  pelvis  narrowed.  Even  in  the  most 
favorable  cases  persons  who  have  once  had  rachitis  usually  remain  somewhat 
smaller  than  those  who  are  perfectly  healthy. 

Some  authorities  describe  an  "  acute  rachitis,"  in  which  painful  swelling  of  the 
epiphyses  is  said  to  be  developed  in  the  course  of  a  few  weeks.  At  the  same  time 
the  child  becomes  emaciated,  and  may  also  suffer  from  diarrhoea  or  ulcerative 
stomatitis.  Recovery  takes  place  in  a  few  months.  How  far  cases  of  this  sort  are 
related  to  genuine  rickets  has  not  yet  been  determined. 

Rachitis  does  not  involve  direct  danger  to  life,  although  many  rachitic  chil- 
dren fall  victims  to  the  attendant  intestinal  catarrh,  or  to  such  complications  as 
catarrhal  pneumonia  or  tuberculosis.  The  prognosis  is,  therefore,  not  unfavorable 
where  the  outward  circumstances  of  the  child  permit  of  good  care  and  nourish- 
ment. The  remote  influences  of  the  thoracic,  spinal,  and  pelvic  deformities  can 
be  readily  inferred. 

The  diagnosis  of  rachitis  is  but  seldom  difficult  if  the  characteristic  changes  in 
the  bones  exist.  In  case  cranial  changes  exist,  we  should  guard  against  confound- 
ing rickets  with  hydrocephalus,  but  we  can  usually  avoid  error.  The  rachitic 
child  holds  its  head  erect,  and  is  free  from  mental  or  other  functional  nervous  dis- 
turbances. 

Treatment. — The  most  experienced  specialists  agree  that  the  first  aim  in  treat- 
ing most  cases  of  rachitis  is  to  improve  the  general  nutrition.  It  is  often  possible 
to  bring  about  recovery  simply  by  means  of  proper  diet  (milk,  the  yolk  of  eggs, 
and  perhaps  meat),  good  air  (in  the  country),  and  baths  (brine,  malt,  and  medi- 
cated baths).  Digestive  disturbances  should  be  corrected  by  such  remedies  as 
hydrochloric  acid  or  tincture  of  rhubarb ;  and  iron  should  be  administered  if  the 
patient  be  anaemic. 

It  is  very  important  that  the  child  should  be  placed  upon  a  good  mattress,  and 
should  neither  attempt  to  walk  too  early,  nor  be  needlessly  taken  up  and  carried 


OSTEOMALACIA.  93g 

about.  The  best  way  to  avoid  the  development  of  deformities  in  the  bones  is  to 
avoid  all  such  unfavorable  mechanical  influences. 

Attempts  have  also  been  made  to  check  the  disease  by  specific  remedies.  Upon 
theoretical  grounds,  lime  has  been  very  frequently  prescribed  in  the  form  of 
phosphate  of  calcium,  of  which  fifteen  to  forty-five  grains  may  be  given  in  powder 
several  times  a  day;  or  in  the  form  of  lime-water,  of  which  one  or  two  teaspoon- 
fuls  are  added  to  the  milk  which  the  child  drinks.  The  benefit  of  tbese  remedies 
is  seldom  very  obvious.  Kassowitz  has  given  a  fresh  impetus  to  the  employment 
of  phosphorus.  To  support  his  belief  he  brings  forward  numerous  clinical  obser- 
vations as  well  as  facts  obtained  from  experiment.  We  may  either  dissolve  the 
phosphorus  in  cod-liver  oil  (0"01-100),  giving  one  or  two  small  teaspoonfuls  of  this 
solution  every  day,  or  we  may  write  for  the  following  mixture,  which  is  more 
elegant,  but  is  also  more  apt  to  spoil : 

5  Phosphori O'Ol; 

Olei  amygdalae  expressi 10'0. 

Misce,  deinde  adde : 

Pulv.  acaciae, 

Syrupi  simplicis ää    5*0; 

Aquae  destillatae 80"0. 

M.     Sig. :  Two  to  four  small  teaspoonfuls  a  day. 

We  can  state  from  our  own  experience  that  the  remedy  is  usually  very  well  borne, 
and,  in  fact,  often  shows  its  beneficial  action  after  a  few  weeks,  the  fontanelles 
growing  smaller  and  the  bones  becoming  firm. 

It  may  be  eventually  necessary  to  resort  to  orthopaedic  or  surgical  treatment 
in  order  to  correct  the  deformities  of  the  bones. 

[The  comparative  rarity  of  rickets,  especially  in  its  extreme  degrees,  in  this 
country  strikes  all  observers  who  have  studied  in  Germany.  With  a  fairly  exten- 
sive experience  among  the  poorer  classes  of  the  city,  the  writer  can  recall  scarcely 
half  a  dozen  cases  of  craniotabes.  The  colored  race  furnishes  a  large  contingent 
of  cases  of  rickets,  although,  as  is  shown  by  Haven,  in  attention  to  diet  and  fresh 
air  its  members  are  superior  to  the  Irish  laboring  classes,  as  a  rule.  The  more 
pure  the  negro  blood,  the  greater  does  the  liability  to  rickets  seem  to  be  in  this 
latitude — an  indication,  perhaps,  that  a  northern  climate  is  unsuitable  to  the  Afri- 
can race.l 


CHAPTER  V. 
OSTEOMALACIA. 

iEtiology  and  Pathology. — As  a  rule,  osteomalacia  does  not,  like  rachitis,  con- 
sist in  a  disturbance  of  development.  The  growing  bones  are  not  prevented  from 
ossifying,  but,  having  already  undergone  normal  development  and  acquired 
normal  firmness,  they  afterward  become  soft.  It  is  mainly  a  disease  of  adults,  say 
between  thirty  and  forty  years*  of  age.  The  female  sex  is  noticeably  predis- 
posed to  the  disease,  although  occasionally  it  has  been  observed  in  men. 

The  true  cause  of  osteomalacia  has  not  yet  been  ascertained.  It  is  a  remarkable 
fact  that  the  disease  is  much  more  frequent  in  certain  regions  than  in  others.     It 

*  Eehn  maintains  that  genuine  osteomalacia  may  occur  in  children  ;  but  his  statement  has  not  yet 
been  fully  corroborated. 


926  DISEASES  OF  THE  ORGANS  OF  LOCOMOTION. 

is  very  common  along  the  Rhine,  and  in  Westphalia,  in  eastern  Flanders,  and 
northern  Italy.  This  suggests  that  there  is  some  specific  cause  for  the  disease, 
endemic  in  certain  localities.  Among  exciting  causes,  child-bearing  is  certainly 
the  most  important,  for  both  the  first  signs  of  osteomalacia,  and  also  fresh 
exacerbations  of  the  disease,  usually  date  from  a  pregnancy.  Another  factor  said 
to  promote  the  development  of  the  disease  is  found  in  unfavorable  hygienic  sur- 
roundings, such  as  damp  dwellings  and  the  like. 

The  anatomical  process  of  osteomalacia  consists  in  a  disappearance  of  the 
earthy  salts  of  the  bone,  which  begins  interiorly  and  spreads  outward,  and  causes 
a  corresponding  softening  of  the  bony  structure.  The  marrow  is  at  first  extremely 
hyperamiic;  and  extravasations  of  blood  are  not  infrequently  found  here  and 
there.  The  bony  substance  surrounding  the  myeloid  spaces  and  the  Haversian 
canals  becomes  transformed  into  a  soft  fibrous  tissue,  while  the  irregularly 
arranged  bone-corpuscles  are  either  destroyed  or  lose  their  characteristic  shape. 
The  softening  process  gradually  extends  over  the  spongy  substances  outward  to  the 
cortex.  The  central  cavity  grows  larger  and  larger,  so  that  finally  the  cortical 
substance  is  as  thin  as  paper,  and  the  whole  bone  like  an  "  inflated  and  dried  coil 
of  intestine."  At  this  stage  the  original  hyperemia  of  the  marrow  has  vanished. 
The  marrow  acquires  a  yellow  color,  and  may  finally  be  entirely  transformed  into 
a  yellow,  viscid  fluid.  The  affected  bones  are  now  flexible  and  soft,  they  can  be 
easily  cut,  and  they  are  of  less  specific  gravity  than  normal.  The  periosteum  is  also 
at  first  thickened  and  hyperaemic,  as  if  inflamed.  When  it  is  removed,  the  surface 
of  the  bone  beneath  it  is  found  to  be  rough  and  uneven.  The  attendant  altera- 
tions in  the  shape  of  the  bones  will  be  mentioned  below. 

Upon  chemical  examination  of  the  bones  in  osteomalacia,  we  naturally  find  a 
marked  diminution  in  the  proportion  of  lime-salts.  It  is  also  stated  that  lactic 
acid  has  been  discovered  in  the  bones.  This  is  an  interesting  fact,  as  it  may  be 
that  the  acid  plays  an  important  chemical  part  in  the  process  of  decalcification. 

Clinical  History. — Osteomalacia  begins  very  gradually  in  most  cases.  Usually 
the  first  thing  noticed  is  an  ill-defined,  deep-seated  pain,  most  often  felt  in  the 
sacral  region,  the  nape  of  the  neck,  and  the  back  and  thighs.  The  affected  parts 
are  also  sensitive  upon  pressure. 

The  pain  is  persistent.  While  it  still  keeps  on,  motion  becomes  gradually 
impaired.  The  patient  experiences  more  and  more  difficulty  in  walking,  partly 
because  of  the  pain  and  partly  because  of  muscular  weakness.  The  gait  is  either 
uncertain  and  tottering,  or  characterized  by  short  painful  steps,  the  lower  limb 
and  the  pelvis  being  jerked  forward  as  if  in  one  piece.  Sooner  or  later  it  becomes 
impossible  to  walk,  and  the  patient  is  permanently  bedridden.  Even  now  the 
pains  usually  persist  in  great  severity.  They  are  not  actually  spontaneous,  but 
the  mere  pressure  of  the  mattress  and  the  bedclothes  is  sufficient  to  excite  them. 

In  the  meanwhile  many  of  the  bones  will  probably  have  become  distorted. 
Usually  the  deformity  of  the  spinal  column  is  the  first  change  which  attracts 
attention.  This  is  generally  kyphotic ;  less  often  the  curvature  is  in  the  opposite 
direction.  At  the  same  time  the  head  approaches  the  sternum  more  and  more, 
and  the  patient  is  thus  made  to  appear  much  shorter  than  she  really  is.  In  most 
cases,  also,  the  thorax  is  much  distorted.  It  is  compressed  laterally,  while  the 
sternum  becomes  very  prominent,  and  is  sharply  bent.  The  change  in  the  shape 
of  the  pelvis  in  osteomalacia  is  less  obvious  externally,  but  it  can  be  detected  on 
internal  examination.  It  is,  of  course,  of  great  importance  from  an  obstetrical 
point  of  view.  The  pelvis,  like  the  chest,  is  compressed  laterally,  while  the  sym- 
physis is  made  to  project  forward  like  a  beak.  The  sacrum  and  its  promontory 
are  also  pushed  forward,  and  the  superior  strait  thus  acquires  somewhat  of  a  heart 
shape. 


OSTEOMALACIA.  927 

The  extremities  are  less  often  distorted,  particularly  if  the  patient  becomes  bed 
ridden  at  an  early  period.  Manifold  changes  are,  however,  possible.  Sometimes 
there  is  also  fracture.  In  a  few  reported  cases  the  softness  of  the  bones  of  the 
extremities  was  so  extreme  that  one  could  bend  the  limbs  at  will,  like  wax,  and 
give  them  the  most  extraordinary  positions.  In  cases  so  far  advanced  as  these, 
the  pain  in  the  bones  seems  finally  to  cease. 

The  bones  of  the  head  and  face  seldom  undergo  noticeable  change,  but  we  often 
find  the  teeth  carious  or  lost.  In  the  muscles,  several  observers  have  noticed 
trembling  and  fibrillary  contractions.  It  is  also  said  that  sometimes  even  a  slight 
irritation  of  the  skin  suffices  to  excite  painful  contractions  of  the  underlying  mus- 
cles.    These  phenomena  have  not  yet  been  thoroughly  investigated. 

The  general  condition  of  the  patient  is  often  unimpaired  for  a  long  while, 
except  for  the  pain  and  the  impairment  of  motion.  The  internal  organs  perform 
their  functions  in  a  normal  manner,  and  the  appetite  is  good.  Fever  is  observed 
only  when  the  disease  is  undergoing  some  temporary  exacerbation.  With  regard 
to  changes  in  the  urine,  there  have  been  a  good  many  statements  made,  but  their 
significance  is  extremely  doubtful.  It  is  said  that  the  amount  of  phosphoric  acid 
excreted  is  diminished.  With  regard  to  the  amount  of  lime,  no  definite  statement 
can  be  made.  Lactic  acid  has  been  repeatedly  detected  in  the  urine,  as  has  also 
albumen.     Concretions  of  lime  have  been  found  in  the  bladder  and  the  kidneys. 

The  disease  runs  a  chronic  course,  occupying  seldom  less  than  two  or  three 
years,  and  sometimes  even  five  or  ten.  Apparent  arrest  of  the  disease  is  not  infre- 
quently observed,  but  this  is  followed  by  fresh  exacerbations.  The  most  frequent 
termination  is  in  death.  This  results  either  from  general  debility,  or,  more  often 
still,  from  the  dyspnoea  caused  by  the  compression  of  the  lung,  or  by  some  such 
disease  as  lobular  pneumonia.     Eecovery  is  exceptional,  although  not  impossible. 

Diagnosis.— In  well-developed  cases  it  is  not  difficult  to  recognize  the  disease, 
but  at  first  a  correct  diagnosis  is  often  impossible,  unless  the  endemic  frequency 
of  osteomalacia  suggests  it.  In  the  onset  of  the  disease  we  may  often  be  led  to  the 
false  belief  that  there  is  incipient  disease  of  the  cord  on  the  vertebrae.  An  exam- 
ination of  the  pelvis  is  then  of  distinct  diagnostic  importance,  as  its  peculiar  de- 
formity can  be  recognized  early.  The  very  peculiar  hobbling  gait  of  osteomalacia 
is  also  unlike  anything  that  is  seen  in  spinal  disease.  As  the  disease  is  almost  en- 
tirely confined  to  adults,  we  are  seldom  in  danger  of  confounding  it  with  rachitis. 
Besides,  osteomalacia  does  not  produce  swelling  of  the  epiphyses,  nor  changes  in 
the  bones  of  the  skull.  It  is  said  that  osteomalacia  is  occasionally  confounded 
with  diffuse  carcinosis  of  the  bones,  as  this  may  produce  similar  symptoms  and 
deformities. 

Treatment. — As  has  been  already  implied,  therapeutic  efforts  have  thus  far 
proved  in  severe  cases  almost  unavailing  in  this  disease.  In  the  onset  of  the  dis- 
ease we  can  obtain  a  distinct  improvement  by  the  use  of  hygienic  remedies,  good 
air,  proper  food,  etc.  Internally  we  give  cod-liver  oil  and  iron.  Many  patients 
praise  warm  baths,  with  or  without  salt. — The  exhibition  of  lime  seems  to  be  of 
no  special  use,  but,  from  our  own  experience,  we  must  urgently  advise  trying  small 
doses  of  phosphorus  in  the  form  given  above  (page  925). 

The  changes  in  the  bony  pelvis  produced  by  osteomalacia  may  eventually 
demand  obstetrical  interference,  but  we  need  not  discuss  such  procedures  hei'e. 
We  should  invariably  warn  women  who  suffer  from  the  disease  of  the  dangers  of 
becoming  pregnant. 


DISEASES   AFFECTING  THE  BLOOD  AND  TISSUE- 
METAMORPHOSIS. 

(CONSTITUTIONAL  DISEASES.) 


CHAPTER  I. 
ANEMIA  AND   CHLOROSIS. 


Definition  and  iEtiology. — The  word  "  anaemia "  might  properly  be  taken  to 
signify  diminution  of  the  total  volume  of  the  blood,  such  as,  for  example,  is 
directly  brought  about  by  a  severe  haemorrhage.  Usually,  however,  the  word  is 
employed  to  signify  not  so  much  diminution  in  quantity  as  deterioration  in  qual- 
ity. The  total  volume  of  the  blood  is  not  liable  to  nearly  so  great  variation  as  is 
the  number  of  its  most  important  constituents — the  red  corpuscles — inasmuch  as 
the  total  volume  is  dependent  merely  upon  the  amount  of  watery  constituents, 
and  even  after  large  haemorrhages  the  water  is  quite  rapidly  replaced  by  absorp- 
tion. This  is  undoubtedly  the  case  in  most  instances  of  sudden  loss  of  blood. 
Even  in  chronic  anaemia  there  is  usually  no  reason  to  assume  that  the  total 
amount  of  blood  is  diminished,  although  it  may  be  where  there  is  general  emacia- 
ation,  or  diminished  supply  of  liquids  (persistent  vomiting,  dysphagia),  or  large 
watery  discharges  (as  in  cholera).  The  essential  element  in  anaemia  is,  therefore, 
a  diminution  in  the  number  of  the  red  blood-corpuscles,  or  so-called  oligocy- 
thaemia.  Changes  in  the  character  of  the  red  blood-corpuscles,  however  impor- 
tant, are  not  taken  into  consideration  here ;  nor  is  there  usually  any  stress  laid 
upon  any  incidental  variations  in  the  proportion  of  albumen,  especially  as  oligo- 
cythaemia  is  not  invariably  accompanied  by  a  diminution  in  the  amount  of  serum 
albumen  ("  hypalbuminosis  "). 

The  circumstances  under  which  anaemia  is  observed  are  manifold.  They 
admit,  however,  of  our  distinguishing  the  two  great  classes  of  anaemia — primary 
and  secondary.  Primary  anaemia  is  developed  as  an  apparently  primary  and 
idiopathic  disease  in  people  previously  healthy,  while  secondary  anaemia  is  merely 
a  symptom  of  some  already  existing  disease.  However  simple  this  theoretical 
distinction,  yet  in  actual  practice  it  is  often  quite  difficult  to  determine  whether 
the  particular  case  before  us  should  be  regarded  as  primary  or  secondary.  A  sec 
ondary  anaemia  may  occur  where  the  true  primary  cause  can  not  be  at  all  readily 
determined.  There  are,  nevertheless,  quite  a  large  number  of  cases  which  would 
seem  to  deserve  the  name  of  primary  or  essential,  in  which  we  feel  compelled  to 
assume  that  some  pathogenetic  influence  acts  directly  upon  the  blood  and  the 
haematopoietic  processes. 

In  the  first  place,  we  would  class  as  primary,  cases  which  may  best  be  described 


ANiEMIA  AND  CHLOROSIS.  929 

as  "simple  constitutional  anaemia."  These  often  stand  close  to  the  borderland 
between  health  and  disease.  There  are  not  a  few  individuals  who  pres<  at  a  strik- 
ing pallor  for  a  large  part,  if  not  all,  of  their  lives.  These  persons  may  feel  so 
well  and  vigorous  that  we  scarcely  have  a  right  to  regard  the  existent  anaemia  as 
an  actual  disease.  Sometimes,  however,  such  individuals  do  betray  some  diminu- 
tion of  energy,  are  easily  fatigued,  and  are  subject  to  headache.  We  may  then 
certainly  regard  the  condition  as  pathological.  In  many  instances  the  cause  of 
this  simple  anaemia  is  fount!  in  the  general  hygienic  surroundings  of  the  patient, 
for  such  cases  are  most  often  met  with  among  the  poorer  classes.  Deficient  nutri- 
tion, bad  air,  unhealthy  occupation  in  factories  or  the  like,  not  only  affect  the 
general  health,  but  more  especially  interfere  with  the  processes  of  normal  blood- 
making.  Other  cases  of  constitutional  anaemia,  apparently  primary,  occur  in 
individuals  who  are  entirely  beyond  the  reach  of  such  influences  as  have  just  been 
mentioned,  in  whom  the  anaemia  has  developed  and  persists  despite  the  best  of 
food  and  air.  Here  we  are  forced  to  the  conclusion  that  the  organs  engaged  in 
the  manufacture  of  the  blood  are  in  some  way  prevented  from  performing  their 
proper  functions.  The  trouble  often  seems  to  be  congenital,  for  such  individuals 
may  present  the  symptoms  of  anaemia  in  their  earliest  infancy.  There  are  persons 
who  have  always  been  pale  and  feeble.  Or,  again,  anaemia  does  not  develop  until 
later  on,  in  which  case  it  not  infrequently  associates  itself  with  certain  phases  of 
physiological  development,  as  when  growth  is  particularly  rapid,  or  when  adoles- 
cence occurs.  Virchow  has  directed  attention  to  another  factor,  which  he  regards 
as  potent  in  many  of  these  cases  of  congenital  anaemia.  He  has  found  that  the 
arteries  may  be  congenitally  small,  or  that  the  whole  arterial  system  may  be 
imperfectly  developed.  The  condition  may  be  associated  with  a  congenitally  weak 
and  small  heart.  The  importance  of  this  factor  has  not  yet  been  fully  determined. 
Possibly  the  condition  of  the  circulatory  system  just  mentioned  may  be  the  result 
rather  than  the  cause  of  the  anaemia. 

A  second  division  of  primary  anaemia  includes  cases  which  present  a  far  more 
definite  and  distinct  group  of  symptoms.  They  quite  often  appear  in  persons  pre- 
viously healthy,  last  for  a  certain  length  of  time,  and  then  end  in  complete  recov- 
ery. The  typical  form  of  this  variety  is  chlorosis  (xXwpo?  =  greenish  yellow),  or 
"greensickness."  This  well-known  disease  is  especially  frequent  in  young  girls 
fourteen  to  twenty  years  of  age — that  is,  at  puberty.  It  often  comes  on  quite  rap- 
idly without  any  ascertainable  cause.  There  are  not  infrequently  predisposing 
influences  in  the  outward  circumstances  of  the  patient.  Thus  it  is  promoted  by 
an  unhealthy  sedentary  mode  of  life,  as  in  seamstresses;  bad  air,  as  in  factory 
operatives;  mental  and  physical  over-exertion,  as  in  teachers,  governesses,  and 
students ;  and,  finally,  by  mental  influences.  It  is,  nevertheless,  true  that  chlorosis 
also  appears  in  girls  who  have  lived  under  the  most  favorable  hygienic  conditions 
possible.  Sometimes  the  disease  seems  to  be  merely  a  temporary  exacerbation  of 
a  simple  constitutional  anaemia  which  has  existed  a  long  while;  but  it  may  also 
appear  in  young  women  who  were  previously  healthy,  and  even  robust. 

The  true  cause  of  chlorosis  is  unknown.  In  all  probability  it  is  a  disease  of  the 
blood  itself,  or  a  process  interfering  with  its  normal  manufacture.  Its  pathological 
physiology  is,  however,  as  yet  entirely  beyond  our  grasp.  The  old  view,  that 
chlorosis  was  referable  mainly  to  sexual  derangement,  such  as  disturbance  of  men- 
struation, or  defective  development  of  the  genital  organs,  must  be  regarded  as  a 
confusion  of  cause  and  effect,  although  it  is  true  that  such  disturbances  are  often 
seen  in  the  disease.  Furthermore,  cases  of  marked  temporary  anaemia,  precisely 
like  ordinary  chlorosis  in  their  symptoms  and  behavior,  occur  in  men  and  in 
elderly  individuals. 

A  third  variety  of  primary  essential  anaemia  is  the  so-called  progressive  perni- 
59 


930  CONSTITUTIONAL  DISEASES. 

cious  anaemia.  This  is  likewise  an  idiopathic  disease,  distinguished  from  chlorosis 
mainly  by  its  continuous  progress  and  fatal  termination.  We  must  confess  that 
in  our  opinion  it  is  not  possible,  at  least  from  a  clinical  point  of  view,  to  draw  a 
sharp  dividing  line  between  ''ordinary  chlorosis"  and  "pernicious  anaemia." 
Some  future  investigator  may  discover  aetiological  as  well  as  anatomical  differ- 
ences between  the  two  diseases,  which  will  separate  them  widely.  In  the  mean- 
while we  have  only  the  clinical  phenomena  to  guide  us,  and  must  acknowledge 
our  inability  to  make  any  sharp  distinction.  There  are  "severe  cases  of  chlorosis" 
which  resemble  "  pernicious  anaemia "  in  every  respect,  except  that  they  finally 
get  well  ;  so  that  the  only  point  which  would  enable  us  to  distinguish  them  from 
the  fatal  disease  is  the  mode  of  termination.  To  take  this  for  a  criterion  is 
evidently  unscientific.  Cases  of  "  severe  essential  anaemia  "  also  have  many  points 
in  common  with  certain  other  diseases,  such  as  pseudo-leukaemia  and  splenic 
anaemia.     These  will  be  discussed  later. 

The  forms  of  secondary  anaemia  offer  a  contrast  to  the  forms  of  primary  or 
essential  anaemia  just  described  in  the  much  greater  number  of  their  causes. 
Under  this  head  come  cases  of  anaemia  which  do  not  occur  idiopathically,  but  as 
a  result  of  other  abnormal  processes.  The  simplest  variety  is  anaemia  from 
haemorrhage.  This  is  produced  by  profuse  loss  of  blood,  whether  from  the 
stomach,  lungs,  uterus,  intestines,  kidneys,  or  some  wound.  Repeated  small 
haemorrhages  finally  produce  the  same  result  as  a  single  large  one.  Thus  the 
most  profound  anaemia  may  be  observed  where  there  is  a  very  frequent  epistaxis 
(haemorrhagic  diathesis),  or  where  cancer  of  the  womb  gives  rise  to  a  constant 
oozing  of  blood. 

Other  cases  of  secondary  anaemia  may  be  divided  into  two  great  groups.  In 
one  class  the  anaemia  is  a  symptom  of  impaired  nutrition.  This  is  seen  in  almost 
every  severe  disease,  acute  or  chronic,  and  is  usually  associated  with  more  or  less 
emaciation  and  loss  of  strength.  The  bad  appetite,  the  lack  of  fresh  air  and  exer- 
cise, and  perhaps  an  impairment  of  digestion,  or  fever,  or  some  abnormal  drain 
upon  the  system,  as  in  suppuration — these  injure  the  entire  body.  It  is  not  sur- 
prising that  the  blood  shares  in  the  universal  misfortune.  This  is  why  most 
chronic  invalids  seem  pale,  particularly  if  they  suffer  from  disease  of  the  stomach, 
kidneys,  chest,  or  nervous  system.  In  the  second  class,  the  anaemia  is  secondary 
to  some  other  disease,  but  assumes  especial  prominence  as  a  symptom,  independ- 
ently of  any  general  impairment  of  nutrition.  Of  course,  it  is  often  associated 
with  emaciation,  but  nevertheless  its  extraordinary  intensity  offers  a  striking  con- 
trast to  the  condition  of  the  rest  of  the  body.  This  "  specific  secondary  anaemia  " 
must,  like  essential  anaemia,  be  due  to  a  special  lesion  of  the  blood  itself,  and  is, 
therefore,  to  be  regarded  as  in  a  certain  sense  a  special  complication  or  localiza- 
tion of  the  primary  disease.  General  malnutrition  never  directly  produces 
anaemia  of  this  grade.  This  fact  is  illustrated  in  stenosis  of  the  oesophagus. 
Here  the  ingestion  of  food  is  very  greatly,  if  not  completely,  impaired,  and  there 
is  the  greatest  emaciation,  with  a  subnormal  temperature  and  slow  pulse.  Of 
course,  such  a  patient  appears  pale  and  wretched,  but  he  does  not  present  that 
peculiar  waxy  pallor  which  is  the  infallible  sign  of  genuine  anaemia. 

The  exact  mode  of  origin  of  specific  secondary  anaemia  is  often  obscure.  We 
have  already  reported,  in  a  preceding  chapter,  a  very  instructive  example.  In 
cancer  of  the  stomach  we  find  usually  emaciation  and  pallor.  This  is  natural 
enough ;  but  sometimes  the  carcinoma  is  complicated  by  an  extraordinarily  pro- 
found anaemia,  comparable  only  to  the  pernicious  variety.  In  one  such  case  we 
found,  at  the  autopsy,  an  extensive  secondary  carcinosis  of  the  bone-marrow. 
Here,  therefore,  the  anaemia  certainly  was  not  the  result  of  the  general  impair- 
ment of  nutrition  occasioned  by  the  gastric  carcinoma,  but  of  the  disease  of  the 


ANEMIA  AND  CHLOROSIS.  931 

marrow,  which  tissue  undoubtedly  plays  an  important  part  in  the  manufacture  of 
the  blood. 

Some  cases  of  specific  secondary  anaemia  deserve  special  mention,  although  it 
is  seldom  possible  to  demonstrate  their  precise  cause.  In  the  first  place  come  such 
cases  as  develop  after  certain  acute  diseases,  usually  of  an  infections  character. 
For  example,  there  may  be  great  anaemia  after  typhoid  fever,  or  less  often  after 
acute  articular  rheumatism.  A  peculiar  form  of  anaemia  is  often  observed  during 
tbe  secondary  stage  of  syphilis,  although  nutrition  seems  to  be  otherwise  well 
maintained.  This  is  known  as  "syphilitic  chlorosis."  Tuberculosis,  chronic 
malarial  poisoning,  and  other  cases  of  chronic  poisoning  (lead;,  as  well  as  amy- 
loid disease,  renal  disease,  etc.,  may  also  be  attended  by  anaemia  of  such  intensity 
as  to  justify  the  conclusion  that  there  is  some  special  disturbance  of  secondary  ori- 
gin affecting  the  manufacture  of  the  blood  or  the  blood  itself.  [Chronic  arsenical 
poisoning  from  wall  papers,  dress  fabrics,  furniture  covering,  and  the  like,  is  a  not 
infrequent  cause  of  anaemia  and  debility,  which  resists  treatment  as  long  as  the 
exposure  to  the  toxic  influence  lasts.  The  classical  symptoms  of  chronic  arsenical 
poisoning  are  not  necessarily  present.  The  number  of  cases  in  which  prompt 
recovery  has  taken  place  after  the  removal  of  the  poison  which  was  proved  to 
exist  in  the  surroundings  as  well  as  in  the  urine  of  the  patient  is  too  large  and  too 
striking  to  explain  by  simple  coincidence.  Recovery  may,  however,  be  slow  in 
those  whose  toleration  of  arsenic  is  slight,  or  in  whom  the  cause  of  the  symptoms 
has  remained  long  undetected.] 

We  shall  now  proceed  to  describe  the  symptoms  common  to  all  forms  of 
anaemia.  Upon  this  will  follow  a  sketch  of  chlorosis.  A  special  chapter  is 
assigned  to  the  grave  form  of  essential  anaemia  known  as  progressive  pernicious 
anaemia;  and  in  the  same  connection  will  be  set  forth  the  little  that  is  known  with 
regard  to  the  relations  of  anaemia  to  pathological  changes  in  the  haematopoietic 
organs. 

Symptomatology  of  Anaemia.— The  first  symptom  which  attracts  the  attention 
of  the  physician  in  any  case  of  anaemia  is  the  altered  appearance,  the  pallor  of  the 
skin  and  visible  mucous  membranes.  This  is  especially  striking  in  the  face,  but 
it  is  sufficiently  evident  everywhere.  Special  value  is  usually  assigned  to  pallor 
of  the  mucous  membranes,  for  example,  of  the  lips  and  conjunctivae,  inasmuch  as 
their  color  is  not  liable  to  be  interfered  with  by  pigmentation  or  opacity  of  the 
epidermis.  The  degree  of  pallor,  of  course,  varies  greatly.  The  whole  body  may 
present  a  waxy  appearance.  Such  pallor,  of  course,  indicates  a  very  decided 
diminution  in  the  number  of  the  red  blood-corpuscles,  which  elements  impart  to 
the  blood  its  normal  color.  More  information  about  this  and  other  changes  in  the 
blood  will  be  found  below,  under  chlorosis  and  pernicious  anaemia. 

Besides  the  alteration  in  complexion,  there  is  always  a  group  of  symptoms  ulti- 
mately referable  to  an  impairment  of  the  normal  processes  of  innervation  result- 
ing from  a  lack  of  arterial  blood.  First  among  these  phenomena  comes  general 
weakness  of  the  motor  system.  The  voluntary  muscles  are  easily  fatigued,  and 
the  patient  suffers  from  constant  languor.  When  the  anaemia  is  very  great,  as 
after  severe  haemorrhage,  this  weakness  may  be  so  pronounced  that  the  patient 
can  neither  walk  nor  stand. 

This  diminished  nervous  energy  is  also  shown  by  the  mental  condition. 
There  is  no  intellectual  vigor.  The  patient  is  incapable  of  any  great  mental  exer- 
tion, and  experiences  a  constant  feeling  of  weariness  and  sleepiness.  Whether 
the  special  senses  are  blunted  in  anaemia  has  not  yet  been  determined.  It  is  very 
probable  that  a  careful  investigation  would  reveal  an  impairment  of  the  percep- 
tive powere,  corresponding  to  the  muscular  weakness.  If  the  anaemia  reaches  a 
certain  degree,  the  patient  becomes  unconscious.      This  explains  the  frequent 


932  CONSTITUTIONAL  DISEASES. 

fainting  attacks  (compare  page  708),  which  are  referable  to  a  temporary  aggrava- 
tion of  the  cerebral  anaemia,  and  are  therefore  apt  to  come  on  after  the  patient 
lias  been  standing  for  some  time,  or  when  he  rises  from  a  horizontal  position.  It 
is  an  extremely  interesting  fact  that  a  circumscribed  portion  of  the  nervous  sys- 
tem may  alone  suffer ;  thus  we  may  have  an  anaemic  amaurosis  after  profuse 
haemorrhage:  There  is  no  doubt  that  this  blindness  is  due  to  anaemia  of  the 
optical  nervous  apparatus.  The  only  question  is  whether  the  anaemia  affects 
chiefly  the  retina  or  the  central  portion  of  the  optic  tract  (cortex  of  the  occipital 
lobe). 

If  the  anaemia  be  at  all  marked,  many  other  organs  exhibit  functional  derange- 
ment. In  particular,  the  secretory  organs  are  disturbed.  The  mouth  and  tongue 
are  frequently  dry.  This  is  in  part  due  to  the  diminished  secretion  of  mucus  and 
saliva.  Of  course,  where  there  is  a  sudden  great  loss  of  blood,  the  condition  is 
also  in  part  a  result  of  the  compensatory  abstraction  of  water  from  the  tissues. 
Other  and  still  more  important  glands  belonging  to  the  digestive  system  are 
affected.  Our  knowledge  in  this  regard  is  as  yet  very  far  from  complete;  but 
Manassem  has  called  attention  to  the  interesting  fact  that  the  amount  of  hydro- 
chloric acid  in  the  gastric  juice  is  considerably  less  than  normal,  and  that  the  dys- 
pepsia so  often  seen  in  anaemic  patients  must  in  part  be  referable  to  this  condi- 
tion. Analogous  disturbances  in  the  functions  of  other  digestive  organs  are  pre- 
sumably present,  but  they  have  not  yet  been  actually  proven  to  exist.  We  would 
add  only  that  the  constipation  to  which  anaemic  persons  are  very  liable  is  usually 
due  to  diminished  energy  of  peristaltic  action. 

The  symptoms  thus  far  described  are  all  referable  to  diminished  functional 
activity.  On  the  other  hand,  anaemia  gives  rise  to  certain  symptoms  of  irritation 
in  the  nervous  system.  It  would,  of  course,  be  illogical  to  say  that  these  symp- 
toms are  the  direct  result  of  a  lack  of  oxygen-carrying  blood.  They  are,  in  all 
probability,  expressive  of  the  irritation  excited  in  certain  portions  of  the  nervous 
system  by  the  products  of  abnormal  tissue-metamorphosis.  It  may  be  that  these 
products  are  themselves  the  result  of  a  deficiency  in  the  supply  of  oxygen. 

The  symptoms  of  cerebral  irritation  observed  in  anaemia  include  vertigo,  spots 
before  the  eyes,  and  tinnitus  aurium.  This  last  is  an  almost  constant  symptom,  if 
the  anaemia  be  at  all  severe,  and  it  may  cause  the  patient  great  discomfort.  It  is 
usually  aggravated  if  the  patient  lies  upon  his  side.*  Another  irritative  symptom 
is  eructations.  We  also  have  anaemic  vomiting,  and  no  doubt  this  is  usually  of 
central  origin.  It  may  be  very  troublesome.  Sometimes  violent  hiccoughs  are 
observed,  as  well  as  frequent  yawning  of  a  convulsive  character.  Anaemic  head- 
ache may  be  very  severe.  It  is  usually  referred  either  to  the  entire  head  or  the 
forehead;  there  is  a  painful  feeling  of  pressure,  which  may  attain  great  se- 
verity. 

Other  important  evidences  of  irritation  are  to  be  found  in  the  behavior  of  the 
pulse  and  the  respiration.  The  changes  here  are  apparently  in  part  of  a  compen- 
satory character.  The  pulse  is  accelerated  in  most  cases  of  any  severity,  reaching 
SO  to  100  beats  per  minute,  or  even  more.  It  is  also  very  excitable,  so  that  compara- 
tively slight  external  influences  suffice  to  increase  its  rapidity  for  the  time  being. 
This  increase  in  frequency  would  not,  of  course,  necessitate  an  increase  of  intra- 
vascular tension,  or  of  the  rapidity  of  the  circulation ;  but  it  may  exert  a  favor- 
able influence  in  this  direction,  and  so  be  teleologic.  Respiration  is  also  usually 
accelerated  in  anaemia.  In  cases  of  great  severity  the  breathing  may  be  so  deep 
and  noisy  as  to  justify  the  term  "anaemic  dyspnoea."     This  is  the  direct  expres- 

*  We  may  also  state  that  the  tinnitus  of  the  anaemic  is  sometimes  nothing  but  the  jugular  venous 
hum  (bruit  de  (liable)  heard  by  the  patient. 


ANEMIA  AND  CHLOROSIS.  933 

sion  of  the  body's  hunger  for  oxygen.  It  is  obvious  that  tbis  increase  in  the  num- 
ber of  respirations  favors,  to  a  certain  extent,  the  absorption  of  tbat  gas. 

There  are  still  other  symptoms  referable  to  the  circulatory  system.  It  has 
beenalready  stated  that  the  total  volume  of  the  blood  is  not  diminished  in  anaemia 
unless,  of  course,  there  has  just  been  an  actual  haemorrhage.  This  explains  why 
the  pulse  in  anaemia  is  often  comparatively  full  and  strong.  Quit,  frequently 
there  is  a  peculiar  quickness  of  the  pulse.  This  seems  to  be  due  to  a  vigorous 
cardiac  systole,  in  conjunction  with  a  low  intra- arterial  tension.  This  supposition 
explains  the  fact,  which  we  have  often  observed,  that  there  may  be  in  profound 
anaemia  a  loud  sound  in  the  femoral  artery  similar  to  that  heard  in  aortic  regur- 
gitation. 

It  has  long  been  known  that  anaemia  may  produce  functional  cardiac  mur- 
murs, often  called  "anaemic  murmurs."  Their  mode  of  origin  is  not  yet  fully 
explained.  They  are  usually  heard  loudest  over  the  base  of  the  heart,  in  the 
neighborhood  of  the  pulmonary  valves,  although  sometimes  at  the  apex  of  the 
heart.  As  a  rule,  they  are  purely  systolic  in  time,  but  we  certainly  heard  in  one 
case  of  pernicious  anaemia  a  loud  diastolic  murmur  of  anaemic  origin.  The  mur- 
murs are  of  a  blowing  character.  Sometimes  they  are  so  rough  as  to  simulate 
pericardial  friction-murmurs;  it  has  therefore  been  suggested  that  many  anaemic 
murmurs  are  actually  due  to  the  rubbing  upon  each  other  of  the  abnormally  dry 
folds  of  the  pericardial  sac.  Another  explanation  of  their  occurrence  is,  that  the 
movements  of  the  cardiac  valves  are  interfered  with,  as  a  result  perhaps  of  fatty 
degeneration  of  the  myocardium  (vide  infra).  It  is  also  possible  that  they  are 
due  in  some  eases  to  relative  insufficiency,  resulting,  for  instance,  from  dilatation 
of  the  heart  or  imperfect  action  of  the  papillary  muscles. 

Murmurs  in  the  large  veins  of  the  neck  are  very  often  heard  in  anaemia,  either 
with  or  without  cardiac  murmurs.  They  are  often  called  bruit  de  diable.  No 
less  an  authority  than  A.  Weil  has  maintained  that  murmurs  in  the  jugular  veins 
are  just  as  frequent  in  healthy  persons  as  in  the  anaemic;  but  our  experience 
obliges  us  to  differ  from  this  view.  We  believe  that  the  loud  venous  murmurs  are 
more  frequent  in  the  anaemic  than  in  other  persons.  We  can  not  claim,  however, 
that  they  are  of  any  great  diagnostic  value. 

The  processes  of  tissue  metamorphosis  in  profound  anaemia  are  of  great  in- 
terest, but,  unfortunately,  they  have  not  yet  been  thoroughly  investigated.  It  is 
extremely  probable  that  the  absorption  of  oxygen  in  severe  anaemia  is  less  than 
normal,  and  that  the  body  must,  therefore,  suffer  from  a  diminished  supply  of 
oxygen.  It  has  been  demonstrated  by  the  experiments  of  A.  Fränkel  that  there 
is  an  increased  destruction  of  albuminoids  within  the  body  and  a  correspondingly 
increased  excretion  of  nitrogen  through  the  kidneys.  This  experimental  deduc- 
tion we  were  the  first  to  confirm  in  a  case  of  very  severe  essential  anaemia ;  and 
later  various  observers  have  in  other  cases  arrived  at  similar  conclusions.  Of 
course,  the  excretion  of  nitrogen  is  influenced  by  many  different  factors,  so  that 
the  truth  of  the  above  statement  is  not  easily  established.  There  can  be  no  doubt, 
however,  that  in  many  instances  of  profound  anaemia  a  larger  amount  of  nitrogen 
is  excreted  than  is  ingested.  This  fact  acquires  a  special  significance  when  taken 
in  connection  with  certain  anatomical  lesions  produced  by  anaemia:  there  is  almost 
invariably  a  well-marked  fatty  degeneration  of  many  organs,  particularly  of  the 
heart  and  kidneys.  This  fatty  degeneration  is  the  direct  result  of  the  abnormal 
destruction  of  albuminoid  structures.  The  fat  represents  the  non-nitrogenous 
remnants  of  the  decomposed  albuminoids.  The  reason  why  the  fat  itself  does  not 
undergo  oxidation  is  the  same  that  leads  to  the  destruction  of  the  albuminoids — 
namely,  a  lack  of  oxygen.  This  explains  why  the  panniculus  adiposus  is  for  a 
long  while  preserved  in  many  cases  of  anaemia. 


934  CONSTITUTIONAL  DISEASES. 

It  is  evident  that  the  fatty  degeneration  once  produced  must,  in  its  turn,  lead 
to  unfavorable  results.  It  has  already  been  suggested  that  the  fatty  degeneration 
of  the  heart  may  be  the  cause  of  certain  irregularities  in  its  functional  activity; 
but  it  should  be  said  that  this  is  not  invariably  the  case,  for  often  the  heart 
exhibits  a  surprising  energy  despite  marked  fatty  degeneration  of  its  muscular 
tissue.  The  corresponding  changes  in  the  walls  of  the  blood-vessels  are,  how- 
ever, of  great  importance,  as  they  frequently  occasion  disturbance,  above  ail  by 
haemorrhage.  In  many  instances  (for  example,  in  leukaemia,  vide  infra)  an 
actual  hemorrhagic  diathesis  is  developed ;  but  we  shall  find  later  (see  the  chapter 
on  pernicious  anaemia)  that  the  condition  of  haemoglobinaemia  and  the  chronic 
fi  brine-  ferment  intoxication  caused  by  it  play  a  part  in  producing  capillary 
haemorrhages  in  severe  anaemia.  There  is  also  strong  evidence  in  many  cases 
that  there  is  an  abnormal  permeability  of  the  vascular  walls.  From  this  results 
the  mild  grade  of  oedema  frequently  seen  in  anaemic  patients,  although  in  some 
few  cases  this  oedema  may  be  ascribed  to  passive  congestion,  resulting  from  the 
cardiac  debility  {vide  supra).  The  increased  permeability  of  the  renal  blood- 
vessels is  sometimes  shown  by  polyuria. 

The  urine  is  usually  rather  light-colored,  if  the  anaemia  be  at  all  marked.  It  is 
evident  that  there  is  a  diminished  production  of  urinary  pigment,  the  material  for 
which  is  the  coloring  matter  of  the  blood.  Another  reason  for  the  light  color  of 
the  secretion  is  the  polyuria  above  mentioned.  There  may  be  fifty  to  seventy 
ounces  (1,500-2,000  c.  c),  or  more,  secreted  in  twenty-four  hours.  The  specific 
gravity  may  nevertheless  be  comparatively  high,  and  higher  than  one  would 
expect  from  the  appearance  of  the  urine,  not  infrequently  ranging  between  1015 
and  1021.  This  indicates,  of  course,  that  the  amount  of  solid  constituents  is  com- 
paratively large;  and  in  fact  we  find  a  corresponding  amount  of  urea,  say  four 
or  five  hundred  grains  (grm.  25-32)  in  twenty-four  hours.  This  is  a  large  figure 
when  we  consider  the  amount  of  ingesta.  As  to  the  other  constituents  of  the 
urine,  we  possess  as  yet  little  definite  knowledge.  The  amount  of  phosphoric 
acid  is  sometimes  surprisingly  small,  compared  with  the  amount  of  nitrogen. 
Albuminuria  is  exceptional  in  cases  of  simple  anaemia. 

The  bodily  temperature  is  very  often  affected  in  anaemia.  An  "anaemic 
fever  "  is  very  frequently  associated  with  pernicious  anaemia,  and  even  with  cases 
of  profound  secondary  anaemia,  as  after  a  large  haemorrhage  from  the  stomach. 
There  are  irregular  elevations  of  temperature,  usually  occurring  at  evening,  and 
attaining  101°-102°  (38-5°-39°  C),  or  even  still  higher  figures.  This  fever  is  not 
due  to  inflammatory  organic  changes,  but,  in  all  probability,  is  rather  the  result 
of  the  presence  of  fibrine  ferment  in  the  blood. 

Clinical  History  of  Chlorosis.— Chlorosis,  or  "green-sickness,"  as  already  ex- 
plained, is  a  term  applied  to  the  mild  forms  of  essential  anaemia,  such  as  are  most 
often  seen  in  females  at  the  time  of  puberty.  The  disease  sometimes  develops  in 
previously  healthy  girls  with  considerable  rapidity,  and  may  completely  vanish 
again  at  the  end  of  a  few  weeks  or  months.  In  other  cases  it  runs  a  more  tedious 
course,  without  sharp  limits,  so  that  the  condition  resembles  that  of  constitutional 
anaemia,  or  it  may  be  described  as  an  habitual  chlorosis.  In  many  instances  the 
disease  may  be  said  to  undergo  repeated  relapses. 

The  various  symptoms  of  chlorosis  are  almost  all  direct  results  of  the  anaemia, 
so  that  they  have  already  been  described.  Their  intensity  and  variety  are,  how- 
ever, very  different  in  different  cases.  There  are  mild  cases  where  the  patient 
can  hardly  be  called  ill.  She  feels  perfectly  well,  but  is  "a  little  pale."  From 
these  cases  there  is  a  gradual  and  unbroken  transition  to  the  other  extreme  of 
severity. 

A  constant  and  essential  symptom  is  the  greater  or  less  pallor  of  the  face  as 


ANEMIA  AND  CHLOROSIS.  935 

well  as  of  the  rest  of  the  surface  of  the  body,  and  of  the  mucous  membranes  so 
far  as  visible.  There  is  also  almost  invariably  general  languor;  the  patient  is 
easily  fatigued,  and  has  neither  the  desire  nor  the  ability  to  make  any  great 
bodily  or  mental  exertion.  There  is  also  a  tendency  to  headache  and  vertigo. 
Other  nervous  or  "  hysterical "  symptoms,  if  they  occur,  are  not  directly  ascribable 
to  the  disease  itself,  but  are  merely  complications.  Chlorotic  patients  of  ten  com 
plain  of  dyspepsia.  Tbe  appetite  is  usually  diminished,  and  tbero  is  often  a  sense 
of  pressure  in  the  epigastrium  after  meals.  There  may  also  be  severe  cardial;.!:*. 
This  is  usually  of  a  purely  nervous  origin,  but  is  sometimes  produced  by  a  gastric 
ulcer  existing  as  a  complication  of  tbe  chlorosis.  There  is  not  infrequently  con- 
stipation, as  might  be  expected  from  the  small  amount  of  food  taken,  and  from 
the  diminished  activity  of  intestinal  peristalsis.  Over  the  veins  in  tbe  neck  we 
often  hear  a  loud  murmur,  above  referred  to,  and  called  bruit  de  (liable.  Some- 
times the  heart  is  found  to  be  slightly  dilated.  This  is  probably  a  result  of  the 
diminished  power  of  resistance  of  the  cardiac  tissues.  Anaemic  cardiac  murmurs 
are  not  infrequent ;  the  pulse  is  accelerated  and  easily  excited.  Otherwise  phys- 
ical examination  does  not  reveal  any  abnormal  condition  of  the  internal  organs. 
It  is  a  very  great  exception  to  find  any  indications  of  disturbance  in  the  spleen 
or  lymph-glands,  or  the  bone-marrow.  Fever  is  rare  in  cases  of  sinqne  chlorosis, 
but  in  severe  cases  we  sometimes  see,  especially  at  night,  a  slight  rise  of  tempera- 
ture, up  to  101°  F.  (SB'S0  C).  The  urine  is  usually  pale,  but  seldom  differs 
greatly,  either  in  amount  or  constituents,  from  the  normal  character.  It  is 
noteworthy  that  chlorotic  girls  are  very  apt  to  suffer  from  disorders  of  men- 
struation. The  menses  may  not  appear  until  late,  or,  if  they  occur,  they  are  very 
scanty.  It  is  only  in  exceptional  instances  that  chlorotic  patients  have  menor- 
rhagia. 

Examinations  of  the  blood  have  been  made,  in  the  hope  of  gaining  a  clearer 
insight  into  the  true  character  of  chlorosis.  The  blood  is  usually  pale.  Upon 
microscopic  examination,  we  notice  that  the  red  blood-corpuscles  do  not  tend  to 
form  rouleaux  so  much  as  normally,  and  sometimes  we  can  perceive  that  the  glob- 
ules are  comparatively  light-colored,  and  are  not  all  of  the  same  size.  There  are 
some  of  the  normal  dimensions,  others  are  notably  small  (microcytes),  while  there 
are  a  few  which  are  unusually  large  (macrocytes).  Here  and  there  we  see  corpus- 
cles of  irregular  shape  (poikilocytes).  Often  there  is  some  increase  in  the  number 
of  white  blood-corpuscles— that  is,  there  is  a  slight  degree  of  leucocytosis  {vide  in. 
fro).  In  occasional  instances  there  are  considerable  numbers  of  "  granular  bodies  " 
in  the  blood.  These  are  usually  regarded  as  products  of  the  disintegration  of  white 
blood-corpuscles.  Malassez,  Hayem,  Thoma,  and  others  have  endeavored  to  deter- 
mine the  number  of  blood- corpuscles  in  chlorosis  and  allied  diseases  by  means  of 
special  methods  of  counting.  In  general,  we  may  say  that  in  most  cases  of  chlo- 
rosis the  number  of  red  blood-corpuscles  is  decidedly  diminished.  In  a  cubic  mil- 
limetre of  blood  we  find  perhaps  only  3,000,000  to  3,500,000  red  blood-corpuscles, 
instead  of  the  normal  number  of  5,000,000.  The  diminution  may  be  even  greater 
than  this.  On  the  other  hand,  it  should  be  noted  that  Duncan,  Hayem,  and  Laache 
have  met  with  cases  where  the  number  of  corpuscles  was  not  diminished.  Proba- 
bly here  the  amount  of  haemoglobin  in  the  blood-corpuscles  was  diminished.  An 
intelligent  and  satisfactory  explanation  of  all  these  isolated  facts  has  not  yet  been 
given.  There  are  certain  hypotheses  which  have  been  brought  forward,  and  these 
we  shall  discuss  in  the  following  chapter,  where  also  a  more  extensive  description 
will  be  found  of  the  changes  presented  by  the  blood. 

We  have  already  intimated  that  there  is  great  variety  in  the  general  course  of 
chlorosis.  Many  cases  which  seem  severe  at  first  terminate  in  complete  recovery 
by  the  end  of  four  to  six  weeks,  or  a  few  months.     Other  cases  are  much  more 


936  CONSTITUTIONAL  DISEASES. 

obstinate,  resist  all  modes  of  treatment,  and  undergo  frequent  relapses.  The  prog- 
nosis may  therefore  be  regarded  as  favorable  on  the  whole,  but  it  should  always  be 
given  with  a  certain  degree  of  reserve.  It  is  true  that  ordinary  chlorosis  never 
involves  direct  danger  to  life.  "We  shall,  however,  find  that  there  is  no  sharp 
dividing-line  between  "simple  chlorosis "  and  "pernicious  anaemia";  and  in  any 
individual  case  it  may  not  at  first  be  possible  to  decide  which  variety  of  anaemia 
is  before  us. 

Diagnosis. — The  diagnosis  of  chlorosis  may  be  regarded,  therefore,  either  as 
extremely  easy  or  extremely  difficult  to  make,  according  to  the  point  of  view.  It 
is  easy  in  that  we  can  readily  perceive  the  characteristic  symptoms  of  pallor  and 
the  like ;  but  it  is  difficult  in  that  the  term  chlorosis  should  be  applied  to  those 
cases  only  where  the  anaemia  is  primary  and  essential.  We  therefore  have  no 
right  to  declare  the  diagnosis  of  chlorosis  until  we  have  made  a  careful  and 
thorough  physical  examination,  and  have  found  that  no  factors  are  present  which 
might  produce  a  secondary  anaemia.  We  should,  above  all,  bear  in  mind  the 
possibility  of  incipient  tuberculosis,  and  examine  the  lungs,  the  expectoration, 
and  the  general  condition  of  the  patient,  and  also  consider  hereditary  and  other 
predisposing  influences.  We  should  also  bear  in  mind  the  possibility  of  some 
organic  disease  of  the  stomach,  such  as  ulcer,  catarrh,  or  dilatation,  or  chronic 
renal  disease,  or  possibly  constitutional  syphilis,  giving  rise  to  the  syphilitic 
chlorosis  before  mentioned.  In  many  cases  it  is  easy  to  exclude  all  these  sec- 
ondary forms  of  anaemia,  but  occasionally  the  task  is  a  very  difficult  one. 

Treatment  of  Ansemia  and  Chlorosis. — The  first  indication  in  treating  chlorosis, 
as  well  as  every  other  form  of  anaemia,  is  to  promote  the  regeneration  of  the 
blood.  There  are  two  ways  in  which  we  can  endeavor  to  fulfill  this  indication : 
first,  by  general  hygienic  and  dietetic  measures,  and,  secondly,  by  employing 
certain  internal  remedies. 

First  among  general  measures  comes  a  care  for  pure  air  and  proper  food. 
Many  a  pale  city  girl  regains  her  ruddy  cheeks  after  a  few  weeks  spent  either  in 
the  country,  or  on  the  mountains,  or  at  the  seashore.  The  choice  of  a  place  must, 
of  course,  depend  mainly  upon  the  circumstances  of  the  patient.  In  many 
instances,  boarding  in  any  suitable  country  place  answers  as  well  as  a  long  and 
expensive  journey.  „  If  the  seashore  be  chosen,  some  bathing  resort  on  the  North 
Sea  will  usually  be  preferable.  There  are  other  places  where  the  patient  can 
combine  the  advantages  of  pure  forest  air  and  ferruginous  mineral  water;  these 
will  be  mentioned  below. 

The  diet  of  anaemic  patients  should  be  easily  digestible  and  rich  in  albumen ; 
carbo-hydrates  and  fat  should  be  given  in  but  limited  amounts  to  patients  in 
whom  the  panniculus  adiposus  is  already  well  developed.  Lean  patients,  on  the 
other  hand,  require  such  ingredients  in  their  diet,  and  should  be  recommended  to 
take  simple  puddings,  extract  of  malt,  butter,  and  cod-liver  oil.  If  milk  be  well 
borne  it  is  an  excellent  article  of  diet  for  the  anaemic;  but  what  is  called  the 
"milk  cure" — that  is,  an  almost  exclusively  milk  diet — is  not  advisable,  as  we 
have  already  had  occasion  to  observe  (see  the  chapter  on  tuberculosis).  Some 
authors  ascribe  an  exaggerated  value  to  alcoholic  beverages.  They  may  be 
allowed  in  moderate  amount  if  the  patient  asks  for  them  and  finds  the  appetite 
improve  under  their  use.  The  best  to  choose  for  an  emaciated  patient  are  porter 
and  other  varieties  of  beer  rich  in  extractive  principles,  but  wine  is  often  ill  borne 
by  chlorotic  girls. 

Many  physicians  also  insist  upon  "abundant  exercise  in  the  open  air."  This 
can,  however,  be  carried  too  far.  A  chlorotic  girl  is  often  made  to  take  long 
walks  in  spite  of  her  own  reluctance  to  do  so,  with  the  result  of  becoming  more 
languid  and  exhausted  than  she  was  before.     We  even  believe  that  a  case  of  pro- 


ANiEMIA  AND  CHLOROSIS.  937 

found  anaemia  will  be  benefited  by  a  certain  degree  of  bodily  rest.  Thus  any 
needless  tax  upon  the  muscles  is  avoided.  The  most  brilliant  results  we  have 
ever  observed  in  the  treatment  of  chlorosis  have  been  within  the  hospital.  The 
patients,  who  are  usually  factory  operatives  and  shop-girls,  are  often  kepi  in  bed 
for  the  first  week.  We  admit  that  pure  country  air  maybe  very  beneficial,  but 
we  would  strongly  advise  moderation  in  bodily  exercise.  If  the  patienl  begins  to 
feel  more  vigorous,  she  will  of  herself  take  more  exercise,  and  may  safely  indulge 
in  long  walks  or  extended  excursions  on  foot. 

Of  internal  remedies,  the  preparations  of  iron  have  long  occupied  the  first 
place  in  the  treatment  of  all  varieties  of  anaemia.  The  manner  in  which  their 
good  effects  are  exerted  was  until  recently  unknown,  for  careful  investigation  had 
established  the  fact  that  the  salts  of  iron  are  absorbed  by  the  intestines  only  in  an 
extremely  small  amount,  and  that  the  system  needs  so  little  iron  that  the  iron  in 
ordinary  food  ought  to  be  entirely  sufficient.  Bunge  has  recently  enabled  us  to 
understand  why  iron  possesses  therapeutic  value,  at  least  in  some  cases.  He  has 
shown  that  the  iron  contained  in  ordinary  food  does  not  exist  in  an  inorganic 
form,  but  in  a  very  complex  organic  combination,  to  which  he  has  given  the  name 
of  haematogen.  The  inorganic  salts  of  iron  given  as  a  medicine  protect  the 
haematogen  from  being  decomposed,  a  danger  to  which  it  is  liable  from  the 
sulphides  which  are  generated  in  the  intestinal  canal. 

Hence  it  follows  that  iron  can  not  act  in  the  same  way  in  all  cases  of  anaemia, 
and,  in  fact,  we  often  see  that  iron  may  be  taken  by  anaemic  patients  for  a  long 
time  without  any  effect;  but,  on  the  other  hand,  the  action  of  iron  is  often  appar- 
ently so  beneficial  that,  in  spite  of  our  unsatisfactory  theoretical  knowledge,  we 
still  give  one  of  the  many  iron  preparations,  together  with  general  dietetic  pre- 
scriptions, in  severe  anaemia  and  especially  in  chlorosis.  It  may  be  regarded  as  a 
general  rule  to  give  not  too  small  doses,  and  to  give  these  two  or  three  times  a 
day,  directly  after  meals.  Ferrum  redactum  is  perfectly  pure  iron,  in  a  state  of 
very  fine  subdivision,  and  may  be  given  either  as  a  powder  or  in  pills,  several 
times  a  day,  in  the  dose  of  one  to  three  grains  (grm.  0 -05-0-20).  Avery  good 
preparation  for  children  consists  of  pastiles  made  of  chocolate  containing  reduced 
iron.  Two  other  powders  are  contained  in  the  list  of  the  German  pharmacopoeia, 
ferrum  carbonicum  saccharatum,  and  ferrum  oxydatum  saccharatum,  the  dose 
of  each  being  half  a  teaspoonful  to  a  teaspoonful  in  water  three  times  a  day. 
The  second  of  these  preparations,  ferrum  oxydatum,  has  the  advantage  of  not 
blackening  the  teeth.  An  easily  digestible  preparation  is  ferri  lactas,  which  may 
be  given  either  as  a  powder  or  in  pills,  the  dose  being  five  to  twelve  grains  (grm. 
0-3-075).  Finally,  the  sulphate  of  iron  should  be  mentioned.  This  is  one  con- 
stituent of  the  well-known  and  very  valuable  Blaud's  pills  (ferri  sulphatis  exsic- 
cat.,  potassii  carbonat.,  ää  grm.  15;  pulv.  tragacanth,  q.  s.  Misce  et  div.  in  pil. 
No.  100.  Sig. :  Three  to  five  pills  three  times  a  day).  The  German  pharmacopoeia 
contains  three  tinctures  of  iron— viz.,  tinctura  ferri  acetici  aetherea,  tinctura  ferri 
chlorati  aetherea  [resembling  tinctura  ferri  chloridi,  U.  S.  P.].  and  tinctura  ferri 
pomata.  We  must  also  praise  the  liquor  ferri  albuminati,  a  teaspoonful  three 
times  a  day,  which  often  has  a  good  effect  on  the  appetite.  Repeated  trials  have 
lately  been  made  with  successful  results,  in  giving  haemoglobine  internally,  espe- 
cially Pfeufer's  haemoglobine  pastiles,  made  of  ox  blood,  giving  six  of  them  a  day. 
Often  iron  is  given  in  combination  with  other  remedies,  of  which  quinine  is  chief. 
This  is  said  not  only  to  increase  the  tonic  action,  but  to  lessen  the  headaches  to 
which  anaemic  patients  are  subject.  Stomachic  tonics,  such  as  gentian,  or  laxa- 
tives, such  as  aloes,  are  also  combined  with  iron. 

Exceptionally  iron  is  not  well  borne,  and  causes  digestive  disturbances  or  diar- 
rhoea.    We  must  then  try  another  preparation  or  diminish  the  dose.     It  is  com- 


93S  CONSTITUTIONAL  DISEASES. 

mon  to  forbid  the  ingestion  of  sour  articles  of  diet  while  taking  iron,  but  the 
injunction  is  due  mainly  to  prejudice. 

The  use  of  mineral  waters  containing  iron  is  quite  common,  although  the 
amount  of  iron  thus  introduced  into  the  system  is  so  small  that  it  is  hard  to  under- 
stand their  thei'apetitic  value.  Of  those  artifically  produced,  tbat  which  contains 
the  pyrophosphate  of  iron  is  the  best,  and  does  not  irritate  even  a  delicate  stom- 
ach. The  natural  .chalybeate  waters  are  also  bottled  and  sent  to  distant  places. 
Tbey  are  often  more  effective  if  drunk  upon  the  spot,  but  merely  because,  in  that 
case,  the  general  bygienic  surroundings  of  the  patient  are  better  than  they  would 
be  at  home.  Tbe  best-known  and  most  popular  ferruginous  springs  in  Germany 
and  Switzerland  are  situated  at  Cudowa,  Eippoldsau,  Homburg,  Elster,  Schwal- 
bacb,  Pyrmont,  Driburg,  Liebenstein,  St.  Moritz,  and  Tarasp.  "  Steel  baths  "  are 
also  much  employed;  but  the  effect  is  not  due  to  the  iron  contained  in  the  water, 
but  to  tbe  temperature  of  the  water  and  the  carbonic-acid  gas  it  contains.  Baths 
generally  seem  to  be  of  distinct  service  in  chlorosis,  and  hence  we  often  prescribe 
simple  baths  or  salt  baths,  giving  a  bath  of  fifteen  or  twenty  minutes  duration,  at 
a  temperature  of  90°-95°  F.,  two  or  three  times  a  week,  adding  five  or  six  pounds 
of  salt  to  the  bath . 

No  other  remedies  for  chlorosis  approach  iron  iu  popularity.  Arsenic  is  the 
only  one  which  needs  to  be  mentioned.  Its  effects  are  often  very  beneficial, 
and  it  deserves  a  trial,  especially  in  severe  cases.  It  may  be  given  alone  or  in 
combination  with  hon.  Hydrochloric  acid  also  deserves  special  mention,  and 
often  does  good  service  in  cases  with  digestive  troubles,  pressure  in  the  stomach, 
etc.  We  give  ten  or  fifteen  drops  of  the  dilute  acid  in  a  quarter  of  a  tumbler 
of  water,  half  an  hour  after  meals.  Scholz  and  Strübing  recommend  the  use  of 
sulphur — one  part  of  purified  sulphur  to  two  parts  of  milk  sugar— giving  as 
much  as  will  go  on  the  point  of  a  knife,  three  times  a  day.  We  must  refer  to  the 
following  chapter  for  the  experiments  with  subcutaneous  injections  of  blood. 

If  there  be  constipation,  it  is  desirable  to  remedy  it  rather  by  suitable  diet  than 
by  laxatives.  Thus  we  may  prescribe  fruit,  Graham  bread,  and  other  foods  which 
promote  peristaltic  action  by  the  mechanical  irritation  which  they  exert. 


CHAPTEE  II. 

PROGRESSIVE   PERNICIOUS  ANEMIA. 

( Grave  Form  of  Essential  Anoimia.) 

We  term  pernicious  anaemia  that  variety  of  essential  anaemia  which  does  not, 
like  chlorosis,  terminate  in  recovery,  or  maintain  a  low  degree  of  severity,  but 
which  goes  on  uninterruptedly  from  bad  to  worse,  in  many  instances  leading  to 
a  degree  of  anaemia  which  of  itself  proves  the  immediate  cause  of  death.  The 
word  "  essential  "  is  here  used  to  signify  that  the  anaemia  is  a  primary  one,  the 
result  of  some  pathogenic  cause  acting  upon  the  blood  itself,  or  the  haematopoi- 
etic system.  We  must  hold  fast  to  this  conception  of  the  disease,  especially  as  the 
attempt  has  been  repeatedly  made  of  late  to  degrade  pernicious  anaemia  from  the 
rank  of  an  idiopathic  disease,  and  regard  it  as  merely  a  grave  form  of  secondary 
anaemia  which  may  result  from  any  one  of  the  most  various  causes. 

Of  course,  the  diagnosis  of  primary  anaemia  may  be  wrongly  made  in  cases 
where  a  more  careful  search  will  detect  some  special  cause  for  the  condition. 
Such  a  mistake  may  become  evident  at  the  autopsy.     Thus,  in  repeated  instances, 


PROGEESSIVE  PERNICIOUS  ANOSMIA.  939 

cases  which  have  been  during1  life  regarded  as  "pernicious  ana;mia"  hav<  been 
shown  to  he  cancer  of  the  stomach  {vide  page  391).  In  other  cases,  however,  it,  is 
much  more  difficult  to  discover  the  primary  cause  of  the  anaemia.  Tims  the  pro- 
found anaemia  which  attacked  the  men  at  work  upon  the  St.  Gothard  Tunnel  was 
at  first  regarded  as  idiopathic,  but  more  careful  investigation  showed  that  the  dis- 
ease was  really  due  to  anchylostoma  (vide  page  448),  the  ravages  of  which  parasite 
have  in  other  cases  also  been  confounded  with  the  symptoms  of  pernicious  anae- 
mia. Reyher  and  Runeberg  have  lately  called  attention  to  the  fact  that  the  pres- 
ence of  bothryocephalus  latus  in  the  intestine  may  produce  an  affection  resem- 
bling severe  and  apparently  primary  ana3mia.  Of  late  there  have  been  a  number 
of  cases  reported  where  the  post-mortem  examination  showed  that  the  progressive 
marasmus  and  anaemia  of  the  patient  had  "resulted  from  an  extensive  atrophy  of 
the  coats  of  the  stomach  and  intestine,  associated  in  some  instances  with  well- 
marked  lesions  of  the  sympathetic  plexus.  These  cases  are  very  interesting,  but 
have  nothing  whatever  to  do  with  pernicious  anaemia,  except  in  so  far  as  the  changes 
are  of  a  secondary  nature,  analogous  to  the  fatty  degeneration  seen  in  other  organs 
{vide  infra).  Often  the  symptoms  even  during  life  differ  not  a  little  from  those  of 
pernicious  anaemia,  so  that  we  can  not  think  it  right  to  establish  what  is  called  a 
u  gastro-intestinal  variety  of  pernicious  anaemia."  It  is  proper  to  group  and 
classify  the  forms  of  secondary  anaemia  according  to  their  various  causes,  but 
not  the  cases  of  primary  idiopathic  anaemia,  which  are  all  essentially  alike. 

The  credit  of  having  been  the  first  to  study  pernicious  anaemia  as  a  special 
form  of  disease  belongs  to  Biermer  (1868),  although  occasional  instances  of  the 
disease  had  long  before  been  noticed.  Its  occurrence  during  pregnancy  was  first 
pointed  out  by  Gusserow. 

[The  puerperal  form  of  pernicious  anaemia  was  described  by  Walter  Channing 
in  1842.] 

With  regard  to  the  special  aetiology  of  progressive  pernicious  anaemia,  it  must 
be  confessed  that  we  have  as  little  definite  information  as  about  the  aetiology  of 
chlorosis.  Klebs,  and  more  lately  Frankenhäuser,  have  discovered  micro-organ- 
isms in  the  blood,  to  which  they  have  given  the  names  " cercomonas  globulus'1'' 
and  "  cercomonas  navicula  " ;  and  they  ascribe  to  them,  a  pathogenic  influence. 
These  discoveries,  however,  have  not  yet  been  satisfactorily  confirmed.  It  is  a 
noteworthy  fact  that  pernicious  anaemia  is  much  more  frequent  in  some  countries 
than  in  others;  thus,  it  is  seen  far  more  frequently  in  Switzerland  than  in  North 
Germany.  This  would  be  one  argument  for  assuming  that  the  disease  is  an  infec- 
tious one.  In  Leipsic,  pernicious  anaemia  was  comparatively  frequent  several 
years  ago,  while  of  late  it  seems  to  have  become  decidedly  less  common.  There 
do  not  usually  seem  to  be  any  special  exciting  causes.  It  has  been  maintained 
that  unfavorable  hygienic  surroundings  and  insufficient  nourishment  promote  the 
development  of  the  disease;  and  this  would  apply  perhaps  to  some  cases,  but 
certainly  it  does  not  to  all.  We  are  inclined  to  regard  it  as  characteristic  of  this 
disease,  as  well  as  of  chlorosis,  that  the  anaemia  may  develop  despite  the  most 
favorable  outward  circumstances.  There  is,  however,  one  factor  which  seems  to 
have  a  decided  influence,  and  that  is  the  condition  associated  with  pregnancy  and 
childbirth.  The  first  symptoms  of  pernicious  anaemiaain  women  are  very  apt  to 
date  from  this  period.  It  is  a  very  interesting  but  somewhat  puzzling  fact,  that 
the  disease  may  appear  as  a  sequel  to  a  great  loss  of  blood,  whether  from  one  or 
several  haemorrhages.  It  seems  as  if  the  body  were  sometimes  unable  to  recover 
from  the  effects  of  large  haemorrhages  of  this  sort,  so  that  the  acute  merges  into  a 
chronic  and  progressive  anaemia,  which,  despite  nursing  and  treatment,  advances 
to  a  fatal  termination.  It  is  quite  doubtful,  however,  whether  such  cases  should 
be  classed  as  genuine  pernicious  anaemia. 


940  CONSTITUTIONAL  DISEASES. 

Most  of  the  cases  occur  during  middle  life,  between  twenty-five  and  forty 
years  of  age.  Both  sexes  are  equally  liable  to  the  disease,  except  for  those  cases 
already  referred  to  which  seem  to  be  especially  connected  with  the  sexual  func- 
tions. 

Pathology. — Pernicious  anaemia  so  often  terminates  fatally  that  there  has  been 
abundant  opportunity  to  make  accurate  anatomical  investigations  of  the  lesions 
it  produces.  We  shall  not  here  discuss  the  changes  in  the  blood  itself,  inasmuch 
as  they  will  more  properly  be  described  among  the  clinical  phenomena.  The 
changes  in  the  internal  organs  are  divisible  into  two  groups:  First,  such  as  are 
secondary  and  the  result  of  the  anaemia ;  and,  secondly,  such  as  may  perhaps  be 
primary  and  pathognomonic.  All  the  internal  organs  are,  of  course,  anaemic. 
Another  striking  change  is  fatty  degeneration.  This  is  usually  best  marked  in 
the  heart,  but  it  also  affects  the  kidneys,  liver,  and  the  walls  of  the  stomach  and 
intestines,  as  well  as  the  intima  of  the  blood-vessels  (compare  page  934).  We  have 
already  pointed  out  that  this  fatty  change  is  to  be  regarded  as  the  direct  result  of 
the  anaemia,  or  more  particularly  of  the  diminished  supply  of  oxygen  in  the  tis- 
sues ;  and  we  have  also  explained  that  the  destruction  of  albuminoids  indicated  by 
this  fatty  degeneration  maintains  a  direct  ratio  to  the  increase  of  nitrogen  in  the 
urinary  secretion. 

The  second  important  lesion  found  at  the  autopsies  of  those  who  die  of  per- 
nicious anaemia  is  the  frequent  haemorrhages,  usually  small,  but  occasionally  large ; 
these  are  found  in  all  sorts  of  locations.  The  most  important  of  these  haemor- 
rhages are  into  the  retina,  because  they  can  be  demonstrated  by  means  of  the  oph- 
thalmoscope during  life.  They  are  very  frequent.  We  may  also  find  minute 
haemorrhages  in  the  serous  membranes,  such  as  the  pleura  or  pericardium,  in  the 
brain  and  in  the  mucous  membranes.  Cutaneous  ecchymoses  are  also  occasion- 
ally found.  As  we  shall  note  later,  the  haemorrhages  are  probably  due  to  little 
capillary  embolisms  caused  by  the  formation  of  fibrine  ferment  in  the  blood. 

Still  another  secondary  symptom  is  an  abundant  deposit  of  iron  in  the  cells  of 
many  organs.  This  can  usually  be  determined  only  by  the  aid  of  the  microscope 
or  micro-chemical  tests.  It  is  most  abundant  in  the  peripheral  zone  of  the  hepatic 
lobules,  but  it  also  occurs  in  the  kidneys,  pancreas,  and  other  organs.  Quincke 
has  studied  this  point  very  carefully,  and  finds  that  the  total  amount  of  iron  con- 
tained in  the  liver  in  pernicious  anaemia  is  much  larger  than  normal.  The  most 
natural  and  most  probable  interpretation  of  this  fact  is  that  the  iron  originates 
from  the  destruction  of  large  numbers  of  red  blood-corpuscles. 

The  changes  thus  far  described  are  the  result  of  anaemia,  and  hence  are  the 
same  in  all  severe  anaemias,  whatever  their  cause.  On  the  other  hand,  search  has 
been  made  for  specific  changes  which  could  be  regarded  as  the  primary  disease, 
and  thus,  of  course,  our  attention  has  been  especially  directed  to  the  organs  en- 
gaged in  the  formation  of  the  blood.  The  lymph-glands  do  not  usually  pi'esent 
any  special  changes  in  pernicious  anaemia.  If  they  are  much  altered,  it  is  proba- 
ble that  the  disease  is  quite  a  different  one,  which  we  shall  later  have  an  oppor- 
tunity to  study  (vide  pseudo-leukaemia).  The  spleen  is  in  many  cases  normal. 
In  exceptional  instances,  however,  it  is  decidedly  enlarged,  although  never  enor- 
mous. Even  when  the  «pgan  is  enlarged  thei'e  are  no  important  histological 
changes  to  be  detected.  Cases  of  pernicious  anaemia  with  marked  splenic  tumor 
are  often  termed  splenic  anaemia  (vide  infra),  but  we  do  not  ourselves  see  how 
such  cases  differ  essentially  from  others  in  which  the  spleen  is  not  enlarged.  The 
changes  in  the  bone-marrow  are  by  far  the  most  constant.  This  structure  plays 
a  much  more  important  part  in  the  formation  of  the  blood  than  does  the  spleen. 
C.  Wood,  and  after  him  Cohnheim,  called  attention  to  the  fact  that  the  bone- 
marrow  is  almost  invariably  affected  in  pernicious  anaemia.     Instead  of  its  normal 


PEOGRESSIVE  PERNICIOUS  ANAEMIA.  !i  1 1 

yellow  color,  it  has  a>  reddish -purple  appearance.  Tin's  is  due  mainly  to  (lie  fact 
that  the  numerous  fat-cells  of  the  marrow  are  all,  or  nearly  all,  destroyed.  This 
is  the  more  surprising  as  the  fatty  tissues  in  other  parts  of  the  body  are  offo  □ 
very  little  affected  in  pernicious  anaemia.  The  specific  cellular  elements  of  the 
marrow  also  exhibit  certain  changes.  There  is  a  decided  hyperplasia,  arid  often, 
although  not  always,  there  are  found  large  numbers  of  nucleated  red  blood-cor- 
puscles. Cohnheim  is  inclined  to  regard  the  disease  of  the  bone-marrow  as 
specific  and  primary,  but  it  must  be  confessed  that  there  are  many  real 
which  strongly  oppose  this  view,  and  suggest  the  possibility  of  this  change  in 
the  marrow  being  merely  a  secondary  phenomenon,  a  sign  of  the  extremely  ac- 
tive formation  and  regeneration  of  the  red  blood-corpuscles.  Neumann's  i n  vst  Na- 
tions would  lead  to  the  belief  that  the  nucleated  red  blood-corpuscles  are  young 
blood-cells  in  the  process  of  development.  Furthermore,  these  vigorous  processes 
of  regeneration,  and  the  corresponding  changes  in  the  bone-marrow,  are  often 
found  in  cases  of  profound  anaemia  which  are  beyond  a  doubt  of  secondary 
origin. 

We  can  not,  therefore,  feel  certain  that  the  lesion  of  the  bone-marrow  is  the 
primary  anatomical  disturbance,  and  we  are  therefore  obliged  to  assume  that 
essential  anaemia  may  be  a  disease  of  the  blood  itself — that  is,  some  process  which 
does  direct  injury  to  the  red  blood-corpuscles,  possibly  of  an  infectious  char- 
acter (?). 

Symptoms. — As  already  stated,  the  symptoms  of  pernicious  anaemia  usually 
begin,  independently  of  any  demonstrable  cause,  in  individuals  previously  healthy, 
and  develop  so  slowly  and  gradually  that  it  is  hardly  ever  possible  to  determine 
the  precise  date  of  the  commencement  of  the  disease.  This  is  still  more  likely  to 
be  the  case  if  the  trouble  occurs,  as  indeed  it  may,  in  individuals  who  were  pre- 
viously feeble  and  pale  without  being  actually  ill.  Occasionally  a  more  acute 
onset  is  observed  in  pregnant  women. 

The  first  symptoms  are  almost  invariably  traceable  to  the  incipient  anaemia. 
They  include  the  subjective  disturbances  and  the  objective  changes  which  are  seen 
in  ordinary  chlorosis.  The  patient  feels  languid  and  is  easily  fatigued,  is  liable  to 
headache,  vertigo,  palpitation,  and  tinnitus  aurium;  there  are  anorexia,  frequent 
nausea,  and,  above  all,  a  striking  pallor  of  the  skin  and  mucous  membranes. 
While  these  symptoms,  however,  usually  remain  of  slight  or  moderate  severity  in 
chlorosis,  they  attain,  in  pernicious  anaemia,  the  greatest  conceivable  intensity. 
Of  course,  it  would  be  impossible  to  describe  all  the  stages  through  which  the 
patient  passes,  but  we  append  a  sketch  of  those  symptoms  which  are  almost  sure 
to  be  present,  in  greater  or  less  completeness,  in  any  well-marked  case  of  perni- 
cious anaemia. 

If  the  anaemia  be  profound,  the  patient  may  be  so  weak  as  to  be  confined  to  the 
bed.  If  he  sits  up  for  any  length  of  time,  symptoms  of  increasing  cerebral  anaemia 
develop,  and  he  is  apt  to  faint.  Usually  the  patient  lies  upon  his  back,  with  his 
head  rather  low,  and  presents  a  countenance  of  waxy  pallor.  Very  frequently  a 
slight  but  distinct  yellowish  hue  may  be  detected.  Occasionally  there  are  cutane- 
ous ecchymoses,  but  those  are  exceptional.  The  mucous  membrane  of  the  lips, 
the  gums,  and  the  conjunctivae  are  likewise  pale  and  colorless.  The  intellect  is 
unimpaired,  but  all  answers  to  questions  are  slow,  apathetic,  and  delivered  in  a 
low  and  feeble  tone  of  voice.  The  patient  is  usually  incapable  of  any  great  men- 
tal exertion.  If  the  body  be  moved,  and  especially  if  an  upright  position  be  sub- 
stituted for  a  horizontal  one,  there  is  gi-eat  liability  to  syncope,  as  already  men- 
tioned. This  may  result  from  other  slight  physical  exertions,  and  is  often  accom- 
panied by  a  peculiar  spasmodic  rigidity  of  the  body.  The  main  subjective  symp- 
toms are  weakness,  and  more  especially  intense  headache ;  this  often  assumes  a 


942  CONSTITUTIONAL  DISEASES. 

pulsating  character,  and  is  located  mainly  in  the  temples  or  forehead.  There  is 
also  an  annoying  ringing  in  the  ears,  described  as  a  rushing  or  roaring  sound. 
There  are  certain  other  subjective  sensations,  namely,  nausea,  a  sense  of  thoracic 
oppression,  and  pain  in  the  bones,  which  will  be  further  considered  below. 

If  we  now  proceed  to  a  systematic  physical  examination,  we  are  struck,  in  the 
first  place,  by  the  condition  of  the  eyes.  The  pupils  are  often  somewhat  enlarged, 
but  react  in  a  normal  manner.  Vision  is  often  disturbed  by  spots  before  the  eyes. 
The  anaemic  amaurosis  seen  after  a  sudden  large  haemorrhage  has  not  yet  been 
observed  in  pernicious  anaemia.  The  ophthalmoscopic  examination  of  the  fundus 
has  very  great  diagnostic  importance.  We  find  in  a  majority  of  cases,  although 
not  in  all,  retinal  haemorrhage.  There  may  be  either  one  or  many  haemorrhages. 
If  they  are  extensive  enough  to  involve  the  macula  lutea  or  the  disk,  they  may 
disturb  vision  greatly.  Retinal  haemorrhages  invariably  signify  that  the  anaemia 
is  profound,  and  are,  with  considerable  justice,  regarded  as  distinguishing  perni- 
cious anaemia  from  chlorosis. 

Respiratory  Symptoms. — Breathing  is  usually  accelerated,  and,  in  the  most 
advanced  cases,  is  often  remarkably  deep  and  noisy  (anaemic  dyspnoea,  vide  supra). 
Sometimes  there  is  a  very  annoying  and  almost  painful  sense  of  thoracic  oppres- 
sion, which  is  evidently  connected  with  the  dyspnoea.  There  is  a  "  hunger  for  air." 
Physical  examination  of  the  lungs  gives  negative  results.  Sometimes  there  is  a 
little  cough,  and  there  may  be  sufficient  haemori'hage  into  the  mucous  membrane 
of  the  air-passages  to  give  rise  to  a  slight  haemoptysis.  Even  in  this  case  no  ana- 
tomical changes  can  be  detected  during  life.  We  may  also  mention  in  this  con- 
nection that  epistaxis  is  not  very  infrequent. 

Phenomena  referable  to  the  circulatory  system  are  of  still  greater  clinical 
importance.  The  area  of  cardiac  dullness  is  usually  normal,  although  sometimes 
slightly  increased.  Upon  palpation,  we  often  find  that  the  heart's  action  is  exag- 
gerated, and  that  its  beat  is  felt  over  a  larger  area  than  normal.  The  pulse  is  usu- 
ally decidedly  rapid  (100-120),  but  it  is  regular,  and  sometimes,  but  by  no  means 
invariably,  small.  It  is  often  surprisingly  strong.  The  loud  "  anaemic  murmurs  " 
are  very  characteristic.  They  can  be  appreciated  at  the  apex  of  the  heart,  but  are 
usually  still  better  heard  at  its  base.  We  generally  hear  a  loud  bruit  de  diable  in 
the  veins  of  the  neck. 

Digestive  Organs. — The  tongue  is  usually  pale,  smooth,  and  dry.  The  appe- 
tite is  often  very  poor.  The  most  prominent  distui'bances,  however,  are  not  due 
directly  to  the  condition  of  the  stomach,  but  they  result  from  the  cerebral  anaemia 
— that  is,  they  are  symptoms  of  the  irritation  of  the  nervous  centers.  We  refer  to 
eructations  and  vomiting,  which  may  be  very  frequent  and  distressing.  There  is 
usually  a  tendency  to  constipation.     Occasionally  there  is  diarrhoea. 

The  liver  is  usually  normal;  as  is  also  the  spleen  in  many  instances,  while  in 
others  it  is  shown  by  percussion  and  palpation  to  be  enlarged.  It  is  sometimes 
possible,  as  we  can  ourselves  bear  witness,  to  observe  an  enlargement  of  the  spleen 
increasing  as  the  anaemia  grows  more  profound,  and  again  decreasing  if  improve- 
ment occurs  (vide  infra).  On  ordinary  examination,  the  urine  does  not  usually 
differ  essentially  from  normal.  With  few  exceptions  it  is  free  from  albumen, 
and  it  never  contains  sugar.  As  already  set  forth,  however,  accurate  quantitative 
analysis  often  furnishes  important  evidence  of  changes  in  tissue-metamorphosis 
resultant  upon  the  anaemia  (cf.  page  934).  We  will  merely  mention  once  more 
the  comparative  increase  in  the  amount  of  urea  excreted,  and  the  occasional 
excess  of  uric  acid.  Sometimes  the  urine  gives  an  unusually  vivid  reaction  for 
indican. 

In  regard  to  what  has  already  been  said  about  the  bones,  it  is  an  interesting 
fact  that  they  are  very  sensitive  to  pressure  in  many  cases  of  pernicious  anaemia. 


PROGRESSIVE  PERNICIOUS  ANiEMIA.  943 

The  sternum  in  particular  is  painful  upon  light  percussion  ;  and  sometimes  press- 
ure will  cause  pain  in  the  hones  of  the  extremities.  In  rare  instances  swelling  of 
the  knee  and  other  joints  has  been  observed. 

The  blood  has  been  made  the  subject  of  numerous  and  careful  investigations; 
nevertheless,  no  characteristic  change  has  been  discovered.    The  change«  pre  <  nted 
in  pernicious  anaemia  likewise  occur  in 
cases    of   profound    secondary   anaemia. 
This  seems  the  more  readily  intelligible 
to  us  because  of  the  view  which  we  have 
already  expressed  on  page  930  with  re-     6"" 
gard  to  the  origin  of  secondary  anaemia. 
To  the  naked  eye  the  blood  seems  ex-  ^_    '' -■    .      C\ 

tremely  pale  and  watery.     The  number  i£j(  ?  C-^     v '  r  ■  r>. 

of  red  blood -corpuscles  is  sometimes  so    a -— -— Q  {)  /  ,.    "°    > 

diminished  that  it  seems  incredible  that  **  0  q  ( -"  ■  Or 

life  should  persist.     It  is  not  at  all  un-  (""■■      „  (3\    /fOV«    /  -     \/, 

usual,  in  the  last  stages  of  the  disease,  to  n    -1   (~\     a  ".  -,.    )-    Ij  -J 

find  less  than  500,000  red  blood-corpuscles  ^--°    f  /)  q° -c 

per  cubic  millimetre — that  is,  about  one   c -■-''  i  @ 

tenth  of  the  normal  amount.     The  red  /      ggg^  9 

blood  -  corpuscles  are  found   to   present  /        v . 

striking  varieties  in  size  and  form  (vide  •'  ■ 

Fig.  118).     While  some  corpuscles  have   ^     1io    ~,  .    ,,        ,  .,     ,  .      . 

0            '                                              r  p-IG.  118.— Changes  in  the  red  blood-corpuscles  in 
a  normal   appearance,  others  may  be  of  pernicious  anaemia.    (From  Quincke.)    a.  Nor- 
-1,       -,                           ,                     ,      s  mal  blood-corpuscles,     b.   Macrocytes.    c.  Mi- 
an   unusually  large    size    (macrocytes).  crocytes.    d.  poikilocytes. 

These  "  giant  corpuscles  "  appear  normal 

except  in  dimensions,  and  some  observers  (Laache)  have  thought  that  they  were 
even  possessed  of  an  unusual  amount  of  haemoglobin.  It  is  therefore  surmised 
that  they  represent  an  effort  on  the  part  of  nature  toward  compensation.  In 
contrast  with  these  large  cells  are  found  a  varying  number  of  minute  red  cells  of 
a  spherical  shape ;  these  were  first  described  by  Vanlair  and  Masius,  and  called 
microcytes.  Their  mode  of  origin  and  significance  are  not  known.  Finally, 
there  are  numerous  red  blood-corpuscles  of  abnormal  shax>e.  These  Quincke  was 
the  first  to  notice.  They  present  remarkable  forms,  being  biscuit-shaped,  ham- 
mer-shaped, or  anvil-shaped,  and  so  on,  as  illustrated  in  the  accompanying  cut. 
These  "  poikilocytes  "  are  found  in  perfectly  fresh  undiluted  blood,  so  that  there  is 
no  reason  to  suppose  that  they  are  artificial  products.  Both  the  microcytes  and 
poikilocytes  are  at  present  generally  regarded  as  blood-corpuscles  which  have  un- 
dergone imperfect  or  abnormal  development,  or  suffered  changes  due  to  disease. 
Nucleated  red  blood-corpuscles  have  also  been  seen  by  Ehrlich  a  number  of  times 
during  life.  The  white  blood-corpuscles  are  not  usually  increased  in  number:  in 
occasional  instances,  however,  a  temporary  leukocytosis  has  been  found.  "Gran- 
ule-masses "  are  often  found  in  considerable  abundance.  Chemical  examination 
of  the  blood  has  not  as  yet  brought  to  light  any  facts  of  great  importance.  Of 
course  there  is  a  great  diminution  in  the  total  amount  of  haemoglobin.  The 
amount  of  albumen  in  the  blood-serum  remains  nearly  normal. 

We  observe  in  pernicious  anaemia  the  tendency  to  fever  common  to  all  varie- 
ties of  profound  anaemia.  In  many  cases  the  evening  temperature  will  for  weeks 
reach  100°-101°  (38°-38-5°  C),  or  even  higher.  Previous  to  death,  however,  the 
temperature  may  become  subnormal,  falling  to  86°  (30°  C),  or  even  lower. 

As  to  the  origin  of  all  these  symptoms  we  must,  as  we  have  said,  regard  the 
impairment  of  the  blood,  especially  its  poverty  in  red  blood-corpuseles,  as  the 
essential  morbid  process.     How  this  impairment  is  produced,  whether  by  injury 


944  CONSTITUTIONAL  DISEASES. 

to  the  blood-corpuscles  themselves  or  to  the  place  where  they  are  formed,  we  do 
not  know.  A  large  part  of  the  other  morbid  symptoms — the  pallor  of  the  skin, 
the  weakness,  the  "  anaemic  cerebral  symptoms,"  tinnitus,  vertigo,  nausea,  faint- 
ness,  etc.,  are  due  directly  to  the  anaeuiia.  In  regard  to  certain  other  important 
symptoms,  however,  another  factor  is  probably  of  great  significance,  namely,  an 
auto-intoxication  of  the  body  with  fibrine  ferment. 

By  the  destruction  of  many  red  blood-corpuscles,  probably  a  certain  amount 
of  haemoglobin  is  always  set  free,  and  enters  the  blood  plasma.  There  is  then 
a  haemoglobinaemia.  From  many  experiments,  however  (Dorpat  school  of  Alex- 
ander Schmidt,  Ponfick,  Silbermann,  etc.),  we  know  that  haemoglobin  dissolved 
in  the  blood  destroys  the  white  blood-corpuscles,  and  in  some  way  produces  from 
them  fibrine  ferment.  Chronic  "  ferment  intoxication  "  of  the  body  causes  certain 
symptoms,  which  are  almost  never  absent  in  pernicious  anaemia — capillary  haemor- 
rhages and  fever.  The  haemorrhages  are  usually  associated  with  embolism  of  the 
smaller  vessels,  seldom  with  local  thrombi.  Many  severe  nervous  symptoms  may 
perhaps  also  be  referred  to  this  intoxication. 

General  Course,  Duration,  and  Prognosis. — As  the  very  name  "pernicious" 
indicates,  the  disease  generally  terminates  unfavorably.  Death  usually  seems  to 
be  the  direct  result  of  the  extreme  anaemia ;  special  complications  are  exceptional. 
The  disease  often  maintains  a  slow  but  gradual  progress  to  the  end.  Its  dura- 
tion, reckoning  from  the  appearance  of  the  first  symptoms,  may  not  exceed  three 
to  six  months.  It  may  even  run  its  course  in  a  still  shorter  time.  It  seldom  lasts 
more  than  a  year.  Sometimes  its  course  is  interrupted ;  there  may  be  an  arrest 
of  the  process,  or  improvement,  or  even  apparent  recovery.  Usually,  however, 
there  are  fresh  relapses.  In  a  certain  class  of  cases  the  disease  lasts  two  or  three 
years,  and  is  marked  by  a  number  of  "  attacks  of  anaemia  "  so  intense  that  the 
subsequent  improvement  of  the  patient  seems  simply  marvelous.  It  is  in  cases 
of  this  sort  that  splenic  tumor  has  been  made  out  at  the  time  the  anaemia  was  at 
its  height;  yet  we  do  not  perceive  the  necessity  of  establishing  "splenic  anaemia" 
as  an  affection  essentially  different  from  progressive  pernicious  anaemia.  It  is 
merely  a  clinical  variety  of  the  disease  under  discussion.  Apparently,  it  likewise 
has  an  invariably  fatal  termination. 

Permanent  recovery  may  occur  in  cases  of  idiopathic  anaemia  so  profound  that 
we  are  at  first  inclined  to  regard  them  as  pernicious.  These  cases  are  unfortu- 
nately very  rare,  and  even  where  there  is  a  marked  improvement  the  danger  of  a 
relapse  is  to  be  borne  in  mind.  The  prognosis  is  therefore  always  very  grave, 
if  not  absolutely  vmfavorable.  Of  course,  general  hygienic  surroundings  and 
good  care  may  exert  some  influence  upon  the  course  of  the  disease.  It  is  note- 
worthy that  if  pregnancy  be  complicated  by  profound  anaemia  there  is  a  great 
liability  to  premature  delivery,  after  which  there  is  often  a  rapid  change  for  the 
worse.     There  are  exceptions  to  this  rule. 

Diagnosis.— It  is  seldom  difficult  to  make  out  the  existence  of  a  profound 
anaemia,  or  to  determine  the  degree  of  clanger  which  the  consequent  symptoms 
indicate.  We  have,  however,  the  same  difficulty  here  as  in  chlorosis  in  proving 
that  the  anaemia  is  primary  and  idiopathic.  The  factors  essential  to  this  diag- 
nosis have  been  already  indicated.  We  should  bear  in  mind  the  possibility  of 
incipient  tuberculosis,  organic  diseases  of  the  stomach,  or  such  parasites  as  the 
anchylostoma  and  tapeworm. 

Treatment. — For  treating  progressive  pernicious  anaemia  we  have  only  the 
same  remedies  as  for  the  benign  variety  of  anaemia.  Abundant  and. suitable 
nourishment  is  requisite,  and  all  hygienic  influences  should  be  carefully  regu- 
lated. Internally,  our  main  reliance  is  to  be  put  upon  the  preparations  of  iron. 
With  us,  a  favorite  remedy  in  pernicious  anaemia  is  the  tinctura  ferri  chlorati 


LEUKEMIA.  945 

aetherea  (analogous  to  tinctura  ferri  chloridi,  U.  8.  P.),  of  which  ten  drops  in 
sweetened  water  maybe  given  several  times  a  day.  It  would  also  be  extremely 
advisable  to  try  the  effect  of  arsenic.  This  remedy  sometimes  accomplishes  strik- 
ing results  in  the  whole  group  of  blood  diseases,  including  Leukaemia  and  pseudo- 
leukaemia  as  well  as  anaemia.  It  is  much  better  administered  in  pill  form  tban  in 
Fowler's  solution.  Iron  may  be  given  at  the  same  time  with  arsenic.  Some 
authorities  recommend  phosphorus. 

If  the  case  be  not  too  far  advanced,  baths  may  prove  useful  adjuvants  to  the 
internal  treatment.  Salt  baths  or  artificial  carbonic-acid  baths  may  be  employed. 
Symptomatic  treatment  is  often  indicated:  the  dyspepsia  may  call  for  dilute 
hydrochloric  acid,  or  the  troublesome  vomiting  may  require  bits  of  ice,  bromide 
of  potassium,  or  opium. 

The  transfusion  of  blood  has  been  employed  in  pernicious  anaemia.  Some- 
times the  effect  seems  to  be  favorable.  Experience  thus  far,  however,  would  not 
lead  one  to  expect  very  great  benefit  from  it.  Von  Ziemssen  lias  lately  recom- 
mended in  all  severe  forms  of  anaemia  the  subcutaneous  injection  of  blood.  It  is 
done  by  injecting  under  the  skin,  by  thoroughly  disinfected  instruments,  fifty 
cubic  centimetres  of  defibrinated  human  blood,  divided  into  two  parts,  twenty-five 
cubic  centimetres  being  injected  into  each  thigh.  The  point  of  injection  is  vigor- 
ously rubbed,  and  thus  the  injected  blood  is  forced  into  the  lymph-channels.  In 
severe  cases  this  procedure  should  be  frequently  repeated.  Experiments  on  this 
method  are  thus  far  very  favorable.  Not  only  the  subjective  symptoms,  but  the 
objective  condition  of  the  blood,  the  number  of  red  blood-corpuscles,  sometimes 
show  a  striking  improvement  after  the  injection. 

[In  the  experience  of  American  and  English  clinicians,  arsenic,  long  continued 
and  in  as  large  doses  as  are  tolerated,  is  of  far  greater  value  than  iron. 

The  inhalation  of  oxygen  is  expensive,  but  seems  to  be  of  distinct  service  in 
some  cases  of  grave  anaemia  of  all  forms.] 


CHAPTER  III. 

LEUKEMIA. 

( Leiicocythmmia. ) 

Definition  and  iEtiology.— Virchow,  in  1845,  was  the  first  to  obtain  an  insight 
into  the  disease  leukaemia  ("white  blood").  He  detected  the  great  increase  of 
white  corpuscles  occasioned  by  it,  and  from  this  time  these  constituents  of  the 
blood  were  subjected  to  observation  in  all  sorts  of  diseases.  It  was  soon  found 
that  there  may  be  a  temporary  increase  of  the  white  corpuscles  in  various  primary 
diseases,  and  that  in  certain  instances  this  increase  may  actually  constitute  the 
essential  symptom.  In  this  latter  case  the  increase  is  due  to  a  depraved  condition 
of  certain  internal  organs.  In  the  temporary  cases,  where  the  increase  of  white 
blood-corpuscles  is  usually  not  very  great,  we  find  one  white  corpuscle  to  one 
hundred  red.  or  even  one  to  fifty — the  normal  ratio  being  one  to  six  hundred  or 
more.  This  is  usually  termed  leukocytosis,  in  distinction  from  leukaemia  proper. 
Leukocytosis  is  most  frequent  in  acute  infectious  diseases,  such  as  typhoid  fever, 
recurrent  fever,  intermittent  fever,  and  pyaemia,  and  is  also  often  seen  in  anaemia. 

Genuine  leukaemia  is  a  rather  rare  disease.     Its  characteristics  are  well  marked 

in  most  cases,  but  of  its  true  nature  we  remain  entirely  ignorant.     In  a  majority 

of  the  cases  the  change  in  the  blood  is  associated  with  marked  changes  in  the 

spleen  and  the  bone-marrow,  and  often  also  in  the  lymph-glands.     The  organs 

60 


946  CONSTITUTIONAL  DISEASES. 

just  enumerated  being  concerned  in  the  manufacture  of  the  blood,  it  is  very- 
reasonable  to  suppose  that  leukaemia  is  a  disease  which  primarily  affects  these 
organs,  and  that  the  increase  in  white  corpuscles  results  from  the  disturbance 
thus  occasioned.  The  cause  of  the  disease  in  the  organs  mentioned  is  as  yet 
unknown.  Various  authors  have  suggested  that  there  may  be  some  specific  infec- 
tion, but  they  have  not  been  able  thus  far  to  produce  any  evidence  of  the  truth 
of  their  surmise.  -  In  few  cases  can  we  discover  even  any  exciting  cause.  The 
illness  seems  to  develop  spontaneously  in  perfectly  healthy  persons.  In  some 
cases,  on  the  other  hand,  leukaemia  does  seem  to  be  a  sequel  of  some  other  disease. 
Thus  it  is  occasionally  preceded  by  a  tedious  attack  of  intermittent  fever.  It  has 
also  been  asserted  that  syphilis  and  other  infectious  diseases,  such  as  typhoid,  may 
give  rise  to  leukaemia,  but  this  is  not  very  probable.  Finally,  trauma  of  the  spleen 
or  bones  has  in  repeated  instances  been  regarded  as  the  occasion  of  the  disease. 

The  hygienic  surroundings  of  the  patient  have  also  been  regarded  as  causes  of 
leukaemia.  The  disease  is  more  frequent  among  the  poorer  classes  than  among 
the  wealthy ;  but  there  are  numerous  exceptions  to  this  rule.  .^Etiological  impor- 
tance has  also  been  ascribed  to  anxiety,  trouble,  and  mental  depression  in  general, 
but  with  how  much  justice  is  doubtful. 

Leukaemia  is  most  common  in  middle  life,  between  thirty  and  forty-five  years 
of  age,  but  well-marked  cases  have  been  observed  repeatedly  even  in  childhood, 
as  also,  though  less  frequently,  in  old  age.  Men  are  somewhat  more  liable  to 
the  disease  than  women.  It  has  been  repeatedly  stated  that  in  female  patients 
the  disease  is  sometimes  referable  to  sexual  derangement,  but  this  has  not  been 
proven. 

Pathological  Anatomy. — The  pathognomonic  change  in  leukaemia  is  an 
increase  in  the  number  of  white  blood-corpuscles;  this  may  be  so  considerable 
that  there  may  be  one  white  to  three  red,  or  even  one  white  to  two  red  corpuscles. 
The  characteristics  of  the  blood  can  be  studied  during  the  life  of  the  patient,  and 
upon  them  the  diagnosis  is  mainly  based.  They  will  therefore  be  discussed 
under  symptomatology,  while  we  shall  here  confine  ourselves  to  the  lesions  pre- 
sented by  the  spleen,  bone-marrow,  and  lymph-glands. 

Of  the  organs  just  enumerated,  the  spleen  is  the  one  most  frequently  affected 
(splenic  leukaemia).  It  is  often  greatly  increased  in  size,  not  seldom  attaining  a 
weight  of  six  to  thirteen  pounds  (3-6  kilogrammes)  and  a  length  of  a  foot  (30 
ctm.).  There  is  a  true  hyperplasia  of  the  whole  organ:  all  the  histological  con- 
stituents are  increased.  The  cut  surface  is  usually  a  rather  vivid  red  in  early 
cases,  but  later  on  it  often  has  a  lighter,  yellowish  color.  The  consistence  is  usually 
diminished,  but  in  the  later  stages  it  may  be  greater  than  normal.  Upon  micro- 
scopic examination,  we  find  enlargement  of  the  blood-vessels  and  a  great  increase 
in  the  cells  of  the  pulp  and  of  the  follicles.  Sometimes  the  hyperplasia  of  the 
follicles  predominates,  giving  the  spleen  a  spotted  appearance,  like  marble.  In 
such  cases  the  pulp  usually  presents  retrograde  metamorphosis,  with  atrophy  and 
fatty  degeneration  of  its  cells  and  deposits  of  pigment.  In  advanced  cases  a  con- 
siderable amount  of  firm  connective  tissue  may  be  present.  There  are  often 
haemorrhagic  infarctions,  presenting  the  appearance  of  circumscribed  spots,  dark 
red,  or  in  the  later  stages  brownish  yellow,  in  color. 

Lesions  of  the  bone-marrow  are  next  in  frequency  to  those  of  the  spleen 
(medullary  and  myelogenous  variety  of  leukaemia).  Neumann  and  a  few  other 
authorities  regard  changes  in  the  bone-marrow  as  an  essential  lesion,  and  hold 
that  they  can  be  demonstrated  in  every  case  of  leukaemia.  There  would  certainly 
seem  to  be  exceptions  to  this  last  rule,  but  nevertheless  in  a  majority  of  cases  the 
marrow  does  present  a  peculiar  yellowish  or  almost  puriform  appearance.  By 
means  of  the  microscope  we  can  detect  a  great  increase  in  the  lymphoid  cells  of 


LEUKAEMIA.  947 

the  marrow  and  the  presence  of  a  considerable  number  of  nucleated  red  blood- 
corpuscles. 

In  many  cases  the  lymph-glands  remain  perfectly  normal;  but  in  others  they 
become  considerably  enlarged,  and  form  actual  tumors  in  various  parts  of  the 
body,  such  as  the  axilla,  neck,  and  groin,  and  sometimes  the  internal  lymph-gland 
Such  cases  are  examples  of  lymphatic  leukaemia.     Histologically,  the  change  here 
is  simple  hyperplasia  of  the  glandular  tissue. 

These  three  forms  of  leukaemia — splenic,  myelogenous,  and  lymphatic— can  not 
be  regarded  as  distinct  diseases,  inasmuch  as  cases  occur  which  present  all  sorts  of 
combinations  of  these  different  lesions.  Purely  myelogenous  cases  are  very  rare,  if 
they  occur  at  all;  and  we  rarely  meet  with  cases  which  are  purely  splenic  or 
purely  lymphatic.  Most  cases  present  lesions  of  the  spleen  and  marrow  con- 
jointly. In  less  frequent  instances  splenic  disease  is  associated  with  that  of  the 
lymphatic  glands.  The  fact  that  these  combinations  exist  indicates  that  there  is 
one  common  cause  for  the  disease,  which  assails  sometimes  one,  sometimes  two,  or 
sometimes  all  three  of  the  organs  named. 

Just  what  the  connection  is  between  the  changes  in  the  blood  and  the  lesions 
of  these  various  organs  is  an  unanswered  question.  A  view  which  seems  to  us 
very  plausible  regards  the  disturbance  in  the  spleen,  or  marrow,  or  lymph-glands, 
as  the  case  may  be,  as  the  primary  one,  and  the  alteration  in  the  blood  as  a  result 
of  this  primary  disturbance;  there  is  an  increase  in  the  number  of  colorless  cor- 
puscles formed,  and  a  consequent  increase  in  the  number  of  them  introduced  into 
the  circulatory  fluid.  Some  authorities  have  taken  for  granted  that  the  colorless 
blood-corpuscles  normally  undergo  transformation  into  red  blood-corpuscles,  and 
believe  that  in  leukaemia  this  metamorphosis  is  hindered;  but  the  assumption 
lacks  support.  It  is  true,  however,  that  the  number  of  red  blood-corpuscles  is 
diminished  in  leukaemia.  This  diminution  in  number  might  be  ascribed  either 
to  scantiness  of  supply  or  to  increase  in  the  processes  of  destruction,  but  which 
factor  is  in  reality  the  important  one  must  remain  undetermined. 

Changes  in  Other  Organs. — Leukaemia  sometimes  causes  new  growths  of  a 
lymphatic  character  in  certain  organs  other  than  those  already  mentioned.  The 
growths  may  either  be  diffuse  or  circumscribed  and  nodular.  They  are  observed 
in  the  tonsils,  Peyer's  patches,  and  the  intestinal  follicles.  They  are  also  very  fre- 
quent in  the  liver,  kidneys,  and  retina,  and  more  rarely  in  the  lungs  and  the 
pleura.  These  various  lesions  may  be  regarded  as  in  a  certain  sense  analogous  to 
the  metastatic  tumors  of  cancer  or  sarcoma,  and  suggest  the  possibility  of  the  diffu- 
sion of  the  pathogenic  poison  throughout  the  whole  body.  In  one  or  two  cases 
a  well-marked  leukaemia  has  been  found  independent  of  any  demonstrable  organic 
lesions.  It  is  impossible,  at  present,  to  explain  such  occurrences.  Leube  and 
Fleischer  have  reported  a  case  of  this  sort,  and  are  inclined  to  believe  that  the 
blood  itself  was  diseased.  There  is  little  known  as  yet  as  to  changes  in  the  chem- 
ical characters  of  the  blood  and  viscera  in  leukaemia.  Xanthine  and  hypoxanthine 
have  been  found  in  the  blood,  as  have  also  lactic  acid  and  formic  acid.  It  is  also 
noteworthy  that  octahedral  crystals  are  often  found  after  death  in  the  blood, 
spleen,  and  marrow,  and  in  other  parts.  These  are  known  as  Chai'cot's  crystals, 
and  have  already  been  described  as  occurring  in  the  sputum  in  certain  pulmonary 
diseases  (compare  page  169). 

Symptoms. — The  clinical  phenomena  of  leukaemia  are  in  many  respects  similar 
to  those  of  progressive  pernicious  anaemia,  and  need  not  be  enumerated  again 
here.  In  leukaemia,  however,  we  have,  in  addition,  symptoms  referable  to  the 
spleen  or  lymph-glands  or  bone-marrow  (as  the  case  may  be),  and  also  the  char- 
acteristic alterations  in  the  blood.  The  blood-changes,  being  pathognomonic, 
demand  a  full  description. 


948 


CONSTITUTIONAL  DISEASES. 


Fig.  119.  —  AtiEemic  blood. 
White  blood-corpuscles, 
cles. 


(From   Funke.) 


The  pallor  and  watery  character  of  the  blood  in  leukaemia  are  noticeable  even 
to  the  naked  eye  in  advanced  stages  of  the  disease.  They  can  not,  however,  be 
distinguished  without  the  aid  of  the  microscope  from  the  changes  present  in  grave 
anaemia  (vide  Fig.  119).  Looking  through  that  instrument,-  we  frequently  per- 
ceive at  once  an  enormous  increase  in  the 
number  of  the  white  blood- corpuscles. 
As  already  stated,  there  may  be  almost  as 
many  white  as  red  corpuscles.  The  size 
of  the  white  corpuscles  varies  in  different 
cases,  and  also  in  the  same  case.  Vir- 
chow  has  called  attention  to  the  fact  that 
the  smaller  cells  originate  mainly  in  the 
lymph-glands,  and  are  therefore  especial- 
ly numerous  where  the  leukaemia  is  of  a 
lymphatic  type.  The  larger  cells  are  re- 
ferred mainly  to  the  spleen  and  the  mar- 
row. The  marrow  is  also  said  to  contrib- 
ute certain  extremely  large  nucleated 
cells,  the  dimensions  of  which  considei*a- 
bly  exceed  those  of  the  normal  white 
blood-corpuscles.  It  is  not  always  possi- 
b.  Red  blood-corpus-  We  to  determine  the  origin  of  the  white 
cells  from  their  size.  Ehrlich  has  suc- 
ceeded in  making  out  various  forms  of  white  corpuscles  by  staining.  What  are 
called  "  eosinophilous  cells "  are  especially  increased  in  the  blood  of  leukaemia. 
These  are  colorless  cells,  the  granules  of  which  take  a  deep  stain  with  acid  pig- 
ments, but  not  with  basic.  Coincident  with  this  increase  in  the  white  cells  in 
leukaemia  there  is  almost  invariably  a  considerable  diminution  in  the  number  of 
red  blood-corpuscles.  We  also  find  an  occasional  nucleated  red  blood-corpuscle  in 
leukaemic  blood,  and  sometimes  also  microcytes,  poikilocytes,  and  almost  always 
a  large  number  of  "  granule-masses  "  interspersed  between  the  blood-corpuscles. 

Splenic  tumor  is  the  most  frequent  and  important  of  the  organic  lesions  pro- 
duced by  leukaemia.  It  is  rarely  possible  to  observe  its  development.  In  most 
instances  the  spleen  is  already  large  when  the  patient  first  comes  under  observa- 
tion. It  projects  from  under  the  ribs  as  a  firm,  hard  mass,  the  lower  and  anterior 
extremity  of  which  often  extends  to  the  median  line  of  the  body.  The  inner  edge 
of  the  tumor  is  somewhat  characteristic ;  it  is  rather  sharp,  and  presents  one  or 
two  notches.  At  first  there  is  little  subjective  disturbance  or  pain  referred  to  the 
spleen.  Where  the  enlargement  is  very  great,  there  is  often  an  annoying  or  even 
distressing  feeling  of  distention  and  fullness  in  the  abdomen.  Respiration  may 
also  be  interfered  with  by  the  crowding  up  of  the  diaphragm. 

The  lesion  of  the  bone-marrow  can  never  be  determined  absolutely  during  life. 
The  only  symptom  which  renders  its  existence  probable  is  pain  in  the  bones,  but 
even  this  is  not  an  infallible  symptom.  There  is  seldom  pain  except  lipon  pressure. 
It  is  usually  brought  out  by  percussion  of  the  sternum,  but  there  may  be  well- 
marked  disease  of  the  marrow  without  this  "  sternal  pain." 

As  already  stated,  the  lymph-glands  often  remain  perfectly  normal.  If  they 
are  affected,  the  disturbance  is  betrayed  by  their  increase  in  size.  Not  only  may 
the  glands  in  the  neck,  axilla,  and  groin  be  enlarged,  but  occasionally  also  those 
of  the  mesentery  and  retroperitoneum,  as  can  be  demonstrated  upon  palpation  of 
the  abdomen.  The  enlarged  lymph-glands  rarely  cause  severe  pain,  if  any  at  all. 
We  have  already  referred  to  leukaemic  new  growths  in  other  internal  organs. 
These  possess,  for  the  most  part,  merely  a  scientific  interest,  as  they  cause  no  spe- 


LEUKEMIA.  949 

cial  symptoms.  Sometimes  hepatic  enlargement  occurs,  as  the  result  of  a  diffuse 
leuksemic  infiltration.  The  changes  in  the  retina  associated  with  leukaemia  are  of 
importance,  as  they  can  be  detected  by  means  of  the  ophthalmoscope.  The  retina 
presents  white  spots  or  stripes  running  parallel  with  the  blood-vessels.  They  are 
due  to  collections  of  lymphoid  cells,  or  to  actual  lymphoid  growths.  These  lesions 
have  been  inappropriately  called  leuksemic  retinitis.  Retinal  haemorrhages  occur 
also  in  leukaemia,  as  in  grave  cases  of  idiopathic  anaemia. 

All  the  other  clinical  phenomena  of  leukaemia  result  from  the  abnormal  con- 
dition of  the  blood,  meaning  thereby  the  anaemia.  Tbe  ability  of  the  blood  to 
perform  its  normal  functions  is  impaired  mainly  through  the  loss  of  red  blood- 
corpuscles;  the  resulting  symptoms  are  therefore  precisely  the  same  as  in  essen- 
tial anaemia,  and  we  do  not  need  to  describe  them  again.  They  usually  are  the 
most  prominent  symptoms  of  the  disease,  and  include  noticeable  pallor  of  the 
skin,  equal  to  that  sometimes  seen  in  anaemia;  anaemic  murmurs  over  the  heart 
and  the  veins  of  the  neck;  general  debility;  anorexia,  and  digestive  disturbances; 
palpitation  and  dyspnoea;  and,  finally,  the  whole  group  of  the  "cerebral  symptoms 
of  anaemia,'1  that  is,  headache,  vertigo,  syncope,  and  ÜDnitus  aurium.  Sometimes 
there  is  a  troublesome  pruritus.  We  would  also  call  attention  once  more  to  the 
frequent  haemorrhages.  These  must  be  due  to  impaired  nutrition  of  the  vascular 
walls,  and  sometimes  justify  our  speaking  of  a  "  hemorrhagic  diathesis."  Obsti- 
nate epistaxis  is  particularly  frequent.  Less  often  we  have  haemorrhage  from  the 
intestine,  stomach,  kidneys,  or  into  the  skin  or  muscles,  etc.  We  may  have  cere- 
bral haemorrhage,  with  hemiplegia,  or  sometimes  immediate  death,  consequent 
upon  it.  Severe  cases  may  present  a  slight  oedema  of  the  skin  and  serous  effusions 
into  the  various  cavities  of  the  body. 

The  urine  in  leukaemia  is  essentially  like  that  excreted  in  pernicious  anaemia. 
Fleischer  and  Penzoldt  have  shown  that  in  leukaemia  as  well  as  in  pernicious 
anaemia  there  is  increased  destruction  of  albuminoids,  and  a  consequent  increase  in 
the  excretion  of  nitrogen.     There  is  often  also  a  considerable  increase  of  uric  acid. 

The  temperature  is  apt  to  undergo  slight  elevations,  as  in  severe  cases  of  anaemia. 
In  advanced  stages  there  may  be  quite  high  fever  of  an  intermittent  character,  reach- 
ing 103°-104°  (39'5°-40°  C).  The  fever  is  sometimes  accompanied  by  chills,  and 
when  the  temperature  falls  there  is  often  a  profuse  and  debilitating  perspiration. 

Complications  are,  on  the  whole,  rare.  Sometimes  we  observe  pulmonary 
tuberculosis,  or  some  acute  intercurrent  disease  such  as  pneumonia.  We  saw  one 
case  end  in  death  from  hemorrhagic  angina  and  oedema  of  the  glottis. 

In  regard  to  the  pathogenesis  of  the  different  symptoms  the  conditions  are 
manifestly  very  like  those  of  simple  severe  anaemia.  Poverty  of  the  blood  in  red 
blood-corpuscles  and  chronic  ferment  intoxication  are  the  most  important  factors. 
We  may  therefore  refer  to  what  was  said  on  page  944. 

Clinical  History.— Leukaemia  is  almost  always  chronic  in  its  course.  The  dis- 
ease begins  insidiously  and  progresses  gradually;  the  patient  grows  pale,  feels  lan- 
guid, and  has  slight  and  apparently  insignificant  symptoms,  which  gradually 
give  place  to  alarming  phenomena.  The  patient  may  himself  notice  the  organic 
lesions  incident  to  the  disease.  If  the  leukaemia  be  of  the  lymphatic  type,  he  is  apt 
to  be  struck  by  the  swelling  of  the  lymph-glands,  while  in  splenic  leukaemia  his 
attention  is  attracted  by  the  feeling  of  tension  and  pressure  in  the  abdomen,  the 
increasing  prominence  of  the  left  side,  and  the  unusual  sense  of  resistance  present 
in  that  part  of  the  abdomen.  Sometimes  it  is  obstinate  epistaxis,  or  haemorrhage 
from  some  other  source,  which  first  attracts  attention  and  leads  to  a  careful  exam- 
ination of  the  blood  and  spleen. 

The  disease  usually  lasts  several  years.  Many  cases  are  rather  mild  and  grad- 
ual in  their  progress,  while  in  others  there  is  a  rapid  development  of  all  the  symp- 


950  CONSTITUTIONAL  DISEASES. 

toms.  Some  cases  go  on  so  rapidly,  occupying  but  a  few  months,  that  they  might 
almost  he  termed  ''acute  leukaemia."  Instances  of  this  form  are  most  frequently 
seen  in  children.  Apparent  arrest  of  the  disease  is  frequent,  as  is  also  temporary 
improvement,  followed  by  fresh  exacerbations.  The  final  termination  is  almost 
invariably  unfavorable.  Death  is  usually  preceded  by  symptoms  of  the  most  pro- 
found anaemia,  and  is  caused  directly  by  the  general  debility.  It  is  sometimes 
hastened  by  the  occurrence  of  haemorrhages,  for  instance,  obstinate  epistaxis  or 
cerebral  haemorrhage. 

Recovery  is  not  absolutely  impossible,  but  still  it  is  very  rare,  and  it  is  out  of  the 
question  after  the  disease  has  passed  its  first  stages.  In  an  advanced  case,  there- 
fore, the  prognosis  must  be  regarded  as  hopeless. 

Diagnosis. — Leukaemia  can  be  easily  and  unmistakably  recognized  by  a  micro- 
scopic examination  of  the  blood.  In  a  very  early  stage  of  the  disease  the  increase 
of  white  blood-corpuscles  may  be  so  slight  that  a  definite  decision  can  not  be  made ; 
but  the  later  developments  will  afford  absolute  certainty  in  any  typical  case. 

"We  can  not  fail  to  recognize  a  case  of  leukaemia  if  the  blood  be  examined. 
Such  an  examination  is  therefore  demanded  in  every  case  of  obstinate  anaemia, 
and,  above  all,  in  such  patients  as  have  a  chronic  enlargement  of  the  spleen,  or 
swelling  of  the  lymph-glands  in  various  parts  of  the  body.  The  enlarged  lymph- 
glands  are  readily  recognizable.  The  splenic  tumor  can  usually  be  diagnosticated 
from  its  characteristic  position  and  shape,  and  especially  from  its  internal  edge, 
with  the  notches  already  spoken  of.  It  may  be  simulated  by  hydronephrosis  and 
other  diseases  causing  enlargement  of  the  kidneys,  and  in  women  by  ovarian 
tumors.  In  cases  of  doubt  the  blood  should  be  examined,  and  if  the  result  be  a 
positive  one,  we  may  feel  certain  of  our  diagnosis.  If  there  is  a  chronic  enlarge- 
ment of  the  spleen  without  a  leükaemic  change  in  the  blood,  we  must  consider  all 
the  possible  causes  of  such  an  enlargement;  thus  there  may  be  a  passive  conges- 
tion of  the  spleen,  with  enlargement,  as  the  result  of  hepatic  disease,  portal  throm- 
bosis, or  disease  of  the  heart,  or  a  splenic  tumor  from  malarial  poisoning.  Again, 
there  are  cases  where  we  have  the  signs  of  a  gradually  progressive  anaemia, 
apparently  idiopathic,  and  a  chronic  enlargement  of  the  spleen,  or  still  more 
frequently  enlargement  of  the  lymph-glands  in  various  parts  of  the  body,  without 
increase  in  the  number  of  white  blood-corpuscles.  Such  cases  are  termed  pseudo- 
leukaemia,  and  are  described  in  the  next  chapter. 

Treatment. — Nearly  the  same  remedies  are  employed  in  leukaemia  as  in  idio- 
pathic anaemia.  Of  course  the  greatest  attention  should  be  paid  to  general  nutri- 
tion. Of  internal  remedies,  the  prepai-ations  of  iron  have  been  mainly  employed. 
They  seldom  produce  any  brilliant  or  permanent  effects.  We  have  much  more 
confidence  in  the  administration  of  arsenic,  and  this  remedy  should  certainly  be 
tried  in  large  doses.  It  may  be  given  either  in  the  shape  of  pills,  or,  possibly  with 
still  more  advantage,  subcutan eously.  Of  course  no  permanent  benefit  is  to  be 
hoped  for  even  from  this,  except  in  the  early  stages  of  the  disease. 

What  are  called  "splenic  remedies"  have  been  often  employed,  but  do  not 
seem  very  effectual  in  leukaemia.  Mosler  obtained  good  results  from  the  long- 
continued  use  of  quinine  (5-8  grains  =  0-30-0 "50  grm.,  or  more,  in  twenty-four 
hours).     He  also  recommends  a  trial  of  piperin  and  oil  of  eucalyptus: 

5  Olei  eucalypti gtt.  100 ; 

Piperini, 

Cerae  albae ää  3  j  (grm.  4'0) ; 

Pulv.  altheae 3  i j  (grm.  7'5). 

M.  et  fiant  pilulae  no.  c. 

S.  Three  to  five  pills  three  times  a  day. 


PSEUDO-LEUKEMIA.  g  5  j 

Local  treatment  of  the  spleen  has  also  been  attempted.  If  an  ice-bag  be  con- 
stantly kept  on  the  splenic  region,  it  will  sometimes  diminish  the  size  of  the  tumor, 
and  may  also  relieve  pain.  Botkin  has  recommended  faradization  of  the  spleen, 
but  we  can  scarcely  expect  any  great  benefit  from  such  a  procedure,  [njections 
of  quinine,  arsenic,  and  other  remedies,  have  been  made  into  the  substi  ace  of  the 
spleen.  We  do  not  believe  that  this  is  advisable.  The  splenic  tumor  of  leukaemia 
has  actually  been  extirpated  surgically;  but  the  proceeding  is  so  ineffectual  and  so 
fatal  that  it  is  now  universally  abandoned.  The  transfusion  of  healthy  human 
blood  has  also  been  tried,  but  without  satisfactory  results.  Subcutaneous  injec- 
tions of  blood  (vide  supra)  have  been  tried  in  only  a  few  cases,  hut  they  may, 
perhaps,  have  good  results.  In  some  recent  cases  inhalations  of  oxygen  have 
acted  favorably. 

Many  other  particulars  of  treatment  have  been  mentioned  under  anaemia. 


CHAPTER  IV. 

FSEUDO-LEUK2EMIA. 

(Hodghin's  Disease.     Adenia.     Malignant  Lymphosarcoma.     Pseudo-leucocythamia.) 

It  was  mentioned  in  the  preceding  chapter  that  there  are  cases  in  which  the 
organic  lesions  are  apparently  the  same  as  in  genuine  leukaemia,  and  yet  there  is 
little  if  any  increase  in  the  number  of  white  corpuscles  in  the  blood.  There  is 
generally,  however,  a  diminution  in  the  number  of  red  corpuscles.  These  cases 
usually  receive  the  name  which  Cohuheim  gave  them  of  pseudo-leukaemia.  It  is 
nevertheless  doubtful  whether  they  are  to  be  regarded  as  a  special  form  of  dis- 
ease, and  there  are  various  facts  which  indicate  that  they  are  at  least  very  closely 
allied  to  genuine  leukaemia.  There  is  a  great  similarity  in  most  of  the  symptoms 
of  the  two  diseases  and  in  their  general  course,  as  well  as  in  the  organic  changes 
they  produce.  Furthermore,  a  case  of  pseudo-leukaemia  may  finally  assume  the 
character  of  genuine  leukaemia,  with  its  characteristic  blood  chauges. 

The  purely  splenic  type  of  pseudo-leukaemia  is  the  least  frequent  one.  As  yet 
very  few  such  cases  have  been  reported.  There  is  a  gradually  increasing  anaemia 
with  the  usual  symptoms,  and  associated  with  these  increasing  enlargement  of 
the  spleen.  It  is  impossible  to  draw  any  sharp  dividing  line  between  such  cases 
and  cases  of  pernicious  anaemia  attended  with  moderate  enlargement  of  the  same 
organ  (splenic  anaemia).  It  may  be  said  to  be  a  matter  of  taste  which  name  the 
physician  shall  give  to  a  case  of  this  sort.  The  bone-marrow  seems  to  present  the 
same  characteristics  in  splenic  pseudo-leukaemia  as  in  pernicious  anaemia. 

Pseudo-leukaemia  Lymphatica.— Pseudo-leukaemia  of  a  lymphatic  type  is  a 
much  more  frequent  and  well-defined  disease.  It  was  first  described  in  1832  by  the 
Englishman  Hodgkin,  and  is  sometimes  called  Hodgkin's  disease.  Wunderlich 
was  the  first  in  Germany  to  study  the  disease  thoroughly ;  he  described  it  in  1S58 
under  the  name  of  "  progressive  multiple  hypertrophy  of  the  lymph-glands  " ;  and 
later  Billroth  termed  it  "multiple  malignant  lymphoma."  Trousseau  gave  it  the 
name  of  "  adenia." 

Little  is  known  about  the  aetiology  of  lymphatic  pseudo-leukaemia.  It  is  said 
to  be  connected  with  malarial  poisoning,  syphilis,  and  some  other  diseases :  but 
such  statements  are  without  a  satisfactory  basis.  The  tendency  of  late  is  to  assign 
adenia  to  the  group  of  infectious  tumors,  although  the  reasons  for  this  belief  are 
as  yet  purely  theoretical.     Pseudo-leukaemia  is  most  common  in  young  and 


952  CONSTITUTIONAL  DISEASES. 

middle-aged  people,  and  is  apparently  rather  more  frequent  in  men  than   in 
women. 

Pathological  Anatomy.— The  hyperplasia  of  the  lymph-glands  may  be  very 
great,  producing  large  tumors  of  varying  consistency.  These  have  been  called 
lymphoma,  lymphadenoma,  and  lymphosarcoma.  On  section,  the  tumors  dis- 
play a  white  or  grayish-red  surface,  and  are  seen  to  be  made  up  of  a  number 
of  swollen  glands  fused  into  nodular  masses.  Upon  microscopic  examination,  we 
find  a  very  abundant  proliferation  of  lymph-cells,  sufficient  to  obscure  the  reticu- 
lum of  the  gland  completely.  The  new  growth  may  even  escape  beyond  the 
capsule  of  the  gland  and  invade  surrounding  structures.  Inflammatory  adhesions 
often  take  place  between  the  tumor  and  the  overlying  skin.  There  does  not  seem 
to  be  any  essential  difference  between  the  harder  and  the  softer  varieties  of  these 
tumors. 

These  changes  in  the  lymph-glands  are  often,  though  not  invariably,  associated 
with  a  swelling  of  the  spleen.  Its  increase  in  size  is  usually  slight.  Lymphomata 
may  also  develop  in  the  tonsils,  the  intestinal  lymphatics,  liver,  kidneys,  and  other 
organs.  Whether  there  are  changes  in  the  bone-marrow  has  not  yet  been  deter- 
mined. 

The  symptoms  are  very  gradually  developed.  It  is  almost  invariably  the 
swelling  of  the  lymph-glands  which  first  attracts  the  attention  of  the  patient  or 
his  physician.  The  glands  upon  one  or  both  sides  of  the  neck  are  usually  the 
first  to  be  enlarged,  and  they  may  finally  grow  to  tumors  the  size  of  the  fist,  or 
even  larger,  producing  great  disfigurement.  To  the  changes  in  the  neck  succeed 
swelling  of  the  axillary,  inguinal,  and  perhaps  also  the  internal  lymph-glands. 
The  changes  are  gradual,  and  vary  in  their  rapidity  and  extent. 

At  first  the  general  health  is  hardly  at  all  affected,  but  as  the  disease  progresses 
its  constitutional  effects  become  more  and  more  marked.  The  patient  grows  pale 
and  languid,  and  finally  presents  all  the  symptoms  of  profound  anaemia.  We 
may  also  have  certain  symptoms  due  to  mechanical  compression  occasioned  by 
the  growth  of  the  lymphomata.  The  tumors  in  the  neck  may  cause  dysphagia, 
from  compression  of  the  pharynx  and  oesophagus ;  dyspnoea,  from  compression  of 
the  larynx  and  trachea;  and  perhaps  alarming  cardiac  disturbance,  from  inter- 
ference with  the  vagus.  Hypertrophy  of  the  bronchial  glands  sometimes  occa- 
sions great  difficulty  in  respiration ;  enlargement  of  the  abdominal  glands  may 
produce  ascites  or  jaundice ;  and  enlargement  of  the  glands  in  the  groin  may  give 
rise  to  cedema  in  the  lower  extremities.  In  advanced  stages  we  may  have  "  cere- 
bral symptoms  of  anaemia  "  precisely  similar  to  those  seen  in  genuine  leukaemia  or 
in  pernicious  anaemia.  There  may  be  a  tendency  to  haemorrhage  and  pruritus, 
and  the  urinary  secretion  and  temperature  may  be  abnormal.  For  particulars  the 
reader  is  referred  to  the  preceding  chapters. 

Upon  examination  of  the  blood,  there  are  usually  found  the  changes  charac- 
teristic of  ordinary  anaemia,  without  increase  in  the  number  of  white  blood-cor- 
puscles. Sometimes,  however,  there  may  be  a  slight  leukocytosis ;  and  sometimes, 
as  already  said,  lymphatic  pseudo-leukaemia  may  merge  into  genuine  leukaemia. 
The  examination  of  the  blood  must  therefore  be  repeated  from  time  to  time.  The 
spleen  should  also  be  examined.  It  is  usually  somewhat  enlarged,  and  in  some 
cases  the  enlargement  may  be  considerable.  Such  cases  might  be  properly  denomi- 
nated splenic-lymphatic  pseudo-leukaemia.  We  may  also  discover  a  tenderness  of 
the  sternum  or  other  bones. 

The  disease  often  lasts  but  a  few  months ;  it  may,  in  rare  instances,  extend  over 
two  or  three  years  or  more.  Eecovery  is  not  absolutely  impossible  in  the  early 
stages  of  the  disease  (vide  infra),  but  at  a  later  period  the  prognosis  is  absolutely 
unfavorable.     The  fatal  termination  results  either  from  increasing  debility  and 


H^EMOGLOBIN^MIA  AND  HEMOGLOBINURIA.  053 

anaemia,  or  from  the  effects  of  mechanical  compression,  or  from  haemorrhage,  or 
from  some  intercurrent  disease. 

The  diagnosis  of  pseudo-leukaemia  is  usually  easy.  It  is  to  be  \>:>s<;<\  upon  the 
objective  signs  and  the  condition  of  the  blood.  The  disease  is  most  apt  to  be 
confounded  with  swelling  of  the  lymph-glands  occasioned  by  tubercular  infec 
tion;  but  in  this  latter  case  the  changes  are  seldom  seen  in  so  many  parts  of 
the  body,  and  the  patient  usually  presents  other  indubitable  evidences  of  tubercu- 
losis. 

Treatment. — We  possess  only  one  remedy  capable  of  promoting  absorption  of 
the  lymphomata,  namely,  arsenic.  We  have  ourselves,  in  common  with  a  great 
number  of  observers,  had  the  most  convincing  evidence  of  the  favorable  influence 
of  arsenic.  It  must,  however,  be  given  in  sufficient  doses:  for  example,  a  pill  con- 
taining one  fifteenth  of  a  grain  (0'004  grm.),  or  even  a  larger  amount  of  arseuious 
acid,  three  times  a  day;  and  its  use  must  be  persisted  in  for  a  long  time.  It 
might  also  be  tried  subcutaneously.  We  have  also  seen  apparent  benefit  from 
associating  with  the  arsenic  inunctions  of  iodoform  (iodoform  one  part,  vaseline 
fifteen  parts)  over  the  tumors. 

In  early  stages  decided  benefit  may  be  expected  from  this  mode  of  treatment. 
At  a  later  period  we  may  obtain  a  decrease  in  the  size  of  the  tumors,  but  we  can 
hardly  hope  for  any  permanent  improvement.  Operative  interference  is  out  of 
the  question,  except  at  the  very  beginning  of  the  disease.  Later  on.  it  would  be 
perfectly  useless,  and  could  seldom  be  carried  out. 

Other  suggestions  with  regard  to  treatment  may  be  obtained  from  the  chapters 
on  anaemia  and  leukaemia. 


CHAPTER  V. 
HiEMOGLOBIN-ffiMIA  AND  HEMOGLOBINURIA. 

Definition  and  General  ./Etiological  Considerations. — If  any  cause  produces  a 
solution  of  the  red  blood-corpuscles  in  the  blood-serum,  haemoglobin  is  excreted 
through  the  kidneys.  The  haemoglobinaemia — the  presence  of  free  haemoglobin 
in  solution  in  the  blood — excites  hemoglobinuria,  i.  e.,  the  excretion  of  haemo- 
globin in  the  urine.  The  causes  of  haemoglobinaemia  and  its  correlative  haemo- 
globinuria  are  ra  anif old.  In  the  first  place,  there  are  a  whole  series  of  poisons 
which,  if  introduced  into  the  blood  in  sufficient  amount,  exercise  a  directly  de- 
structive influence  upon  the  red  blood-corpuscles,  and  thus  excite  haemoglobinu- 
ria.  To  this  list  belong  chlorate  of  potash  (Marchand),  pyrogallic  acid  and  naph- 
thol  (Neisser),  glycerine,  toluyleudiamine,  and  many  other  substances.  Distilled 
water  is  also  in  this  sense  a  poison.  Boström  has  discovered  a  fact  of  practical 
importance  which  deserves  mention  in  this  connection.  It  is,  that  a  certain  kind 
of  mushroom  (Helvetia  esculenta),  when  fresh,  contains  a  poison  which  is  capable 
of  producing  intense  haemoglobinuria,  and  such  grave  symptoms  as  jaundice, 
delirium,  drowsiness,  and  tetanic  convulsions,  with  perhaps  a  fatal  termination. 
This  poison  is,  however,  so  evanescent  and  so  readily  soluble  in  hot  water  that 
the  mushroom  becomes  perfectly  harmless  if  thoroughly  soaked  and  then  boiled, 
or  if  it  has  been  dried. 

Secondly,  haemoglobinuria  may  be  developed  in  connection  with  infectious 
diseases.  In  this  case,  also,  it  may  be  referable  to  the  action  of  poisons  created 
within  the  system.  Thus  haemoglobinuria  has  been  observed  in  the  course  of  a 
severe  attack  of  scarlet  fever  or  typhoid  fever.     Possibly  malarial  poisoning  and 


954  CONSTITUTIONAL  DISEASES. 

syphilis  may  give  i*ise  to  paroxysmal  haemoglobinuria.  This  question  will  be  dis- 
cussed later  on. 

There  is  a  third  mode  of  origin  which  also  possesses  practical  importance.  If 
blood  from  one  animal  be  injected  into  another  of  a  different  species,  haemoglo- 
binuria  is  almost  sure  to  result.  Not  only  do  the  injected  blood-corpuscles  undergo 
solution,  but  also  the  injected  serum  acts  as  a  poison  upon  the  original  blood- 
corpuscles,  destroying  and  dissolving  them.  This  transfusion-haemoglobinuria 
has  been  described  by  Prevost,  Dumas,  Ponfick,  and  Landois.  It  can  be  pro- 
duced in  human  beings,  as  there  was  only  too  good  opportunity  to  obseiwe  dur- 
ing tlie  brief  period  when  the  transfusion  of  lamb's  blood  was  in  vogue.  The 
practical  deduction  is  evident,  that  we  should  not  use  for  injection  into  the  circu- 
latory system  of  a  patient  anything  but  an  unirritating  salt  solution,  or  human 
blood. 

A  fourth  and  very  important  etiological  factor  is  exposure  to  extremes  of 
temperature.  Haemoglobinuria  is  a  very  frequent  result  of  severe  burns.  The 
blood-corpuscles  in  that  region  of  the  periphery  exposed  to  the  heat  are  destroyed. 
Cold  is  capable  of  producing  precisely  analogous  results.  This  is  particularly 
evident  in  the  cases  of  so-called  paroxysmal  haemoglobinuria  described  by  Wick- 
ham  Legg,  Lichtheim,  and  Küssner.  [Raynaud's  disease  (see  page  588)  and  haemo- 
globinuria are  associated  in  a  sufficiently  large  proportion  of  cases  to  show  some 
relationship  between  the  two.] 

Pathology  and  Symptoms  of  HsemGglobinsemia,  particularly  the  Paroxysmal 
Variety. — In  most  of  the  cases  above  enumerated,  haemoglobinuria  is  the  result  of 
an  obvious  or  easily  demonstrable  cause.  There  is,  however,  another  variety 
which  appears  paroxysmally  in  individuals  who  are  otherwise  perfectly  well.  Its 
symptoms  are  extremely  characteristic.  Although  not  a  very  frequent  disease, 
there  has  been  abundant  opportunity  to  study  it. 

As  just  intimated,  the  disease  is  paroxysmal.  Very  often  an  attack  is  ushered 
in  by  frequent  and  persistent  yawning.  To  this  symptom  are  soon  added  pain  in 
the  limbs,  headache,  nausea,  vomiting,  and  coolness  of  the  periphery.  The  tem- 
perature speedily  rises  to  102°  (39°  C.)  or  more.  With  this  is  often  associated  a 
decided  chill.  Sometimes  there  is  a  violent,  cramp-like  pain  in  the  hepatic  region. 
Then  the  temperature  falls  again,  perspiration  appears,  and  the  patient,  although 
languid  and  depressed,  soon  recovers.  A  slight  icteric  hue  can  almost  invariably 
be  detected  toward  the  end  of  the  attack,  the  ordinary  duration  of  which  is  from 
two  to  twelve  hours.  An  eruption  of  urticaria  is  noticeably  frequent  in  connec- 
tion with  the  attacks. 

The  most  interesting  phenomenon  of  all  remains  to  be  described.  We  refer  to 
the  condition  of  the  urine  during  and  directly  after  the  paroxysm.  This  secretion 
presents  a  dai'k  brownish-red  color  resembling  blood ;  it  may  even  appear  almost 
black.  Its  reaction  is  almost  invariably  acid;  its  specific  gravity  is  usually 
rather  low,  say  1008-1012.  On  boiling  the  urine,  the  haemoglobin  is  decomposed 
and  a  brown  coagulum  of  albumen  formed.  If  the  excretion  be  examined 
through  a  spectroscope,  we  find  the  stripes  characteristic  of  haemoglobin,  and 
sometimes  also  the  narrow  stripes  indicative  of  methaemoglobin.  It  is  therefore 
impossible  to  doubt  the  existence  of  haemoglobin  in  the  urine;  and  yet,  upon 
microscopic  examination,  we  find  no  red  blood-corpuscles  in  the  urine,  or,  in 
other  words,  no  "  haematuria. "  Frequently  there  are  great  numbers  of  opaque 
red  granules  in  the  urine,  the  shape  of  which  is  extremely  irregular.  These  are, 
doubtless,  granules  of  haemoglobin.  Some  of  them  are  free  in  the  urine,  some 
are  attached  to  casts.  Of  the  latter,  we  find  hyaline  and  a  few  epithelial  casts 
present.  Sometimes  masses  of  haemoglobin  assume  the  appearance  of  casts.  The 
sediment  may  also  contain  a  few  cells  of  renal  epithelium.     The  presence  of  this 


HJEMOGLOBINiEMIA  AND  HEMOGLOBINURIA.  955 

and  of  hyaline  casts  indicates  that  the  kidneys  have  been  slightly  irritated  by  the 
excretion  of  haemoglobin. 

If  now  we  examine  the  blood  during  a  paroxysm,  we  sball  find  tlmf  haemoglo- 
binaemia  is  associated  with  haemoglobinuria  of  the  paroxysmal  type,  as  well  as 
with  that  occasioned  by  the  action  of  various  poisons.  Küssner  obtained  blood 
from  a  patient  during  a  paroxysm,  andfound  that  its  serum  bad  a  ruby-red  color, 
and  contained  haemoglobin  in  solution.  This  proves  tbat  the  dest  ruction  of  blood- 
corpuscles  takes  place  within  the  circulatory  system.  Indubitable  tokens  of  tins 
destructive  process  are  to  be  seen  upon  microscopic  examination  of  the  blood 
during  a  paroxysm,  especially  when  the  paroxysm  has  been  produced  artificially 
in  the  manner  described  below.  The  red  blood-corpuscles  have  little  tendency  to 
form  rouleaux.  They  are  pale,  and  many  of  them  are  irregular  in  shape  (poikilo- 
cytes).  Irregularly  shaped  flakes  of  haemoglobin  are  also  present,  and  often  large 
numbers  of  decoloinzed  red  blood-corpuscles  are  to  be  seen.  To  these  latter  Pon- 
fick  has  given  the  name  of  "  shadows. "  Haemoglobinaemia  is  also  of  the  greatest 
clinical  importance,  because  it  probably  must  lead  to  a  ferment  intoxication  of  the 
body  (vide  supra,  p.  944),  to  which  a  great  part  of  the  symptoms  of  the  haemo- 
globinuric  attack,  such  as  chill,  fever,  and  nervous  disturbances,  must  be  referred. 
The  origin  of  .jaundice  will  be  considered  below. 

In  many  cases  the  exciting  cause  of  each  separate  paroxysm  is  perfectly  evi- 
dent. There  is  a  cooling  off  of  peripheral  portions  of  the  body — that  is,  the  tem- 
perature of  the  blood  in  those  parts  is  lowered  (or  the  cold  acts  on  the  walls  of  the 
vessels  ?)  and  this  leads  to  a  destruction  of  red  corpuscles.  Patients  are  free  from 
attacks  unless  they  have  been  out  in  cold  or  stormy  weather,  or  have  been  wet 
through  in  a  cold  rain.  As  we  might  expect,  the  paroxysms  are  extremely  rare 
in  summer;  they  may,  however,  as  Rosenbach  showed  by  experiment,  be  artifi- 
cially produced  at  any  time,  by  exposing  the  surface  of  the  body  to  severe  cold, 
as  by  giving  the  patient  foot-baths  of  ice-cold  water.  Ehrlich  and  Boas  have  both 
performed  experiments  which  show  that  the  action  of  cold  is  a  purely  local  one. 
They  have  separated  a  finger  of  the  patient  from  the  general  circulation  by  means 
of  an  elastic  ligature,  and  then  immersed  it  for  a  quarter  of  an  hour  in  iced 
water.  Blood  taken  from  this  finger  invariably  exhibited  the  above-mentioned 
changes,  while  the  condition  of  the  rest  of  the  blood  in  the  patient's  body  remained 
almost  perfectly  normal. 

There  can,  therefore,  be  no  doubt  that  in  certain  cases  cold  affects  any  portion 
of  the  peripheral  circulation  exposed  to  it  in  such  a  way  as  to  excite  a  paroxysm 
of  haemoglobinuria.  The  paroxysms  cause  headache,  fever,  nausea,  and  other 
symptoms,  the  immediate  origin  of  which  is  not  perfectly  understood.  Several 
authorities  believe  that  these  phenomena  are  uraemic;  and  it  has  indeed  been 
proven,  both  from  the  post-mortem  appearances  in  such  patients  as  have  from 
some  coincidence  come  to  autopsy,  and  from  experiments  upon  animals,  that  the 
kidneys  may  be  plugged  up  with  granules  of  haemoglobin  in  sufficient  amount 
to  give  them  a  dark-brown  hue.  The  granules  collect  chiefly  in  the  straight 
tubules,  and  also  in  the  convoluted  tubes  and  the  glomeruli.  Such  a  condition 
may  present  a  considerable  obstacle  to  the  excretion  of  the  urine,  and  more  espe- 
cially to  the  elimination  of  its  solid  constituents.  In  point  of  fact,  the  urine  is 
usually  of  low  specific  gravity.  This  retention  of  urinary  constituents  in  the 
blood  certainly  might  produce  some  of  the  symptoms  observed ;  but  it  is  not  cer- 
tain whether  we  must  not  consider  other  influences. 

No  explanation  has  yet  been  offered  for  the  liability  of  certain  unfortunate 
individuals  to  paroxysms  of  this  sort,  from  which  most  men  are  exempt.  It  may 
be  mentioned  that  most  patients  have  had  a  syphilitic  history ;  so  that  a  connec- 
tion between  these  two  affections  is  in  many  cases  very  probable  (Mum).     Par- 


956  CONSTITUTIONAL  DISEASES. 

oxysmal  hemoglobinuria  lias  also  been  observed  in  hereditary  syphilis.  It  is  doubt- 
ful whether  hemoglobinuria  can  have,  as  is  claimed,  any  relation  to  malaria.  We 
must  note,  however,  that  the  individual  attacks  may  be  due  not  only  to  cold  but 
sometimes  to  other  influences,  especially  great  physical  exertion,  long  walks,  etc. 
In  conclusion,  certain  pathological  facts  should  be  mentioned.  The  kidneys  are 
not  the  only  receptacles  of  the  debris  resulting  from  the  destruction  and  solution 
of  the  blood-corpuscles.  Ponflck  has  been  led  by  the  result  of  certain  experi- 
ments to  believe  that  the  spleen  and  liver  are  also  affected.  The  spleen  appropri- 
ates the  undissolved  remnants  of  the  corpuscles,  and,  as  a  consequence,  may 
undergo  considerable  enlargement.  The  liver  absorbs  a  large  part  of  that  portion 
of  the  hemoglobin  which  has  undergone  solution,  and  converts  it  into  bile.  As 
a  result  there  seems  to  be  an  increased  secretion  of  bile.  Jaundice  is  probably  due 
to  local  biliary  stasis  and  biliary  absorption  in  the  liver  itself  ("  hemo-hepatoge- 
nous  jaundice  "  of  Afanassiew).  It  is  not  yet  established  whether  a  part  of  the 
haemoglobin  dissolved  in  the  blood  can  be  changed  into  bile  pigment  (true 
"  hematogenous  jaundice  "). 

Prognosis. — When  hemoglobinuria  is  merely  a  symptom  of  other  abnormal 
processes  caused  by  poisoning  or  by  some  specific  infection,  the  future  of  the 
patient  depends  entirely  upon  the  severity  of  the  primary  disease.  An  attack  of 
paroxysmal  hemoglobinuria  would  not  seem  to  involve  any  direct  danger  to  life. 
Recurrence  of  the  paroxysms  is  always  to  be  feared  if  the  patient  be  exposed  to 
those  influences  which  produce  it.  There  are  no  certain  means  of  decreasing  the 
patient's  liability  to  attacks.  In  a  few  cases,  however,  where  there  had  been 
syphilis,  the  paroxysms  are  said  to  have  been  permanently  banished  by  mercurial 
inunctions.     Likewise,  if  we  suspect  malarial  influences,  quinine  should  be  tried. 

No  special  treatment  is  required  during  the  paroxysm  itself.  The  patient 
must  escape  as  soon  as  possible  from  the  exciting  cause ;  it  is  then  advisable  for 
him  to  lie  quietly  in  bed,  and  to  drink  a  large  amount  of  fluid,  so  as  to  wash  out 
the  masses  of  haemoglobin  from  the  kidneys. 


CHAPTER  VI. 

SCURVY. 

(Scorbutus.) 

Prefatory  Remarks.— Scurvy  is  one  of  a  group  of  diseases  which  may  be 
termed  "hemorrhagic."  They  all  have  one  predominant  symptom,  namely,  a 
decided  hemorrhagic  diathesis,  respectively  associated  in  the  different  diseases 
with  various  other  more  or  less  pronounced  disturbances.  This  tendency  to  spon- 
taneous hemorrhage  is  in  many  cases,  particularly  the  milder  ones,  more  or  less 
exclusively  confined  to  the  skin,  but  in  numerous  other  instances  hemorrhage 
also  takes  place  into  the  underlying  tissues,  such  as  the  muscles  or  joints,  as  well 
as  into  the  mucous  membranes. 

The  distinctions  between  these  various  diseases  are  founded  upon  the  manner 
in  which  the  hemorrhages  occur  and  the  symptoms  which  attend  them.  We 
may  mention  scorbutus,  purpura  simplex,  purpura  hemorrhagica,  and  peliosis. 
It  should,  however,  be  stated  that,  although  it  is  possible  to  distinguish  several 
varieties  of  disease,  each  one  of  which  presents  a  tolerably  characteristic  picture, 
there  are  innumerable  transitional  forms.  It  may,  indeed,  be  almost  a  matter  of 
taste  in  any  particular  case  what  name  shall  be  applied  to  it.  The  existence  of  so 
many  intermediate  forms  renders  it  evident  that  the  various  members  of  this 


scurvy.  or>7 

group  of  diseases  are  at  least  closely  related  if  not  actually  identical.  We  shall 
even  find,  upon  careful  consideration,  that  certain  other  diseases  not  usually 
regarded  as  hemorrhagic  are  nearly  akin  to  the  group  now  under  consideration. 
We  refer  to  certain  skin  diseases,  which  are  characterized  mainly  by  inflamma- 
tory and  exudative  lesions  of  the  skin.  Chief  among  these  should  be  mentioned 
erythema  exsudativum  multiforme,  which  not  very  infrequently  exhibits  some 
tendency  to  haemorrhages,  and  thus  presents  external  appearances  closely  simu- 
lating the  forms  of  purpura. 

In  order  to  understand  the  underlying  connection  between  these  various  dis- 
orders, a  precise  knowledge  of  their  aetiology  is  requisite.  Already  considerable 
evidence  has  been  gathered  pointing  to  the  importance  of  infectious  influences  in 
their  production  {vide  infra),  but  no  absolute  proof  has  yet  heen  obtained.  In 
the  meanwhile,  we  must  be  guided  mainly  by  the  purely  clinical  phenomena. 
These,  again,  indicate  that  sharp  distinctions  between  the  various  haemorrhagic 
diseases  would  be  purely  artificial.  In  this  and  the  following  chapters  we  shall 
discuss  the  two  main  types  of  hemorrhagic  disease. 

iEtiology  of  Scurvy.— Scurvy  is  sometimes  sporadic,  and  sometimes  epidemic 
and  endemic  in  its  occurrence.  There  were  formerly  very  extensive  and  fatal 
epidemics  of  the  disease,  at  a  time  when  the  laws  of  health  with  regard  to  large 
aggregations  of  human  beings  were  little  regarded.  The  disease  was  prone  to 
attack  armies,  or  the  inhabitants  of  besieged  cities,  or,  especially,  seamen.  It  was, 
and  to  a  certain  extent  is  still,  one  of  the  diseases  most  dreaded  by  the  mariner. 
It  has  often  swept  away  an  entire  ship's  crew.  To-day  endemics  of  scurvy  are  by 
no  means  infrequent,  although  not  so  extensive  as  formerly.  They  are  most  apt 
to  occur  in  prisons  and  similar  institutions,  and  in  barracks. 

These  facts,  under  the  light  of  our  present  views  in  regard  to  such  matters, 
would  almost  force  us  to  seek  some  organic  infectious  poison  as  the  origin  of  the 
disease.  Formerly  men  were  inclined  to  direct  their  sole  attention  to  such  cir- 
cumstances as  the  character  of  the  food,  the  dwelling,  the  climate,  and  similar 
conditions;  nor  can  it  indeed  be  denied  that  these  hygienic  factors  do  exert  a 
decided  influence  upon  the  spread  of  the  disease.  It  is,  however,  evident  that  they 
can  not  be  its  proper  cause,  for,  beyond  a  doubt,  scurvy  may  occur  independently 
of  any  of  the  factors  usually  regarded  as  essential  to  its  development.  These 
causes  must  therefore  be  regarded  as  simply  predisposing  influences. 

Great  etiological  importance  has  long  been  ascribed  to  certain  errors  in  diet. 
These  include  the  use  of  bad  or  insufficient  food,  the  undue  predominance  of 
certain  kinds  of  food,  and  in  particular  of  the  salt  meats  so  much  employed  on 
shipboard ;  or,  again,  the  deficiency  of  certain  varieties  of  food,  in  particular  the 
lack  of  vegetable  food,  and  still  more  of  fresh  vegetables.  Much  industry  and 
acuteness  have  been  expended  in  defending  the  theory  that  the  lack  of  vegetable 
food  is  injurious  because  of  the  deficient  supply  of  potassium  salts  under  such 
circumstances  (Carrod).  Nevertheless,  this  view  does  not  reach  the  heart  of  the 
matter,  for  in  numerous  epidemics  of  scurvy  there  has  been  no  such  lack  of  vege- 
table nourishment ;  and  in  some  instances  the  diet  employed  has  contained  an 
unusual  abundance  of  potassium  compounds. 

A  like  predisposing  but  not  specific  influence  is  exerted  by  the  other  factors  to 
which  etiological  importance  has  been  assigned.  They  are  indeed  often  present 
in  epidemic  as  well  as  in  sporadic  cases,  but,  as  previously  stated,  they  may  not 
exist  at  all.  To  this  class  belong  damp  and  unfavorable  quarters,  cold,  moisture, 
persistent  heat,  and  excessive  muscular  exertion. 

Age  and  sex  exert  no  great  influence  upon  the  disease.  Weakly  persons  seem 
to  be  somewhat  more  liable  to  be  attacked  than  are  the  vigorous.  The  possibil- 
ity of  contagion  has  been  maintained  repeatedly,  but  contagion  has  not  been 


958  CONSTITUTIONAL  DISEASES. 

proven  to  exist,  and  unprejudiced  observation  would  incline  one  to  doubt  its  ex- 
istence. 

[It  seems  pi'obable  tbat  the  dietetic  causes  of  scurvy  lie  rather  in  a  want  of 
variety  in  the  food  than  in  the  absence  of  any  one  class  or  order  of  foods.  Wales 
says  (Pepper,  "  System  of  Medicine  ") :  "  No  single  natural  order  contains  plants 
that  supply  all  the  elements  essential  to  the  nutrition  of  the  body  and  the  right 
composition  of  the  blood.  The  graminaceous  and  leguminous  articles  of  food,  for 
instance,  are  numerous  but  not  various ;  they  all  affoi'd  the  same  or  analogous 
albuminous  elements,  which  have  about  the  same  nutrient  value  as  the  corre- 
sponding substances  in  animal  food,  and  hence  health  and  vigor  can  not  be  sus- 
tained on  a  diet  of  flesh  combined  with  wheat,  rice,  and  oatmeal,  or  with  beans 
and  peas,  or  with  all  of  them  together.  Outbreaks  of  scurvy  have  occurred  on 
shipboard  where  the  ration  is  made  up  principally  of  these  articles — as  in  Anson's 
ship  when  supplied  with  an  abundance  of  fresh  animal,  farinaceous,  and  legumi- 
nous foods.  It  is  clear,  therefore,  that,  in  order  to  obtain  a  variety  of  materials 
required  in  nutrition,  we  must  resort  to  several  of  the  natural  groups,  those  par- 
ticularly which  comprise  the  succulent  vegetables  and  fruits." 

It  is  certain  that  scurvy  is  a  disease  which  we  can  produce  artificially,  and  that 
it  is  preventable  in  the  vast  majority  of  cases.  It  is  now  as  rare  among  seamen  as 
it  was  formerly  common — a  change  which  is  the  result  chiefly  of  care  to  vary  the 
diet,  especially  on  long  voyages.  The  United  States  law  requires  that  lime-  or 
lemon-juice,  sugar,  and  vinegar  shall  be  carried  by  all  sailing  vessels  bound  on 
ocean  voyages  or  engaged  in  the  fisheries,  specifies  the  circumstances  and  mini- 
mum doses  under  which  the  antiscorbutics  are  to  be  given,  and  provides  penalties 
for  violation  or  neglect.] 

Clinical  History.— The  disease  does  not  usually  begin  suddenly.  There  is  a 
gradual  onset,  marked  by  certain  constitutional  symptoms.  The  chief  of  these 
are  languor  and  debility,  a  sense  of  thoracic  oppression,  palpitation,  and  usually 
a  "  rheumatic,  dragging  pain  "  in  the  loins  and  extremities,  especially  in  the  lower 
extremities.  The  patient  is  obliged  to  take  to  his  bed  if  the  case  be  at  all  severe ; 
he  is  very  sensitive  to  cold,  and  often  is  drowsy  and  apathetic.  These  somewhat 
indefinite  premonitory  symptoms  last  for  a  few  days  or  a  week,  when  other  and 
more  characteristic  phenomena  appear. 

Among  these  new  appearances  are  spontaneous  haemorrhages,  occurring  chiefly 
in  the  lower  extremities.  There  are  cutaneous  haemorrhages,  producing  dark-red 
macules  of  varying  size,  most  of  them  with  a  hair-follicle  in  their  center,  and 
there  are  almost  invariably  haemorrhages  into  the  deeper  tissues  also.  The  sub- 
cutaneous connective  tissue  and  muscles,  and  sometimes  the  periosteum,  are 
affected.  These  deeper  extravasations  are  a  peculiarity  of  scurvy.  They  can 
sometimes  be  felt  as  hard,  painful  swellings  in  the  parts  affected,  and  are  some- 
times discernible  from  the  discoloration  of  the  skin,  which  soon  results  from  the 
solution  and  diffusion  of  the  blood-pigment.  The  patches  present  a  diffuse  bluish 
color,  merging  into  greenish  or  yellowish  at  the  periphery,  and  they  are  often 
quite  large.  They  have  a  precisely  similar  appearance  to  "  black-and-blue  "  spots 
resulting  from  injury.  Of  course,  the  more  abundant  and  the  more  superficial 
the  extravasation,  the  more  extensive  and  darker  is  the  macule.  Similar  appear- 
ances may  sometimes  be  observed  in  the  upper  extremities  and  trunk,  mainly  in 
severe  cases.     The  face  and  scalp  rarely  present  ecchymoses. 

Sometimes  a  haemorrhage  results  in  the  necrosis  and  sloughing  away  of  a  por- 
tion of  the  skin.  The  necrosis  is  succeeded  by  ulceration  (''  scorbutic  ulcers "). 
Under  unfavorable  hygienic  influences  this  process  may  assume  a  grave  signifi- 
cance. It  should  also  be  stated  that  we  may  observe  other  cutaneous  disturbances, 
such  as  erythema,  wheals,  vesicles  (the  contents  of  which  may  be  tinged  with 


SCURVY.  950 

blood — "scorbutic  pemphigus"),  papules,  and  pustules.  These  eruptions  are  more 
frequent  in  some  epidemics  than  in  others;  they  may  either  be  associated  with  or 
replace  the  cutaneous  ecchymoses. 

In  the  ordinary  sporadic  cases  of  scurvy  which  occur  among  us,  haemorrhages 
into  the  mucous  membrane,  except  of  the  gums,  are  very  rarely  seen.  The  same 
is  true  of  haemorrhages  from  the  stomach  and  other  internal  organs.  In  severe 
cases,  during  epidemics  and  under  bad  hygienic  surroundings,  it  is  otherwise; 
haemorrhage  may  take  place  from  the  nose,  stomach,  intestines,  bronchi,  and  kid 
neys,  and  blood  may  be  effused  into  the  serous  membranes. 

Next  in  importance  to  haemorrhage  is  another  peculiar  symptom,  presented  by 
the  mucous  membrane  of  the  mouth,  and  particularly  that  of  the  gums.  In  order 
to  establish  a  diagnosis  of  scurvy  in  sporadic  cases,  we  must  demonstrate  the  exist- 
ence of  these  two  main  symptoms — namely,  the  haemorrhage  into  the  skin  or  mus- 
cles, and  the  changes  in  the  gums  now  to  be  described. 

The  scorbutic  changes  in  the  gums  usually  appear  quite  early  in  the  course  of 
the  disease,  being  in  many  cases  simultaneous  with  the  haemorrhages,  although 
they  may  either  precede  or  follow  the  latter.  The  gums  assume  a  bluish  hue, 
become  swollen  and  spongy,  are  painful,  and  have  a  tendency  to  bleed.  The 
changes  are  usually  most  pronounced  in  the  salient  parts  of  the  gums  between 
the  teeth.  It  is  a  remarkable  fact  that  they  are  hardly  visible  at  all  at  places 
where  there  are  no  teeth ;  and  the  gums  of  very  young  children  and  of  aged 
patients  remain  almost  intact.  In  severe  cases  the  gums  are  not  only  swollen  but 
necrosed ;  the  change  is  at  first  a  superficial  one,  but  it  may  extend  inward  and 
produce  dirty -looking  ulcers.  Other  parts  of  the  mouth  are  liable  to  become 
involved  in  the  ulceration,  producing  a  diffuse  ulcerative  stomatitis,  and  giving 
the  breath  a  most  offensive  odor. 

Certain  other  local  and  constitutional  phenomena  are  not  infrequent,  though 
less  characteristic  than  the  haemorrhages  and  the  alterations  in  the  gums.  Chief 
among  the  general  disturbances  is  scorbutic  anaemia.  This  is  often  in  part  refera- 
ble to  the  unfavorable  hygienic  influences  surrounding  the  patient,  but  the  disease 
seems  itself  to  impair  the  general  nutrition.  The  patient  looks  pale,  has  a  dry  skin, 
and  loses  flesh  rapidly.  The  temperature  is  often  normal.  Sometimes  there  may 
be  an  occasional  rise  of  temperature,  either  in  the  beginning  or  in  the  further 
course  of  the  disease.  If  complications  occur,  they  are  not  infrequently  accom- 
panied by  considerable  fever. 

Among  more  localized  symptoms  should  be  mentioned  the  premonitory  sore 
throat  which  sometimes  occurs.  It  is  usually  of  the  ordinary  catarrhal  variety, 
but  it  may  assume  a  haemorrhagic  character.  Bronchitis  may  also  occur.  Lobular 
pneumonia  and  genuine  lobar  pneumonia  have  been  repeatedly  seen  in  severe 
cases.  Pleurisy,  pericarditis,  and  inflammations  of  other  serous  membranes  occa- 
sionally complicate  the  disease.  They  may  likewise  display  a  haemorrhagic  tend- 
ency in  the  exudations  to  which  they  give  rise.  Disturbances  in  the  joints  are 
sometimes  seen,  and  are  characterized  by  an  effusion  of  liquid  into  the  articular 
cavities,  which  effusion  may  be  either  serous  or  haemorrhagic.  This  is  a  favora- 
ble opportunity  to  call  attention  to  a  peculiarity  common  to  all  the  haeinoriliagic 
diseases  and  allied  affections  {vide  supra) — they  are  apt  to  be  associated  with 
articular  swelling. 

The  pulse  may  be  somewhat  accelerated,  or  may  be  slower  than  normal.  It  is 
usually  small  and  compressible.  Endocarditis  may  occur,  but  it  is  very  exceptional. 
The  blood  does  not  present  any  constant  and  characteristic  alterations  in  scurvy. 
The  spleen  may  be  decidedly  enlarged,  particularly  in  severe  cases.  Albuminuria 
has  been  repeatedly  observed,  but  it  is  almost  wholly  confined  to  severe  cases,  in 
which,  indeed,  a  typical  acute  nephritis  may  be  developed. 


960  CONSTITUTIONAL  DISEASES. 

Varieties  of  Scurvy.  Prognosis. — The  sporadic  cases  usually  met  with  in  this 
region  almost  invariably  pursue  a  favorable  course.  The  symptoms  are  mainly 
confined  to  constitutional  disturbance,  ecchymoses  in  the  lower  extremities,  and 
the  affection  of  the  gums,  the  grave  complications  above  mentioned  being  rarely 
met  with.  The  average  duration  of  the  disease  is,  nevertheless,  some  weeks. 
Recovery  is  deferred  in  proportion  as  the  hygieuic  surroundings  are  unfavorable, 
but  even  then  the  termination  is  almost  sure  to  be  favorable. 

The  prognosis  in  grave  cases,  occurring  under  unfavorable  hygienic  influences, 
and  aggravated  by  the  lack  of  proper  food  and  attention,  is  far  otherwise.  Here 
death  is  not  infrequent,  sometimes  as  a  result  of  progressive  cachexia,  some- 
times because  of  pneumonia,  pericarditis,  cerebral  haemorrhage,  or  a  similar 
intercurrent  disease. 

Anomalous  or  rudimentary  cases  of  scorbutus  may  occur.  They  are  most  apt 
to  be  seen  when  the  disease  is  epidemic  or  endemic.  As  a  rule,  the  symptoms  are 
mild.  We  find,  for  example,  a  scorbutic  gingivitis  and  stomatitis  without  haemor- 
rhage, or,  on  the  other  hand,  haemorrhage  into  the  skin  and  mucous  membranes 
unattended  by  alteration  in  the  gums.  There  have  even  been  cases  reported  of 
simple  scorbutic  anaemia  without  any  local  symptoms. 

[The  experience  of  army  surgeons  during  our  late  civil  war  deserves  mention 
in  this  connection.  Hammond,  Woodward,  and  others  state  that  many  cases 
classed  in  the  sick  reports  as  "  general  debility  "  were  cases  of  incipient  or  imper- 
fectly developed  scurvy,  haemorrhage  from  mucous  membranes  or  into  the  skin 
being  absent.] 

Diagnosis. — The  diagnosis  of  scorbutus  is  almost  self-evident  when  the  two 
chief  symptoms  of  haemorrhage  and  alteration  in  the  gums  are  both  present.  If, 
however,  one  or  the  other  of  these  symptoms  is  suppressed  or  imperfectly  devel- 
oped, it  may  be  difficult  to  determine  what  disease  we  have  before  us,  or  to  exclude 
ordinary  stomatitis,  rheumatic  peliosis,  and  similar  diseases.  If  we  remember  the 
statements  made  at  the  beginning  of  this  chapter,  and  bear  in  mind  that  these 
various  diseases  are  probably  aetiologically  related  to  one  another,  we  shall  be 
less  disturbed  by  these  uncertainties.  It  may  be  mentioned,  in  conclusion,  that 
various  septic  disorders,  and  also  acute  ulcerative  endocarditis,  may  occasion  the 
appearance  of  numerous  haemorrhages,  and  thus  simulate  scurvy. 

Treatment.— The  essential  requisites  in  the  treatment  of  scurvy  are  proper 
hygiene  and  diet.  Fresh  air,  suitable  nourishment,  and  good  nursing,  if  promptly 
supplied,  are  usually  of  themselves  sufficient  to  induce  recovery,  while  the  physi- 
cian possesses  no  remedies  which  compensate  for  their  absence. 

The  belief  that  a  main  cause  of  scurvy  lies  in  a  deficiency  of  fresh  vegetables 
has  given  rise  to  a  practice,  still  in  vogue,  of  prescribing  a  great  abundance  of 
fresh  vegetables,  such  as  lettuce,  spinach,  and  sorrel,  fruit,  lemonade,  and  other 
drinks  prepared  from  fruit  syrups.  There  is  no  reason  to  deviate  from  a  course 
to  which  experience  has  given  its  sanction,  although  we  have  repeatedly  had 
opportunity  to  see  that  the  administration  of  fresh  vegetables  is  by  no  means 
essential  to  rapid  recovery.  Patients  supplied  with  any  other  proper  nourishment 
thrive  equally  well.  Certain  varieties  of  plants  have  attained  a  special  reputa- 
tion as  "antiscorbutics,"  such  as  the  spoon  wort  (Cochlearia  officinalis),  so  fre- 
quently mentioned  in  accounts  of  early  polar  expeditions.  None  of  these  plants, 
however,  possess  the  specific  properties  assigned  to  them.  The  administration  of 
vegetable  acids  and  the  salts  of  potassium  (bitartrate  and  nitrate  of  potassium),  in 
a  chemically  pure  form,  has  also  been  repeatedly  tried,  but  it  has  not  gained  popu- 
larity. 

The  drugs  most  employed  are  the  bitters  and  tonics.  They  have  no  specific 
value,  but  are  perhaps  as  good  remedies  to  prescribe  as  any.     We  may  give  a 


PURPURA.     MORBUS  MACULOSUS  WERLHOFII.    PELIOSIS.    961 

decoction  of  cinchona,  to  which  may  be  added  a  small  amount  of  dilute  sulphuric 
acid  and  sirup,  or  some  preparation  of  gentian  or  a  similar  bitter.  It  was  once 
believed  that  the  internal  administration  of  the  mineral  acids  exerted  a  specially 
favorable  influence  upon  the  hemorrhagic  diathesis;  but  this  is  very  doubtful. 

Certain  symptoms  may  demand  attention;  in  particular,  the  affection  of  (lie 
mouth  and  gums.  It  is  of  great  importance  to  cleanse  the  mouth  frequently  with 
disinfectants  and  mild  astringents,  such  as  chlorate  of  potassium  or  sage  tea.  It 
is  also  advisable  to  paint  the  inflamed  and  spongy  gums  at  short  intervals  with 
tincture  of  myrrh  or  tincture  of  rhatany.  The  absorption  of  the  ecchymoses  in 
the  lower  extremities  will  be  promoted  by  cautious  massage.  Inunctions  of  lini- 
mentum  chloroformi  and  the  like  give  great  relief  from  the  pain  caused  by  the 
extravasations  into  the  deeper  tissues.  In  severe  cases  stimulants  are  often  de- 
manded, such  as  camphor,  ether,  and  alcohol.  Such  complications  as  appear  may 
also  demand  special  treatment. 

Convalescence  is  promoted  by  continued  attention  to  diet,  bathing,  and  the 
administration  of  iron  and  quinine. 


CHAPTER  VII. 
PURPURA.     MORBUS   MAOULOSUS   WERLHOFII.     PELIOSIS. 

As  already  stated  in  the  preceding  chapter,  the  various  "  hemorrhagic  dis- 
eases" are  so  intimately  related  to  one  another  that  it  is  quite  impossible  to  make 
a  rigid  categorical  division  of  them.  The  numerous  names  which  have  been 
introduced  into  the  literature  of  this  subject  certainly  contribute  more  to  obscure 
than  to  elucidate  the  attendant  phenomena. 

From  a  clinical  standpoint  this  fact  is  the  all-important  one — namely,  that 
there  are  cases  in  which  the  foremost  symptom  is  the  spontaneous  occurrence  of 
haemorrhage.  There  are  cutaneous  ecchymoses,  and  there  may  be  at  the  same  time 
haemorrhages  in  the  internal  organs  and  into  the  mucous  membranes.  In  the 
milder  cases  of  this  sort  these  haemorrhages  constitute  almost  the  only  symptom 
of  disease ;  but  they  may  be  associated  with  considerable  general  disturbance,  indi- 
cated by  fever  and  weakness,  or  with  certain  local  complications.  The  true  cause 
of  these  diseases  has  not  yet  been  discovered.  There  is  seldom  any  evidence  of  an 
exciting  cause,  and  the  disorder  may  attack  either  the  well-nourished  or  the  poorly 
nourished,  the  old  or  the  young,  men  or  women.  There  is,  however,  an  indisput- 
able relationship  between  these  diseases  and  certain  others— namely,  scurvy,  ery- 
thema exsudativum,  and  perhaps  acute  rheumatism  and  endocarditis.  This  simi- 
larity indicates  that  the  process  is  of  an  infectious,  or  toxic,  character.  Such  an 
assumption  promotes  greatly  a  proper  understanding  of  the  phenomena  under 
consideration.  It  is  also  said  that  subcutaneous  injections  of  blood  from  patients 
with  morbus  maculosus  may  cause  a  like  affection  in  rabbits  (Petrone  and  other's). 
In  some  few  cases  the  weight  of  evidence  would  seem,  however,  to  point  to  an 
antecedent  impairment  of  nutrition  in  the  walls  of  the  blood-vessels.  A  good  ex- 
ample of  this  is  seen  where  cutaneous  ecchymoses  occur  in  old  and  marantic  indi- 
viduals (peliosis  senilis).  There  is  some  doubt  whether  these  exceptional  cases 
belong  with  the  others. 

The  mildest  forms  of  the  diseases  under  discussion  are  termed  purpura.  The 
haemorrhages  are  seen  mainly  in  the  skin  of  the  lower  extremities,  and  are  apt  to 
take  place  into  the  follicles.  There  may  also  be  ecchymoses  upon  the  trunk  and 
61 


962  CONSTITUTIONAL  DISEASES. 

upper  extremities,  but  the  mucous  membranes  and  the  deeper  tissues  remain  intact. 
A  means  of  distinguishing  purpura  from  scorbutus  lies  in  the  fact  that  in  purpura 
there  are  no  haemorrhages  into  the  muscles  and  no  lesions  of  the  gums,  although  it 
should  be  confessed  that  transitional  forms  between  the  two  occur.  The  disorder 
is  called  purpura  simplex  if  the  cutaneous  ecchymoses  constitute  the  only  symp- 
tom, or,  at  any  rate,  the  only  important  one.  These  cases  almost  invariably  ter- 
minate in  recovery,  and  are  over  at  the  end  of  ten  days  or  three  weeks.  Some- 
times elevations  of  the  skin  are  formed  resembling  wheals,  and  haemorrhages  take 
place  here  and  there  into  them.  This  subvariety  has  been  called  by  some  pur- ' 
pura  urticans.  It  forms  a  connecting  link  between  purpura  simplex  and  those 
cases  of  erythema  exsudativum  which  are  associated  with  haemorrhage.  Further 
particulars  may  be  found  in  special  works  upon  dermatology. 

Quite  often  the  haemorrhages  are  attended  by  ''  dragging  rheumatic  pains " : 
such  cases  are  termed  purpura  rheumatica  or  rheumatic  peliosis  (Schönlein). 
There  may  also  be  constitutional  disturbance,  slight  fever,  anorexia,  and  indis- 
position to  either  bodily  or  mental  exertion.  There  may  sometimes  be  actual 
arthritis,  with  an  inflammatory  effusion  into  the  joints.  The  knee  and  other  joints 
of  the  lower  extremities  are  most  apt  to  suffer  in  this  way.  The  gums  are  usually 
normal ;  nor  is  there,  as  a  rule,  haemorrhage  into  the  mucous  membranes  or  the 
viscera.  These  cases  may  last  but  two  or  three  weeks.  Often,  however,  they  are 
more  tedious,  being  marked  by  the  recurrence  of  the  ecchymoses  and  articular 
pain.     Most  of  them  get  well  at  last. 

No  sharp  dividing  line  can  be  drawn  between  the  forms  of  purpura  thus  far 
described  and  certain  graver  cases.  These  latter  are  most  of  them  grouped  under 
the  name  of  purpura  hemorrhagica,  or  its  preferable  because  more  distinctive 
synonym — every  purpura  being  haemorrhagic — morbus  maculosus  Werlhofii.  The 
cutaneous  ecchymoses  in  this  class  of  cases  are  usually  extensive ;  and,  further- 
more, we  have  haemorrhages  into  the  mucous  membranes  of  the  nose,  mouth,  soft 
palate,  stomach,  and  intestinal  canal,  as  well  into  internal  organs  (the  brain  and 
kidneys),  and  also  into  the  serous  membranes.  The  constitutional  disturbance  is 
apt  to  be  severe.  The  condition  may  be  distinctly  "typhoidal."  Fever  maybe 
entirely  absent,  even  in  grave  cases,  although  sometimes  there  is  a  considerable 
rise  in  temperature. 

There  are  usually  no  local  symptoms  beyond  those  already  mentioned.  In 
typical  cases  the  gums  remain  intact.  Swelling  of  one  or  more  joints  has  been 
repeatedly  observed,  as  have  also  endocarditis  and  acute  haemorrhagic  nephritis. 
If  marked  cerebral  symptoms  are  developed,  suggesting  an  apoplectic  shock,  we 
may  surmise  that  a  cerebral  haemorrhage  has  taken  place.  It  should  also  be  stated 
that  marked  gastro-intestinal  disturbance  may  occur.  Cases  of  this  sort  have  been 
observed  by  Henoch  in  children.  They  may  also  occur  in  adults.  In  rare  in- 
stances there  may  be  intestinal  ulceration,  with  perforation  and  consequent  peri- 
tonitis.    The  spleen  may  undergo  acute  enlargement. 

The  prognosis  in  purpura  haemorrhagica  should  always  be  a  guarded  one;  the 
patient  is  in  danger  both  from  the  general  depression  and  anaemia,  and  from 
certain  special  lesions.  Even  a  severe  case  may,  however,  recover.  The  disease 
sometimes  proves  very  tedious ;  it  may  occupy  several  months. 

Treatment. — The  general  regimen  to  be  prescribed  is  similar  to  that  directed  in 
scurvy.  The  physician  must  strive  to  support  his  patient's  strength  by  means  of 
proper  nourishment.  A  great  many  internal  remedies  have  been  recommended, 
most  of  them  on  purely  theoretic  grounds.  It  is  difficult  to  say  whether  they 
actually  exert  a  favorable  influence  upon  the  course  of  the  disease.  The  following 
drugs  are  chiefly  employed :  Ergotine,  perchloride  of  iron,  dilute  sulphuric  acid, 
and  cinchona.     If  there  be  swelling  of  the  joints  or  endocarditis,  we  should  ad- 


HAEMOPHILIA.  96g 

vise  a  trial  of  salicylic  acid  or  antipyrine.     Such  special  symptoms  as  demand 
attention  should  be  treated  according  to  general  principles. 


CHAPTER  VIII. 
HEMOPHILIA. 

Definition  and  iEtiology. — Haemophilia  is  the  term  used  to  denote  a  peculiar 
constitutional  anomaly,  exhibited  in  a  remarkable  tendency  to  spontaneous  and 
traumatic  haemorrhage.  The  condition  is  probably  in  every  instance  congenital, 
and  is  usually  hereditary ;  the  existence  of  families  of  "  bleeders  "  has  long  been 
known.  Generation  after  generation  displays  frequent  cases  of  haemophilia,  both 
among  the  direct  descendants  and  the  lateral  branches.  Bleeders  are  very  apt  to 
have  a  numerous  progeny.  Not  all  of  the  children,  however,  fall  victims  to  the 
disease.  Grandidier  has  pointed  out  two  facts  which  are  of  interest  in  this  con- 
nection, as  they  might  aid  in  deciding  as  to  the  marriageability  of  certain  persons. 

If  a  man  belonging  to  a  family  of  bleeders  marries  a  healthy  women,  neither  a 
bleeder  herself  nor  inheriting  a  pi*edisposition  to  haemophilia,  his  children  are 
almost  certain  to  be  healthy,  even  though  the  father  himself  be  a  bleeder.  On  the 
other  hand,  a  woman  belonging  to  a  family  of  bleeders,  even  though  she  herself 
be  healthy,  will  almost  always  have  some  children  who  are  subject  to  haemophilia. 
In  other  words,  hereditary  predisposition  is  transmitted  much  oftener  through  the 
female  than  through  the  male  members  of  the  family.  Haemophilia  itself,  is,  on 
the  contrary,  much  more  frequent  in  the  male  sex  than  in  the  female ;  at  least 
this  is  true  of  the  pronounced  cases.  Hössli,  who  has  lately  published  a  very 
careful  family  tree  of  bleeders  of  Tenna  (Canton  Graubünden),  comes  to  the  fol- 
lowing conclusions:  "The  inheritance  of  haemophilia  is  often  from  the  father, 
through  the  daughter,  to  the  grandson,  also  from  the  mother,  through  the  daughter, 
to  the  grandson,  and  most  rarely  directly  from  the  father  to  the  son."  It  is  doubt- 
ful whether  race  and  place  of  residence  are  of  aetiological  importance.  So  far  as 
is  known,  haemophilia  appears  to  occur  in  all  countries,  although  it  is  fortunately 
rare  anywhere. 

[A  similar  transmission  through  the  females,  who  themselves  usually  escape,  is 
seen  in  color-blindness  and  in  pseudo-hypertrophic  paralysis.] 

The  real  causes  of  haemophilia  are  entirely  unknown  to  us.  We  can  make  one 
or  two  steps  toward  finding  the  source  of  the  haemorrhage,  but  we  are  unable  to 
proceed  further.  It  would  seem  that  the  bleeding  must  depend,  in  the  first  place, 
upon  an  abnormal  delicacy  of  the  walls  of  the  vessels  predisposing  them  to  rupture, 
and,  secondly,  upon  deficient  coagulability  of  the  blood.  This  latter  abnormality 
is  evident  from  the  fact  that  in  haemophilia  it  is  difficult  to  check  even  the  most 
insignificant  haemorrhage.  Thus  far  all  attempts  to  discover  any  anatomical  or 
chemical  explanation  of  this  imperfect  coagulability  have  been  vain.  It  has  not 
been  possible  to  detect  any  variation  in  the  saline  constituents  of  the  blood,  or  in 
the  amount  of  albuminoids,  such  as  fihrinogen,  that  it  contains,  or  in  its  morpho- 
logical elements.  And  likewise  no  anatomical  change  in  the  vascular  walls  or  the 
heart  has  yet  been  reported  which  throws  light  upon  the  character  of  the  disease. 
Various  authorities  have  laid  stress  upon  the  small  diameter  of  the  arteries  and 
the.thinness  of  the  intima,  but  these  conditions  may  occur  independently  of  haemo- 
philia. Fatty  degeneration  of  the  intima  is,  to  be  sure,  often  found  in  connec- 
tion with  this  disease,  but  it  is  doubtless  rather  a  result  of  the  coincident  anaemia 
than  the  cause  of  the  haemophilia.     The  observations  with  regard  to  the  heart  are 


964  CONSTITUTIONAL  DISEASES. 

very  contradictory ;  sometimes  it  is  found  to  be  very  small,  sometimes  of  normal 
size,  and  again  actually  hypertrophied. 

The  subjects  of  haemophilia  do  not  present  any  distinctive  constitutional  pecul- 
iarities. It  has  been  stated  that  they  are  very  apt  to  be  blondes  with  a  delicate 
white  skin,  and  superficial  and  abnormally  distended  cutaneous  veins;  but  the 
exceptions  to  this  rule  are  not  a  few. 

Clinical  History. — Haemophilia  does  not  display  equal  malignity  in  all  cases. 
If  we  have  opportunity  to  obtain  thorough  information  with  regard  to  families  of 
bleeders,  we  shall  find  that  quite  often  rudimentary  varieties  occur  side  by  side 
with  typical  and  severe  cases.  There  is,  to  be  sure,  a  striking  tendency  to  haemor- 
rhage even  in  them;  but  the  haemorrhage  never  assumes  threatening  proportions. 
By  perseverance  and  industry  it  is  possible  to  collect  an  almost  unbroken  series 
of  cases,  varying  in  degree  from  extreme  mildness  to  extreme  severity.  The  fol- 
lowing sketch  applies  mainly  to  typical  and  severe  cases. 

That  haemophilia  is  a  hereditary  constitutional  disease  is  shown  by  the  fact 
that  it  sometimes  appears  in  earliest  infancy.  Many  cases  of  umbilical  haemor- 
rhage in  the  newborn  are  referable  to  haemophilia.  Of  course  this  does  not 
apply  to  all  cases.  In  Jewish  children  the  disease  may  betray  itself  for  the  first 
time  when  the  rite  of  circumcision  is  performed.  In  many  cases  the  disease  does 
not  betray  itself  at  so  early  a  period ;  but  this  is  no  proof  that  the  disease  is  not 
already  developed,  inasmuch  as  the  young  child  is  not  much  exposed  to  trauma- 
tism and  other  causes  which  naturally  occasion  haemorrhage. 

The  most  striking  symptom  in  a  fully  developed  case  of  haemophilia  is  the 
occurrence  of  severe  haemorrhage  as  a  result  of  the  most  insignificant  causes.  A 
slight  blow  produces  a  "  black-and-blue  spot  "  such  as  is  ordinarily  seen  only  after  a 
very  violent  injury.  The  prick  of  a  pin,  a  slight  cut  on  the  finger,  or  the  extrac- 
tion of  a  tooth,  may  give  rise  in  haemophilia  to  an  obstinate  and  alarming  haemor- 
rhage. Epistaxis  may  be  caused  by  blowing  the  nose,  and  haemorrhage  from  the 
gums  by  brushing  the  teeth,  and  so  on.  Whether  there  is  ever  a  perfectly  spon- 
taneous haemorrhage  is  uncertain.  It  is  true  that  in  severe  cases  haemorrhages 
take  place  independently  of  any  visible  cause.  This  may  be  seen  in  the  skin  and 
mucous  membranes  (nose  and  gums) ;  and  in  rare  instances  we  may  even  have 
free  haemorrhage  from  the  stomach,  intestines,  or  urinary  passages.  Yet  it  may 
be  doubted  whether  these  occurrences  are  not  the  result  of  comparatively  insig- 
nificant mechanical  injuries  which  escape  our  notice.  At  any  rate,  we  scarcely 
ever  find  haemorrhage  taking  place  into  the  parenchyma  of  the  viscera,  in  places 
where  injury  from  external  sources  is  entirely  out  of  the  question.  This  fact  con- 
stitutes an  important  point  of  distinction  between  haemophilia  and  the  acquired 
haemorrhagic  diathesis. 

The  second  important  symptom  of  haemophilia  has  been  already  referred  to: 
it  is  extremely  difficult,  and  may  even  be  impossible,  to  check  by  artificial  means 
any  free  haemorrhage  which  may  occur.  It  is  this  which  makes  the  disease  so 
dangerous,  and  prevents  most  patients  from  reaching  old  age.  It  has  frequently 
happened  that  an  apparently  trifling  wound  of  the  skin,  or  some  insignificant 
operation,  or  a  leech-bite,  or  in  women  childbirth,  has  started  up  a  haemorrhage, 
which  eventually  became  fatal.  In  other  cases  the  haemorrhage  is  finally  checked, 
but  not  until  it  has  caused  profound  anaemia.  Bleeders  are  apt  to  recover  with 
remarkable  rapidity  from  the  effects  of  excessive  haemorrhage ;  yet  continually 
repeated  haemorrhages  may  lead  to  a  persistent  and  profound  anaemia,  attended  by 
all  the  symptoms  described  in  preceding  chapters. 

We  see,  therefore,  that  the  general  condition  in  haemophilia  varies  with  the 
severity  of  the  individual  case,  and  with  the  more  or  less  fortuitous  circumstances 
which  develop  its  dormant  characteristics.     If  no  special  accident  occurs,  the 


DIABETES  MELLITUS.  9#5 

patient  may  maintain  the  appearance  of  perfect  health  for  years.  In  the  worst 
cases,  however,  such  a  state  is  very  temporary,  if  it  exists  at  all,  because  the  haem- 
orrhages can  he  so  easily  excited.  As  a  consequence,  the  skin  almost  always  pre- 
sents a  greater  or  less  number  of  eccbymoses,  while  haemorrhages  from  the  intern;  I 
organs  contribute  from  time  to  time  to  tbe  general  debility  and  anaemia.  Certain 
complications  may  occur  in  haemophilia,  but  they  are  little  characteristic.  There 
is  a  noticeable  tendency  to  "  rheumatic  "  inflammation  of  the  muscles  and  swelling 
of  the  joints,  wherein  is  seen  a  striking  analogy  to  the  "haemorrhagic  diseases." 
Often  there  is  an  actual  effusion  of  blood  into  the  joints.  This  may  cause  consid- 
erable functional  disturbance  of  the  joints,  and  eventuate  in  anchylosis.  Various 
writers  have  also  called  attention  to  the  comparative  frequency  of  neuralgia,  espe- 
cially in  the  trigeminus. 

Prognosis. — In  only  too  many  instances  the  victims  of  haemophilia  die  in 
childhood ;  in  other  cases  the  patient  attains  an  advanced  age.  A  fact  of  great 
practical  importance  is  that  often,  although  not  invariably,  haemophilia  grows 
gradually  milder  with  advancing  years.  If,  therefore,  the  patient  have  survived 
the  period  of  adolescence,  we  may  believe  that  his  prospects  are  gradually  improv- 
ing. The  prognosis  of  haemophilia  is  obvious.  The  amount  of  danger  at  any 
given  time  depends  upon  the  severity  of  the  haemorrhage  and  the  consequent 
anaemia.  The  comparative  severity  of  the  case  must  be  judged  from  its  previous 
history;  as  has  just  been  said,  the  prognosis  grows  more  favorable  as  the  patient 
grows  older. 

Treatment. — Prophylaxis  assumes  a  very  important  place  in  the  treatment  of 
haemophilia.  First,  children  who  inherit  a  tendency  to  the  disease,  or  who  have 
given  evidence  of  its  existence,  should  be  treated  with  a  view  to  improve  their 
general  constitutional  condition,  so  as  to  check  the  development  of  the  disease  as 
far  as  possible.  The  means  to  this  end  need  not  be  described  at  length.  They 
comprise  good  nourishment,  fresh  air,  cautious  endeavors  to  harden  the  system, 
baths,  and  tonics.  Secondly,  when  haemophilia  already  exists,  the  patient  should 
be  guarded  as  much  as  possible  from  any  mechanical  injury,  such  as  might  excite 
haemorrhage.  Thus  caution  is  demanded  in  performing  vaccination  and  other 
apparently  trifling  operations. 

As  regards  direct  treatment  of  the  disease,  no  effectual  remedy  is  known.  Tbe 
general  tonic  treatment  already  referred  to  should  not  be  neglected;  but  the 
administration  of  ergotine,  acetate  of  lead,  and  similar  drugs  is  indicated,  if  at  all, 
only  when  haemorrhage  is  actually  taking  place,  and  even  then  it  is  very  apt  to 
fail.  The  only  way  to  stop  the  haemorrhage  is  by  surgical  methods,  and  these 
need  not  be  described  here.  They  do  not  differ  essentially  from  those  employed 
when  haemoi'rhage  occurs  independently  of  haemophilia.  If  mechanical  efforts 
to  check  the  bleeding  fail,  we  can  expect  nothing  from  the  remedies  above  men- 
tioned, nor  from  sulphate  of  sodium  and  the  other  laxatives  which  have  been 
recommended.  For  the  symptomatic  treatment  of  the  anaemia  and  of  its  results, 
we  may  refer  to  the  first  chapter  of  this  section. 


CHAPTER  IX. 

DIABETES   MELLITUS. 

Definition  and  iEtiology. — Under  normal  circumstances  the  blood  always  con- 
tains a  slight  amount  of  sugar;  but  this  ingredient  does  not  usually  pass  over  in 
appreciable  quantities  into  the  urinary  excretion.     If,  however,  the  amount  of 


966  CONSTITUTIONAL  DISEASES. 

sugar  in  the  blood  exceeds  certain  limits — that  is,  if  there  exists  an  abnormal 
"glyksemia" — then  sugar  is  excreted  in  the  urine,  and  we  have  glycosuria.  This 
is  seen  as  a  more  or  less  temporary  phenomenon  under  the  most  varied  conditions. 
The  amount  of  sugar  in  the  urine  is  usually  comparatively  slight,  and  it  soon  dis- 
appears again.  Its  presence  does  not  imply  any  persistent  abnormal  condition. 
This  phenomenon  has  been  termed  glycosuria  or  melituria,  in  contrast  with  the 
peculiar  disease  which  has  for  its  chief  symptom  a  persistence  of  sugar  in  the 
urine,  and  has  therefore  received  the  name  of  diabetes  mellitus. 

The  causes  of  glycosuria  need  not  be  discussed  here  at  any  length.  We  will 
briefly  state  that  sugar  may  appear  temporarily  in  the  urine  as  a  result  of  poison- 
ing from  various  substances,  chief  among  which  are  carbonic-acid  gas,  morphine, 
hydrocyanic  acid,  mercury,  nitrite  of  amyl,  and  curare.  Von  Mehring  has  lately 
discovered  in  phloriclzine,  a  glucoside  in  the  bark  of  the  roots  of  apple  and  cherry 
trees  a  substance  which  causes  a  very  large  amount  of  sugar  in  the  urine  if  given 
to  dogs,  rabbits,  etc.  A  marked  glycosuria  may  also  be  produced  in  man  by  giving 
phloroglucine,  or  by  other  disturbances  of  the  general  condition.  Temporary 
glycosuria  has  also  been  seen  in  connection  with  the  acute  infectious  diseases — 
for  example,  malignant  pustule,  cholera,  typhus  or  typhoid  fever,  scarlet  fever, 
diphtheria,  and  malarial  poisoning.  A  far  more  frequent  cause  is  disturbance  of 
the  nervous  system.  Thus,  glycosuria  may  result  from  severe  concussion  of  the 
brain,  fracture  of  the  skull,  cerebral  haemorrhage,  cerebro-spinal  meningitis,  and 
after  epileptic  fits.  It  is  especially  apt  to  occur  when  there  is  disease  of  the 
medulla ;  and  we  need  hardly  point  out  how  close  is  the  connection  between  this 
clinical  fact  and  the  famous  discovery  of  Claude  Bernard,  who  found  by  experi- 
ment that,  when  certain  injuries  are  inflicted  upon  the  floor  of  the  fourth  ventri- 
cle, glycosuria  inevitably  follows.  It  has  been  thought  that  diseases  of  the  stom- 
ach and  liver  may  occasion  glycosuria ;  but  this  is  doubtful.  With  regard  to  the 
theory  of  diabetes  (vide  infra),  it  is  an  interesting  fact  that  extensive  disease  of  the 
liver — as  seen  in  phosphorus  poisoning  or  cirrhosis — occasions  no  glycosuria,  even 
when  the  patient's  diet  contains  large  amounts  of  sugar  (Frerichs) ;  but  atrophy 
of  the  pancreas  seems  to  have  a  definite  relation  to  diabetes  (vide  infra).  As 
Minkowski  and  Von  Mehring  have  found,  we  can  produce  a  severe  diabetes  in 
dogs  by  extirpation  of  the  pancreas.  Ligature  of  the  duct  of  the  gland  does  not 
produce  this  condition.  There  must  therefore  be  some  special  function  of  the 
pancreas  not  yet  known,  and  after  this  function  ceases  to  be  performed  the  con- 
sumption of  sugar  in  the  animal  economy  ceases  to  be  complete. 

Diabetes  mellitus  is  a  disease  in  which  a  considerable  amount  of  sugar  is  con- 
stantly present  in  the  blood,  and  consequently  in  the  urine.  The  immediate  cause 
and  the  true  nature  of  this  strange  disease  are  entirely  unknown.  It  is  therefore 
difficult  to  determine  whether  all  cases  of  "diabetes  mellitus"  are  essentially 
identical.  In  most  of  the  typical  cases  this  question  may,  indeed,  be  answered 
affirmatively  with  little  hesitation;  but  other  cases,  particularly  many  of  what 
are  called  the  "  milder  varieties  "  of  diabetes,  afford  more  room  for  doubt.  We 
must  not  forget  that  diabetes  mellitus  is  at  present  known  to  us  only  through  its 
symptoms,  and  that  the  individual  cases  do  not  exhibit  any  uniformity  either  as 
to  causation  or  as  to  anatomical  changes. 

As  has  been  said,  we  know  practically  nothing  of  the  true  causes  of  diabetes. 
All  that  the  physician  can  do  in  any  particular  case  is  to  search  for  certain  excit- 
ing or  predisposing  causes,  the  significance  of  which  has  been  learned  from  clinical 
experience.  It  must,  however,  be  borne  in  mind  that  in  many  cases  of  diabetes, 
and  some  of  them  most  severe,  no  cause  whatever  can  be  made  out ;  the  disease 
seems  to  have  developed  of  itself  in  persons  who  were  previously  perfectly  well. 
We  append  a  list  of  such  exciting  influences  as  seem  to  be  most  frequent  and 


DIABETES  MELLITUS.  967 

important.  First,  heredity:  diabetes  has  been  repeatedly  observed  to  occur  in 
several  generations  of  the  same  family,  or  in  several  brothers  und  sisters.  It  is 
noteworthy  that  the  disease  may  also  occur  in  families  where  there  is  a  heredi- 
tary predisposition  to  nervous  diseases.  Second,  improper  modi;  of  life:  by  this 
is  meant  chiefly  unsuitable  diet,  especially  the  persistent  overindulgence;  in  starch  v 
foods  and  sugar;  sedentary  habits  are  also  considered  harmful,  especially  if  asso- 
ciated with  overeating.  This  is  said  to  be  the  reason  why  diabetes  is  more  fre- 
quent among  the  wealthy  classes,  and  why  it  is  quite  common  in  corpulent  persons. 
Third,  taking  cold  and  getting  wet  seem,  in  occasional  rare  instances,  to  determine 
the  appearance  of  diabetes.  Fourth,  emotional  disturbances,  excessive  mental 
exertion,  anxiety,  and  passion,  are  sometimes  thought  to  occasion  the  disease. 
Fifth,  it  is  very  remarkable  that  sometimes  the  same  factors  which  we  have 
already  seen  to  be  possible  causes  of  temporary  melituria,  may  also  occasion  a 
chronic  diabetes  mellitus  ;  thus,  cases  of  diabetes  have  been  known  to  follow 
injuries  to  the  head,  and  such  acute  infectious  diseases  as  typhus,  typhoid,  or 
scarlet  fever,  cholera,  and  malarial  poisoning.  Sixth,  certain  chronic  constitu- 
tional and  infectious  diseases,  particularly  gout  and  syphilis,  may  perhaps  promote 
the  development  of  diabetes.  The  disease  also  appears  in  connection  with  certain 
organic  diseases;  this  list  includes  cerebral  diseases,  such  as  hasmorrhage,  tumor, 
or  sclerosis,  particularly  when  in  the  region  of  the  fourth  ventricle;  other  nervous 
disorders,  such  as  organic  disease  of  the  peripheral  nerves,  and  functional  dis- 
eases; and,  in  rare  instances,  disease  of  the  pancreas,  such  as  suppuration  and 
cancer.  It  is  obvious  that  such  cases  of  diabetes  should  be  regarded  as ''acci- 
dental," in  distinction  from  the  true  idiopathic  disease. 

Diabetes  occurs  everywhere,  but  certain  countries  and  districts  seem  to  be 
particularly  liable  to  it — for  example,  India,  Ceylon,  and  Italy.  In  Germany, 
Würtemberg  and  Thüringen  are  said  to  present  the  largest  relative  number  of 
cases.  Jews  are  very  liable  to  the  disease.  Most  cases  occur  in  patients  between 
thirty-five  and  fifty  years  of  age.  Next  in  liability  to  the  disease  come  younger 
individuals,  under  thirty-five  and  over  twenty  years  old.  After  the  fiftieth  year 
diabetes  is  not  very  exceptional ;  but,  in  the  other  direction,  children  under  ten 
are  very  seldom  attacked  by  it,  although  they  are  not  absolutely  exempt.  With 
regard  to  sex,  males  are  much  more  often  attacked  than  females. 

Clinical  History. — With  few  exceptions,  the  symptoms  of  diabetes  mellitus  come 
on  slowly  and  gradually.  Sometimes  the  symptoms  are  merely  general  and  indefi- 
nite, such  as  languor,  emaciation,  weakness,  and  deficient  endurance.  Sometimes 
we  have  mild  nervous  disturbances,  including  headache,  mental  depression,  wake- 
fulness, and  neuralgia,  and  in  still  other  cases  gastro-intestinal  symptoms,  includ- 
ing nausea,  eructations,  and  irregularity  of  the  bowels.  At  last  the  patient's 
attention  is  called  to  the  altered  character  of  the  urine,  and  particularly  to  its 
increased  amount.  He  also  notices  that  he  is  very  thirsty,  and  that,  in  spite  of 
his  enormous  appetite,  he  is  constantly  growing  weaker.  Sometimes  quite  dif- 
erent  symptoms  first  arouse  suspicion  of  the  existence  of  diabetes ;  these  will  be 
mentioned  later.  In  order  to  make  a  diagnosis  of  diabetes  mellitus,  a  knowledge 
of  the  abnormal  character  of  the  urine  is  indispensable.  We  shall  therefore 
proceed  to  describe  the  changes  produced  in  the  urinary  excretion  as  a  result  of 
diabetes  mellitus. 

1.  Character  of  the  Urine.  Demonstration  of  Sugar. — Usually  the  first 
point  that  attracts  attention  is  the  increased  amount  of  urine.  There  are  often  a 
hundred  to  a  hundred  and  fifty  ounces  (three  to  five  quarts,  3,000-5.000  c.  c.)  ex- 
creted in  twenty -four  hours,  and  sometimes  there  may  even  be  as  much  as  ten  or 
twelve  quarts  (8,000-12,000  c.  a).  Under  suitable  treatment  and  with  proper  diet 
the  amount  may,  of  course,  be  much  smaller.     In  some  cases  the  polyuria  will 


968  CONSTITUTIONAL  DISEASES. 

almost  cease  from  time  to  time  ("  diabetes  decipiens ").  Often  the  amount  of 
urine  undergoes  diminution,  when  some  intercurrent  disease  appears,  or  when 
death  is  imminent. 

In  color  the  urine  is  light  yellow,  corresponding  to  its  amount.  It  often  has 
something  of  a  greenish  hue,  but  a  small  quantity  of  it  may  seem  almost  as  color- 
less as  water.  Ordinarily  the  urine  is  clear  and  without  sediment;  but  after  it 
has  stood  for  some  time  it  may  become  cloudy,  usually  as  a  result  of  the  abundant 
development  of  fermentation  spores. 

The  odor  may  be  somewhat  aromatic,  suggesting  acetone  (vide  infra).  Its 
taste,  as  determined  by  earlier  observers,  may  be  distinctly  sweetish.  The  reaction 
is  acid,  and  the  acidity  of  the  urine  may  increase  on  standing,  because  of  the 
alcoholic  and  lactic-acid  fermentation  processes  which  the  sugar  undergoes. 

The  specific  gravity  is  almost  invariably  greatly  increased,  as  a  result  of  the 
large  amount  of  sugar.  If  a  pale  urine  is  found  to  have  a  specific  gravity  of  more 
than  1025,  we  may  feel  almost  certain  that  it  contains  sugar.  Specimens  often 
have  a  specific  gravity  of  1030-1045,  and  even  higher.  In  exceptional  instances 
the  specific  gravity  may  fall  below  1020 ;  this  may  occur,  for  instance,  where  the 
patient  is  very  much  debilitated. 

The  diagnosis  requires  that  sugar  be  detected  in  the  urine.  The  sugar  found  in 
both  the  blood  and  the  urine  of  diabetic  patients  is  grape-sugar  (glucose,  dextrose). 
The  amount  of  sugar  secreted  in  twenty-four  hours  often  reaches  half  a  pound  to 
a  pound  (grm.  200-500).  Of  course  the  amount  varies  greatly  according  to  the 
diet,  mode  of  life,  and  treatment  of  the  patient.  The  greatest  amount  ever  known 
to  be  produced  in  twenty-four  hours  was  more  than  two  and  one  fifth  pounds 
(grm.  1,000).  The  percentage  of  sugar  in  the  urine  varies  between  0-5-l  per  cent, 
at  the  lowest  extreme,  and  8-10  per  cent,  as  the  maximum;  usually  it  is  about  2-4 
per  cent.  It  is  noteworthy  that  in  the  last  weeks,  or  just  before  death,  the  sugar  in 
the  urine  may  become  greatly  diminished  in  amount,  or  may  absolutely  disappear. 

The  most  important  tests  for  sugar  in  the  urine  are,  first,  Trommer's  test:  To 
urine  in  a  test-tube  sufficient  potassic  or  sodic  hydrate  is  added  to  make  the  reac- 
tion strongly  alkaline;  then  a  solution  of  sulphate  of  copper  (about  one  part  of 
the  salt  to  ten  of  water)  is  added,  drop  by  drop.  If  the  urine  contain  sugar,  the 
hydrated  cupric  oxide,  which  is  at  first  formed  in  large  amounts,  is  dissolved,  and 
usually  the  fluid  assumes  a  beautiful  deep-blue  color.  We  ought,  properly,  to  go 
on  adding  the  sulphate  of  copper  until  the  hydrated  cupric  oxide  ceases  to  be  dis- 
solved. The  urine  is  then  heated,  whereupon  the  cupric  oxide  is  reduced  and  a 
yellow,  or  reddish-yellow,  precipitate  of  cuprous  oxide,  or  hydrated  cuprous  oxide, 
is  formed.  The  application  of  heat  should  not  be  continued  long  after  the  precipi- 
tation begins  to  take  place,  lest  the  test  be  obscured ;  the  i-eduction  will  go  on  even 
without  heat.  If  the  urine  contains  more  than  0'5-l  per  cent.,  this  test  is  perfectly 
reliable.  If  the  reaction  be  a  doubtful  one— that  is,  if  there  be  no  precipitate  of 
cuprous  oxide,  although  the  urine  becomes  yellow — we  should  be  cautious  in  mak- 
ing a  diagnosis,  as  the  urine  may  contain  substances  other  than  sugar  capable  of 
reducing  the  copper,  such  as  uric  acid,  kreatinine,  murine,  etc.  Second,  the  bis- 
muth test  (Böttger's) :  Sodic  hydrate  or  sodic  carbonate  is  added  to  the  urine,  and 
then  a  small  pinch  of  subnitrate  of  bismuth.  Upon  boiling,  the  urine,  if  it  con- 
tains sugar,  quickly  assumes  a  perfectly  black  color,  the  oxide  being  reduced  to 
the  metallic  state.  Third,  the  potassium  test  (Moore's) :  Potassic  hydrate  is  added 
to  the  urine  in  the  test-tube  and  the  uppermost  layer  cautiously  heated ;  if  it  con- 
tains sugar,  the  urine  quickly  assumes  a  deep-brown  color,  as  a  result  of  the  action 
of  the  potassium  on  the  sugar ;  and  this  upper  dark-colored  layer  contrasts  strongly 
with  the  clear  urine  below. 

[Fehling's  test  is  justly  a  favorite  in  this  country,  and  has  the  advantage  of 


DIABETES  MELLITUS.  969 

being  applicable  to  the  quantitative  as  well  as  to  the  qualitative  analysis.  The  diffi- 
culty of  its  not  keeping  well  can  be  met  by  having  separate  bottles  for  the  copper 
and  tartrate  solutions,  and  making  the  mixture  at  the  time  of  using  the  test.  The 
Fehl ing's- test  pellets  put  up  by  chemists  are  convenient  for  the  qualitative 
analysis,  but,  on  the  whole,  they  are  inferior  to  the  solution.] 

If  the  above-described  tests  leave  us  still  in  doubt,  there  can  be  only  a  small 
amount  of  sugar,  if  any,  present.  We  may,  however,  attain  certainty  by  employ- 
ing the  fermentation  test  (which  causes  a  decomposition  of  the  sugar  into  alcohol 
and  carbonic  dioxide),  or  circumpolarization  (deflection  of  the  plane  of  polarization 
to  the  right  by  the  grape-sugar).  Further  particulars  in  regard  to  these  and  other 
tests,  and  also  in  regard  to  the  quantitative  estimation  of  sugar,  may  be  found  in 
works  on  medical  chemistry. 

Diabetic  urine  sometimes  contains  other  varieties  of  sugar  in  small  amounts — 
namely,  levulose,  which  deflects  the  plane  of  polarization  toward  the  left,  and 
inosite ;  these  are,  however,  of  no  practical  importance. 

The  amount  of  urea  is  usually  somewhat  increased  {vide  infra).  Uric  acid,  on 
the  contrary,  is  excreted  in  small  amounts.  The  amount  of  kreatine  is  normal  or 
even  increased  (Senator).  The  amount  of  phosphoric  acid  and  sulphuric  acid 
usually  corresponds  to  the  amount  of  urea,  or,  in  other  words,  to  the  decomposi- 
tion of  albuminoids.  Occasionally,  according  to  Teissier,  the  amount  of  phos- 
phates is  surprisingly  great,  and  may  either  correspond  with  the  amount  of  sugar 
simultaneously  excreted,  or  replace  the  sugar  in  the  urine.  This  subject  has  not 
yet  been  fully  investigated.  The  amount  of  sodic  chloride  excreted  depends,  as  in 
health,  merely  upon  the  amount  ingested. 

Hallervorden  has  discovered  an  important  fact  in  regard  to  the  excretion  of 
ammonia.  In  many  cases  of  diabetes,  although  not  in  all,  it  is  much  increased : 
forty-five  to  ninety  grains  (grm.  3-6),  or  even  more,  may  be  excreted  in  twenty- 
four  hours.  Despite  this,  diabetic  urine  has  an  acid  reaction;  and,  as  Stadel rnann 
has  shown,  the  basic  elements  are  considerably  out  of  proportion  to  the  acids  known 
to  us.  It  is,  therefore,  evident  that  diabetic  urine,  since  it  contains  a  large  amount 
of  ammonium  and  yet  has  an  acid  reaction,  must  have  among  its  constituents  some 
unusual  acid.  Stadelmann  was  at  first  inclined  to  believe  that  this  was  crotonic 
acid.  Minkowsky  and  Külz  have,  however,  shown,  by  their  more  recent  investi- 
gations, that  the  acid  in  question  is  really  oxybutyric  acid,  or,  more  accurately, 
beta-oxybutyric  acid.  This  acid  is  readily  decomposed  into  crotonic  acid,  which 
explains  Stadelmann's  error.  Another  interesting  fact  is  that,  upon  oxidation 
oxybutyric  acid  changes  to  acet-acetic  acid,  a  substance  easily  decomposed  into 
carbonic-dioxide  gas  and  acetone.  This  suggests  the  possibility  that  oxybutyric 
acid  may  give  rise  within  the  system  to  acetone,  a  substance  which  has  occupied 
an  important  place  in  the  literature  of  diabetes. 

Acetone  was  first  discovered  by  Petters  in  diabetic  urine.  This  was  regarded 
as  an  important  discovery,  because  it  was  believed  that  the  accumulation  of  this 
substance  in  the  blood  produced  those  grave  nervous  disturbances  (vide  infra,  dia- 
betic coma)  sometimes  observed  in  diabetes.  More  recent  developments  have  ren- 
dered this  view  extremely  improbable,  but  it  is  an  established  fact  that  acetone  is 
quite  often  present  in  the  urine  of  diabetic  patients.*  Whether  it  is  a  primary  or 
secondary  product  remains  uncertain.  It  was  formerly  believed  that  acetone  was 
formed  from  ethyldiacetic  acid  (acet-acetic  ether),  but  of  late  the  tendency  is 
rather  to  regard  acet-acetic  acid  as  the  source  of  acetone  (Deichmüller  and  Tol- 
lens,  Jaksch).     Acetone  is  probably  the  cause  of  the  reaction  to  which  Gerhardt 

*  It  should  be  added  that  acetone  has  been  found  by  Kaulieh  and  Jaksch  to  occur  frequently  in  the 
urine  during  many  other  diseases,  both  febrile  and  nonfebrile,  and  even  in  normal  urine. 


970  CONSTITUTIONAL  DISEASES. 

has  called  attention — namely,  the  development  of  a  Burgundy-red  color  in  the 
urine  upon  the  addition  of  ferric  chloride.  This  is  quite  often  to  be  observed  in 
the  urine  of  diabetic  patients.  In  speaking  of  diabetic  coma  we  sball  have  occa- 
sion to  revert  to  this  ferric-chloride  reaction. 

Albumen  may  be  found  in  diabetic  urine,  as  will  be  seen  below  under  renal 
complications;  small  amounts,  to  be  detected  only  after  careful  examination,  are 
common. 

2.  Tissue  Metamorphosis  in  Diabetes.  Sources  of  the  Sugar  and  Vari- 
ations in  its  Amount  occasioned  by  External  Influences. — Inasmuch  as  the 
presence  of  sugar  in  the  urine  is  the  most  prominent  symptom  in  diabetes,  the 
question  of  its  origin  is  all-important.  One  fact  is  indubitable — namely,  that  the 
secretion  of  sugar  depends  in  large  part  upon  the  amount  of  potential  sugar  in- 
gested— that  is,  upon  the  proportion  of  starches  in  the  food.  The  amount  of  sugar 
excreted  with  the  urine  increases  and  diminishes  with  the  amount  of  starchy  food 
eaten.  If  a  diabetic  patient  abstains  totally  for  any  length  of  time  from  such  arti- 
cles of  food  as  contain  starch,  sugar  will,  in  many  instances,  entirely  disappear 
from  the  ui'ine.  In  other  words,  the  system  of  a  diabetic  patient  is  almost,  if  not 
quite,  incapable  of  oxidizing  sugar  into  carbonic-dioxide  gas  and  water.  Voit  and 
Pettenkofer  have  made  an  experiment  the  result  of  which  confirms  this  statement. 
By  means  of  the  great  Munich  respiration  apparatus,  they  have  demonstrated  that 
in  diabetes  the  amount  of  oxygen  absorbed  from  the  air,  and  of  carbonic-dioxide 
gas  and  water  given  off  from  the  body,  is  less  than  in  health,  the  diet  being  pre- 
cisely the  same  in  both  cases.  Previously  to  this  many  investigators  had  shown 
that  there  was  a  diminution  in  the  amount  of  the  "  insensible  exci*eta." 

The  oxidation  of  sugar  is  not  absolutely  nil  in  diabetes.  Ktiiz  has  proved  by 
numerous  experiments  that  not  all  the  starch  is  excreted  in  the  form  of  sugar,  and 
he  has  also  found  that  many  varieties  of  sugar,  such  as  mannite,  fruit  sugar,  and 
inosite,  are  decomposed  even  in  diabetes,  so  that  their  ingestion  does  not  lead  to 
an  increase  of  sugar  in  the  urine. 

The  disturbances  in  metamorphosis  affect  other  substances  than  the  carbohy- 
drates. While  they  escape  oxidation,  on  the  other  hand,  the  destruction  of  albu- 
minoids is  increased.  We  have  already  stated  that  diabetic  urine  contains  a  large 
amount  of  urea.  Gäthgens  and  others  have  shown,  by  means  of  carefully  conducted 
investigations,  that  this  increase  in  the  amount  of  urea  is  not  merely  relative,  but 
absolute.  The  system  of  the  patient  destroys  a  larger  amount  of  albumen  than 
does  the  system  of  a  healthy  man,  the  ingesta  in  both  cases  being  alike.  Whether 
this  is  true  in  all  cases  of  diabetes  is  quite  doubtful,  but  the  fact  is  established  with 
regard  to  severe  cases.  It  is  also  certain  that  in  severe  cases  a  part  of  the  albumen 
is  transformed  into  sugar,  escapes  oxidation,  and  is  excreted  in  the  urine.  The 
proof  of  this  is  that  in  some  cases  of  diabetes  sugar  continues  to  be  present  in  the 
urine,  although  the  diet  is  exclusively  nitrogenous.  Seegen  accordingly  divides 
all  cases  of  diabetes  into  two  varieties :  a  milder  form,  where  sugar  ceases  to  be 
excreted  if  starchy  food  be  excluded  from  the  diet,  and  a  severer  form,  where  sugar 
persists  upon  an  exclusively  meat  diet. 

Muscular  exertion  is  one  of  the  external  influences  which  modify  the  excretion 
of  sugar  in  diabetes.  According  to  our  present  views,  muscular  activity  wastes 
mainly  non-nitrogenous  substances,  and,  accordingly,  we  find  in  diabetes  that  an 
increase  of  muscular  exertion,  other  things  being  equal,  diminishes  the  amount  of 
sugar  excreted. 

Emotional  excitement  is  said  to  increase  the  amount  of  sugar  excreted. 

Intercurrent  acute  febrile  diseases  may  cause  a  great  diminution  in  the  amount 
of  sugar,  but  sometimes  there  is  no  essential  change.  Probably  the  altered  diet 
of  the  patient  plays  an  important  part  in  this  connection,  although  doubtless  the 


DIABETES  MELLITUS.  !)T1 

special  modifications  of  tissue-metamorphosis  occasioned  by  the  high  temperature 
or  by  the  disease  itself  also  exert  some  influence. 

3.  Constitutional  Symptoms  in  Diabetes  Mellitus. — In  many  of  the  milder 
cases  there  is  for  a  long  time  little  apparent  disturbance  of  the  general  health. 
The  patient  is  well  nourished,  and  suffers  little  discomfort,  except  the  incon- 
venience occasioned  by  the  polyuria  and  the  polydipsia.  In  severer  cases  the  sys- 
tem is  deeply  affected  by  the  drain  upon  it.  The  patient  becomes  emaciated,  weak, 
and  easily  exhausted,  and  at  length  there  may  be  profound  marasmus.  Mentally, 
the  patient  is  apt  to  be  depressed  and  irritable.  The  intellectual  powers  art:  Dot 
impah'ed,  but  there  is  indisposition  to  mental  effort.  The  temperature  is  normal 
or  subnormal.     Fever  invariably  indicates  some  complication. 

4.  Symptoms  referable  to  the  Digestive  Organs. — We  have  already  men- 
tioned the  excessive  thirst  experienced  in  diabetes.  This  may  be  a  source  of  great 
discomfort,  obliging  the  patient  to  drink  at  short  intervals,  even  through  the 
night.  The  interdependence  of  polyuria  and  polydipsia  is  not  yet  fully  under- 
stood. The  most  natural  view  seems  to  be  that  the  increased  excretion  of  water 
by  the  kidneys  is  the  primary  factor,  and  the  increased  thirst  secondary  thereto. 
One  cause  of  the  polyuria  is  the  excretion  of  sugar,  in  order  to  dissolve  which  a 
large  amount  of  water  is  necessary,  but  certain  nervous  factors  would  also  seem 
to  be  implicated.  That  they  exert  some  influence  is  rendered  probable  by  the  fact 
that  the  amount  of  urine  does  not  always  correspond  to  the  amount  of  sugar 
excreted.  A  very  large  amount  of  urine  may  be  excreted  containing  little  or  no 
sugar;  and,  on  the  other  hand,  there  ai*e  genuine  cases  of  diabetes  mellitus  where 
the  amount  of  urine  is  normal,  and  the  patient  feels  no  unusual  thirst  {diabetes 
decipiens).  It  has  also  been  suggested  that  the  sugar  may  irritate  the  nerves  of 
the  mouth  and  throat,  and  thus  cause  thirst.  According  to  this  idea,  the  polyuria 
would  be  merely  the  result  of  the  excessive  ingestion  of  liquids.  The  abnor- 
mally great  appetite  in  diabetes  seems  in  most  cases  to  be  due  to  defective  assimi- 
lation of  the  food.  Many  patients  are  never  able  to  eat  enough.  They  have  a 
longing,  in  many  cases,  for  carbohydrates.  Occasionally  the  hunger  becomes 
ravenous,  and  is  associated  with  headache  and  a  general  sense  of  weakness,  all 
these  symptoms  being  alleviated  when  food  is  taken.  This  rule  has  rare  excep- 
tions in  which  the  appetite  is  not  unusually  great,  even  though  the  case  be  severe. 

The  tongue  is  frequently  dry ;  it  is  broad  and  thick,  with  an  irregular  and  fis- 
sured surface,  sometimes  coated  and  sometimes  red.  The  gums  may  be  spongy, 
and  may  exhibit  a  tendency  to  bleed.  The  teeth  frequently  decay  rapidly.  The 
saliva  is  invariably  found  to  give  an  acid  reaction.  This  is  true  of  the  isolated 
secretion  of  the  parotic  gland  also,  and  is  said  to  be  due  to  the  presence  of  lactic 
acid.  It  is  only  in  exceptional  instances  that  sugar  can  be  demonstrated  in  the 
saliva.     Thrush  quite  often  appears  on  the  soft  palate. 

There  are  no  marked  gastric  symptoms.  There  is  usually  constipation,  but 
sometimes  there  is  a  severe,  though  temporary,  diarrhoea.  The  liver  and  spleen 
are  seldom  much  affected ;  the  liver  rarely  is  somewhat  enlarged.  Jaundice  is 
frequently  observed,  but  it  is  always  referable  to  some  complication.  As  a  rule, 
the  secretion  of  the  bile  goes  on  as  in  health. 

5.  Symptoms  referable  to  the  Eespiratory  Organs. — In  many  cases  the 
organs  of  respiration  are  unimpaired  for  a  long  while.  It  may  be  mentioned  that 
often  patients  have  a  decidedly  fruity  odor  to  the  breath  (acetone  odor).  In  the 
later  stages  of  the  disease  pulmonary  complications  are  very  frequent.  Almost 
one  half  of  all  diabetic  patients  perish  from  secondary  disease  of  the  lungs.  Most 
frequently  there  is  pulmonary  tuberculosis ;  its  course,  symptoms,  the  presence  of 
tubercle  bacilli,  and  all  other  details  are  the  same  as  in  ordinary  cases  of  tuber- 
culosis.    Next  in  point  of  frequency  is  pulmonary  gangrene.     Sometimes  there  is 


972  CONSTITUTIONAL  DISEASES. 

a  diffuse  gangrenous  process,  and  sometimes  there  are  isolated  foci  of  necrosis, 
which  become  liquid,  and  have  an  acid  reaction,  but  they  often  have  compara- 
tively little  odor.  The  expectoration  in  these  cases  may  be  odorless.  Croupous 
pneumonia  may  also  occur.  It  often  terminates  unfavorably,  and  may,  as  we 
have  ourselves  observed,  result  in  gangrene. 

6.  Symptoms  referable  to  the  Circulatory  System. — In  many  instances 
the  circulatory  apparatus  presents  no  special  lesions.  The  pulse  is  either  of  a  nor- 
mal rate  or  a  trifle  slow.  It  is  usually  soft,  although  exceptionally  it  may  exhibit 
increased  tension.  There  is  often  distinct  evidence  of  cardiac  weakness  (Schmitz) ; 
the  pulse  is  small,  intermittent,  sometimes  very  slow  (50  or  even  40  beats  -per  min- 
ute), and  sometimes  accelerated  (100  to  120  beats  per  minute).  There  are  shortness 
of  breath,  faintness,  nausea,  and  the  like.  Sometimes  sudden  and  profound  car- 
diac disturbance  occurs,  and  may  occasion  speedy  death  (vide  infra,  coma).  Not 
very  rarely  diabetes  is  combined  with  general  arterio-sclerosis.  This  is  particu- 
larly apt  to  be  the  case  in  patients  who  have  been  subject  to  gout. 

7.  GtENIto-urinary  Symptoms. — Despite  the  great  demands  made  upon  them, 
the  kidneys  usually  maintain  a  normal  condition.  As  we  shall  see  when  we  come 
to  the  pathological  anatomy  of  diabetes,  the  kidneys  are  often  very  large.  Some- 
times a  chronic  nephritis  is  developed  as  a  complication,  usually  in  the  later  stages 
of  the  disease.  The  urine  contains  albumen,  and  there  are  oedema  and  other 
symptoms  of  renal  disorder.  It  was  formerly  a  common  opinion  that  the  nephri- 
tis results  from  the  irritation  of  the  sugar  excreted  by  the  kidneys,  but  in  such 
cases  other  irritants  are  probably  to  be  considered,  especially  as  in  most  cases  of 
nephritis  complicating  diabetes  there  are  usually  present  at  the  same  time  other 
disorders  to  which  the  nephritis  may  be  referable,  such  as  pulmonary  consump- 
tion or  cardiac  disease.  We  have  seen  well-marked  suppurative  pyelo-nepkritis 
as  a  complication  of  diabetes.  If  the  amount  of  albumen  in  the  urine  becomes 
considerable,  the  excretion  of  sugar  usually  undergoes  marked  diminution.  Many 
physicians  therefore  consider  the  transition  of  diabetes  into  chronic  renal  disease 
(contracted  kidney)  as  a  comparatively  favorable  symptom. 

Saccharine  urine  is  apt,  as  it  decomposes,  to  cause  irritation  of  the  skin.  This 
is  the  explanation  of  the  troublesome  pruritus  pudendi,  which  is  especially  marked 
in  women.  It  may,  indeed,  be  this  symptom  which  first  directs  attention  to  the 
disease.  Sometimes  the  external  genitals  are  attacked  by  eczema  or  furunculosis. 
Men  often  suffer  from  balanitis,  with  inflammatory  phimosis,  or  paraphimosis.  A 
frequent  and  important  symptom  in  men  is  impotence.  This  sometimes  occurs 
very  early  in  the  disease,  but  it  may  afterward  undergo  improvement.  The  oi'igin 
of  it  is  not  determined.  Some  authorities  state  that  diabetes  is  apt  to  occasion 
atrophy  of  the  testicles. 

8.  Disturbances  of  the  Organs  of  Special  Sense. — An  important  and  not 
infrequent  result  of  diabetes  is  cataract.  This  may  occasion  almost  total  blind- 
ness. The  cause  of  cataract  in  diabetes  is  not  known.  It  was  formerly  supposed 
that  the  sugar  in  the  blood  absorbed  water  from  the  crystalline  lens,  and  thus 
occasioned  its  opacity ;  but  this  has  not  been  confirmed.  Diabetic  patients  are  also 
subject  to  disturbances  of  accommodation.  Eetinitis,  atrophy  of  the  optic  nerve, 
and  purulent  choroiditis  may  also  occur,  but  they  are  very  rare,  and  perhaps  are 
merely  chance  complications. 

None  of  the  other  special  senses  are  peculiarly  affected  in  diabetes. 

9.  Cutaneous  Affections. — In  most  cases  the  skin  is  remarkably  dry  and 
rough.  There  may,  however,  be  abundant  perspiration.  Several  authorities  claim 
to  have  found  sugar  in  the  perspiration,  but  this  statement  has  not  been  confirmed 
by  later  investigators.  Sometimes  there  is  a  troublesome  pruritus.  We  often  see 
a  rapid  loss  of  hair  and  a  shedding  of  the  nails.     In  many  cases  there  is  a  great 


DIABETES  MELLITUS.  973 

tendency  to  furunculosis.  This  may  be  the  first  symptom  to  suggest  the  existence 
of  diabetes.  In  the  later  stages  there  are  sometimes  extensive  carbuncles,  and 
multiple  phlegmonous  abscesses  in  the  subcutaneous  cellular  tissue,  which  may 
prove  fatal.  Once  we  saw  an  eruption  resembling  pemphigus  appear  a  short  lime 
previously  to  death.  Gangrenous  processes  have  been  repeatedly  observed,  and 
in  particular  necrosis  of  one  or  more  toes,  which  may  take  the  form  of  perforating 
ulcer  {mal  perforanf),  or  rarely  of  an  entire  extremity.  This  gangrene  often 
seems  to  be  due  to  arterial  sclerosis;  in  other  cases  its  cause  is  obscure. 

CEdema  of  the  subcutaneous  cellular  tissue  may  occur  independently  of  nephri- 
tis.    It  is  then  probably  occasioned  by  the  cardiac  weakness. 

[Another  skin  affection  which  deserves  mention  is  eczema.  In  the  neighbor- 
hood of  the  genitals  it  is  more  common  in  women  than  in  men,  and  is  attributable 
to  the  irritating  properties  of  sugar  contained  in  the  urine  acting  on  a  skin  the 
nutrition  of  which  is  impaired  owing  to  the  morbid  condition  of  the  blood.  Some- 
times the  eczema  involves  other  portions  of  the  integument,  is  generally  acute, 
and  has  an  angry  appearance.] 

10.  Symptoms  referable  to  the  Nervous  System. — It  has  already  been 
mentioned  that  there  is  frequently  in  diabetes  a  moderate  disturbance  of  the 
whole  nervous  system,  as  indicated  by  headache,  physical  and  mental  hebetude, 
and  depression  of  spirits.  Still  more  characteristic  is  neuralgia.  This  is  most 
often  located  in  the  sciatic  nerve,  and  an  obstinate  bilateral  sciatica  may  be  one  of 
the  first  symptoms  of  diabetes.  Occipital  or  trigeminal  neuralgia  or  hemicrania, 
and,  on  the  other  hand,  anaesthesia,  have  also  been  repeatedly  observed.  We 
once  saw  peripheral  paralysis  of  the  peroneus  come  on  without  any  discoverable 
cause.  Bouchard  has  called  attention  to  the  frequent  absence  of  the  patellar  ten- 
don reflex  in  diabetes.  To  what  this  is  due,  or  what  relation  it  bears  to  the  pri- 
mary disease,  is  not  known.  Possibly  it  is  caused  by  degeneration  of  the  periph- 
eral nerves  from  toxic  (?)  influences. 

The  most  important  nervous  symptom  of  all  is  a  peculiar  disturbance  which 
occurs  in  a  considerable  proportion  of  all  cases  with  more  or  less  suddenness,  and 
usually  terminates  in  a  surprisingly  speedy  death.  This  strange  phenomenon 
was  first  thoroughly  investigated  by  Kussmaul,  although  known  long  before.  It 
is  termed  diabetic  coma.  The  condition  sometimes  develops  without  any  evident 
cause.  In  other  instances  it  is  apparently  brought  on  by  violent  muscular  exer- 
tion, mental  excitement,  or  some  trifling  illness,  such  as  gastric  catarrh,  bron- 
chitis, or  sore  throat. 

Frequently  certain  mild  prodromata  herald  its  onset.  There  may  be  nausea, 
headache,  a  sense  of  thoracic  oppression,  and  general  uneasiness.  Soon  the  con- 
dition becomes  aggravated.  The  patient  is  geized  with  a  feeling  of  great  anxiety, 
and  becomes  delirious,  sometimes  jumping  out  of  bed  and  growing  uncontrol- 
lable. Gradually,  however,  the  excitement  gives  place  to  an  ever-increasing 
drowsiness,  usually  terminating  in  the  most  profound  coma.  One  of  the  most 
frequent  and  striking  symptoms  attending  this  condition  is  the  peculiar  alteration 
in  respiration.  The  breathing  becomes  remarkably  deep  and  noisy.  Its  rate  may 
remain  nearly  normal ;  or  it  may  be  considerably  increased,  so  as  to  justify  the 
term  "diabetic  dyspnoea."  The  patient  is  sometimes  cyanotic.  The  pulse  is  usu- 
ally very  rapid  and  small.  The  temperature  gradually  sinks,  and  has  in  repeated 
instances  fallen  to  86°  (30°  C),  or  even  lower.  In  most  instances,  also,  the  breath 
has  a  very  noticeable  odor,  resembling  fruit  or  chloroform,  which  may  be  per- 
ceived on  entering  the  room.  Even  the  urine  may  have  this  same  odor;  and 
it  almost  invaluably  becomes  dark  red  on  the  addition  of  ferric  chloride  {vide 
supra). 

Diabetic  coma  does  not  pursue  the  same  course  in  all  cases;  sometimes  the 


974:  CONSTITUTIONAL  DISEASES. 

patient  lingers  on  for  several  days  before  death,  while  in  other  instances  the 
change  is  extremely  rapid  and  death  speedy.  The  early  stage  of  excitement  may 
be  wanting.  The  patient  becomes  somnolent  and  then  comatose,  and  never 
regains  consciousness.  Temporary  improvement,  and  even  complete  cessation  of 
the  threatening  symptoms,  are  not  impossible,  but  they  are  very  exceptional. 

We  have  no  definite  information  as  to  the  cause  of  diabetic  coma.  Of  course 
the  cases  where  an  autopsy  discloses  some  marked  organic  lesion,  such  as  cerebral 
hgemorrhage,  capable  of  producing  the  nervous  symptoms,  are  not  true  diabetic 
coma.  Nor  do  the  cases  of  sudden  death  reported  by  Frerichs  deserve  to  be 
classed  as  diabetic  coma,  where  death  occurred  with  the  symptoms  of  acute  car- 
diac failure— namely,  collapse,  coolness  of  the  extremities,  small  and  rapid  pulse, 
and  unconsciousness.  Besides,  these  patients  never  have  the  acetone  odor,  the 
exaggerated  respiration,  nor  the  ferric-chloride  reaction,  and  usually  the  myocar- 
dium is  found  to  be  in  an  advanced  state  of  degeneration. 

In  genuine  diabetic  coma,  on  the  other  hand,  everything  seems  to  indicate 
that  the  system  has  been  poisoned  by  some  noxious  product  of  the  abnormal  pro- 
cesses of  metamorphosis.  Great  effort  has  been  made  to  discover  what  this  prod- 
uct is,  but  in  vain.  Kussmaul  regarded  acetone  as  the  injurious  substance,  and 
therefore  called  diabetic  coma  "acetonemia."  Other  investigators  believe  that 
acet-acetic  acid  (Jaksch)  is  the  cause  of  the  phenomenon  in  question,  or  at  least 
regard  the  coma  as  a  result  of  poisoning  from  some  of  the  unusual  acids  present 
in  diabetes  (Stadelmann,  vide  supra).  No  one  view  has  obtained  general  accept- 
ance, nor  has  it  been  possible  to  produce  diabetic  coma  in  animals  by  the  employ- 
ment of  acetone,  acet-acetic  acid,  crotonic  acid,  or  similar  substances  (Brieger  and 
others).  It  is,  nevertheless,  extremely  probable  that  these  substances  do  have 
some  close  connection  with  "  diabetic  intoxication  "  (Frerichs). 

Pathological  Anatomy  and  Histochemistry  of  Diabetes  Mellitus.— The  mysteri- 
ous phenomena  of  diabetes  mellitus  present  a  problem,  the  solution  of  which  has 
been  most  industriously  sought  post  mortem ;  but  no  satisfactory  result  has  been 
reached,  even  in  this  way. 

'  If  we  exclude  the  organic  diseases,  such  as  pulmonary  tuberculosis  and  nephri- 
tis, which  are  merely  complications,  the  pathological  changes  in  diabetes  are 
trifling.  Bernard's  discovery,  that  an  injury  inflicted  in  a  certain  spot  on  the 
floor  of  the  fourth  ventricle  produces  glycosuria  in  animals,  has  directed  the 
attention  of  investigators  to  the  condition  of  the  nervous  system  in  this  disease. 
In  some  instances,  tumors,  sclerosis,  or  similar  troubles  have  been  found  in  the 
medulla  and  cerebellum ;  but  in  these  cases  the  diabetes  was  evidently  not  idio- 
pathic {vide  siqora).  In  idiopathic  cases  the  central  nervous  system  presents  no 
striking  macroscopic  changes.  By  means  of  the  microscope,  Frerichs  has  found 
lesions  of  the  medulla  oblongata  in  frequent  instances.  The  minute  blood-vessels 
are  widely  dilated ;  there  are  small  capillary  haemorrhages,  some  of  a  more  recent 
and  others  of  a  more  remote  date ;  and  occasionally  there  are  microscopic  foci  of 
myelitis.  The  nervous  elements  proper,  the  nerve-fibers  and  ganglion-cells,  be- 
tray no  alteration.  The  significance  of  these  changes  must  be  determined  by 
further  investigation. 

The  stomach  and  intestines  present  no  constant  alterations  of  importance. 

The  liver  has  naturally  been  the  object  of  repeated  and  careful  examinations, 
because  of  its  well-known  part  in  the  manufacture  of  glycogen.  Yet  this  organ 
seldom  presents  any  special  abnormality.  It  is  usually  of  the  natural  size,  and 
may  contain  either  considerable  or  very  little  blood.  The  amount  of  glycogen  in 
the  hepatic  cells  can  be  demonstrated  with  iodine  by  a  micro-chemical  reaction. 
It  appears  that,  other  things  being  equal,  there  is  less  glycogen  present  than 
normal.     It  is  usually  found  only  in  the  cells  situated  upon  the  periphery  of  the 


DIABETES  MELLITUS.  9 


10 


lobules,  and  in  small  quantities.  In  an  extremely  advanced  case  of  diabetes 
Ebrlicb  obtained,  by  means  of  a  hollow  needle,  small  amounts  of  the  hepatic 
parenchyma  for  examination  during  life,  and  found  that  glycogen  was  almost 
completely  absent.  In  other  cases  the  liver  has  been  examined  as  early  as  possible 
after  death,  and  presented  no  trace  of  glycogen,  but  it  sometimes  has  been  found. 

The  spleen  is  usually  of  normal  size.  Occasionally  it  is  atrophied,  or  on  the 
other  hand,  slightly  enlarged.     No  other  changes  in  it  have  been  observed. 

Many  cases  have  presented  a  striking  atrophy  of  the  pancreas  (Bouchardat),  a 
fact  which  has  acquired  great  significance  from  Minkowsky's  discovery,  already 
mentioned,  that  glycosuria  may  come  on  after  extirpation  of  the  pancreas.  It  is 
uncertain  whether  the  coeliac  plexus  may  also  sometimes  take  part  in  the  atrophy 
of  the  pancreas.  We  must  also  state,  however,  that  atrophy  of  the  pancreas  is  not 
a  constant  lesion  in  diabetes,  so  that  it  is  not  proper  to  regard  the  disease  of  the 
pancreas  as  the  special  cause  of  diabetes  in  all  cases. 

The  kidneys  are  often  enlarged,  from  functional  hypertrophy.  Ehrlich  dis- 
covered in  them  a  glycogenic  degeneration  *  of  the  loops  of  Henle.  This  change 
is  a  constant  one.  The  epithelial  cells  in  the  loops  are  enlarged,  and  the  proto- 
plasm in  these  cells,  although  apparently  homogeneous,  is  found,  by  the  addition 
of  a  solution  of  iodine  in  mucilage,  to  contain  glycogen,  in  flakes  and  clumps  of 
varying  size.  How  important  this  glycogenic  degeneration  of  the  kidneys  may 
be  has  not  yet  been  determined.  Perhaps  the  glycogen  represents  sugar  which 
has  been  absorbed  by  the  cells.  That  chronic  nephritis  may  complicate  diabetes 
has  already  been  mentioned. 

No  thorough  investigation  of  the  chemical  composition  of  the  blood  in  diabetes 
has  yet  been  made.  One  important  and  constant  characteristic  is  the  gradually 
increased  proportion  of  sugar  in  the  blood.  There  is  usually  somewhere  between 
0-2  and  0'45  per  cent,  of  sugar,  while  in  health  the  blood  rarely  contains  over  O'l 
per  cent.  The  lymph,  and  such  serous  effusions  as  are  found,  contain  sugar,  but 
the  saliva,  perspiration,  bile,  gastric  juice,  and  other  secretions  rarely  furnish  evi- 
dence of  its  existence. 

Varieties,  Course,  and  Prognosis  of  the  Disease. — The  study  of  a  large  number 
of  cases  of  diabetes  will  show  great  variations  in  the  course  and  duration  of  the 
disease.  As  already  stated,  we  may  in  practice  distinguish  between  mild  and 
severe  forms  of  diabetes.  In  the  mild  cases,  sugar  ceases  to  be  excreted  if  the 
patient  be  put  upon  a  diet  containing  no  carbohydrates.  Sometimes  it  is  even 
possible  for  the  patient  to  eat  a  small  amount  of  starchy  food  without  occasioning 
glycosuria,  particularly  if  he  take  enough  exercise  {vide  supra).  In  the  severe 
form,  sugar  persists  in  the  urine  even  upon  a  purely  meat  diet;  and  upon  the 
ingestion  of  carbohydrates  there  will  be,  at  the  end  of  half  an  hour  or  so,  a  large 
increase  of  sugar.  Most  of  the  other  symptoms  are  alike  in  both  forms  of  the  dis- 
ease, varying  only  in  degree.  The  moderate  form  may  finally  assume  a  severe 
character;  and  sometimes,  although  the  secretion  of  sugar  remains  permanently 
small,  fatal  complications,  such  as  tuberculosis  of  the  lungs,  finally  develop. 

The  general  course  of  diabetes  varies  in  different  cases,  exclusive  of  the  differ- 
ences already  referred  to.  In  a  few  instances  the  disease  occupies  only  a  few 
weeks,  and  may  almost  be  termed  "acute  diabetes."  Other  cases  last  one  or  two 
years,  and  still  others  ten  or  twenty  years.  The  patient's  condition  may  vary 
from  time  to  time.  We  have  repeatedly  seen  the  sugar  disappear  temporarily 
from  the  urine,  and  the  patient  apparently  completely  recover ;  but  sooner  or  later 
the  disease  breaks  out  again.     These  cases,  which  are  commoner  in  old  people, 

*  Ebstein  and  Armanni  noticed  and  described  this  condition ;  but  they  regarded  it  as  a  necrosis  of 
the  epithelium. 


976  CONSTITUTIONAL  DISEASES. 

have  been  called  "  intermittent  diabetes."  The  relapse  is  often  brought  about  by 
emotional  excitement  or  some  grave  error  in  diet.  Again,  the  disease  may  under- 
go apparent  arrest  and  the  patient  enjoy  comparative  comfort  for  years.  As  a 
general  rule,  it  may  be  said  that  older  patients  are  more  apt  to  have  the  niild  form 
of  diabetes,  while  in  young  adults  and  children  the  disease  is  wont  to  pursue  a 
more  rapid  and  unfavorable  course. 

Different  cases  also  differ  in  the  relative  severity  of  particular  symptoms. 
Thus,  the  clinical  picture  presented  by  diabetes  may  be  modified  by  the  general 
constitution  of  the  patient — for  instance,  his  corpulence  or  emaciation ;  by  such 
complications  as  diseases  of  the  lungs,  kidneys,  or  brain,  or  syphilis  and  gout; 
and  by  many  other  conditions.  In  practice,  especially  in  practice  among  the 
better  classes,  it  is  very  important  to  have  a  knowledge  of  the  milder  forms  of 
diabetes,  in  which  sugar  is  present  in  the  urine  only  at  times,  and  not  in  very 
large  amount.  The  more  we  are  accustomed  to  examine  every  urine  for  sugar 
the  offener  we  find  such  cases,  as  to  the  pathological  significance  of  which  our 
knowledge  is  still  very  slight.  The  glycosmia  of  the  corpulent  (Seeger)  is  worthy 
of  special  consideration.  It  is  not  uncommon  in  patients  who  have  formerly 
suffered  from  true  gout.  The  tendency  to  the  formation  of  furuncles  and  cataract 
is  noteworthy.  We  must  also  mention  the  cases  of  diabetes  in  neurasthenics — 
that  is,  cases  where  there  is  sugar  in  the  urine,  and  where  the  chief  complaint  is 
of  general  nervous  symptoms,  pressure  in  the  head,  anxiety,  a  dull  feeling,  inca- 
pacity for  mental  work,  neuralgic  pains,  etc.  In  all  such  cases  glycosuria  has  not 
the  serious  significance  that  it  has  in  genuine  and  severe  diabetes. 

We  would  agahi  call  attention  to  the  fact  that  diabetes  may  exist  without 
polyuria  or  abnormal  thirst,  and  so  be  overlooked.  It  is  a  very  interesting  fact 
that  diabetes  mellitus  occasionally  undergoes  gradual  transformation  into  diabetes 
insipidus  (see  Chapter  X).     Frerichs  has  given  some  striking  examples  of  this. 

The  usual  termination  of  diabetes  is  death.  We  have  already  seen  how  great 
a  difference  there  may  be  in  the  length  of  time  preceding  the  fatal  termination, 
and  in  what  various  ways  it  may  be  brought  about.  The  most  frequent  immediate 
causes  of  death  are  marasmus,  diabetic  coma,  pulmonary  consumption,  nephritis, 
furunculosis,  or  the  development  of  carbuncles. 

There  is  no  doubt  that  complete  recovery  may  occur ;  but  this  is  rare,  and  is 
possible  only  in  the  milder  cases.  It  should  also  be  borne  in  mind  that  apparent 
recovery  does  not  exclude  the  possibility  of  a  fresh  outbreak  of  the  disease. 

[It  should  be  clearly  understood  that  the  presence  of  sugar  in  the  urine  does 
not  in  itself  indicate  diabetes ;  and  that  diabetes  is  not  now  considered  nearly  as 
hopeless  a  disease  as  it  was.  The  diagnosis  was  formerly  seldom  made  unless  one 
or  all  of  the  cardinal  symptoms— increased  thirst  and  appetite,  with  progressive 
emaciation  and  polyuria — wTere  markedly  present,  a  condition  of  things  which 
may  be  roughly  compared  to  phthisis  in  the  stage  of  cavity.  The  prognosis  is 
more  grave  in  the  young  than  in  those  past  middle  life,  in  thin  than  in  stout 
people,  and  in  those  from  whose  urine  the  sugar  does  not  disappear  under  dietetic 
treatment  alone.  If  the  bodily  weight  and  the  strength  be  well  maintained,  sugar 
may  be  excreted  for  long  periods  without  any  obvious  ill  effects.] 

Theoretical  Discussion  of  the  Nature  of  Diabetes.— We  have  endeavored  to 
give  an  approximately  complete  summary  of  the  facts  pertaining  to  diabetes.  We 
trust  we  shall  be  excused  from  detailing  all  the  theories  and  hypotheses  which 
have  been  devised  to  explain  the  peculiar  phenomena  of  the  disease,  particularly 
the  glycosuria.  It  is  a  better  way  simply  to  confess  that  the  true  nature  of  dia- 
betes mellitus  as  yet  remains  very  obscure.  We  shall  confine  ourselves  to  a  few 
remarks  upon  the  present  state  of  the  question. 

The  essential  fact  which  demands  explanation  is  the  excess  of  sugar  in  the 


DIABETES  MELLITUS.  977 

blood.  The  source  of  this  sugar  is  probably  the  same  as  of  the  sugar  normally 
contained  in  the  blood.  The  largest  part  of  the  sugar  probably  comes  from  the 
carbohydrates  contained  in  the  food.  These  are,  for  the  most  part,  converted  into 
sugar  in  the  primae  via;,  which  sugar  thereupon  enters  the  portal  system.  It  may 
also  be  assumed  that  glycogen,  so  widely  diffused  throughout  the  system,  is  an- 
other source  of  sugar.  The  liver  is  the  main  seat  of  the  manufacture  of  glycogen  ; 
but  it  is  produced  in  other  parts  as  well,  and  in  particular  in  the  muscles.  The 
question  next  arises,  Erom  what  is  the  glycogen  formed  ?  A  part  of  it  is  probably 
manufactured  from  the  carbohydrates  contained  in  the  food,  hut  another  part  is 
certainly  due  to  the  ingested  albuminoids.  Accordingly,  Von  Mehring  found 
that  in  fasting  animals,  who  have  no  more  glycogen  stored  up  in  the  body,  dia- 
betes may  be  produced  by  giving  phloriclzine  {vide  supra).  The  sugar  excreted 
can  therefore  come  only  from  the  destruction  of  albumen  in  the  body.  Again,  the 
transformation  of  glycogen  into  sugar  is  not  confined  to  the  liver,  but  may  take 
place  wherever  glycogen  is  produced.  How  it  takes  place  is  unknown.  It  is 
usually  assumed  that  there  is  some  "saccharine  ferment." 

It  would  seem,  therefore,  that  the  sources  of  sugar  are  the  same  in  diabetes  as 
in  health.  We  have  next  to  seek  for  the  reason  of  its  excessive  accumulation  in 
the  blood.  Uuder  normal  circumstances,  the  sugar  present  in  that  fluid  rapidly 
undergoes  decomposition  into  other  substances.  In  health  there  is  no  great 
excess  of  sugar  in  the  blood,  even  upon  a  diet  extremely  rich  in  starch;  and  it  is 
possible  to  eat  large  amounts  of  sugar  without  any  glycosuria.  We  see,  there- 
fore, that  diabetes  can  not  be  explained  by  assuming  that  there  is  an  increased 
production  of  sugar  except  in  so  far  as  corresponds  to  the  increased  amount  of 
ingesta.  On  the  other  hand,  everything  points  toward  the  conclusion  that  in 
diabetes  the  ordinary  processes  effecting  the  decomposition  and  destruction  of 
sugar  are  suspended.  The  sugar  is  excreted  by  the  kidneys  unaltered,  for  the  rea- 
son that  it  is  not  destroyed.  It  is  difficult  to  conjecture  what  the  circumstances 
may  be  which  thus  interfere  with  the  decomposition  of  the  sugar.  Perhaps  it 
is  some  special  nervous  influence,  or  perhaps  some  ferment  may  be  wanting  in 
diabetes  which  in  health  promotes  the  metamorphosis  of  the  sugar  (compare  the 
experiments  of  Minkowsky,  above  mentioned,  in  producing  diabetes  by  extirpation 
of  the  pancreas).  Another  point  that  is  difficult  to  understand  is,  that  in  the 
milder  cases  of  diabetes  only  such  sugar  as  originates  from  the  starch  contained 
in  the  food  is  excreted,  while  the  sugar  manufactured  from  albumen  seems  to  be 
completely  decomposed.  The  cause  of  the  excretion  of  sugar  can  not  lie  in  the 
disturbed  condition  of  the  kidney,  for  in  diabetes  insipidus,  as  Prerichs  shows,  no 
glycosuria  is  produced,  even  when  a  very  large  amount  of  sugar  is  ingested. 

Diagnosis. — For  the  diagnosis  of  diabetes  mellitus  it  is  indispensable  that 
sugar  should  be  demonstrated  in  the  urine.  We  have  also  to  decide  whether  the 
condition  be  a  temporary  or  a  permanent  one,  or,  in  other  words,  whether  we 
have  to  deal  with  mere  glycosuria  or  genuine  diabetes  mellitus.  This  point  is  to 
be  determined  by  means  of  the  symptoms  and  general  course  of  the  disease. 

Diabetes  often  exists  for  some  time  unsuspected  even  by  the  physician.  It 
may  therefore  be  well  to  name  over  the  symptoms  which  may  be  the  first  to 
attract  the  patient's  attention,  and  which  should  therefore  always  suggest  to  a 
physician  the  possibility  of  the  existence  of  diabetes.  They  are:  1,  languor  and 
debility;  2,  furunculosis ;  3,  pruritus  pudendi  in  women,  balanitis  in  men;  4.  cata- 
ract ;  5,  sciatica,  especially  if  bilateral ;  6,  impotence.  We  should  also  be  in  the 
habit  of  examining  the  urine  for  sugar  in  all  cases  where  complaint  is  made  of 
indefinite  symptoms,  which  can  not  be  explained  without  further  evidence,  espe- 
cially in  cases  where  the  patient  is  fat  or  nervous. 

If  symptoms  similar  to  those  just  enumerated  lead  to  an  examination  of  the 
62 


978  CONSTITUTIONAL  DISEASES. 

urine,  and  the  result  of  this  is  ambiguous,  it  is  advisable  to  have  the  patient  par- 
take of  a  meal  rich  in  starchy  elements,  and  to  examine  the  urine  thereafter.  If 
even  then  no  sugar  is  found,  diabetes  does  not  exist. 

[The  urine  passed  three  or  four  hours  after  a  f  ull  meal  often  contains  sugar, 
when  that  passed  on  rising  is  quite  free  from  it.] 

Treatment.— Medical  science  does  not  possess  the  power  to  cure  the  disease, 
but  it  can  greatly  benefit  tbe  patient,  both  by  alleviating  his  symptoms  and  by 
shielding  him,  at  least  for  the  time,  from  many  of  the  secondary  effects. 

The  first  requisite  is  to  institute  a  proper  regimen.  All  the  hygienic  circum- 
stances of  the  patient  should  be  regulated.  This  is  more  important  than  any  sort 
of  medicinal  treatment.  We  have  seen  that  a  large  part  of  the  food  taken  by  a 
diabetic  patient  escapes  from  the  body  unutilized,  and  that,  as  a  result  of  this, 
certain  disturbances  are  produced  in  the  tissues;  thus  there  is  a  tendency  to 
furunculosis  and  gangrene  and  cataract.  Furthermore,  the  sugar  contained  in 
the  urine  gives  rise  to  certain  secondary  symptoms,  such  as  balanitis,  and  perhaps 
its  presence  in  other  secretions  has  analogous  bad  effects.  We  must  therefore 
endeavor,  first,  to  promote  the  conversion  of  the  non-nitrogenous  elements  of  the 
food;  and,  secondly,  to  furnish  the  system  with  a  substitute  for  that  portion  of 
the  food  which  it  can  not  assimilate,  and  to  obviate  the  excessive  ingestion  and 
production  of  sugar.  It  would  be  erroneous  to  conclude  that  this  last  point  is 
the  only  essential  one,  and  that  we  accomplish  our  whole  duty  by  reducing  the 
amount  of  sugar  contained  in  the  urine  to  a  minimum.  The  general  condition 
of  the  patient  should  invariably  be  considered.  There  can  be  no  doubt  that  a 
diabetic  patient  whose  strength  is  well  maintained  is  better  off  than  one  whose 
urine  contains  only  one  per  cent,  of  sugar  but  who  yet  is  daily  growing  weaker. 

Mental  excitement  has  been  suggested  as  a  possible  cause  of  the  disease ;  and 
there  can  be  still  less  doubt  that  it  usually  has  a  bad  effect  upon  its  course.  The 
physician  should  therefore  endeavor,  so  far  as  he  is  able,  to  guard  the  patient 
from  excitement,  whether  incidental  to  his  occupation  or  to  his  social  position. 

A  proper  diet  is  of  the  greatest  importance.  It  has  already  been  stated  that  in 
many  instances  the  excretion  of  sugar  may  be  entirely  stopped  by  excluding 
starch  from  the  ingesta;  but  such  exclusion  does  not  always  result  in  permanent 
benefit  to  the  patient.  Cantani,  however,  believes  otherwise,  and  has  laid  down  a 
very  strict  dietetic  regimen.  He  states  that  in  not  a  few  cases  an  almost  exclusive 
meat  diet  may  be  persisted  in  for  years,  and  the  patient  may  at  length  experience 
complete  recovery,  or  even  acquire  the  ability  to  partake  once  more  of  starchy  food 
with  impunity.  That  such  favorable  results  may  occur  we  have  no  doubt;  but 
we  must  call  attention  to  the  fact  that  it  is  frequently  impossible  to  enforce  the 
strict  regimen  of  Cantani,  and  that  many  patients,  while  following  it,  feel  worse 
than  when  they  indulge  in  a  moderate  amount  of  carbohydrates.  The  "cure" 
affords  them  no  relief,  but  merely  distress.  At  present,  authorities  are  generally 
inclined  to  recommend  a  diet  mainly  of  flesh  or  albuminoids,  but  not  absolutely 
devoid  of  carbohydrates.  The  amount  of  starch  which  can  be  safely  ingested 
varies  with  the  individual.  Of  course,  the  best  way  is  to  judge  of  the  system's 
power  to  tolerate  starch  by  means  of  daily  quantitative  estimations  of  the  amount 
of  sugar  excreted.  We  repeat  that,  within  certain  limits,  the  percentage  of  sugar 
should  not  be  the  only  criterion  of  the  suitability  of  the  diet,  but  that  the  general 
condition  should  also  be  taken  into  consideration. 

If  we  consider  the  most  common  articles  of  diet  with  regard  to  the  proportion 
of  carbohydrates  they  contain,  we  shall  find  that  they  may  be  classified  somewhat 
as  follows :  First,  these  articles  may  be  allowed  ad  libitum :  All  sorts  of  fresh 
meat,  ham,  smoked  meat,  tongue,  fish,  crabs,  eggs,  caviare,  sour  milk,  cheese, 
butter,  bacon ;  also  green  vegetables,  lettuce,  spinach,  and  cucumbers.     Secondly, 


DIABETES  MELLITUS.  979 

the  following  may  bo  used  moderately:  Bread,  milk,  fruit,  rice,  turnips,  beets,  as- 
paragus, radishes,  cauliflower;  also  light  beer,  claret,  and  other  dry  wines.  Thirdly, 
if  possible,  the  following  should  be  entirely  abandoned:  Sweet  dishes,  cake,  honey, 
potatoes,  grits,  sago,  peas,  beans,  lentils,  sweet  fruit,  sweet  wine,  and  Liqueurs. 

The  greatest  trial  for  most  patients  is  to  give  up  bread.  Every  physician  has 
had  experience  of  the  cunning  which  patients  exercise  in  order  to  satisfy  th<  ir 
invincible  craving  for  it.  Faults  of  this  kind  are  not  so  apt  to  be  committed  if 
the  patient  is  allowed  a  limited  amount  of  bread,  say  two  or  three  ounces  a  day  in 
divided  portions.  There  have  also  been  many  attempts  to  make  a  bread  out  of 
such  carbohydrates  as  have  been  found  by  experience  not  to  increase  the  excretion 
of  sugar,  and  thus  to  furnish  a  substitute  for  ordinary  bread ;  but  these  succedanea 
have  not  become  popular,  mainly  because  of  their  bad  taste.  They  may,  however, 
be  tried.  We  have  not  space  to  describe  in  detail  the  various  kinds  of  "  diabetic 
bread "  which  have  been  recommended.  The  best  known  are  bread  made  from 
bran  flour  (Prout),  from  almonds  (Pavy),  from  inulin  and  lichenin  (Külz).  Most 
of  these  substances  contain  a  considerable  amount  of  starch. 

Since  we  can  not  supply  the  system  of  a  diabetic  patient  with  carbohydrates  in 
sufficient  amount,  it  suggests  itself  that  we  should  endeavor  to  supply  the  lack  by 
other  non-nitrogenous  substances,  and  that  the  patient  should  be  allowed  a  large 
proportion  of  fat  in  his  diet.  With  regard  to  this,  experience  and  theory  coin- 
cide. Fatty  substances  are  well  borne  in  most  cases,  and  we  should  not  only 
allow,  but  urge  patients  who  are  at  all  emaciated  to  use  butter,  cream,  and  similar 
articles  of  diet.  Cod-liver  oil  is  also  frequently  employed,  and  is  even  regarded 
by  many  physicians  as  having  a  specific  effect.  It  may  be  stated  in  this  connec- 
tion that  for  a  time  it  was  believed  that  glycerine  might  serve  as  a  substitute  for 
sugar  (Schultzen);  two  to  three  ounces  maybe  given  in  a  day;  but,  with  some 
apparent  exceptions,  its  administration  has  not  proved  especially  satisfactory. 

Dühring  claims  that  by  long-continued  boiling  the  carbohydrates  may  be  so 
modified  as  to  cease  to  affect  the  excretion  of  sugar  in  diabetes.  Dühring  gives 
his  patients  mainly  rice  and  fruit,  these  substances  having  previously  been  soaked 
in  water  and  boiled  for  several  hours.  His  method  also  includes  certain  other 
dietetic  and  hygienic  measures,  but  it  has  not  yet  been  satisfactorily  tested. 

To  quench  thirst,  we  may  allow  the  patient  simple  water  or  Seltzer  water,  and 
acidulated  drinks.  If  the  thirst  be  very  troublesome,  the  patient  may  let  little 
pieces  of  ice  melt  in  the  mouth.  Tea  and  coffee  may  be  taken  with  cream,  but 
without  sugar.  In  place  of  sugar,  we  may  make  trial  of  glycerine  or  mannite. 
Milk  does  not  need  to  be  absolutely  banished,  but  few  patients  care  for  it.  Alco- 
holic beverages  may  be  allowed  in  moderation,  particularly  red  wine,  such  as 
Bordeaux,  and  light  beer.  Thirst  may  also  be  moderated  by  weak  brandy  and 
water. 

[The  dietetic  treatment  of  diabetes  is  so  important  that  it  is  desirable  to  go  more 
into  detail. 

There  is  some  discrepancy  between  the  authorities  on  this  point,  a  more  strict 
diet  being  laid  down  by  some  than  by  others.  Ralfe's  list  is  as  rigid  as  any,  and 
is  as  follows : 

To  avoid  milk  (except  very  small  quantities  for  cooking  purposes).  The  liver 
of  all  animals  (as  the  liver  of  oysters  and  all  mollusca  is  large,  and  abounds  in 
glycogen,  these  animals  must  be  forbidden),  so  also  the  interior  of  crabs,  lobsters, 
etc.  Bread,  biscuits,  rusks,  toast,  farinaceous  vegetables,  such  äs  potatoes,  Jeru- 
salem artichokes,  rice,  oatmeal,  corn-flour,  sago,  tapioca,  arrowroot,  etc.  Saccha- 
rine vegetables,  turnips,  carrots,  parsnips,  green  peas,  French  beans,  beet-root, 
asparagus,  tomatoes.  Blanched  vegetables  of  every  sort,  as  celery,  sea-kale,  endive, 
radishes;   also  the  stalks  and  white  parts  of  such  vegetables  as  cabbage,  lettuce, 


980  CONSTITUTIONAL  DISEASES. 

broccoli,  etc.  Fruits  of  all  kinds.  Jams,  sirups,  sugars.  Certain  condiments, 
such  as  chutnee  and  sweet  pickles,  cocoa,  chocolate,  liqueurs,  sweet  wines. 

May  take  meat,  fish,  poultry,  game,  bacon,  ham,  eggs.  Bread  and  biscuits  made 
with  prepared  gluten,  bran,  or  almond-flour.  Green  vegetables,  summer  cabbage, 
turnip-tops,  spinach,  broccoli-tops,  water-cresses,  mustard  and  cress,  laver,  sauer- 
kraut, the  green  parts  of  lettuce,  sorrel,  mushrooms.  Nuts  of  various  kinds  (except 
chestnuts).     Cheese. 

Flint's  list  is  more  lenient,  allowing  oysters  and  a  much  larger  choice  of  vege- 
tables, such  as  asparagus,  string  beans,  artichokes,  cauliflower,  tomatoes,  etc. 
("Journal  of  the  American  Medical  Association,"  July  12,  1884;  also  "Pepper's 
System  of  Medicine,"  vol.  ii,  page  221). 

Donkin's  treatment  by  skim  milk  exclusively  is  highly  approved  by  Tyson. 

Rhenish  and  similar  wines,  moderate  quantities  of  spirits,  or  a  malt  liquor  in 
which  the  sugar  has  been  entirely  converted  into  carbonic  acid  and  alcohol  (Bass's 
ale,  for  instance),  are  permitted. 

In  the  opinion  of  the  writer,  it  is  always  well  to  begin  treatment  with  a  very 
stringent  dietary,  which  may  be  relaxed  gradually  as  circumstances  dictate.  The 
severity  of  the  case  is  to  be  regarded  rather  than  the  name  of  the  disease.  The 
gluten  and  other  diabetic  flours  are  unreliable;  and  I  agree  with  Flint  that,  if 
bread  be  allowed,  it  is  better  to  give  the  crust  of  a  French  roll  the  ingredients  of 
which  are  known.  Saccharine  may  be  vised  to  sweeten  tea  and  coffee,  jellies,  ice 
cream,  and  the  like.] 

Certain  other  general  directions  are  important.  The  patient  should  take  suffi- 
cient exercise.  Külz  has  determined  by  means  of  accurate  experiments  that,  other 
things  being  equal,  the  assimilation  of  sugar  is  increased  upon  increase  of  muscu- 
lar activity,  with  a  consequent  diminution  in  the  excretion  of  sugar.  Practical 
experience  also  shows  that  regular  exercise  is  extremely  beneficial.  A  proper  dis- 
cretion should  be  employed,  however;  nothing  would  be  more  injudicious  than  to 
force  a  feeble  patient  to  exhaustive  efforts.  But  if  the  patient  be  vigorous  and  well 
nourished,  he  should  be  strongly  urged  to  take  a  walking-trip  in  the  mountains, 
or  to  try  horseback  riding  and  the  like.  Methodical  massage  of  the  muscles 
sometimes  has  a  good  effect. 

Proper  care  of  the  skin  is  indispensable.  Baths,  cold  sponging,  and  douching 
may  be  employed.  Strict  attention  should  also  be  given  to  the  teeth,  lest  they  be- 
come carious.     Thorough  ventilation  should  be  maintained,  both  day  and  night. 

Of  internal  remedies,  opium  should  be  named  first.  One  good  effect  of  this  drug 
is  that  it  lessens  the  annoying  thirst.  It  sometimes  also  causes  decided  diminution 
in  the  amount  of  urine  and  sugar  excreted.  It  is  further  indicated  when  there  is 
general  restlessness  or  sleeplessness.  It  is  often  well  borne  by  diabetic  patients, 
even  in  large  doses.  A  patient  sometimes  can  take  four  to  eight  grains  (grm. 
0"25-0"5),  or  even  more,  of  opium  in  twenty -four  hours  without  any  bad  effects. 
It  is  noteworthy  that  the  alkaloids  of  opium,  such  as  morphine  and  codeia,  possess 
much  less  value  than  opium  itself. 

[If  sugar  does  not  disappear  from  the  urine  under  diet  alone,  or  if  a  strict  diet 
be  not  tolerated  for  any  reason,  opium  is  indicated.  The  drug  is  usually  well  tol- 
erated, and  can  be  given  in  divided  doses  or  in  one  dose  at  bedtime.  If  the  latter 
course  be  adopted,  one  grain  can  be  given  and  increased  until  the  sugar  either  dis- 
appears or  ceases  to  diminish  in  amount;  this  dose  varies  with  different  individ- 
uals, but  when  reached  it  can  be  maintained  without  increase  for  a  long  time. 

The  inhalation  of  oxygen  is  worthy  of  mention  as  a  remedial  measure. 

Purdy  seems  to  show  that  diabetes  attains  its  highest  mortality  in  those  States 
which  combine  relatively  high  altitude  with  low  temperature.  A  residence  in  the 
Gulf  States  or  Southern  California  may  therefore  be  curative  or  prolong  life.] 


DIABETES  MELLITUS.  'jSJ 

Belladonna,  cannabis  indica,  chloral,  and  bromide  of  potassium  arc  also  given, 
but  they  are  less  efficient  than  opium.  Bromide  of  potassium  would  probably  be 
the  best  of  these,  particularly  if  there  were  a  condition  of  nervous  excitement. 

The  alkalies,  and  still  more  the  alkaline  mineral  waters,  enjoy  a  reputation 
second  only  to  that  of  opium.  Hundreds  of  patients  visit  Carlsbad,  Neuenahr, 
and  Vichy  every  year  to  return  much  benefited.  Of  course  it  must  not  be  for- 
gotten tbat  it  is  not  merely  the  waters  which  produce  these  beneficial  changes. 
Other  factors  are  also  important,  in  particular  the  strict  diet,  fresh  air,  and  free- 
dom from  the  cares  of  the  household  and  business.  Why  the  alkalies  should  act 
favorably  we  do  not  know.  Griesingcr,  and  later  Kürz,  as  well  as  others,  have 
made  careful  comparisons  of  the  amounts  of  sugar  excreted  under  like  circum- 
stances, with  and  without  the  ingestion  of  bicarbonate  of  soda  or  of  Carlsbad 
water  and  similar  substances,  and  for  the  most  part  have  not  been  able  to  per- 
ceive any  benefit  from  these  remedies.  Practical  experience,  however,  shows  the 
value  of  these  alkaline  springs;  and  their  use  is  to  be  recommended,  although  the 
expectations  of  the  patient  should  not  be  wrought  to  too  high  a  pitch. 

From  a  theoretical  point  of  view,  there  is  interest  in  the  fact  that  certain  reme- 
dies which  are  antagonistic  to  fermentation  have  been  shown  by  Ebstein  and 
Müller  to  diminish  the  excretion  of  sugar  in  many  cases  of  diabetes.  Chief  among 
these  are  carbolic  acid  and  salicylate  of  sodium.  The  carbolic  acid  is  given  in  the 
amount  of  ten  to  twenty  grains  (grm.  0"5-l-5)  per  diem.  The  amount  of  salicyl- 
ate of  sodium  is  one  to  two  and  a  half  drachms  (grm.  5-10)  daily.  There  is  no 
doubt  that  these  drugs  possess  the  property  ascribed  to  them ;  but  they  are  not 
advantageous  to  the  patient,  inasmuch  as  the  general  condition  is  seldom  improved 
by  their  tise.     On  the  contrary,  very  unpleasant  effects  are  sometimes  observed. 

We  need  not  enumerate  all  the  remedies  which  have  been  recommended  in 
diabetes.  We  have  already  mentioned  those  that  possess  any  extended  reputation. 
We  may  therefore  merely  refer  to  certain  drugs  which  have  been  lately  introduced. 

Cantani  has  suggested  the  employment  of  lactic  acid  in  the  amount  of  one  to 
two  and  a  half  drachms  (grm.  5-10)  per  diem,  dissolved  in  half  a  pint  of  water. 
This  drug  may  perhaps  serve  as  a  physiological  substitute  for  sugar,  as  glycerine 
is  supposed  to  do  {vide  supra),  but  it  has  no  specific  virtues. 

Certain  salts  of  ammonia,  such  as  the  carbonate  and  acetate,  are  said  to  dimin- 
ish the  excretion  of  sugar,  and  have  therefore  long  been  employed  in  diabetes, 
but  without  special  benefit. 

Iodoform  has  been  recommended  by  Moleschott  to  the  amount  of  three  to  six 
grains  (grm.  0-2-0"4)  per  diem.  It  is  said  not  only  to  diminish  the  amount  of 
sugar  in  the  urine,  but  also  to  alleviate  other  symptoms.  Arsenic,  tincture  of 
iodine,  and  quinine  have  also  been  employed;  and  we  may  mention  that  even 
electricity  has  been  tried — we  need  hardly  say,  in  vain. 

It  is  evident,  in  brief,  that  the  best  mode  of  treating  diabetes,  at  least  according 
to  our  present  knowledge,  is  by  regulating  the  diet,  and  that  it  is  well,  in  addition, 
to  recommend  the  employment  for  a  time  of  the  above-mentioned  mineral  waters, 
with  opium  and  other  internal  remedies  to  combat  special  symptoms.  The  treat- 
ment of  such  complications  as  phthisis  or  cutaneous  eruptions  need  not  be 
described  here. 

In  diabetic  coma,  camphor  or  ether,  subcutaneously,  should  be  employed, 
together  with  lukewarm  baths  and  douching.  As  it  is  possible  that  the  coma 
may  be  due  to  poisoning  from  the  acids  in  the  blood  {vide  supra),  we  should  also 
try  bicarbonate  of  sodium  in  large  doses,  and  in  some  cases  use  intravenous  in- 
jections of  a  three  to  five  per  cent  solution,  or  give  it  subcutaneously;  but  the  effi- 
ciency of  such  treatment  remains  to  be  decided.  Experience  thus  far  is  not  very 
encouraging:  for  further  trials. 


982  CONSTITUTIONAL  DISEASES. 


CHAPTER  X. 
DIABETES   INSIPIDUS. 

Definition  and  ^Etiology. — In  the  preceding  chapter  a  distinction  was  drawn 
between  diabetes  mellitus  and  the  symptomatic  condition  termed  glycosuria. 
There  is  a  similar  distinction  to  be  made  between  diabetes  insipidus  and  polyuria. 
Polyuria  is  an  increase  in  the  volume  of  urine,  and  mainly  in  the  amount  of 
water  excreted  by  the  kidneys.  It  is  a  symptom  which  may  be  produced  in  many 
different  ways.  In  the  first  place,  it  is  a  natural  consequence  of  the  ingestion  of 
large  amounts  of  water,  or  of  the  absorption  of  serous  effusions ;  it  also  occurs  in 
certain  diseases  of  the  nervous  system,  especially  of  the  medulla  and  cerebellum; 
it  is  also  occasionally  seen,  as  we  have  had  opportunity  to  observe,  in  chronic 
hydrocephalus,  and  is  a  not  very  infrequent  phenomenon  in  hysteria.  Large 
amounts  of  urine  are  also  secreted  in  certain  renal  diseases  (interstitial  nephritis 
and  amyloid  degeneration),  and  often  during  convalescence  from  acute  diseases, 
such  as  typhoid  fever,  or  after  the  ingestion  of  certain  drugs,  called  diuretics. 

Diabetes  insipidus,  on  the  other  hand,  is  a  disease  which  may  develop  idio- 
pathically  in  people  otherwise  perfectly  healthy.  Its  aetiology  is  unknown. 
It  occasionally  seems  to  be  excited  by  emotional  disturbance,  concussion  or  other 
injury  of  the  brain,  or  some  previous  acute  disease,  such  as  typhoid  or  typhus 
fever,  malarial  poisoning,  and  cerebro-spinal  meningitis.  The  disease  sometimes 
appears  in  the  syphilitic,  and  may,  therefore,  in  many  instances,  be  due  to  syphilis. 
Patients  frequently  state  that  their  symptoms  began  immediately  after  drinking 
a  very  large  amount  of  some  fluid,  as  on  a  very  hot  day  or  after  a  long  march. 
In  such  cases  the  assumption  is  a  probable  one  that  the  primary  symptom  is  not 
polyuria,  but  an  abnormally  great  thirst  (polydipsia),  the  increase  in  urinary 
secretion  being  a  result  of  the  large  amount  of  water  ingested.  Finally,  the  dis- 
ease may. be  hereditary  (vide  infra).  The  true  nature  of  diabetes  insipidus  is 
entirely  unknown  to  us. 

The  view  which  seems  most  probable  of  any  is,  that  some  nervous  disturbance 
is  its  direct  cause.  In  support  of  this,  we  have  the  appearance  of  a  "  symptomatic 
diabetes  insipidus"  in  connection  with  organic  disease  of  the  brain  (vide  supra), 
and  the  fact  that  polyuria  may  be  artificially  excited  by  injury  to  a  definite  spot 
in  the  floor  of  the  fourth  ventricle  or  by  section  of  the  vagus  nerve.  Diabetes 
insipidus  presents  a  most  striking  analogy  with  diabetes  mellitus.  This  is  shown 
both  by  the  similarity  in  aetiology  and  symptomatology,  and  still  more  by  the  fact 
that  occasionally  one  disease  merges  into  the  other. 

Diabetes  insipidus  is  a  disease  of  very  infrequent  occurrence,  and,  at  least  in 
Germany,  is  decidedly  less  often  seen  than  diabetes  mellitus.  Most  patients  are  in 
young  adult  or  middle  life.  Males  are  somewhat  more  liable  to  the  disease  than 
females. 

Clinical  History. — Diabetes  insipidus  may  be  developed  gradually  or  with  con- 
siderable abruptness ;  the  latter  case  is  especially  frequent  when  there  is  some  defi- 
nite cause,  such  as  the  ingestion  of  a  large  amount  of  liquid,  or  traumatism. 

The  essential  and  characteristic  symptom  is  an  increase  in  the  volume  of  urine. 
This  is  usually  very  considerable.  Often  eight  or  ten  quarts  (8000  to  10,000  c.  c.) 
are  excreted  in  twenty-four  hours,  and  cases  have  even  been  reported  where  the 
amount  reached  the  almost  incredible  volume  of  thirty  to  forty  quarts  (litres).  If 
a  healthy  person  and  a  sufferer  from  diabetes  insipidus  are  each  given  the  same 


DIABETES  INSIPIDUS.  983 

amount  of  water  in  food  and  drink,  the  sick  man  will  excrete  more  urine  than  the 
healthy.  In  color  the  urine  is  very  pale,  and  sometimes  almost  like  water.  The 
specific  gravity  is  very  low,  being  usually  1004  to  1002,  or  even  1001.  The  reaction 
is  slightly  acid,  sometimes  almost  neutral. 

The  percentage  of  solid  constituents  in  the  urine  is,  of  course,  trifling.  The 
total  amount  of  solids,  however,  corresponds  perfectly  with  the  ingesta,  or  indeed 
is  even  somewhat  above  normal.  The  amount  of  urea  in  particular  seems  to  be 
increased,  but  it  has  also  been  stated  that  other  constituents  of  the  urine  have  been 
excreted  in  abnormally  large  amounts — namely,  phosphoric  acid,  sulphuric  acid, 
lime,  and  kreatinine.  Inosite  has  been  found  in  the  urine  by  Strauss  and  other 
observers,  so  that  it  has  even  been  proposed  to  give  diabetes  insipidus  the  name  of 
"  diabetes  inositus,"  in  distinction  from  diabetes  mellitus.  Inosite  is  not  invariably 
present,  however,  in  the  urine  of  diabetes  insipidus.  In  cases  of  true  diabetes 
insipidus,  albuminuria  is  extremely  exceptional. 

Another  important  symptom  is  the  excessive  thirst.  To  make  up  for  the  great 
loss  of  water  by  way  of  the  kidneys  the  patient  is  obliged  to  drink  great  quantities 
of  liquid,  and.  indeed,  it  is  always  found  that  the  amount  of  water  ingested,  in  the 
way  of  drink  and  solid  food,  somewhat  exceeds  the  total  volume  of  urine  excreted. 
Despite  this,  the  tongue  is  usually  dry,  as  is  also  the  skin,  the  insensible  perspira- 
tion being  considerably  below  the  normal  amount.  The  f urunculosis  seen  in  dia- 
betes mellitus  is  exceptional  in  diabetes  insipidus.  The  same  is  true  of  pruritus  and 
balanitis.     Occasionally  profuse  salivation  has  been  associated  with  the  disease. 

Symptoms  referable  to  the  various  internal  organs  are  few.  Cataract  has  been 
occasionally  observed,  but  it  is  much  less  frequent  than  in  diabetes  mellitus.  The 
same  may  be  said  of  pulmonary  tuberculosis.  In  most  cases  the  appetite  is  not 
excessive.  The  bowels  are  regular  or  slightly  constipated.  There  is  seldom  much 
gastro-intestinal  disturbance,  unless  from  some  chance  complication.  The  sexual 
functions  are  usually  unimpaired. 

The  general  health  is  considerably  affected  in  cases  of  any  severity.  The 
patient  becomes  emaciated,  languid,  and  feeble,  and  has  no  inclination  to  mental 
or  physical  exertion.  Sleep  is  often  disturbed,  the  mind  depressed.  The  tempera- 
ture is  normal,  or  even  a  trifle  below  normal,  probably  as  a  result  of  the  large 
amount  of  cold  water  drunk. 

Diabetes  insipidus  is  a  very  chronic  disease.  If  there  is  no  serious  complication 
it  may  last  for  decades,  yet  there  are  cases  that  run  a  more  rapid  and  unfavorable 
course.  Sometimes  there  are  considerable  vicissitudes  in  the  condition  of  the 
patient,  in  part  dependent  upon  external  circumstances  and  in  part  apparently 
spontaneous.  In  case  some  intercurrent  acute  disease  develops  there  may  be, 
during  its  continuance,  a  considerable  diminution  in  the  amount  of  urine  excreted. 

The  termination  is  usually  unfavorable.  Recovery  is  extremely  rare.  In  the 
more  fortunate  cases  the  condition  finally  becomes  stationary,  and  the  patient 
attains  to  advanced  years.  Sometimes,  however,  death  occurs  more  prematurely, 
being  usually  hastened  by  phthisis  or  some  similar  complication. 

Weil  has  lately  contributed  to  our  knowledge  of  this  disease  the  results  of  an 
accurate  study  of  its  hereditary  and  apparently  congenital  variety.  Weil  narrates 
the  history  of  a  family  in  which  marked  polyuria  and  corresponding  polydipsia 
appeared  in  numerous  members  for  several  generations.  These  persons  all  enjoyed 
excellent  health,  with  this  exception ;  and  most  of  them  attained  old  age.  We 
hardly  need  to  emphasize  the  fact  that  this  form  of  the  disease  is  radically  differ- 
ent from  the  ordinary  acquired  variety.  Perhaps  its  true  cause  is  an  abnormal 
congenital  permeability  of  the  glomeruli,  but  we  have  no  certain  information  in 
regard  to  it. 

Post-mortem  Appearances.— Such  lesions  as  have  been  found  in  diabetes  insipi- 


984  CONSTITUTIONAL  DISEASES. 

dus  are  usually  the  result  of  fortuitous  complications,  such  as  tuberculosis,  carci- 
noma, and  pneumonia.  There  are  but  very  few  changes  referable  directly  to  the 
disease  itself:  among  these  are  enlargement  of  the  kidneys  and  dilatation  of  the 
ureters.  In  rare  instances  a  possible  cause  for  the  symptoms  has  been  found  in 
some  lesion  of  the  central  nervous  system,  but  these  were  properly  cases  of  symp- 
tomatic polyuria  and  not  of  genuine  diabetes  insipidus.  Instances  of  this  sort  are 
seen  in  connection  with  tumors  or  inflammatory  changes  in  the  medulla  or  cere- 
bellum, and  exostoses  at  the  base  of  the  skull. 

Diagnosis. — The  characteristic  urinary  phenomena  usually  render  the  diagnosis 
of  diabetes  insipidus  an  easy  matter.  It  is  of  course  necessary  to  exclude  such  dis- 
eases as  might  occasion  symptomatic  polyuria  {vide  supra)  ;  but  this  is  seldom 
difficult  if  we  make  a  careful  physical  examination  and  carefully  consider  all  the 
attendant  symptoms.  The  differential  diagnosis  between  diabetes  insipidus  and 
diabetes  mellitus  can  almost  invariably  be  made  by  means  of  the  urinometer.  If 
the  specific  gravity  is  below  normal,  it  is  scarcely  necessary  to  test  for  sugar. 

Treatment. — No  special  injunctions  with  regard  to  diet  are  required.  It  would 
of  course  be  a  mistake  to  forbid  the  patient  to  assuage  his  excessive  thirst ;  but  we 
may  possibly  lessen  the  amount  of  water  drunk  by  prescribing  bits  of  ice,  or 
lemonade  and  other  acid  drinks.  Opium  sometimes  lessens  both  the  thirst  and  the 
amount  of  urine  excreted.  It  is  also  important  that  the  skin  should  be  well  cared 
for  by  means  of  baths  and  friction,  and  every  effort  should  be  made  to  promote 
the  general  vigor  of  the  patent.     He  should  have  nourishing  food  and  good  air. 

Numerous  internal  remedies  have  been  recommended  as  specific,  but  few  of 
these  have  won  any  great  reputation.  Valerian  appears,  on  the  whole,  to  be  the 
most  efficient  drug,  and  may  be  given  in  powder  or  infusion  to  the  amount  of 
one  to  two  and  a  half  drachms  (grm.  5-10)  per  diem.  Ergotine  may  also  be  tried. 
Carbolic  acid,  salicylate  of  sodium,  and  nitric  acid  have  been  said  to  prove  benefi- 
cial. It  is  also  said  that  galvanization  of  the  medulla  and  upper  part  of  the  spinal 
cord  sometimes  accomplishes  good  results. 

Occasionally  we  may  find  an  apparent  cause  for  the  disease  and  endeavor  to 
remove  it.  If  there  is  a  suspicion  of  syphilis,  mercurial  inunctions  should  be 
tried.  Sometimes,  as  we  can  confirm  by  our  own  experience,  they  have  an  ex- 
cellent effect.  Of  course,  where  there  is  symptomatic  polyuria,  the  primary  dis- 
ease, such  as  hysteria,  demands  treatment. 

[Da  Costa  and  others  report  very  good  results  as  following  the  administration 
of  ergot.] 


CHAPTER  XI. 
GOUT. 

{Podagra.) 

iEtiology. — Thomas  Sydenham  was  the  first  to  write  a  careful  clinical  descrip- 
tion of  gout.  He  himself  suffered  from  the  disease  for  about  forty  years,  and  has 
given  a  detailed  description  of  his  own  case  in  the  treatise  which  he  published  in 
1683,  under  the  title  ''Tractatus  de  podagra  et  hydrope."  It  was,  bowever,  Wol- 
laston  who,  in  1797,  threw  the  first  light  upon  the  peculiar  anomaly  of  tissue-meta- 
morphosis which  exists  in  this  disease.  He  demonstrated  that  the  gouty  deposits 
found  in  the  joints  and  other  parts  of  tbe  body  are  mainly  uric  acid.  From  his 
time  an  all-important  point  with  regard  to  the  nature  of  the  disease  has  been  the 
relation  between  the  symptoms  of  gout  and  disturbances  in  the  manufacture  and 
excretion  of  uric  acid.  In  1848  G-arrod  showed  that  in  gout  the  blood  contains  an 
excess  of  uric  acid,  and  that  the  excretion  of  uric  acid  by  the  kidneys  is  dimin- 


GOUT.  985 

ished.  He  was  thus  in  a  position  to  frame  a  theory  consistent  with  all  the  clinical 
facts.  Numerous  investigations  have  heen  undertaken  since  his  day:  but  we  still 
remain  with  regard  to  gout  in  a  position  analogous  to  that  which  we  bold  toward 
diabetes.  We  are,  it  is  true,  in  the  possession  of  a  considerable  number  of  well- 
established  facts  relating  to  it,  but  we  do  not  know  why  the  normal  chemical  pro- 
cesses are  disturbed,  and  are  unable  to  explain  the  connection  between  the  yarioui 
phenomena  observed. 

Clinical  experience  has  taught  us  certain  remote  causes  of  gout,  first  of  which 
comes  heredity.  About  fifty  per  cent,  of  all  cases  occur  in  patients  whose  families 
have  already  suffered  from  the  disease,  and  it  is  sometimes  possible  to  trace  this 
transmitted  taint  through  many  generations.  It  is  decidedly  more  apt  to  pass 
down  through  the  male  members  of  the  family  than  through  the  female. 

Next  in  importance  to  hereditary  influences  is  the  mode  of  life.  From  time 
immemorial  this  has  been  regarded  as  an  exciting  cause  of  the  disease.  It  has 
been  a  matter  of  universal  belief  that  over-feeding,  and  especially  the  ingestion  of 
too  large  a  quantity  of  albuminoids,  is  strongly  provocative  of  the  disease.  The 
same  'opinion  has  been  held  with  regard  to  persistent  over-indulgence  in  alco- 
holic beverages.  Seneca  relates  that  at  the  time  of  the  decay  of  the  Roman 
Empire  women  practiced  such  excesses  that  they  were  as  subject  to  gout  as  the 
men,  and  an  old  verse  runs :  "  Wine  is  the  father  of  gout,  feasting  is  its  mother, 
and  Venus  is  the  midwife."  This  view  is,  however,  an  exaggerated  one.  It  can 
not  he  denied  that  there  is  some  truth  in  it,  but,  on  the  other  hand,  gout  is  not 
exclusively  an  "  arthritis  of  the  rich."  It  occurs  also  among  the  poor,  who  have 
had  only  too  little  acquaintance  with  the  pleasures  of  the  table ;  and  many  a  bon 
vivant  has  reached  old  age  without  ever  experiencing  pain  in  his  great  toe. 

[Gout  is  a  disease  so  much  more  common  in  England  than  in  Germany  or  this 
country  that  English  opinions  in  regard  to  it  are  deserving  of  especial  weight. 
The  most  commonly  accepted,  though  by  no  means  the  only,  view  as  to  its  nature 
is  that  it  depends  on  defective  oxidation,  which  may  be  brought  about  in  two 
ways:  either  by  the  ingestion  of  more  food  than  can  be  properly  oxidized,  or  by 
the  presence  of  such  conditions  that  even  a  moderate  supply  of  food  can  not  be 
worked  up  and  undergo  its  proper  transformations.  This  theory  will  account  for- 
gout  in  the  poor  as  well  as  in  the  rich. 

There  can  be  no  question  that  the  use  of  malt  liquors,  especially  in  the  stronger 
forms,  consumed  so  enormously  in  England,  is  much  more  favorable  to  the  devel- 
opment of  gout  than  is  the  use  of  distilled  spirits ;  so  also  the  stronger  wines — 
such  as  port,  sherry,  Madeira,  and  the  heavy  Burgundies — are  more  dangerous 
than  are  the  lighter  and  more  acid  wines  of  France  and  Germany.  In  this 
country  gout  is  becoming  more  common,  a  fact  which  may  be  fairly  explained  by 
the  accumulation  of  wealth  and  the  consequent  growth  of  luxury.] 

There  is  a  noteworthy,  although  mystei'ious,  connection  between  gout  and 
chronic  lead-poisoning.  The  fact  is  well  established  that  persons  who  have  to  do 
with  lead,  such  as  type-setters  and  house-painters,  are  subject  to  genuine  gout 
with  deposits  of  uric  acid  in  the  joints. 

With  regard  to  still  other  alleged  setiological  factors,  confirmatory  evidence  is 
lacking.  Possibly,  however,  when  the  foundation  for  the  disease  is  already  laid, 
an  attack  may  be  excited  by  certain  determining  causes — namely,  trauma,  taking 
cold,  errors  in  diet,  and  mental  emotion. 

The  geographical  distribution  of  gout  is  remarkably  unequal.  The  disease  is 
much  more  frequent  in  England  than  in  Germany,  although  in  the  latter  country 
certain  regions  appear  to  be  more  affected  by  it  than  others.  In  Leipsic,  in 
Saxony  generally,  and  in  Bavaria,  gout  is  decidedly  rare. 

Gout  is  rarely  seen  in  young  persons.     It  is  a  disease  of  advanced  life,  rarely 


986  CONSTITUTIONAL  DISEASES. 

appearing  previously  to  the  fortieth  year.     Men  are  much  more  often  attacked 
than  are  women. 

Clinical  History. — Gout  may  produce  symptoms  in  many  different  organs ;  hut 
its  effect  upon  the  joints  is  so  characteristic  that  the  arthritic  disturbance  has  long 
been  termed  "  normal  or  regular  gout,"  in  contradistinction  from  "  atypical, 
internal  gout."  This  distinction  is  of  course  an  artificial  one,  for  the  various  phe 
nomena  of  gout  present  the  most  manifold  gradations  and  transitions.  It  will, 
however,  be  advantageous,  in  attempting  to  gain  a  practical  insight  into  the  vari- 
ous symptoms  of  the  disease,  if  we  first  discuss  the  so-called  "  typical  attack  of 
gout,"  subsequently  appending  a  description  of  the  other  manifestations  of  the  dis- 
ease. Furthermore,  the  regular  attack  of  gout  is,  in  at  least  a  majority  of  cases 
{vide  infra),  the  first  and  earliest  symptom  of  the  disease. 

1.  The  typical  attack  of  gout  is  seldom  abrupt.  It  is  usually  preceded  for  a 
longer  or  shorter  period  by  certain  premonitory  symptoms,  the  meaning  of 
which,  though  not  evident  to  one  who  is  about  to  suffer  from  his  first  attack,  is 
sufficiently  clear  to  more  experienced  patients,  particularly  as  each  individual 
case  is  apt  to  present  a  marked  similarity  in  the  prodromata  of  the  separate 
paroxysms.  These  premonitory  symptoms  vary  in  different  individuals.  Some- 
times they  consist  in  dyspeptic  disturbances  ;  sometimes  in  a  feeling  of  languor 
and  mental  depression  ;  very  often  in  dragging,  muscular  pains  or  cramps  in  the 
calves  of  the  legs ;  or  again  in  slight  feverishness,  with  chilliness,  sense  of  heat, 
and  perspiration.  On  the  other  hand,  it  must  be  confessed  that  a  patient  may 
feel  unusually  well  just  before  an  attack. 

The  attack  is  noticeably  apt  to  begin  in  the  night-time,  or  very  early  in  the 
morning.  The  patient  is  awakened  by  a  sudden  and  very  violent  pain  in  the 
metatarso-phalangeal  joint  of  one  of  the  great  toes  ("podagra").  The  joint 
becomes  swollen,  the  skin  over  it  red,  hot,  and  tense,  the  veins  in  the  neighbor- 
hood distended.  At  the  same  time  there  is  chilliness  and  moderate  fever.  This 
condition  persists  till  morning.  Then  the  pain  is  almost  sure  to  abate,  the  fever 
to  remit  at  the  same  time  that  sweating  begins,  and  the  patient  to  feel  tolerably 
well  during  the  day.  The  joint,  however,  remains  swollen,  with  inflammation 
and  oedema.  The  next  night  the  pain  begins  again,  and  there  is  a  fresh  fever  ; 
and  these  alternations  are  repeated,  as  a  rule,  for  three  to  ten  days.  Even  where 
the  attack  is  more  persistent  than  this,  the  pain  is  usually  much  less  severe  after 
the  first  two  or  three  nights.  After  that  time  it  gradually  abates  ;  and  it  is  com- 
monly said  that  an  attack  is  brief  in  proportion  to  the  violence  of  its  first  symp- 
toms. When  the  pain  ceases,  swelling  soon  disappears,  the  skin  undergoes  a 
slight  desquamation  and  resumes  its  normal  appearance,  the  general  health  of 
the  patient  rapidly  improves,  and  he  is  often  found  to  be  much  better  after  an 
attack  than  he  was  before. 

For  theoretical  purposes  (vide  infra)  it  would  be  very  advantageous  to  possess 
a  more  accurate  knowledge  of  the  condition  of  the  urine,  and  in  particular  of  the 
excretion  of  uric  acid  during  the  attack.  As  yet,  however,  there  have  been  few  care- 
ful investigations  made.  Garrod  has  made  a  very  important  observation,  which 
has  been  confirmed  by  Cantani :  it  is,  that  the  amount  of  uric  acid  excreted  dimin- 
ishes several  days  before  the  commencement  of  an  attack,  and  remains  diminished 
during  the  attack.  Subsequently  to  the  attack  the  excretion  of  uric  acid  is  said  to 
be  above  normal,  while  the  amount  of  uric  acid  in  the  blood  varies  in  precisely 
the  opposite  way — that  is,  during  the  attack  it  is  increased,  and  after,  it  is  dimin- 
ished. It  has  not  yet  been  determined  how  far  this  variation  in  the  excretion  of 
uric  acid  may  be  referable  to  the  altered  diet  of  the  patient,  and  how  far  to  a 
diminished  formation  of  uric  acid  or  a  deposition  of  that  substance  in  the  diseased 
joints  (vide  infra). 


GOUT.  UH7 

If  there  has  been  one  attack  of  gout,  there  are  almost  sure  to  be  others.  They 
come  sooner  or  later,  at  regular  or  irregular  intervals,  and  separated  by  weeks, 
months,  or  even  years.  The  attacks  recur  at  long  intervals  in  mild  cases,  more 
frequently  and  at  gradually  diminishing  intervals  in  the  severe.  Spring  and 
autumn  are  regarded  as  the  time  when  attacks  of  gout  are  most  apt  to  occur.  In 
these  subsequent  attacks  the  great  toe  still  remains  the  part  most  constantly  and 
severely  affected  ;  but  other  joints  may  also  suffer -for  example,  the  wrist,  the 
knee,  or  the  shoulder.  Sometimes  traumatism  or  some  previous  affection  of  the 
joints — such  as  rheumatism — apparently  determines  the  localization  of  the  gouty 
disturbance.  In  each  attack,  the  trouble  is  usually  confined  to  a  single  joint.  It 
is  only  in  exceptional  or  advanced  cases  that  several  joints  are  simultaneously 
invaded. 

The  longer  the  disease  has  lasted,  the  less  typical  are  the  separate  attacks. 
There  may  now  be  less  suffering  at  the  time  of  an  attack  ;  but  the  articular 
changes  are  more  persistent.  There  are  symptoms  referable  to  other  parts  of  the 
body  ;  and  the  gout  gradually  passes  into  its  second  chronic  or  "  atonic  "  stage. 
Occasionally  the  disease  is  irregular  and  atypical  from  its  incipiency  ;  and  the 
first  manifestations  may  not  be  arthritic,  but  referable  to  the  kidneys  (vide  infra) 
or  other  organs. 

2.  Atypical  Gout.  Gouty  Disturbance  of  other  Parts  than  the  Joints. — Gout 
may  affect  the  mucous  membranes.  A  gouty  dyspepsia  is  very  frequent.  Its 
symptoms  are  more  or  less  severe.  The  gouty  are  also  subject  to  intestinal 
catarrh  of  varying  severity,  and  to  bronchitis  and  conjunctivitis,  as  well  as  to 
catarrh  of  the  urinary  organs.  Ebstein  regards  "  gouty  gonorrhoea "  as  essen- 
tially a  catarrh  of  the  excretory  ducts  of  the  prostate  gland.  It  is  not  an  easy 
matter  to  explain  why  these  various  forms  of  catarrh  should  occur  in  gout.  They 
may  be,  some  of  them,  complications.  In  other  cases  they  are  doubtless  the 
result  of  passive  congestion,  due  to  cardiac  failure  (vide  infra) ;  but  in  still  other 
instances  it  must  be  confessed  that  they  are  apparently  due  to  the  toxic  influence 
of  the  accumulated  uric  acid. 

[My  experience,  though  far  more  limited  than  that  of  Draper,  nevertheless 
leads  me  to  believe,  as  he  does,  that  the  irregular  forms  of  gout  are  by  no  means 
uncommon  in  women  as  an  inheritance  from  a  previous  generation.  The  mani- 
festations in  some  of  these  cases  are  so  ill-defined  that  a  diagnosis  may  be  difficiüt 
without  a  knowledge  of  the  family  history  ;  in  other  cases,  more  or  less  deformity 
of  the  smaller  joints,  or  slight  recurrent  swellings  of  those  parts,  throw  much 
light  on  the  condition  underlying  the  symptoms.] 

Inflammation  of  serous  membranes — for  example,  of  the  pleura— also  occurs  ; 
and  there  may  be  pneumonia.  The  skin  not  infrequently  suffers  from  acute  or 
chronic  eczema,  which  sometimes  appears  to  be  referable  directly  to  the  gout. 
Keratitis,  iritis,  and  other  inflammatory  disturbances  of  the  eye  are  also  said  to  be 
caused  directly  by  gout.  Cirrhosis  of  the  liver  has  been  repeatedly  found,  and  is 
perhaps  referable  to  the  action  of  the  uric  acid  upon  the  hepatic  parenchyma. 
By  far  the  most  important  of  all  these  gouty  manifestations  are  referable  to 
the  kidneys  and  to  the  circulatory  system.  The  disorder  of  the  latter  is  some- 
times symptomatic  of  the  renal  trouble,  but  in  other  instances  it  occurs  inde- 
pendently of  it.  There  may  be  severe  gouty  arthritis  for  years  without  any  lesion 
of  the  kidneys  ;  but  this  is  exceptional.  In  severe  cases  of  gout  it  is  the  rule  that, 
sooner  or  later,  symptoms  of  renal  disorder  present  themselves.  The  so-called 
"  gouty  kidney  "  is  a  form  of  chronic  interstitial  nephritis.  However  important 
this  complication,  its  symptoms  do  not  need  to  be  discussed  here,  as  they  are  pre- 
cisely similar  to  those  seen  in  ordinary  cases  of  contracted  kidney  (vide  page  S56, 
et  seq.).     The  distinctive  symptom  of  this  disturbance  is  albuminuria  ;  and  the 


988  CONSTITUTIONAL  DISEASES. 

gradually  developing  secondary  hypertrophy  of  the  left  ventricle  is  the  pivot  on 
which  turns  the  whole  future  course  of  the  disease.  So  long  as  the  heart  remains 
capable  of  performing  its  functions,  the  condition  of  the  patient  will  probably 
remain  endurable  if  not  actually  comfortable.  Finally,  however,  compensation 
is  sure  to  become  impaired  ;  and  then  appear  oedema,  dyspnoea,  debility,  and 
emaciation — in  short,  all  the  familiar  symptoms  of  cardiac  failure.  A  speedy 
end  may  be  brought  about  by  uraemia,  or  cerebral  embolism,  or  haemorrhage  ; 
but  in  other  cases  the  patient  suffers  for  years,  both  from  the  heart  disease  and 
from  fresh  arthritic  attacks. 

The  cardiac  hypertrophy  just  mentioned  is  the  result  of  the  contracted  kidney. 
Other  disturbances  of  the  circulatory  system  appear  to  be  referable  directly  to  the 
gout  itself.  Among  these  are  chronic  endocarditis  or  myocarditis,  and  perhaps 
certain  "  functional "  symptoms,  such  as  palpitation  and  angina.  An  important 
symptom  is  chronic  endarteritis  or  arterio-sclerosis.  This  is  of  ten  seen  in  gouty 
subjects,  and  in  many  instances  seems  to  be  immediately  connected  with  the  gout. 
Sometimes,  also,  there  are  gouty  lesions  of  the  veins,  such  as  varicosities  or  throm- 
bosis. Of  course,  these  changes  in  the  blood-vessels  may,  in  their  turn,  give  rise 
to  various  disorders. 

In  a  few  very  rare  instances  gout  seems  to  attack  the  brain  and  spinal  cord. 
Usually,  however,  the  nervous  disturbances  seen  in  gout  are,  as  already  stated, 
symptoms  of  uraemia,  or  of  circulatory  disturbance,  and  the  like.  The  patient 
may  also  have  certain  functional  nervous  troubles,  like  neuralgia  or  migraine. 
The  direct  cause  of  these  is  seldom  evident. 

The  joints,  despite  frequent  attacks,  may  yet  maintain  an  almost  normal  appear- 
ance, inasmuch  as  the  acute  inflammatory  changes  completely  vanish  after  each 
separate  attack.  They  may,  however,  undergo  permanent  enlargement  and  de- 
formity from  gouty  concretions  {tophi  arthritici).  In  many  instances  similar 
masses  can  be  felt  here  and  there  in  the  muscles  and  tendons,  the  skin  (for 
instance,  of  the  eyelids),  and  quite  often  in  the  external  ear.  They  consist  essen- 
tially of  accumulations  of  urates  (vide  infra).  Occasionally  these  concretions 
break  externally,  discharging  a  thick  pus  mingled  with  urates,  and  forming  indo- 
lent ulcers,  slow  to  heal.  Sometimes  atmospheric  germs  thus  find  ingress  into 
the  system,  and  give  rise  to  phlegmon. 

It  should  be  stated,  in  conclusion,  that  gout  may  be  complicated  with  other  dis- 
eases. Thus,  it  may  be  associated  with  renal  calculi,  and  sometimes  with  diabetes 
mellitus  (vide  supra). 

Anatomical  and  Chemical  Changes  in  Gout.  Theory  of  its  Nature.— The  essen- 
tial anatomical  lesion  in  gout  consists  of  an  abundant  deposit  of  crystalline  urates 
in  the  tissues.  This  is  most  evident  in  the  affected  joints,  the  cartilaginous  sur- 
faces of  which  are  often  completely  covered  with  white,  chalk-like  material.  In 
severe  cases  the  same  appearance  may  also  be  presented  by  the  articular  ligaments, 
tendons,  and  bursae,  while  there  are  at  the  same  time  numerous  concretions  of 
urates  here  and  there  beneath  the  skin.  These  deposits  are  mainly  composed  of 
acid  sodic  urate,  with  traces  of  calcic  urate,  calcic  phosphate,  and  sodic  chloride. 
Ebstein  has  lately  explained  how  these  collections  are  formed.  He  found  that  the 
deposition  of  uric  acid  is  invariably  preceded  by  a  necrosis  of  the  tissues.  The 
uric  acid  while  still  in  solution  acts  as  a  chemical  irritant  upon  the  cartilage  here 
and  there,  and  thus  produces  necrosis,  whereupon  the  urates  are  crystallized  out 
and  deposited.  Then  a  secondary  inflammation  develops  around  these  foci  of 
necrosis.  By  ligaturing  the  ureters  in  fowls,  Ebstein  succeeded  in  artificially  pro- 
ducing similar  changes. 

The  nephritis  of  gout  corresponds  in  its  pathological  appearances  to  that  of  the 
true  contracted  kidney,  with  one  exception ;  the  organs  usually  present  deposits  of 


GOUT.  989 

uric  acid  or  urates,  in  stripes,  both  in  the  lumen  of  the  urinary  tubules  and  ;ilso 
in  the  epithelial  cells  and  the  interstitial  tissue.  In  the  connective  tissue  it  is 
probable  that  a  necrosis  precedes  the  deposit. 

The  lesions  presented  by  the  heart,  blood-vessels,  and  remaining  parts  of  the 
body  are  not  especially  characteristic  of  the  disease.  The  blood  of  gouty  subjects, 
as  Garrod  demonstrated,  contains  an  excess  of  uric  acid. 

There  are  many  theoretical  questions  which  remain  unanswered:  Wb ether  in 
this  disease  there  is  an  over-production,  or  merely  a  defective  excretion  of  uric 
acid  ?  What  the  true  cause  of  this  strange  anomaly  in  metamorphosis  may  be  ? 
What  conditions  are  essential  to  the  crystallizing  out  of  uric  acid  in  the  tissues  ? 
Why  certain  parts,  particularly  the  joints,  and  still  more  particularly  the  first  joint 
of  the  great  toe,  are  especially  liable  to  suffer  ?  And,  finally,  What  circumstances 
decide  the  course  of  the  disease,  and  determine  its  separate  attacks  ?  Not  one  of 
these  questions  has  been  satisfactorily  answered.  The  fact  that  gout  is  prone  to 
attack  individuals  who  have  led  a  luxurious  life  has  led  to  the  belief  that  in  every 
case  of  gout  the  ingesta  are  not  completely  oxidized,  and  an  excess  of  uric  acid  is 
conseqiiently  accumulated  in  the  system.  We  have  already  pointed  out  that  this 
assumption  is  too  sweeping.  And,  indeed,  our  present  knowledge  with  regard  to 
the  manufacture  of  uric  acid  out  of  the  albuminoids,  and  its  further  transforma- 
tions, is  not  at  all  adequate  for  the  establishment  of  any  hypothesis  of  this  sort. 
We  must  simply  confess  that  the  true  cause  of  the  accumulation  of  uric  acid  in 
the  tissues  is  unknown.  It  may  be  conjectured,  however,  that  the  deposit  of  crys- 
tals of  uric  acid  is  either  occasioned  or  promoted  by  an  excessively  acid  reaction 
of  the  blood  or  lymph  in  which  that  acid  is  dissolved.  It  is  not  known  what  acids 
give  rise  to  this  reaction,  nor  how  they  are  formed.  It  has  been  seen  that  the 
articular  cartilages  are  especially  apt  to  present  a  gouty  deposit.  Perhaps  this  is 
occasioned  by  the  sluggishness  of  the  circulation  in  these  parts.  It  is  doubtful 
whether  the  uric  acid  is  produced  in  the  cartilage  itself.  Ebstein  believes  that  it 
originates  mainly  in  the  muscles  and  bone-marrow,  and  is  thence  conveyed  to  the 
cartilage.  Others,  and  among  them  Cantani,  believe  that  the  m*ic  acid  is  formed 
in  the  cartilage  and  the  connective  tissue. 

Diagnosis. — It  is  usually  easy  to  recognize  an  acute  attack  of  gout.  The  sudden 
onset  of  the  pain  at  night  and  its  localization  in  one  of  the  great  toes  are  very 
characteristic  symptoms,  and  render  it  easy  to  distinguish  between  it  and  other 
acute  affections  of  the  joints.  The  diagnosis  is  more  difficult  in  the  advanced 
stages,  where  symptoms  are  more  confused.  Here  the  history  of  the  case  will 
often  include  the  description  of  typical  attacks  and  also  etiological  factors,  such 
as  heredity  and  mode  of  life,  which  may  assist  in  diagnosis.  It  must  be  said  that 
many  gouty  subjects  are  reticent  as  to  their  past  experiences,  and  sometimes  even 
deny  previous  attacks  of  gout.  If  there  is  a  chronic  gouty  arthritis,  it  may  be 
necessary  to  make  a  differential  diagnosis  between  it  and  arthritis  deformans. 
The  deformities  of  arthritis  deformans  are  usually  seen  first  of  all  in  the  hands 
and  fingers,  and  it  has  a  persistent,  chronic  course.  Furthermore,  in  gout  we 
sometimes  can  feel  the  characteristic  deposits  in  the  tendons  or  skin  (for  instance, 
in  the  eyelids  or  external  ear). 

If  there  is  chronic  nephritis  of  gouty  origin,  its  source  can  be  recognized  only 
from  its  association  with  other  indubitable  symptoms  of  gout,  unless  possibly  the 
knowledge  of  certain  etiological  factors,  such  as  a  history  of  gout  in  the  family 
or  of  chronic  lead-poisoning,  should  put  us  upon  the  right  track.  Ebstein  has 
reported  cases  of  "  primary  renal  gout "  where  there  was  no  arthritis  during  the 
whole  course  of  the  disease.  Such  cases  can  seldom  be  correctly  diagnosticated 
during  life. 

Brief  mention  should  here  be  made  of  an  experiment  performed  by  Garrod, 


990  CONSTITUTIONAL  DISEASES. 

which  may  be  employed  to  demonstrate  the  existence  of  uric  acid  in  the  blood,  for 
diagnostic  purposes.  A  drachm  or  two  of  blood-serum,  or  of  the  serum  obtained 
from  a  fly-blister,  is  put  into  a  shallow  watch-glass,  and  six  or  eight  drops  of  a 
thirty-per-cent.  solution  of  acetic  acid  are  added  to  it.  A  linen  thread  is  then  laid 
in  the  fluid,  and  the  whole  allowed  to  remain  at  a  moderate  temperature  for  about 
a  day.  If  the  proportion  of  uric  acid  in  the  fluid  is  sufficiently  large,  crystals  of 
that  acid  will  how  be  found  on  the  thread  and  may  be  recognized  by  their  shape 
and  chemical  reaction.  This  "  thread  test "  of  Garrod's  is  not  extensively  used, 
because  it  does  not  succeed  unless  there  is  a  comparatively  large  amount  of  uric 
acid  in  the  blood,  and,  furthermore,  uric  acid  may  exist  in  the  blood  in  health,  or 
in  other  diseases  than  gout. 

Prognosis. — However  favorable  the  prognosis  may  be  with  regard  to  the  single 
gouty  attack,  yet  a  permanent  release  from  the  disease  is  rarely  to  be  hoped  for. 
Only  such  patients  as.  from  the  first  appearance  of  gout,  pursue  most  carefully  all 
the  requisite  prophylactic  and  dietetic  measures,  can  expect  that  future  attacks  will 
be  rare  and  conqDaratively  mild,  and  that  severe  lesions  of  the  internal  organs  will 
not  occur.  So  long  as  the  kidneys  and  other  viscera  are  intact,  there  is  no  imme- 
diate danger  to  life,  and  the  patient  may  attain  advanced  years  despite  his  gout. 
The  gradual  and  chronic  alterations  in  the  joints  may,  however,  impede  locomo- 
tion as  well  as  all  other  movements  of  the  body.  Except  for  this,  the  general  con- 
dition of  the  patient  in  the  intervals  between  the  attacks  is  often  one  of  tolerable 
comfort.  Indeed,  it  is  frequently  the  case  that  the  patient  will  feel  his  very  best 
directly  after  a  severe  paroxysm,  while  rudimentary  or  atypical  attacks  are  often 
regarded  as  of  ill  omen.  Really,  however,  there  is  no  serious  danger  until  a 
chronic  nephritis  is  developed.  The  prognosis  then  becomes  as  unfavorable  as  in 
the  other  forms  of  contracted  kidney  (q.  v.),  and  involves  the  same  possibilities. 

Treatment.— All  authorities  agree  that  the  first  essential  in  treating  gout  is  a 
proper  regimen.  Unless  the  patient  has  energy  enough  to  yield  the  most  implicit 
obedience  to  the  injunctions  regarding  diet  and  mode  of  life  in  general,  from  the 
first  appearance  of  his  disease,  no  great  benefit  can  be  obtained  from  treatment. 

Various  aiithorities  have,  of  late,  prescribed  special  diets  for  the  gouty.  These 
differ  considerably  from  one  another,  but  the  discrepancies  are  not  actually  so 
great  as  they  seem  to  be  at  first  glance ;  and,  after  all,  more  importance  attaches  to 
the  quantity  of  the  ingesta  than  to  their  quality.  As  most  gouty  patients  are  cor- 
pulent, the  diet  to  be  prescribed  for  them  is  mainly  that  indicated  by  their  corpu- 
lence. The  first  point  is  to  limit  the  total  amount  of  ingesta.  No  more  shotild  be 
eaten  than  is  absolutely  required  to  satisfy  hunger.  The  diet  may  be  a  mixed 
one — that  is,  may  contain  albuminoids,  carbohydrates,  and  fats ;  but  the  quantities 
of  each  of  these  ingredients  should  be  small  (vide  following  chapter).  The  albu- 
minoids should  not  be  too  abundant,  in  order  that  the  formation  of  uric  acid  may 
be  limited ;  the  fats  and  carbohydrates  should  be  cut  down,  in  order  that  the  albu- 
minoids may  be  thoroughly  oxidized  and  thus  any  further  deposit  of  adipose 
tissue  avoided.  Acid  articles  of  diet  should  be  forbidden,  lest  they  promote  the 
deposit  of  uric  acid  in  the  tissues.  The  experience  of  certain  physicians  tends  to 
show  that  a  diet  mainly  vegetable  is  better  borne  by  gouty  patients  than  animal 
food.  In  this  case  also,  however,  it  will  be  seen  that  the  essential  point  is  the 
quantity.  With  a  vegetable  diet,  the  amount  of  ingested  food,  and  still  more  the 
amount  of  nourishment  absorbed  from  the  prima?  vise,  is  almost  sure  to  be  less 
than  upon  an  exclusive  meat  diet.  The  patient  should,  therefore,  be  told  that  his 
diet  should  consist  mainly  of  lean  meat,  fish,  broth,  green  vegetables,  small 
amounts  of  milk,  eggs,  and  bread.  Sweet  puddings,  fat  meat,  potatoes,  or  sour 
and  acid  food  of  any  kind  should  be  avoided.  Fruit  may  be  allowed  in  small 
quantities.     Water  is  the  best  beverage;  but  it  is  not  advisable,  and  may  even  be 


GOUT.  991 

prejudicial,  to  drink  too  large  an  amount  of  any  fluid  (vide  infra).  Large  quan- 
tities of  alcohol  are  sure  to  injure  the  patient.  If  they  can  not  be  absolutely  pro- 
scribed, yet  at  least  their  amount  should  be  reduced  to  a  minimum. 

[Many  gouty  persons,  especially  those  suffering  from  the  irregular  form  of  the 
disease  and  acid  dyspepsia,  are  more  comfortable  and  seem  to  do  better  on  a  diet 
which  is  largely  nitrogenous,  the  starches  and  sugars  being  greatly  limited  in 
amount.  The  diet,  in  fact,  should  be  similar  to  that  laid  down  for  diabetes  melli- 
tus, though  not  so  strictly  carried  out.  In  chronic  and  irregular  cases  it  is  often 
desirable  to  prescribe  a  stimulant,  for  a  time  at  least;  brandy,  whisky,  or  gin,  well 
diluted  with  water,  is  perhaps  the  best  form.] 

By  thus  limiting  the  amount  of  food  taken,  we  shall  promote  metamorphosis 
and  avoid  any  excessive  formation  of  ui'ic  acid.  A  more  direct  means  of  hasten- 
ing the  conversion  of  the  albuminoids  is  muscular  exercise.  If  a  corpulent 
patient  is  still  vigorous  and  is  not  threatened  by  any  serious  internal  disease,  he 
should  be  urged  to  take  a  large  amount  of  exercise  in  mountain-climbing,  gym- 
nastics, gardening,  or  similar  pursuits.  The  motto  of  such  a  patient  should  be 
"little  sleep  and  great  activity."  This  same  indication  of  accelerating  tissue-meta- 
morphosis is  fulfilled  also  by  bathing.  In  early  stages  cool  baths  and  sponging 
are  useful,  as  are  also  baths  containing  common  salt,  or  perhaps  even  sea-bathing 
cautiously  employed.  In  more  advanced  cases,  particularly  if  the  joints  present 
permanent  lesions,  the  warmer  baths  are  more  desirable,  such  as  are  found  in 
Teplitz,  Wildbad,  Wiesbaden,  Baden-Baden,  Carlsbad,  Ems,  and  Aix. 

The  internal  administration  of  alkalies  is  an  efficient  adjuvant  to  the  dietetic 
and  hygienic  prescriptions  above  enumerated.  For  a  long  period  the  use  of  alka- 
line mineral- waters  has  been  found  to  be  most  beneficial.  Experience  confirms 
the  confidence  which  theoretical  considerations  would  lead  us  to  have  in  their 
value  in  checking  the  deposit  of  uric  acid,  so  far  as  it  is  occasioned  by  excessive 
acidity  of  the  circulatory  fluids  (vide  supra).  The  sodic  chloride  contained  in 
these  waters  stimulates  the  conversion  of  the  albuminoids.  The  waters  also  in- 
crease the  activity  of  the  kidneys,  benefit  gastric  catarrh,  and  overcome  constipa- 
tion, and  in  all  these  ways  combine  to  produce  a  favorable  effect  upon  the  patient's 
health.  Still  another  factor  is  the  judicious  diet  and  mode  of  life  at  such  health 
resorts.  The  waters  of  Carlsbad  and  Vichy  have  gained  the  greatest  repute  in 
gout,  although  the  waters  of  Ems  and  Neüenahr  have  an  analogous  composition 
and  doubtless  would  produce  similar  effects.  Of  the  waters  which  contain  sodic 
chloride,  the  most  advisable  are  Wiesbaden,  Baden-Baden,  Kissingen,  and  Hom- 
burg. The  salts  of  lithium  especially  promote  the  solution  of  uric  acid,  and  of 
late  the  waters  which  contain  lithium  have  been  strongly  recommended.  The 
natural  springs  of  this  sort,  such  as  the  Crown  Spring  in  Obersalsbrunn,  and  those 
of  Assmannshausen  and  Salzschlirf,  contain  comparatively  insignificant  amounts 
of  lithium ;  and  it  might  be  a  better  way  to  use  the  artificial  lithium  waters,  such 
as  are  made  by  Struve  or  Ewich.  Another  way  is  to  prescribe  carbonate  of  lith- 
ium, in  powders  containing  two  or  three  grains  each  (grm.  0"10-0-20),  one  powder 
two  or  three  times  a  day,  in  a  glass  of  Seltzer  or  Biliner  water. 

Other  remedies  formerly  in  vogue  were  said  to  correct  the  "  gouty  diathesis,'' 
but  their  efficacy  is  extremely  dubious,  and  they  need  not  be  especially  mentioned. 

As  to  the  treatment  of  the  acute  attack,  it  has  ceased  to  be  customary  to  employ 
any  potent  remedies.  The  patient  must,  of  course,  keep  his  bed.  The  affected 
joint  should  be  wrapped  up  in  cotton  wool,  the  whole  leg  elevated,  and  a  proper 
diet  strictly  enjoined.  Free  movement  of  the  bowels  should  be  maintained  by 
means  of  an  enema.  If  there  is  considerable  gastric  disturbance,  bicarbonate  of 
sodium,  magnesia,  or  some  bitter  may  be  prescribed.  The  most  certain  remedy 
for  severe  pain  is  a  subcutaneous  injection  of  morphine.     Less  efficient  are  nar- 


992  CONSTITUTIONAL  DISEASES. 

cotics  locally  applied,  and  warm  compresses.  Whether  any  internal  remedies  are 
calculated  to  abbreviate  the  attack  is  doubtful.  Formerly  Colchicum  (twenty  or 
thirty  drops  of  vinum  colchici  seminis  three  or  four  times  a  day)  was  the  favorite 
medicine,  but  it  seems  to  be  going  out  of  use.  Salicylic  acid  and  salicylate  of 
sodium  may  be  administered  in  the  same  way  as  in  acute  articular  rheumatism, 
and  sometimes,  although  not  always,  they  are  followed  by  improvement.  Anti- 
pyrine,  and  perhaps  antifebrine,  sometimes  succeed  in  allaying  the  pain  in  the 
affection  of  the  joints.  Some  physicians  recommend  subcutaneous  injections  of 
antipyrine  in  the  neighborhood  of  the  joint,  but  we  have  no  personal  experience 
on  this  point. 

[One  reason  why  Colchicum  has  fallen  into  relative  disuse  is  that  the  relief 
obtained  from  it  is  often  so  prompt  and  complete  that  patients  are  tempted  into 
continued  indulgence  in  a  faulty  manner  of  life.  It  is  also  supposed  by  some 
that  the  drug  interferes  with  the  effort  of  nature  to  eliminate  the  poison,  which 
becomes  generally  diffused,  and  sets  up  changes  in  the  vessels  and  internal 
organs. 

Precisely  how  Colchicum  acts  we  do  not  know,  but  that  it  does  act,  and  some- 
times with  marvelous  success,  there  can  be  no  question.] 

The  chronic  affections  of  the  joints  in  gout  are  treated  as  are  other  varieties 
of  chronic  arthritis  (vide  page  915).  The  most  efficient  remedies  are  cautious  mas- 
sage and  baths,  including  hot  sulphur  baths  and  mud-and-sulphur  baths.  The 
internal  administration  of  the  alkalies,  lithium,  and  similar  drugs,  to  combat  the 
general  gouty  diathesis,  should  be  associated  with  these  external  remedies.  Some 
physicians  report  that  iodide  of  potassium  favors  the  absorption  of  the  gouty 
deposits. 

The  treatment  of  the  nephritis  and  other  complications  need  not  be  discussed 
at  length.  The  gout  itself  should  always  be  the  main  object  of  our  therapeutic 
efforts,  and  beyond  this  we  may  be  guided  by  general  principles. 


CHAPTER  XII. 

OBESITY. 

(Corpulence.     Polysarcia  adiposa.) 

Definition  and  iEtiology. — The  amount  of  adipose  tissue  in  the  body  is  subject 
to  considerable  variation,  and  it  is  not  possible  to  state  absolutely  what  should  be 
considered  as  normal  and  what  as  abnormal.  For  practical  purposes  we  may 
draw  the  line  where  the  increased  size  grows  burdensome  to  the  individual.  After 
a  certain  point,  any  further  addition  to  the  amount  of  fatty  tissue  is  almost  sure 
to  work  serious  injury,  and  is  therefore  to  be  regarded  as  an  actual  disease,  and 
not  merely  an  inconvenience.  It  should  be  said,  however,  that  in  such  cases  the 
symptoms  of  obesity  are  very  frequently  confounded  with  those  springing  from 
other  disorders — these  latter  possessing,  indeed,  the  same  aetiology  as  obesity,  but 
distinct  from  it. 

The  most  frequent  and  important  cause  of  obesity  is  the  habitual  ingestion  of 
too  large  an  amount  of  food.  By  "  too  large  "  is  meant  an  amount  sufficient  to 
occasion  a  continual  increase  of  the  adipose  tissue  of  the  body,  when  this  is  already 
fairly  well  developed.  It  is  a  matter  of  indifference  whether  the  excess  is  com- 
posed mainly  of  albuminoids,  or  carbohydrates,  or  fats ;  for  in  either  case,  if  the 
quantity  be  sufficient,  an  increase  of  adipose  tissue  may  take  place.  We  shall 
soon  see,  however,  that  the  excess  is  usually  in  fat  and  carbohydrates.    Inasmuch 


OBESITY.  993 

as  this  overfeeding  is  almost  certain  to  be  habitual,  tbe  excess  at  any  one  time 
need  not  be  at  all  large.  We  often  hear  a  corpulent  person  express  bis  surprise 
that  he  grows  heavier  every  day,  although  he  "  does  not  cat  any  more  than  others 
who  are  lean."  The  explanation  is  easy  if  we  consider  tbat  a  daily  increase  oi 
five  grammes  of  fat  (one  and  one  fourth  drachms)  suffices  to  increase  the  weight 
in  ten  years,  or,  say  between  the  thirty-fifth  and  forty-fifth  years,  forty  pounds 
avoirdupois.     In  reality  the  daily  increase  is  sometimes  greater  than  this. 

The  basis  for  a  detailed  consideration  of  the  causes  which  lead  to  tbe  deposit  of 
fat  will  be  gained  by  a  consideration  of  tbe  physiological  laws  relating  to  nutrition 
discovered  by  Voit,  Pettenkofer,  and  their  pupils.  It  has  been  shown  that  both 
the  albuminoids  and  the  carbohydrates  of  the  food  may  be  a  source  of  fat,  formed 
within  the  economy,  and  also  that  the  fat  contained  in  the  food  may  be  to  a  large 
extent  directly  deposited  in  the  fat-cells  of  the  body.  One  product  of  the  decom- 
position of  albuminoid  substances  is  invariably  fat.  This  usually  undergoes  fur- 
ther oxidation,  but  it  is  sometimes  retained  unaltered  in  the  system.  It  would 
even  seem  that  the  albuminoids  give  rise  to  much  more  of  the  fatty  tissues  of  the 
body  than  are  produced  from  the  carbohydrates  ingested,  although  there  is  no 
doubt  that  these  latter  also  yield  fat.  Carbohydrates  do  promote  obesity,  but  less 
because  they  are  a  direct  source  of  fat  than  because  they  are  easily  decomposed, 
and  so  shield  both  the  ingested  fat  and  that  which  is  formed  out  of  the  albu- 
minoids from  oxidation.  In  this  indirect  way  they  do  greatly  favor  a  tendency  to 
corpulence. 

We  thus  perceive  that  various  diets  may,  each  one  of  them,  permit  of  an 
increase  of  adipose  tissue.  In  actual  life,  of  course,  the  most  frequent  conditions 
are  such  as  result  from  the  customs  and  habits  of  the  population  in  general.  The 
diet  is  almost  invariably  a  "  mixed"  one — that  is,  it  contains  albumen  and  fat  and 
carbohydrates — and  in  most  instances  the  obesity  is  due  to  an  excessive  amount  of 
all  three  elements,  or  at  least  of  the  fat  and  carbohydrates.  A  person  may,  how- 
ever, become  corpulent  who  eats  very  little  fat,  provided  he  consumes  a  large 
quantity  of  albuminoids  and  carbohydrates ;  or  if  he  eats  very  little  starchy  food, 
provided  he  consumes  a  large  amount  of  meat  and  fat.  Perhaps  these  facts  may 
be  made  clearer  by  giving  a  concrete  example.  Voit  tells  us  that  a  vigorous  man 
who  requires  daily  118  grin,  of  albumen  and  259  grm.  of  fat  to  maintain  a  physio- 
logical equilibrium  as  regards  fat  and  albumen  will,  other  things  being  equal, 
begin  to  store  up  fat  if  there  is  any  further  increase  in  the  amount  of  fat  in  his 
diet.  The  same  result  will  also  take  place  if,  instead  of  the  rations  previously 
stated,  he  ingests  more  than  118  grm.  of  albumen  and  600  grm.  of  starch,  or  more 
than  661  grm.  of  albumen  alone,  or,  fiually,  more  than  118  grm.  of  albumen,  100 
grm.  of  fat,  and  368  grm.  of  starch.*  It  is  obvious  that  this  last  diet,  which 
closely  resembles  the  average  diet  of  an  adult  t  in  good  circumstances,  whose 
weight  is  neither  increasing  nor  diminishing,  is  the  one  most  likely  to  be  ex- 
ceeded ;  whereupon  there  must  take  place  a  deposition  within  the  system  of  the 
superfluous  fat. 

Among  the  various  kinds  of  food  is  one  group  which  deserves  mention,  as 
being  an  important  factor  in  many  cases  of  obesity ;  we  refer  to  alcoholic  bever- 

*  This  statement  is  founded  upon  an  important  discovery  of  Kubner,  that,  as  far  as  the  storing  up 
of  fat  is  concerned,  the  measure  of  value  for  different  foods  is  the  amount  of  heat  given  off  by  them 
when  they  undergo  oxidation  into  carbonic-dioxide  gas  and  water.  Measured  in  this  "way,  100  grm. 
fat  =  211  grm.  albumen  =  232  grm.  starch  =  234  grm.  cane  sugar  =  256  grm.  grape  sugar. 

t  Probably  the  amount  of  fat  contained  in  the  food  is  often  less  than  the  above,  and  the  amounts 
of  albumen  and  starch  somewhat  larger.     Voit  estimates  tbe  diet  of  a  well-to-do  person  at  127  grm. 
albumen,  89  grm.  fat,  and  362  grm.  starch ;  and  that  for  a  vigorous  laborer  at  118  grm.  albumen,  56 
grm.  fat,  and  500  grm.  starch.     Of  course,  these  figures  are  merely  approximate. 
63 


994  CONSTITUTIONAL  DISEASES. 

ao-es.  There  can  be  no  doubt  that  intemperance  in  this  regard  plays  a  prominent 
part  in  many  instances.  Sufficient  illustration  is  furnished  by  brewers,  hotel- 
keepers,  and  the  inhabitants  of  countries  like  Bavaria,  where  beer  drinking  is 
prevalent.  In  this  particular  it  is  evident  that  beer  works  more  harm  than  does 
wine  or  strong  liquor ;  for  beer  contains,  in  addition  to  the  alcohol,  an  appreciable 
amount  of  starchy  material,  making  the  sum  total  from  the  beer  drunk  during 
the  entire  day  a  considerable  one.  Many  persons  who  would  be  extremely  indig- 
nant if  called  "  tipplers,"  habitually  take  five  or  six  glasses  of  beer  a  day,  equiva- 
lent to  150  grin,  of  starch,  or,  in  other  wTords,  one  half  the  total  amount  of  starch 
required  by  the  system.  Even  this  quantity  is  frequently  exceeded.  Of  course, 
the  three  or  four  per  cent,  of  alcohol  which  the  beer  contains  also  promotes  the 
deposition  of  fat.  Alcohol  is  readily  oxidizable,  and  it  thus  shields  to  a  consid- 
erable extent  the  fat  already  present  in  the  body;  and  it  also,  in  all  probability, 
works  such  an  injury  to  the  tissues  as  to  diminish  their  power  of  effecting  decom- 
position. We  must  also  remember  that  most  beer  drinkers  take  little  exercise. 
The  long  sitting  at  the  beer  table,  and  the  mental  and  physical  sluggishness 
which  immoderate  indulgence  in  beer  always  causes,  and  finally  the  increasing 
corpulence  itself,  make  it  clear  why  most  beer  drinkers  dislike  protracted  exercise. 

We  have  thus  seen  that  in  by  far  the  larger  number  of  cases  obesity  is  mainly 
due  to  the  ingestion  of  too  much  food.  No  weight  need  be  attached  to  the  usual 
statement  of  corpulent  persons,  that  they  eat  no  more  than  others.  Few  of  them 
have  any  idea  how  much  nourishment  they  do  consume.  Others,  having  already 
become  corpulent,  eat  less,  to  be  sure,  than  they  used  to,  but  nevertheless  an. 
amount  sufficient  to  maintain  the  acquired  weight. 

Other  factors  may  no  doubt  exert  an  influence  upon  the  increase  of  adipose 
tissue  by  diminishing  the  consumption  of  fat  in  the  system.  The  most  important 
factor  of  this  class  is  physical  inactivity.  Muscular  contractions  lead  to  the  decom- 
position of  a  large  amount  of  fat.  This  explains  why  people  of  sedentary  habits, 
and  those  who  sleep  long  and  exercise  little,  are  more  apt  to  become  corpulent  than 
are  manual  laborers.  Again,  there  are  certain  diseases  which  seem  to  promote 
corpulence.  In  anaemia  there  is  sometimes  a  striking  tendency  to  obesity,  in  part 
due  to  the  diminished  supply  of  oxygen  and  in  part  to  diminished  muscular 
activity.  This  same  inactivity  is  probably  the  main  cause  of  corpulence  in  paraly- 
sis (hemiplegia).  It  may  be,  however,  that  disturbances  of  the  nervous  system 
may  directly  affect  metamorphosis.  Thus,  idiots  and  other  subjects  of  congenital 
defects  of  the  brain  are  liable  to  obesity.  Disturbances  of  the  circulatory  system 
seem  to  favor  the  production  of  corpulence  by  impairing  oxidation.  This  is  seen 
in  many  young  persons  with  cardiac  disease,  although  it  is  not  easy  to  exclude  in 
this  case  the  influence  of  still  other  factors,  such  as  a  sedentary  life. 

Finally,  some  cases  of  obesity  seem  to  result  from  a  constitutional  and  inborn 
predisposition.  Young  children  sometimes  suffer  from  obesity,  and  the  condi- 
tion seems  in  many  cases  to  be  hereditary.  Many  races  and  nations  exhibit  an 
especial  tendency  to  corpulence — for  example,  the  Jews.  Age  and  sex  have  some 
importance  in  this  regard :  extreme  obesity  is  seldom  seen  previously  to  the  thir- 
tieth year;  and  women  appear  to  be  somewrhat  more  subject  to  the  disease  than 
men.  The  importance  of  a  "  tendency  "  to  obesity  should  not  be  overrated.  Upon 
careful  investigation,  we  shall  almost  invariably  find  in  the  habits  of  the  indi- 
vidual, as  regards  food  and  exercise,  a  satisfactory  explanation  of  his  obesity. 
Strictly  speaking,  the  condition  can  not  be  regarded  as  a  disease  unless  the  habits 
as  to  diet  and  exercise  fail  to  account  for  it. 

Pathology. — After  corpulence  has  passed  a  certain  point  the  condition  is  evi- 
dent at  the  first  glance.  The  subcutaneous  cellular  tissue  is  one  of  the  chief  places 
in  which  the  fat  is  deposited.    Consequently,  the  panniculus  adiposus  soon  attains 


OBESITY.  995 

considerable  thickness.  The  countenance  grows  more  round  and  plump;  beneath 
the  chin  is  formed  a  second  prominence  known  as  the  "double  chin  ";  the  chest 
appears  broadened ;  the  waist  enlarges;  and,  particularly  in  women,  the  breasts 
are  changed  to  great  shapeless  masses,  over  which  tbe  skin  is  so  tightly  stretched 
as  to  present  lineae  albicantes.  The  abdominal  walls  are  greatly  altered.  The 
belly  projects  more  and  more  until  it  becomes  actually  pendulous,  and  ils  lower 
surface  touches  the  interior  surface  of  the  thighs.  Intertrigo  is  apt  to  occur  in 
the  groins,  below  the  breasts,  and  between  the  buttocks.  The  skin  everywhere 
has  a  fatty  feel,  due  to  the  increased  secretion  of  the  sebaceous  glands.  This 
hyperplasia  of  the  fatty  tissue  in  the  panniculus  adiposus  is  associated  with  a 
deposit  of  fat  in  many  parts  of  the  interior  of  the  body,  including  tbe  mesentery, 
mediastinum,  pericardium,  and  the  capsules  of  the  kidneys.  Some  of  these  will 
be  mentioned  again  further  on. 

Of  course,  the  circumference  and  weight  of  the  body  become  greatly  increased. 
As  an  approximate  measure,  it  may  be  stated  that  for  men  of  middle  height  a 
weight  exceeding  90  kilo.  (200  pounds),  and  for  women  75  kilo.  (165  pounds),  may 
be  regarded  as  abnormal.*  This  increase  in  bulk  is  the  first  cause  of  subjective 
symptoms.  An  obese  person  has  to  exert  a  greater  effort  in  making  any  motion 
than  do  other  people,  and  as  a  necessary  consequence  he  gets  easily  tired,  and 
seeks  as  far  as  possible  to  avoid  exertion.  The  increased  demand  upon  the  muscles 
explains  the  familiar  fact  that  corpulent  persons  perspire  so  readily. 

The  graver  symptoms  of  obesity,  and  properly  the  first  pathological  phe- 
nomena of  the  condition,  relate  to  the  respiration  and  the  circulation.  The  patient 
begins  to  complain  of  shortness  of  breath,  and  is  subject  to  marked  dyspnoea  upon 
running  or  climbing  stairs.  There  may  be,  at  the  same  time,  cardiac  disturbance, 
indicated  by  a  rapid  pulse,  palpitation,  intermission  of  the  pulse,  or  other  slight 
irregularities  in  cardiac  action.  All  these  symptoms  grow  gradually  worse ;  and 
to  them  are  added  symptoms  of  cardiac  failure  and  consequent  passive  congestion. 
There  is  a  tendency  to  bronchitis  and  other  catarrhal  troubles.  The  appetite  and 
digestion  are  affected,  and  oedema  appears. 

A  careful  analysis  of  all  these  symptoms  shows  that  many  causes  combine  to 
produce  them,  all  having  a  common  tendency  to  impede  respiration,  and,  still 
more,  circulation.  One  source  of  disturbance  is  the  increased  deposit  of  fat  upon 
the  framework  of  the  body.  It  is  probable  that  the  excess  of  adipose  tissue  cover- 
ing the  thorax  exerts  a  direct  influence  in  obstructing  the  respiratory  motion  of 
the  thoracic  walls,  and  renders  the  respiration  more  superficial.  In  this  way  the 
return  of  venous  blood  to  the  heart  and  the  pulmonary  circulation  are  both 
impeded,  because  the  negative  pressure  in  the  chest  is  less  than  normal.  Likewise 
the  diminished  amount  of  bodily  exercise  affects  the  circulation  unfavorably. 
Brauner  has  shown  how  numerous  are  the  arrangements  connected  with  the 
fasciae  for  promoting  the  venous  currents,  by  means  of  the  negative  pressure 
resulting  from  the  movements  of  the  body.  Whether  the  fat  deposited  around 
the  heart  directly  obstructs  the  cardiac  movements  is  somewhat  doubtful,  though 
this  view  is  held  by  many.  The  fatty  infiltration  of  the  myocardium  is  of  more 
importance:  the  fat  is  deposited  in  the  intermuscular  connective  tissue.  This 
lesion,  however,  is  not  of  very  frequent  occurrence,  nor  does  it  produce  so  grave 
results  as  do  certain  other  cardiac  changes,  which  are  either  secondary  to  the 
obesity  or  complications  of  it. 

There  is  no  doubt  that,  in  almost  all  cases  where  the  corpulence  actually 
induces  grave  disturbance,  the  cardiac  symptoms  are  of  prime  importance.  These 
are  due,  as  has  just  been  indicated,  in  part  to  the  increased  amount  of  adipose 

*Even  150  kilo.  (330  pounds)  has  been  repeatedly  observed. 


996  CONSTITUTIONAL  DISEASES. 

tissue,  and  in  still  greater  part  to  complications,  most  of  which  are  excited  by  the 
same  causes  as  is  the  obesity  itself.  The  abundant  adipose  tissue  may  obstruct 
the  circulation  in  the  smaller  blood-vessels  and  capillaries  inclosed  within  it. 
And,  furthermore,  the  excessive  development  of  fatty  tissue  probably  leads  to  the 
growth  of  new  blood-vessels,  and,  as  a  consequence,  to  an  increase  in  the  total  vol- 
ume of  the  blood.  This  is  one  way  in  which  the  demands  made  upon  the  heart 
are  rendered  greater  than  normal,  and  explains  why  the  corpulent  frequently 
exhibit  cardiac  hypertrophy.  Other  influences  are  also  at  work  to  produce  this 
same  result:  they  are,  in  the  first  place,  the  same  factor  which  occasions  the 
obesity  itself,  namely,  the  ingestion  of  increased  amounts  of  food  and  drink  (see 
the  chapter  on  cardiac  hypertrophy),  antl,  secondly,  certain  other  lesions  which  are 
frequently  associated  with  obesity  and  are  referable  to  the  same  causes  as  it  is. 
Chief  among  this  latter  class  is  general  arterio-sclerosis.  If  this  involve  the  coro- 
nary arteries,  it  may  in  turn  occasion  still  further  damage — for  example,  degenera- 
tive myocarditis  (compare  page  309.)  Chronic  interstitial  nephritis  is  another  not 
infrequent  complication.  This  is  in  part  referable  to  the  same  causes  as  is  the  obe- 
sity.    Gout  and  diabetes  are  less  frequent. 

We  thus  see  that  obesity  is  often  merely  one  of  many  injurious  results  occa- 
sioned by  an  improper  mode  of  life.  It  is,  in  a  certain  sense,  the  first  danger- 
signal,  warning  the  patient  and  his  physician  to  avoid  the  graver  disturbances 
which  threaten.  This  is  a  point  of  great  practical  importance;  for,  when  once 
we  have  a  combination  of  obesity  with  cardiac  hypertrophy,  fatty  infiltration  of 
the  heai't,  arterio-sclerosis,  or  interstitial  nephritis,  the  various  causes  and  effects 
act  and  react  upon  one  another  in  a  way  most  perilous  to  health,  and  even  to  life. 
There  is  no  need  of  describing  the  grave  disturbances  which  invariably  develop 
at  the  close  of  the  scene.  They  are  the  result  of  chronic  cardiac  insufficiency,  and 
have  been  fully  described  under  cardiac  disease. 

In  every  case  of  obesity  the  physician  should  examine  the  heart,  lungs,  vascu- 
lar system,  and  kidneys,  particularly  if  there  be  already  subjective  disturbance. 
The  examination  of  the  heart  may  present  considerable  difficulties,  because  the 
results  of  palpation  and  percussion  are  so  obscured  by  the  thick  cushion  of  fat 
which  covers  the  thorax.  We  can,  however,  have  recourse  to  auscultation,  and 
can  feel  the  pulse.  The  pulse  may  be  either  rapid,  or  slow,  or  irregular.  We 
need  not  mention  any  minute  particulars  as  to  the  examination.  It  may  be  stated, 
however,  that  a  hepatic  enlargement  is  often  found,  but  it  is  much  less  often  the 
result  of  fatty  infiltration  than  of  simple  hypertrophy  or  passive  congestion. 

We  have  thus  seen  that  corpulence  may  sometimes  be  associated  with  grave 
and  dangerous  lesions ;  but,  on  the  other  hand,  it  should  be  stated  that  this  unfor- 
tunate condition  by  no  means  invariably  exists.  Not  infrequently  the  corpulence 
remains  moderate,  in  which  case  it  is  not  really  dangerous,  however  incon- 
venient. This  is  true  of  a  proportion  of  those  cases  which  are  due  to  the  in- 
gestion of  a  large  amount  of  nourishment,  associated  with  defective  oxidation, 
and  where  there  are  no  other  unfavorable  influences  at  work.  The  obesity  of 
hard  drinkers  is  almost  always  a  more  or  less  dangerous  condition,  while  that 
seen  in  many  elderly  persons  and  in  women  is  often  comparatively  free  from 
peril.  These  latter  individuals  are,  to  be  sui'e,  discommoded  by  their  great  weight, 
can  accomplish  less  than  they  used  to,  are  easily  put  out  of  breath,  and  have  a 
certain  tendency  to  catarrhal  inflammations  and  rheumatic  difficulties ;  but  they 
escape  the  severer  lesions  above  enumerated.  Even  these  apparently  harmless 
conditions  should  not  be  disregarded  by  the  physician,  as  he  can  never  be  abso- 
lutely certain  that  grave  complications  may  not  be  developed  eventually. 

Treatment  of  Obesity. — To  cause  the  disappearance  of  the  accumulated  fat,  it  is 
necessary  to  promote  its  oxidation  in  the  system  and  to  prevent  the  ingestion  of 


OBESITY.  997 

new  supplies  of  fat.  To  accomplish  this  purpose  we  possess  only  two  means — first, 
a  limitation  of  the  ingestion  of  such  kinds  of  food  as  may  lead  to  the  formation  of 
fat  in  the  system,  and,  secondly,  stimulation  of  those  factors  which  occasion  th< 
destruction  of  the  fat  already  present.  All  the  various  methods  of  treating 
obesity,  without  exception,  aim  either  to  diminish  the  supply  or  to  increase  the 
destruction  of  fat. 

The  methods  vary  greatly.  It  must  be  borne  in  mind  that  the  diminution  of 
the  adipose  tissue  must  not  involve  injury  to  the  body  itself.  The  treatment 
should  not  weaken  the  constitution,  but  should  invigorate  the  patient,  <m-  at  least 
be  innocuous. 

It  is  of  prime  importance,  in  every  method  of  treatment,  that  the  total  quantity 
of  ingested  food  should  be  diminished.  It  is  a  mistake  to  forbid  the  patient  some 
particular  kind  of  food — for  instance,  the  carbohydrates  or  the  fats — with  the  idea 
that  they  alone  do  harm,  or  to  allow  him  unlimited  quantities  of  other  kinds  of 
food,  in  the  belief  that  they  are  harmless.  Any  person  can  eat  albuminoids,  fat 
and  starch  at  every  meal,  and  yet  not  grow  fat;  while,  on  the  other  hand,  too 
much  of  any  one  of  these  may  lead  to  an  increase  of  adipose  tissue.  The  amount 
of  food  which  a  person  can  take  without  increasing  the  amount  of  adipose  tissue 
varies  with  the  individual.  It  depends  upon  the  amount  of  material  already 
present  in  the  body,  and  upon  the  various  demands  made  upon  the  system,  as 
well  as  other  factors.  This  renders  it  difficult  to  draw  up  a  universal  dietary  for 
the  obese.  We  can  best  judge  of  the  value  of  any  course  of  treatment  by  its 
results,  and  these  are  best  measured  by  the  weight  and  the  subjective  condition  of 
the  patient. 

Of  the  various  elements  of  food,  the  albuminoids  should  be  diminished  least  of 
any,  because  it  would  be  sure  to  work  injury  to  the  system  if  they  were  supplied 
in  too  small  an  amount.  Of  course,  the  albuminoids  must  not  be  eaten  to  such 
an  extent  that  the  fat  into  which  they  decompose  remains  intact  in  the  body.  An 
increase  in  the  amount  of  nitrogenous  tissue  is,  however,  desirable,  because  this 
promotes  the  vigor  of  the  muscles  and  the  heart,  and  so  leads  to  the  oxidation  of 
larger  quantities  of  the  non-nitrogenous  tissues. 

The  amount  of  fat  and  starch  must  be  much  more  limited.  The  fats  and 
starches  are  more  potent  in  increasing  adipose  tissue  and  in  shielding  from  oxida- 
tion the  fat  already  stored  up  in  the  body  than  is  nitrogenous  food.  It  would 
not  be  at  all  advisable  to  forbid  the  use  of  either  one  of  these  two  constituents  of  a 
mixed  diet,  allowing  the  other  alone  to  be  eaten.  A  varied  diet  is  extremely  desir- 
able, even  for  one  who  is  corpulent ;  and  we  should  exclude  neither  fat  nor  starch 
wholly  from  the  dietary,  but  we  should  merely  limit  the  amounts  to  be  taken.  As 
already  indicated,  the  amount  of  albuminoid  food  remaining  unchanged,  a  person 
can  eat  double  the  quantity  of  starchy  food  that  he  can  of  fat,  without  increasing 
his  adipose  tissue.  It  is  therefore  irrational  to  allow  the  corpulent  fat  in  larger 
proportions  than  starchy  foods.  The  diet  which  Ebstein  has  recently  proposed 
for  the  treatment  of  obesity  does  prove  successful,  but  the  explanation  of  its  suc- 
cess lies  in  the  comparatively  small  amounts  of  meat  and  fat  ingested.  Precisely 
the  same  results  would  be  attained  if  a  corresponding  amount  of  starch  were  sub- 
stituted for  all  or  a  portion  of  the  fat;  and  in  practice  it  is  desirable,  at  least  in 
most  cases,  to  allow  the  patient  both  starches  and  fats.  Of  course,  the  likings  and 
experience  of  the  individual  should  be  considered  in  each  separate  case.  The 
Banting  treatment,  introduced  in  1864,  enjoyed  for  a  time  a  great  reputation.  Its 
inventor  applied  it  first  of  all  to  his  own  case,  and  with  success.  It  rests  upon  a 
rational  basis,  inasmuch  as  the  albuminoids  are  allowed  in  abundance,  and  the 
ingestion  of  fat  and  starch  is  limited.  It  lays  too  much  stress,  however,  upon  the 
exclusion  of  fat  as  compared  with  starch. 


998  CONSTITUTIONAL  DISEASES. 

The  principles  here  expounded  are  direct  corollaries  to  the  laws  which  Voit 
has  taught  us  in  regard  to  the  different  kinds  of  food.  The  physician  who  hears 
them  in  mind  can  lay  down  his  own  rules  for  the  diet  of  his  patient.  As  already 
stated,  it  is  impossible  to  give  figures  which  will  apply  to  every  case.  If  we  take 
as  a  basis  the  average  diet  for  an  adult — that  is,  about  125  grm.  albumen,  80  grm. 
fat,  and  350  grm.  starch — we  might  say  that  most  cases  of  obesity  woiild  be  sure 
to  undergo  improvement  upon  a  diet  containing  125  grm.  albumen  (or  possibly 
even  more  than  this),  40  grm.  fat,  and  150  grm.  starch.  The  amounts  of  fat  and 
starch  could  be  even  more  diminished,  but  it  is  usually  best  not  to  be  too  precipi- 
tate. A  gradual  diminution  of,  say,  two  or  three  pounds  a  week,  extending  over 
a  long  period  withoiit  interruption,  is  to  be  preferred  to  the  rapid  treatment  com- 
mon at  many  health  resorts.  Of  course,  the  loss  of  fat  is  greater  at  the  commence- 
ment of  treatment  than  later  on,  when  the  amount  of  adipose  tissue  has  already 
approached  more  nearly  to  normal,  and  the  diet  must  undergo  a  gradual  and  cor- 
responding change.  It  is  of  particular  importance  to  increase  the  amount  of  non- 
nitrogenous  foods  in  the  later  stages  of  treatment,  lest  the  albuminoid  tissues  of 
the  body  become  wasted. 

The  following  dietary  may  be  taken  as  an  illustration  of  what  would  be  suit- 
able for  a  patient  in  the  beginning  of  treatment :  For  breakfast,  a  cup  of  coffee 
with  milk,  and  about  75  grm.  of  bread.  At  noon,  a  plate  of  soup,  150  to  175  grm. 
lean  meat  or  fish,  lettuce,  green  vegetables,  and  about  25  grm.  bread.  For  dessert, 
about  75  grm.  boiled  rice,  or  some  simple  pudding,  or  100  grm.  fruit.  To  quench 
the  thirst,  water,  or  half  a  pint  of  light  wine.  In  the  afternoon,  a  cup  of  coffee, 
and  with  it  not  more  than  20  to  30  grm.  bread.  For  supper,  two  eggs,  or  100  to 
120  grm.  meat,  with  30  grm.  bread,  a  little  fruit,  lettuce,  half  a  pint  of  wine,  or 
one  or  two  cups  of  tea,  not  much  sweetened.  Butter  should  be  entirely  proscribed 
at  first ;  later  on  it  may  be  used  in  small  amounts. 

Some  approach  to  this  bill  of  fare  must  be  enforced  not  merely  for  a  few  weeks, 
but  for  months.  It  is  absolutely  necessary  that  the  patient  should  be  weighed 
every  two  or  three  weeks.  If  the  weight  diminishes  slowly  and  gradually,  with- 
out any  subjective  disturbance,  we  have  the  best  proof  that  the  diet  is  a  suitable 
one.  If  the  weight  does  not  diminish,  then  the  amount  of  ingesta  must  undergo 
further  reduction.  If  more  food  can  be  taken  without  the  weight  increasing 
again,  a  larger  amount  may  be  unhesitatingly  permitted,  and  indeed  may  even 
be  advisable  if  the  patient  be  languid.  The  increase  should  at  first,  however,  be 
mainly  in  the  amount  of  albuminous  food,  the  amount  of  starches  and  fats  not 
being  much  increased.  The  "cure"  can  not  be  regarded  as  complete  until  the 
weight  has  been  brought  down  to  that  of  the  average  individual  of  the  given  age 
and  sex.     This  goal  having  been  reached,  greater  freedom  in  diet  is  permissible. 

The  object  of  the  treatment  just  suggested  is  exclusively  the  limitation  of  the 
production  of  fat.  We  may  also  promote  the  destruction  of  the  fat  already  stored 
up  in  the  system.  A  chief  means  to  this  end  is  muscular  exercise,  which  undoubt- 
edly increases  the  oxidation  of  the  adipose  tissues.  Carried  out  in  a  proper  man- 
ner, it  is  therefore  a  most  valuable  adjuvant  in  treatment.  Oertel  has  recently 
pointed  out  that  muscular  exertion  does  good  in  still  another  way — namely,  by 
promoting  cardiac  activity  and  inducing  deep  respiratory  efforts.  Thus  the  heart 
is  strengthened  and  circulation  promoted.  Mountain-climbing  is  one  of  the  best 
modes  in  which  to  take  the  desired  exercise.  We  need  hardly  say  that  the 
increased  muscular  activity  makes  it  possible  for  the  patient  to  take  an  increased 
amount  of  food  without  injury. 

Baths  also  promote  oxidation,  but  they  are  far  less  potent  than  is  muscular 
exercise.  Cold  baths,  brine  baths,  or  baths  containing  carbonic-acid  gas,  may  be 
employed.     One  way  in  which  they  do  good  is  by  stimulating  the  nervous  system. 


SCROFULA.  999 

Oertel  regards  it  of  great  importance  to  diminish  the  amount  of  water  in  the  sys- 
tem, a  point  which  has  until  very  lately  received  little  attention.  The  diminution 
m  the  amount  of  fluids  may  ameliorate  any  circulatory  disturbance  (vide  supra) 
and  relieve  venous  congestion,  and  it  undoubtedly  has  some  value  in  the  treat- 
ment of  obesity.  Oertel  has  shown  that  a  simple  diminution  in  the  amount  of 
fluids  ingested,  when  there  is  no  other  change  in  the  diet  or  mode  of  life,  will 
effect  a  diminution  of  the  adipose  tissues.  This  result  is  probably  due  mainly  to 
the  diminished  strain  upon  the  heart  and  the  consequent  increase  of  oxidation  ; 
but  the  chief  cause  of  the  rapid  loss  of  weight,  which  we  actually  see  in  the  cor- 
pulent as  a  result  of  the  deprivation  of  fluid,  is  to  be  found  not  in  the  loss  of  fat, 
but  in  the  marked  loss  of  water  contained  in  the  body.  "  Desiccation  "  may  further 
be  promoted  by  stimulating  the  perspiration  by  bodily  exercise  or  by  steam  baths. 
This  withdrawal  of  liquid  from  the  system,  however,  is  advisable  only  in  cases 
where  there  is  already  incipient  cardiac  failure. 

It  is  evident  that  numerous  excellent  methods  are  at  our  disposal  for  the  treat- 
ment of  obesity;  but  their  application  to  any  particular  case  should  be  the  result 
of  a  careful  consideration  of  the  special  circumstances  presented.  A  very  essen- 
tial point  is  that  the  injunctions  of  the  physician  should  not  merely  be  made,  but 
be  carried  out;  and  it  is  precisely  here  that  the  treatment  of  many  cases  suffers 
shipwreck.  We  may  be  baffled  by  the  patient's  lack  of  energy  and  persistency, 
or  by  the  importunate  demands  which  his  profession  or  social  position  make  upon 
him.  Indeed,  it  is  sometimes  absolutely  imj)ossible  to  prosecute  the  treatment  at 
home,  in  which  case  bathing  and  health  resorts  are  to  be  urgently  recommended. 
There  alone  can  the  patient  muster  up  the  resolution  necessary  for  carrying  out 
the  desired  changes  in  his  mode  of  life.  The  incontestable  success  of  treatment  at 
Carlsbad,  Marienbad,  Kissingen,  Tarasp,  and  similar  resorts  is  doubtless  only  to  a 
very  small  extent  the  result  of  their  specific  medicinal  influence,  but  it  is  mainly 
due  to  a  strict  observance  of  the  above-described  diet  and  regimen.  The  internal 
use  of  mineral  waters  is  not  entirely  without  a  beneficial  effect.  Their  laxative 
qualities  diminish  the  absorption  of  food  from  the  intestinal  canal.  It  should  be 
said,  however,  that  the  patient  is  at  the  same  time  exposed  to  the  danger  of  a  waste 
of  his  nitrogenous  tissues.  This  is  why  patients  frequently  complain  of  the  debili- 
tating effect  of  these  mineral  springs ;  to  avoid  which,  it  would  be  well  to  increase 
the  amount  of  albuminoids  in  the  diet.  We  must  also  consider  the  need  of  guard- 
ing against  too  great  a  supply  of  fluid,  with  regard  to  what  was  said  above  as  to 
the  occasional  service  of  "  desiccation  "  of  the  body. 


CHAPTER   XIII. 
SCROFULA. 

Definition  and  Symptoms  of  what  is  called  Scrofula. — We  desire  to  present,  at 
the  close  of  this  section,  a  brief  description  of  scrofula,  but  merely  from  a  practical 
standpoint.  From  a  scientific  point  of  view  scrofula  is  not  to  be  regarded  as  any 
special  variety  of  disease.  The  term  is  applied  to  a  group  of  symptoms  seen  most 
frequently  in  childhood,  the  essential  features  of  which  consist  in  the  appearance 
of  chronic  enlargements  of  the  lymph-glands,  and  in  certain  diseases  of  the  skin 
and  mucous  membranes.  The  simultaneous  appearance  of  these  various  phenom- 
ena does  really  produce  a  somewhat  characteristic  picture,  which  can  frequently 
be  recognized  at  the  first  glance. 

Most  scrofulous  children  appear  pale,  with  a  flabby  skin  and  soft  muscles. 


1000  CONSTITUTIONAL  DISEASES. 

The  panniculus  adiposus  may  nevertheless  be  tolerably  well  developed.  Not 
infrequently  the  face  is  puffy,  with  prominent  lips.  This  is  called  the  "torpid 
habitus."  In  other  cases  the  child  has  small  features  and  a  remarkably  delicate 
white  skin,  which  but  partly  conceals  the  superficial  veins,  and  is  readily  suf- 
fused with  blushes.  To  these  the  name  "  erethitic  habitus  "  is  applied.  Enlarged 
lymph-glands  are  to  be  felt  in  the  throat,  at  the  angles  of  the  lower  jaw,  and  in 
the  back  of  the  neck,  and  occasionally  in  other  parts  of  the  body.  These  glands 
may  remain  indolent  for  a  long  while,  or  they  may  suppurate  and  break  exter- 
nally. Chronic  cutaneous  eruptions  are  often  seen  in  various  places.  The  most 
common  of  these  is  a  scaly  or  impetiginous  eczema,  affecting  the  face,  scalp,  or 
extremities.  More  severe  affections  are  lupus  ("  lupus  scrophulosorum  "_),  prurigo, 
and  lichen  scrophulosorum. 

Of  the  mucous  membranes,  the  conjunctiva  and  the  lining  membrane  of  the 
nostrils  are  most  frequently  affected.  Conjunctivitis  in  various  forms  is  a  char- 
acteristic symptom  of  scrofula ;  as  are  also  blephai'itis  ciliaris,  keratitis,  and  chronic 
rhinitis,  which  last  often  terminates  in  a  pronounced  Ozaena  (q.  v.).  Chronic 
diseases  of  the  ear  are  also  frequent,  such  as  otitis  media,  with  perforation  of 
the  tympanum,  and  occasionally  caries  of  the  mastoid  cells  and  its  unfortunate 
results. 

Of  the  deeper  lying  tissues,  mainly  the  bones  and  joints  suffer.  The  affections 
located  here  are  almost  exclusively  "  fungous  " — namely,  fungous  ostitis  and  peri- 
ostitis, white  swelling,  and  caries.  Formerly  there  was  frequent  use  of  such  terms 
as  "scrofulous  inflammation  of  the  knee-joint,"  or  "scrofulous  caries  of  the  ribs." 

If  we  inquire  into  the  nature  of  this  strange  group  of  symptoms  thus  briefly 
enumerated,  we  shall  find  that  by  far  the  greater  number  of  cases  of  well-marked 
scrofula  are  examples  of  tuberculosis.  Tubercular  bacilli  have  been  demonstrated 
in  connection  with  most  of  the  fungous  or  "  scrofulous  "  diseases  of  the  bones  and 
joints.  Ozaena  is  often  a  tubercular  disease  of  the  nose,  lupus  is  a  tuberculosis  of 
the  skin,  and  many  forms  of  otorrhcea  are  really  tuberculosis  of  the  ear.  The 
aetiology  of  "scrofula"  is  therefore  in  main  part  identical  with  that  of  tuber- 
culosis (q.  v.),  and  this  explains  why  the  old  physicians  habitually  insisted  upon 
the  intimate  relationship  between  the  two  diseases.  It  was  formerly  thought 
that  scrofula  often  terminated  in  tuberculosis — that  is,  a  scrofulous  child  is  apt  to 
suffer  eventually  from  tuberculosis  of  the  lungs,  intestine,  or  brain.  To-day  we 
know  that  most  scrofulous  children  do  not  become,  but  that  they  are  already, 
tuberculous. 

It  must,  however,  be  borne  in  mind  that  in  practice  many  diseases  are  termed 
scrofulous  which  have  nothing  to  do  with  tuberculosis.  Many  cases  of  perfectly 
innocent  eczema  of  the  face  and  scalp  lead  to  swelling  of  the  glands  in  the  throat, 
and  are  therefore  termed  scrofulous  eczema.  These  cases  are  probably  most  of 
them  secondary,  and  the  result  of  external  irritation  and  the  like.  Again,  many 
enlarged  glands  in  the  neck  are  the  result  of  pharyngeal  trouble,  as  after  scarlet 
fever,  and  are  equally  devoid  of  a  tubercular  taint.  Pseudo-leukaemic  lymphomata 
may  also  occur  in  children ;  and  it  should  be  borne  in  mind  that  hereditary  or 
acquired  syphilis  may  produce  in  children  lesions  closely  resembling  those  of 
scrofula. 

It  is  therefore  the  duty  of  the  physician  in  every  case  of  " scrofula"  to  analyze 
the  aetiology  and  symptoms  carefully,  in  order  to  determine  with  what  he  has  to 
deal.  "  Scrofula  "  should  be  regarded  merely  as  a  short  way  of  naming  a  certain 
group  of  symptoms.  It  is  convenient  to  retain  the  term  as  being  less  likely  to 
startle  the  friends  of  the  child  than  would  the  true  name  of  the  disease. 

Treatment. — In  the  treatment  of  scrofula  we  have  first  to  attack  the  various 
local  diseases,  and,  second,  to  invigorate  the  general  health.     We  can  not  here 


CONSTITUTIONAL  DISEASES.  1001 

enter  into  all  the  details  of  local  treatment,  but  we  must  refer  the  reader  to  the 
special  descriptions  already  given  of  the  various  local  affections.  We  may,  how- 
ever, briefly  mention  a  few  facts  with  regard  to  the  treatment  of  scrofulous  swell- 
ing of  the  lymph-glands.  Painting  the  overlying  skin  with  tincture  of  iodine  is 
a  very  common  practice,  but  it  seldom  does  much  good.  We  have  obtained  more 
satisfactory  results  from  iodoform  collodium,  or  iodoform  salve,  or  from  the 
repeated  inunction  of  sapo  viridis.  For  particulars  as  to  the  opening  of  abscesses, 
or  the  extirpation  of  glands,  we  must  refer  to  works  on  surgery. 

Second,  in  the  general  treatment  of  scrofula  every  possible  means  is  to  be 
employed  to  invigorate  the  system.  Abundant  nourishment  and  fresh  air  are 
essential.  The  child  may  be  taken  either  to  the  country,  or  the  mountains,  or  the 
seashore.  Cod-liver  oil  is  regarded  by  some  as  a  specific  in  scrofula;  but  its 
undoubted  value  really  lies  in  the  fact  that  it  is  an  easily  digested  fat.  Some  chil- 
dren can  take  a  considerably  larger  dose  than  others  without  its  disturbing  the 
stomach.  Usually  we  prescribe  two  or  three  tablespoonfuls  per  diem.  Salt  baths 
enjoy  a  great  reputation  as  a  remedy  in  scrofula.  If  circumstances  permit,  the 
best  way  is  to  visit  some  place  where  there  are  brine  baths,  such  as  Kosen,  Suiza, 
Salzungen,  Arnstadt,  Kreuznach,  Münster  am  Stein,  Rehme,  Reichenhall,  Ischl, 
and  Colberg. 

Treatment  at  these  resorts  is  preferable  to  artificial  baths  at  home,  because  it  is 
under  more  favorable  hygienic  surroundings. 

The  chief  internal  remedies  are  iron,  iodine,  and  arsenic.  A  favorite  prescrip- 
tion is  syrup  of  the  iodide  of  iron.  Arsenic  promotes  nutrition,  and  perhaps 
exerts  some  specific  influence  upon  certain  scrofulous  (tubercular)  local  diseases, 
particularly  the  "  fungous  "  affections  and  lupus. 


APPENDIX   I. 


SUMMARY   OP   THE   SYMPTOMS   AND   TREATMENT  IN   CASES   OF 

POISONING. 

1.  Sulphuric  Acid.— Mucous  membrane  of  mouth,  throat,  oesophagus,  and 
stomach  deeply  corroded.  In  the  worst  cases  rapid  death  ushered  in  by  convul- 
sions and  asphyxia,  or  more  rarely  consequent  upon  perforation  of  the  stomach. 
Usually  the  case  is  more  protracted.  The  mouth  and  throat  are  whitened,  or  in 
severe  cases  blackened.  They  are  soon  attacked  by  an  intense  ulcerative  inflam- 
mation. Deglutition  is  extremely  painful,  and  there  are  most  distressing  chok- 
ing and  retching.  The  vomitus  contains  black  lumps.  Profuse  salivation.  Pain 
along  the  oesophagus.  Abdomen  usually  distended  and  very  tender  on  pressure. 
There  may  be  intestinal  discharges  of  a  bloody  character,  resembling  dysentery. 
Urine  is  generally  scanty,  and  often  contains  albumen  and  blood.  Collapse. 
Small  and  rapid  pulse. 

In  mild  cases,  slow  recovery,  the  necrosed  tissues  gradually  sloughing  off. 
Cicatricial  stricture  of  the  oesophagus  frequently  ensues  and  may  prove  fatal. 
Neuralgia,  hyperassthesia,  and  various  other  nervous  disturbances  may  also  occur 
as  sequelse. 

In  fatal  cases,  the  autopsy  discloses  necrosis,  ulceration,  and  inflammation  in 
the  upper  portion  of  the  digestive  tract.  The  lining  of  the  stomach  is  usually 
coal-black.  Well-marked  parenchymatous  degeneration  of  the  liver  and  kidneys. 
Perhaps  nephritis.     In  later  stages,  extensive  cicatrices. 

Treatment :  If  used  at  all,  the  stomach-pump  must  be  introduced  very  cau- 
tiously, for  fear  of  causing  perforation.  The  best  remedy  to  give  at  once  is  several 
teaspoon fuls  of  magnesia  in  water,  or  a  few  drops  of  liquor  soda?  in  mucilage. 
Later,  the  symptoms  are  to  be  combated  with  bits  of  ice,  disinfecting  mouth-washes 
and  gargles,  tonics,  and  cautious  feeding  with  milk,  eggs,  etc.  If  stricture  of  the 
oesophagus  develops  afterward,  an  endeavor  should  be  made  to  dilate  it  with 
bougies. 

2.  Hydrochloric  and  Nitric  Acids.— Symptoms  similar  to  those  of  sulphuric 
acid.  The  most  prominent  symptoms  are  the  local  ones,  intense  stomatitis,  phar- 
yngitis, etc.  There  is  usually  albuminuria,  with  casts  and  blood  hi  the  urine. 
Nitric  acid  sometimes  stains  the  corroded  spots,  especially  the  angles  of  the  mouth, 
yellowish;  and  the  vomitus  may  have  the  same  tinge  (xanthoproteic  acid).  In 
poisoning  from  fuming  nitric  acid  the  inhaled  vapors  cause  pulmo  nary  symptoms. 
Prognosis  and  treatment  as  in  case  of  sulphuric  acid. 

3.  Nitrous  and  Sulphurous  Acid  Fumes.— Intense  local  inflammation  of  the  air- 
passages.  Violent  dyspnoea,  cough,  abundant  bloody  or  yellowish  expectoration. 
There  may  also  be  grave  nervous  disturbance  and  collapse.  Treatment :  Symp- 
tomatic :  sinapisms,  narcotics,  expectorants,  and  inhalations. 

4.  Oxalic  Acid. — Local  corrosive  action  similar  to  that  of  the  other  acids,  only 

(1003) 


1004  APPENDIX  I. 

less  severe.  In  severe  cases  collapse  from  cardiac  paralysis.  Apt  to  occasion  cer- 
tain nervous  symptoms — formication,  anaesthesia  of  the  finger-tips,  tonic  and 
clonic  convulsions,  trismus,  and  tetanus;  later  paresis.  There  is  sometimes 
sugar  in  the  urine,  and  nephritis  may  develop.  Anuria  is  frequent,  and  is  due  to 
plugging  of  the  tubules  by  calcic  oxalate  crystals.  The  treatment  should  be 
symptomatic,  and  should  also  include  the  administration  of  preparations  of  calcium 
— liquor  calcis,  calcii  carbonas,  or  even  egg-shells — to  form  insoluble  calcic  oxalate. 
Magnesia  is  also  useful. 

5.  Ammonia. — The  fumes  affect  the  air-passages  chiefly ;  the  solution,  the  upper 
part  of  the  digestive  tract.  The  specific  local  effect  is  the  production  of  an  intense 
croupous  inflammation  of  the  mucous  membrane.  Accordingly,  the  symptoms 
are  salivation,  dysphagia,  vomiting  of  strongly  alkaline  matter,  and  diarrhoea,  or 
cough,  dyspnoea,  etc.  In  severe  cases  there  is  collapse,  with  rapid  pulse,  and  such 
nervous  symptoms  as  pain,  paresthesia,  vertigo,  convulsions,  etc.  Treatment : 
In  fresh  cases  the  stomach-pump.  The  cautious  use  of  acids— for  instance,  acetic 
or  citric.     Also,  symptomatically,  emulsions  of  oil,  bits  of  ice,  and  narcotics. 

6.  Caustic  Potash,  or  Soda. — Symptoms  and  treatment  as  in  case  of  ammonia. 
In  contrast  to  acid  poisoning,  it  is  to  be  noted  that  alkalies  do  not  withdraw  water 
and  precipitate  albumen,  but  dissolve  it.  The  corroded  spots  are  therefore  not 
dry  and  brittle,  but  softened  ("  colliquation  "). 

7.  Potassic  Nitrate. — Vomiting  and  diarrhoea.  Severe  abdominal  pain.  Col- 
lapse, with  cold  skin  and  rapid,  thready  pulse.  Occasionally  the  pulse  is  slow. 
Nervous  disturbances,  such  as  painful  muscular  contractions,  and,  in  severe  cases, 
convulsions  and  coma.  Treatment :  Symptomatic ;  opium  and  other  narcotics, 
stimulants  (camphor,  ether),  and  bits  of  ice. 

8.  Chlorine  Gas. — Violent  convulsive  cough.  Bloody  expectoration.  Spasm  of 
the  glottis.  Dyspnoea.  Darting  pains  through  the  chest.  Sneezing  and  profuse 
flow  of  tears.  In  severe  cases  pneumonia.  Treatment:  Fresh  air.  Inhalation 
of  warm  aqueous  vapor,  or  of  ammonia  to  form  ammonic  chloride.  Chloroform 
may  also  be  tried,  and  narcotics. 

9.  Iodine. — 1.  Acute  iodism,  as  seen,  for  instance,  after  the  injection  of  large 
amounts  of  tincture  of  iodine  into  ovarian  cysts :  collapse,  with  pallor  and  cya- 
nosis, and  small  and  very  rapid  pulse.  Vomiting.  Often  marked  dyspnoea. 
Suppression  of  urine.  Sometimes  hemoglobinuria.  Later,  the  skin  becomes  very 
red.  There  is  albuminuria ;  also  sore  throat,  coryza,  conjunctivitis,  severe  frontal 
headache,  and  cutaneous  eruptions.  2.  Chronic  iodism,  caused,  for  example,  by 
long-continued  internal  administration  of  potassic  iodide :  coi'yza,  conjunctivitis, 
sore  throat.  Gastric  symptoms.  Vertigo,  headache,  and  similar  nervous  phe- 
nomena of  a  mild  character.  Acne  or  erythema,  sometimes  in  the  form  of  ery- 
thema nodosum.  Treatment:  In  acute  cases,  white  of  egg  and  stimulants. 
Other  than  this,  treatment  must  be  symptomatic.  Prophylaxis  demands  caution 
in  the  internal  administration  of  iodine  or  its  compounds.  According  to  Ehrlich, 
the  symptoms  of  iodism  often  disappear  rapidly  after  the  exhibition  of  about  a 
drachm  and  a  half  (grm.  6)  of  sulpho-nitro-salicylic  acid  (sulphanilic  acid). 

10.  Bromine. — 1.  Acute  poisoning  from  the  fumes  of  bromine  excites  the  same 
symptoms  as  does  chlorine  gas.  2.  Bromism,  resulting  from  the  long-continued 
use  of  potassic  bromide,  causes  languor,  debility,  mental  apathy,  and  impaired' 
intellectual  vigor.  The  reflexes  are  diminished,  particularly  the  reflex  irritability 
of  the  soft  palate  and  pharynx.  Anorexia.  Diarrhoea.  Impotence.  Almost 
invariably  a  characteristic  acne,  the  onset  of  which  may  be  delayed  by  giving 
arsenic  at  the  same  time. 

11.  Lead. — (a)  Acute  lead  poisoning  produces  severe  gastro-enteritis.  The 
best  antidote  is  sulphate  of  sodium  or  magnesium ;  or  phosphates,  white  of  egg, 


APPENDIX  I.  1005 

and  milk.     In  fresh  cases  the  stomach-pump,  or  emetics  and  purgatives.     Other 
than  this  symptomatic  treatment. 

(b)  Chronic  lead  poisoning :  Seen  in  type-setters.,  typefounders,  painters,  pot- 
ters, and  others.  General  symptoms :  Lead  line  on  the  gu  ms,  Lead  anaemia,  and  Lead 
cachexia.  Important  groups  of  symptoms  are:  1.  Lead  colic:  Violent,  colicky 
pains,  radiating  from  the  umbilicus.  Usually  constipation,  exceptionally  diar- 
rhoea. Abdomen  concave  and  hard.  Vomiting.  Hard,  slow  pulse.  Tempera- 
ture usually  normal.  Urine  sometimes  contains  a  trace  of  albumen.  Duration, 
one  or  two  weeks.  Treatment :  If  severe  pain,  opium  and  hot  compresses. 
Atropine  may  also  be  tried.  For  constipation,  enemata  and  gentle  laxatives. 
Warm  baths.  2.  Lead  paralysis  (vide  page  569).  Paralysis  of  the  laryngeal 
muscles  due  to  lead  poisoning  has  been  reported.  3.  Saturnine  encephalopathy  : 
Sudden  development  of  grave  cerebral  symptoms;  convulsions,  coma,  delirium, 
great  mental  uneasiness,  and  excruciating  headache.  Saturnine  amaurosis.  In 
severe  cases,  death.  Cerebral  lesions  are  very  rarely  found  jwst  mortem.  Treat- 
ment is  symptomatic.  Lukewarm  baths,  with  douching,  narcotics,  and  stimu- 
lants. Later,  potassic  iodide.  4.  Lead  arthralgia :  Most  frequently  attacks  the 
knee.  Also  seen  in  the  joints  of  the  upper  extremities.  Sometimes  associated 
with  painful  muscular  contractions.  Objective  lesions  are  rarely  seen.  The 
treatment  consists  in  warm  baths  and  the  administration  of  potassic  iodide.  It 
should  be  remembered  that  chronic  lead  poisoning  may  occasion  gout  and  chronic 
interstitial  nephritis.  The  reader  is  referred  to  the  chapters  describing  these 
diseases. 

12.  Copper  (Blue-Vitriol, Verdigris). — (or)  Acute  copper  poisoning :  Copper  taste. 
Vomiting  of  greenish  matter,  colic,  tenesmus,  and  bloody  stools.  Also  nervous 
symptoms,  headache,  vertigo,  anaesthesia,  paralysis,  delirium.  Collapse.  Dysp- 
noea. Treatment :  White  of  egg,  milk,  wood  charcoal.  Magnesia  is  also  valu- 
able. Yellow  potassic  ferrocyanide,  milk  sugar,  (b)  Chronic  copper  poisoning  is 
rare.  It  occasions  gastro-intestinal  disturbance,  colic,  and  a  reddish  or  greenish 
discoloration  of  the  hair. 

13.  Zinc  (Zinc  Sulp>hate  and  Chloride). — In  acute  poisoning,  symptoms  of 
severe  gastro-enteritis,  especially  vomiting.  Also  albuminuria.  Treatment: 
Albumen,  tannin,  and  alkaline  carbonates.  Chronic  poisoning  (zinc  fumes!)  : 
Fever,  distress,  vertigo,  vomiting,  metallic  taste.  General  anaemia  and  emaci- 
ation. 

14.  Mercury.— (a)  Acute  poisoning  from  corrosive  sublimate :  The  mucous 
membrane  of  the  mouth,  throat,  oesophagus,  stomach,  and  intestines  is  deeply 
corroded.  Metallic  taste.  Vomiting.  Diarrhoea  with  painful  tenesmus.  Ischu- 
ria or  complete  anuria.  Collapse.  Generally  quickly  fatal.  Treatment :  Milk, 
white  of  egg,  reduced  iron,  narcotics,  (b)  Chronic  mercurial  poisoning :  Seen  in 
the  makers  of  thermometers,  scientific  instruments,  and  mirrors.  Rarely  occa- 
sioned by  the  prolonged  use  of  antisyphilitic  remedies.  The  symptoms  are 
anaemia,  emaciation,  with  great  muscular  weakness,  and  gastro-intestinal  disturb- 
ance. In  the  therapeutic  use  of  mercury,  besides  the  rarer  mercurial  enteritis, 
mercurial  stomatitis  is  the  most  important  toxic  symptom ;  onset  of  foul-smelling 
necrosis  of  mucous  membrane,  with  ulceration  of  mucous  membrane  of  cheeks, 
jaws,  gums,  etc.  Treatment :  Immediate  discontinuance  of  medication ;  potassic 
chlorate  as  mouth-wash  and  gargle. 

Mercurial  Tremor. — Tremor  is  common  in  chronic  mercurial  poisoning  and  is 
of  special  interest.  It  is  usually  preceded  by  a  stage  of  pronounced  mental  irri- 
tability ("mercurial  erethism"),  and  often  some  mental  excitement,  fright,  etc.,  is 
the  exciting  cause  of  the  tremor.  The  tremor  itself  is  a  pronounced  intention 
tremor— that  is,  it  is  usually  not  present  when  the  body  is  kept  quiet,  but  it  comes 


1006  APPENDIX  I. 

on  with  all  movements,  like  the  tremor  in  multiple  sclerosis.  The  finer  the 
movements  the  patient  tries  to  make  the  more  marked  is  the  tremor.  Mental 
excitement  usually  increases  the  tremor  considerably.  In  severe  cases  the  tremor 
is  so  great  that  the  patients  can  not  leave  their  beds.  In  rare  cases  there  is  also 
paralysis. 

Treatment :  Dietetic  and  hygienic.  Iodide  of  potassium,  hyoscine,  and  some- 
times galvanism,  are  also  useful. 

15.  Phosphorus. — (i)  Acute  phosphorus  poisoning,  as  from  matches:  Violent 
epigastric  pain,  vomiting — the  vomitus  smells  of  phosphorus,  and  it  may  he  phos- 
phorescent. After  these  initial  symptoms  usually  comes  a  period  of  comparative 
comfort,  lasting  two  or  three  days.  Then  appear  grave  symptoms:  jaundice, 
severe  pain  in  the  hepatic  region  and  whole  abdomen,  hepatic  enlargement,  fever, 
feeble  and  rapid  pulse,  sometimes  gastric  or  intestinal  haemorrhage,  cutaneous 
ecchymoses,  haematuria,  epistaxis,  or  metrorrhagia.  The  intellect  usually  remains 
clear,  except  that  just  before  death  there  may  be  drowsiness  or  convulsions.  The 
urine  contains  albumen,  blood,  casts,  bile-pigment,  and  sometimes  leucine  and  tyro- 
sine. No  urea  is  excreted.  Death  occurs  usually  at  the  end  of  one  or  two  weeks, 
but  it  may  be  more  speedy.  In  mild  cases  the  above  symptoms  are  not  strongly 
marked,  and  recovery  may  ensue.  A  very  grave  prognosis  should  be  made  in 
every  case  at  the  start.  Post-mortem  appearances  in  acute  phosphorus  poison- 
ing :  Jaundice.  Dark  blood.  Numerous  internal  ecchymoses— for  example,  in  the 
serous  and  mucous  membranes  and  kidneys.  Fatty  degeneration  of  most  of  the 
internal  organs,  including  the  liver,  heart,  muscles,  and  kidneys.  Treatment :  In 
fresh  cases,  washing  out  of  the  stomach.  Laxatives.  As  an  emetic,  sulphate  of 
copper.  The  best  antidote  is  old  oil  of  turpentine  (30-40  drops  in  mucilage).  Oily 
substances  should  be  avoided,  as  phosphorus  is  soluble  in  oil.  Narcotics  and 
other  symptomatic  remedies  may  also  be  indicated.  (2)  Chronic  phosphorus 
poisoning:  Necrosis  of  the  lower  jaw,  less  often  of  the  upper  jaw,  extending 
from  caries  of  the  teeth.  Necrosis  of  the  bone,  with  exuberant  growth  of  osteo- 
phytes. 

16.  Arsenic  (Arsenious  Acid,  Schweinfurth  Green,  Scheele's  Green,  Arsenical 
Wall-paper).— (1)  Acute  arsenic  poisoning :  Symptoms  of  intense  gastro-enteritis, 
suggesting  cholera.  Violent  vomiting.  Eice-water  stools.  Severe  abdominal 
pain.  Nervous  symptoms:  Vertigo,  headache,  faintness,  twitchings.  Cardiac 
weakness.  Cyanosis.  Collapse.  Not  infrequently  a  cutaneous  eruption  resem- 
bling urticaria  or  eczema.  Sometimes  albumen  and  blood  are  present  in  the 
urine.  Severe  cases  are  fatal  in  one  or  two  days.  With  regard  to  arsenical 
paralysis,  vide  page  571.  Treatment :  At  first  the  stomach-pump  or  emetics— for 
example,  sulphate  of  zinc.  The  best  antidotes  are  freshly  prepared  ferric  hydrate 
in  water,  two  to  four  tablespoonfuls  every  fifteen  to  thirty  minutes;  ferrum  oxy- 
datum  saccharatum  solubile  (P.  G.),  in  teaspoonful  doses;  magnesia;  and,  best  of 
all,  the  compound  of  magnesia  and  ferric  hydrate  known  as  "  antidotum  arsenici  " 
(P.  G.),  of  which  a  tablespoonful  may  be  given  every  fifteen  to  thirty  minutes. 
(2)  Chronic  arsenic  poisoning :  Acquired  in  arsenic  works  and  glass  factories,  or 
from  arsenical  fabrics,  papers,  and  flowers.  Conjunctivitis,  chronic  gastrointesti- 
nal catarrh,  eczema,  and  cutaneous  ulcerations.  Anaemia  and  cachexia,  falling 
out  of  the  hair,  loss  of  sleep.  Treatment  is  purely  symptomatic,  except  as  regards 
prophylaxis.  In  poisoning  with  arseniuretted  hydrogen,  haemoglobinuria  and 
jaundice  occur,  with  severe  nervous  symptoms. 

17.  Alcohol.— (1.)  Acute  alcoholic  poisoning  :  Unconsciousness;  anaesthesia; 
pupils  either  dilated  or  contracted,  usually  not  reacting  to  light;  pulse  small, 
sometimes  slow ;  skin  cold  and  clammy ;  vomiting;  stertorous  respiration.  There 
may  be  delirium  and  clonic  convulsions  instead  of  coma.     Such  cases  last  three  or 


APPENDIX  I.  1007 

four  days.  Death  has  been  repeatedly  observed.  Treatment:  Bathing  and 
douching'.     Stimulants. 

(2.)  Chronic  alcoholism,  (a)  Physical  and  mental  debility :  Chronic  catarrh 
of  the  throat,  larynx,  stomach,  and  intestines.  Alcoholic  tremor.  Numerous 
organic  diseases,  including  cirrhosis  of  the  liver,  contracted  kidney,  cerebral  dis- 
ease, and  neuritis. 

(b)  Delirium  tremens :  Usually  a  sudden  onset,  as  in  conned  ion  with  some 
acute  disease  or  after  a  surgical  injury.  Disordered  intellect.  Great  restlessness, 
hallucinations  (vermin,  etc.),  excitement,  and  loss  of  sleep.  Treatment :  Bathing 
and  douching.  Injections  of  strychnine.  The  use  of  chloral  and  other  narcotics 
should  be  cautious.  Physical  restraint  should  be  avoided  if  possible.  The  patient 
may  often  be  allowed  to  go  about  the  room  as  he  likes,  if  only  he  be  watched. 
Alcohol  should  be  given  if  collapse  be  threatened. 

18.  Chloroform.— Unconsciousness.  Loss  of  sensibility  and  reflexes.  Slow 
pulse.  Pupils  dilated.  Failure  of  respiration,  and  finally  of  the  heart.  Danger  of 
heart  failure,  especially  in  persons  with  weak  hearts.  Treatment :  Artificial  respi- 
ration.    Injections  of  strychnine.     Stimulants.     Counterirritation. 

19.  Iodoform. — (Repeatedly  seen  from  the  use  of  iodoform  on  wounds).  First 
of  all,  nervous  symptoms:  headache,  vertigo,  sleeplessness.  Peculiar  psychoses, 
maniacal  attacks,  deltisions  of  persecution,  refusal  of  food.  In  severe  cases  con- 
vulsions, deep  coma.  Very  small,  rapid  pulse.  Treatment :  symptomatic,  by 
stimulants,  baths,  etc.  Alkalies  and  atropine  are  recommended,  but  their  action 
is  doubtful. 

20.  Carbonic-oxide  Gas  (Illuminating  Gas).—  At  first,  vertigo,  headache,  throb- 
bing in  the  temples,  ringing  in  the  ears,  and  spots  before  the  eyes.  The  patient 
gradually  becomes  unconscious.  Skin  pale  and  cyanotic.  Respiration  intermit- 
tent. Subnormal  tenmerature.  The  urine  may  contain  albumen  and  sugar.  The 
carbonic  oxide  may  be  demonstrated  in  the  blood  by  means  of  the  spectroscope. 
Its  color  is  clear  cherry-red  (CO-hgemoglobine).  Subsequently  paralysis,  disturb- 
ances of  sensation  and  of  speech.  Treatment :  Fresh  air,  artificial  respiration, 
stimulants,  transfusion. 

21.  Sulphuretted  Hydrogen. — Headache,  vomiting,  diarrhoea.  In  severe  cases, 
unconsciousness,  dyspnoea,  cyanosis,  convulsions,  and  death.  The  blood  is  thin, 
fluid,  and  black  (sulph-hsemoglobine).  Treatment :  Artificial  respiration,  fresh 
air,  and  the  cautious  inhalation  of  chlorine  gas. 

22.  Bisulphide  of  Carbon.— (Workers  in  rubber  factories).  Vomiting.  Severe 
nervous  symptoms.  Incontinence  of  urine,  atrophic  paralyses,  anaesthesia,  men- 
tal disturbances,  especially  loss  of  memory,  spasmodic  conditions,  etc.  The  red 
blood-corpuscles  are  destroyed;  the  black  blood  contains  many  flakes  of  pigment. 
Treatment:  symptomatic. 

23.  Hydrocyanic  Acid  (Potassic  Cyanide;  Bitter  Almonds).— Characteristic 
odor  of  bitter  almonds.  In  severe  cases  death  may  occur  in  a  few  minutes.  If 
the  course  be  more  protracted,  convulsive  and  extremely  slow  respiration,  the 
expiratory  act  being  much  prolonged ;  the  eyeballs  protrude,  and  the  pupils  are 
somewhat  enlarged  and  do  not  react  to  light.  Cardiac  weakness,  cyanosis,  uncon- 
sciousness. Twitching  of  the  muscles.  Trismus.  Treatment :  Merely  symptom- 
atic. Emetics,  artificial  respiration,  cool  douches,  stimulants.  Atropine  may  be 
tried;  also,  hydrated  ferric  oxide  and  chlorine  water. 

24.  Nitrobenzine  (Nitrobenzole,  Oil  of  Mirbane).— Strong  odor  of  bitter  alm- 
onds. At  first,  dizziness.  The  skin  soon  assumes  a  bluish  hue,  rapidly  increas- 
ing to  the  deepest  cyanosis.  Increasing  anxiety,  sense  of  suffocation,  and  gradual 
loss  of  consciousness.  In  severe  cases,  death,  ushered  in  by  convulsions.  In 
milder  cases,  gradual  recovery.     Treatment :  Stomach-pump.     Artificial  respira- 


1008  APPENDIX  I. 

tion.  Stimulants.  In  the  Leipsic  clinique,  transfusion  has  worked  admirably  in 
two  cases.  The  symptoms  caused  by  aniline  and  the  aniline  dyes  closely  resemble 
poisoning  from  nitrobenzole. 

25.  Carbolic  Acid. — Corrosion  of  mouth,  throat,  and  stomach.  In  mild  cases, 
vertigo  and  headache ;  in  severe  cases,  coma,  preceded  in  rare  instances  by  symp- 
toms of  cerebral  irritation.  Contracted  pupils.  Vomiting.  Pulse  slow  at  first, 
then  rapid.  The  urine  has  a  dark,  olive-green  color.  Sometimes  hemoglobinuria 
and  nephritis.  Treatment:  Stomach-punip.  Slaked  lime  and  water.  Large 
doses  of  sulphate  of  sodium  are  especially  to  be  recommended. 

26.  Atropine  {Belladonna). — Dryness  of  the  mouth  and  throat.  Excessive 
thirst.  Dizziness  and  headache.  Peculiar  mental  disturbances:  hallucinations 
are  particularly  frequent.  Pupils  very  widely  dilated.  Cutaneous  erythema 
resembling  that  of  scarlet  fever.  In  severe  cases,  pulse  enormously  accelerated, 
with  violent  pulsation  in  the  arteries.  Convulsions  may  occur.  Nervous  symp- 
toms persist  for  some  time.  Treatment :  The  following  physiological  antidotes 
should  be  tried:  physostigmine  (eserine),  pilocarpine,  and  morphine. 

27.  Digitalis. — Vomiting.  Diarrhoea.  Pulse  very  slow  (forty  beats  per  minute, 
or  less).  Dyspnoea.  Symptoms  of  collapse.  Cold  extremities,  muscular  tremor. 
Somnolence.  In  the  worst  cases,  sopor  and  death.  Even  the  milder  cases  are 
protracted.  Treatment :  Emetics,  stomach-pump.  Tannin.  Camphor,  strong 
cafe  noir,  ether,  ammonia.     Counter-irritation. 

28.  Nicotine  (Smoking;  Tobacco  Juice ;  Tobacco  Enemata).— 1.  Acute :  Pulse 
small  and  slow,  syncope,  sense  of  oppression,  salivation,  vomiting.  In  severe 
cases,  loss  of  consciousness,  tetanic  spasms,  both  pulse  and  respiration  intermittent. 
2.  Chronic  (from  excessive  use  of  tobacco) :  Palpitation,  irregular  action  of  the 
heart,  paroxysms  of  asthma  and  angina  pectoris.  Tremor,  muscular  weakness.  Loss 
of  sleep.  Sometimes  there  are  symptoms  of  ataxia  ("  nicotine  tabes  "  seen  in  cigar 
makers).  Amblyopia,  scintillating  scotoma.  Gastric  disturbance,  chronic  catarrh 
of  the  pharynx  and  larynx.  Treatment :  In  acute  cases,  stimulants.  Chronic 
poisoning  necessitates  the  giving  up  of  tobacco.    Further  treatment  is  symptomatic. 

29.  Strychnine. — Violent  tetanic  reflex  convulsions.  Exaggeration  of  the  cuta- 
neous and  tendon  reflexes.  Trismus.  Opisthotonos.  Pulse  small  and  very  rapid. 
The  convulsions  come  in  paroxysms,  with  intervals  between  them.  The  intellect 
is  usually  perfectly  clear.  Eecovery  occurs  only  in  mild  cases.  Treatment: 
Emetics,  stomach-pump.  Tannin.  Tincture  of  iodine.  Castor-oil.  The  convul- 
sions are  to  be  combated  by  morphine,  chloroform,  chloral,  or  potassic  bromide. 
Curare  has  also  been  tried. 

30.  Coniine  (Hemlock).— In  severe  cases  convulsions,  then  general  paralysis, 
especially  of  the  respiratory  muscles,  loss  of  consciousness,  and  death.  Pupils 
dilated.  In  milder  cases  confusion,  muscular  weakness,  vomiting,  and  diarrhoea. 
Treatment :  Emetics,  tannin,  stimulants. 

31.  Morphine  (Opium).— 1.  Acute:  Begins  with  fatigue,  headache,  darkening 
of  the  visual  field,  nausea,  vomiting.  Then  coma  comes  on  with  slow,  stertorous, 
sometimes  irregular  respiration.  Muscles  completely  lax.  Pupils  usually  very 
small.  Pulse  often  slow,  but  in  other  cases  rapid  and  small.  Toward  the  end  of 
life  Cheyne-Stokes's  respiration.  In  milder  cases  only  vomiting,  stupor,  headache, 
etc.  Treatment :  Sulphate  of  zinc,  or  some  other  emetic ;  stomach-pump.  Tan- 
nin. Cafe  noir.  Atropine  may  be  tried  as  a  physiological  antidote.  Stimulants 
(camphor,  ether)  are  best,  also  cold  baths  with  shower-baths;  artificial  respiration. 
2.  Chronic  (morphine  habit):  Emaciation,  anaemia,  headache,  vertigo,  wakeful- 
ness. Tremor.  Mental  disturbance.  Unconquerable  longing  for  morphine ;  and, 
if  this  be  denied,  the  appearance  of  grave  symptoms.  To  break  up  the  morphine 
habit  is  almost  impossible  except  in  hospitals  and  special  asylums.     The  with- 


APPENDIX  I.  1009 

drawal  of  the  drug  is  abrupt  according  to  the  practice  of   some,  and  gradual 
according  to  others.     For  particulars  consult  monographs. 

32.  Ergot  (Ergotine). — 1.  Acute:  At  first  nausea,  vomiting,  colic,  and  diar 
rhcea.  Then  vertigo,  headache,  and  muscular  weakness.  Pulse  slow,  in  .severe 
cases,  sopor,  disturbance  of  respiration,  and  sometimes  death.  Treatment :  Emet- 
ics and  purgatives.  Tannin.  Ether,  camphor,  and  cafe"  noir  as  stimulants.  2. 
Chronic  ergotism :  Gastric  symptoms,  vertigo,  languor,  cardiac  weakness.  The 
nervous  disturbances  are,  however,  of  especial  importance.  Of  these,  pallesthesia 
has  long  been  recognized.  Recently  attention  has  been  attracted  to  the  great 
resemblance  of  the  nervous  symptoms  to  those  of  tabes  dorsalis;  and  there  is, 
moreover,  an  anatomical  change  in  the  posterior  columns  of  the  cord.  Convul- 
sions and  psychical  phenomena  are  also  observed.  A  second  form  of  chronic 
ergotism  is  called  gangrenous  ergotism.  It  results  in  dry  gangrene  of  the  hands 
and  feet.  A  line  of  demarcation  forms  and  the  gangrenous  parts  slough  off. 
The  process  may  be  attended  by  fever  and  pyaemia.  The  probable  explanation  is 
that  the  minute  blood-vessels  become  spasmodically  contracted  and  thrombi  form 
under  the  influence  of  the  poison.  The  different  symptoms  are  due  in  part  to  the 
different  constituents  of  the  ergot.  The  best  known  are  sphacelinic  acid,  which  is 
probably  the  cause  of  gangrenous  ergotism  and  ergotine  tabes ;  cornutine,  which 
causes  severe  convulsive  symptoms  (convulsive  ergotism)  and  uterine  contrac- 
tions; and  finally  ergotinic  acid.  The  treatment  of  chronic  ergotism  is  purely 
symptomatic. 

33.  Poisonous  Mushrooms. — 1.  Poisoning  from  morels :  Fresh  morels  ("  mor- 
cheln"  or  "  lorcheln  ")  contain  a  poison  which  is  readily  soluble  in  hot  water,  and 
which  evaporates  completely  if  the  morels  be  dried.  Morels  that  have  been  dried 
or  parboiled  are  therefore  perfectly  harmless,  but  the  fresh  ones  are  poisonous. 
The  symptoms  are  nausea,  vomiting,  diarrhoea,  headache,  coma,  and,  above 
all,  haemoglobinaemia  and  haemoglobin uria  (q.  v.),  associated  with  which  is  a 
haematogenous  icterus.  In  severe  cases  death  occurs,  ushered  in  by  convulsions. 
Treatment  is  symptomatic,  and  includes  the  administration  of  emetics,  purgatives, 
and  stimulants.  2.  Poisoning  from  the  red  agaric  (amanita  muscaria);  This 
contains  the  poisonous  alkaloid  muscarine.  Gastric  symptoms  and  diarrhoea. 
Mental  excitement,  delirium,  tetanic  and  epileptiform  convulsions.  A  rapid  pulse, 
small  pupils,  disturbed  vision  from  spasm  of  accommodation,  sweating,  salivation, 
and  in  most  of  the  severe  cases  sopor  and  death.  Treatment :  Emetics,  etc.-  Atro- 
pine, which  acts  as  a  physiological  antidote  to  muscarine.  Also  tannine,  and 
stimulants.  3.  Poisoning  from  tubercular  mushrooms  (amanita  phalloides),  con- 
fused with  young  button  mushrooms  (champignons) .  Digestive  disturbances,  later 
jaundice,  somnolence,  coma.  The  autopsy  shows  fatty  degeneration  of  the  liver, 
kidneys,  and  stomach,  as  in  phosphorus  poisoning. 

34.  Poisoning  from  Sausages  (Botulismus).—  This  sometimes  occurs  as  the  result 
of  eating  partially  decayed  sausages.  The  symptoms  are  pain  in  the  stomach, 
nausea,  vomiting,  colic,  and  diarrhoea.  There  are  also  marked  feebleness,  prae- 
cordial  anxiety,  and  dyspnoea ;  vertigo,  headache,  somnolence ;  and  very  often 
disturbance  of  vision  (amblyopia,  spots  befoi*e  the  eyes),  and,  what  is  surprising, 
ptosis.  In  severe  cases,  dysphagia,  as  a  result  of  more  or  less  complete  paralysis  of 
the  tongue  and  the  constrictors  of  the  pharynx.  The  mouth  is  dry.  The  heart 
is  feeble ;  this  and  the  general  prostration  and  malnutrition  may  prove  fatal.  The 
cases  are  usually  protracted,  rarely  being  very  acute.  The  active  principles  (al- 
kaloids of  putrefaction;  have  lately  become  known  in  part.  In  sausage  and  also 
in  meat  poisoning  the  most  important  substance  is  ptomato-atropine,  a  substance 
which  acts  almost  exactly  like  atropine.  Treatment:  Emetics,  purgatives  (cal- 
omel), stimulants,  and,  if  indicated,  artificial  feeding. 

64 


1010  APPENDIX  I. 

35.  Poisoning  from  Meat. — In  repeated  instances  severe  symptoms  have  been 
occasioned  by  eating  tainted  meat,  or  possibly  that  obtained  from  animals  which 
had  been  diseased.  These  symptoms  are  certainly  due  to  the  products  of  putre- 
faction, substances  which  act  partly  like  muscarine,  partly  like  atropine,  neurine, 
methylguanidine,  etc.  The  special  poison  is  not  yet  fully  known.  Probably  there 
are  several  poisons,  either  chemical  or  organic  and  infectious.  The  usual  symp- 
toms are  vomiting  and  diarrhoea.  The  case  may  closely  simulate  cholera.  In 
most  instances  certain  nervous  phenomena  are  also  observed — wakefulness,  deliri- 
um, headache,  and  changes  in  the  pupils.  Thei'e  may  be  roseola  or  wheals  or 
erythema.  Frequently  there  is  a  high  fever,  but  sometimes  the  temperature  is 
subnormal.  The  pulse  is  small  and  slightly  accelerated,  although  it  may  occa- 
sionally be  slower  than  normal.  There  is  a  sense  of  thoracic  oppression.  The 
cases  are  often  j)rotracted.  Tendency  to  relapses.  Death  may  occur.  Post  mortem, 
there  is  usually  found  an  intense  and  often  hemorrhagic  enteritis  with  secondary 
changes  in  the  spleen,  kidneys,  lungs,  and  other  organs.  Treatment :  Symptom- 
atic: calomel,  emulsions,  stimulants,  and  baths.  Food  should  be  given  cau- 
tiously. 

36.  Poisoning  from  Fish. — The  eating  of  tainted  fish  has  likewise  caused  grave 
disturbance.  The  symptoms  vary.  Usually  there  are  pain  in  the  stomach,  pre- 
cordial anxiety,  vertigo,  dryness  of  the  throat,  aphonia,  and  labored  respiration. 
There  may  also  be  disturbance  of  vision,  amblyopia,  and  colored  vision,  or  paraly- 
sis of  the  motores  oculi  and  of  accommodation.  In  severe  cases  there  may  be 
dysphagia  and  general  paresis.  Sometimes  dyspnoea  and  cardiac  weakness  are 
observed.  The  cases  are  frequently  very  tedious.  Here,  too,  there  are  many  active 
poisonous  products  of  putrefaction,  among  them  one  which  acts  like  muscarine. 
Treatment  similar  to  that  recommended  in  the  two  preceding  paragraphs. 

37.  Poisoning  from  Mussels  (Mytilus  Edulis).  This  is  also  common.  A  draw- 
ing feeling  in  the  neck,  a  blunt  feeling  in  the  teeth,  crawling  and  burning  in  the 
arms  and  legs,  dixllness  in  the  head,  mental  excitability,  feeling  as  if  everything 
were  light,  as  if  the  patient  must  fly ;  in  the  later  stages  dilated,  immobile  pupils, 
difficult  speech,  paresis  and  ataxia  of  the  muscles;  also  nausea,  skin  eruptions 
(urticaria),  fall  of  temperature.  In  severe  cases  death  may  ensue  in  a  few  hours. 
At  the  autopsy  we  find  severe  enteritis,  enlargement  of  the  spleen,  and  often  a 
peculiar  speckling  of  the  liver.  The  poison  of  mussels  that  is  known  has  been 
called  mytilotoxine. 

38.  Poisoning  from  Cheese.— Vomiting,  colicky  pains,  diarrhoea,  vertigo,  sense 
of  thoracic  oppression,  headache,  languor,  and  disturbance  of  vision.  Treatment 
as  in  paragraphs  35  and  36. 


APPENDIX   IL 


TABLE   OF   WEIGHTS   AND   MEASURES. 


Minims- 

Cubic 
Centimetres. 

1 

= 

•06 

2 

= 

•12 

5 

= 

•31 

10 

= 

•62 

15 

= 

•92 

16i 

= 

1-00 

20 

= 

1-23 

Table  of  Relation  op  IT.  S.  Fluid  to  Metric  Measure. 


Cubic 
Centimetres. 

14-79 

22-18 

Cubic 
Centimetres. 

29-57 

59-10 

88-67 


Minims. 

Cubic 
Centimetres. 

Fluid 
Drachms 

30 

=            1-85 

4 

40 

=          2-46 

6 

Fluid 
Drachms. 

Cubic 
Centimetres. 

Fluid 
Ounces. 

1 

=          3-70 

1 

2 

=          7-39 

2 

3 

=        11-09 

3 

Fluid 
Ounces. 

Cubic 
Centimetres. 

4 

=          118-24 

6 

=          177-39 

8 

=           236-53 

12 

=          354-82 

16 

=          473-11 

Table  of  Relation  of  Troy  Weight  to  Grammes. 


rains. 

Grammes. 

Grains. 

i 

= 

•008 

8 

I 

= 

•011 

10 

i 

= 

■016 

15 

i 

= 

•032 

15-43 

l 

= 

•065 

20 

2 

= 

•13 

30 

4 

= 

•26 

40 

5 

= 

•32 

61-73 

6 

= 

•39 

Grammes. 

•52 

•65 

•97 

1-00 

1-29 

1-94 

2-59 

4-00 


Drachms. 
1 

1* 

2 
3 
4 
6 


Grammes. 

3-89 

5-83 

7-77 

11-66 

15-55 

23-3 


Ounces. 

Grammes. 

.1 

= 

31-1 

H 

= 

46-6 

2 

= 

62-2 

3 

= 

93-3 

4 

= 

124-4 

6 

=: 

186-6 

8 

= 

248-8 

The  Metric  System  in  Medicine. 


Old  Style. 

tu  j  or  gr.  j 

f  3  j  or      3-3 


Metric. 

06  grm. 


The  decimal  line,  instead  of  points,  makes  errors  impossible.  As  *06  (drug)  is 
less  than  a  grain,  while  4*  and  32'  (vehicle)  are  more  than  the  drachm  and  ounce, 
there  is  no  danger  of  giving  too  large  doses  of  strong  drugs. 

C.c.  (cubic  centimetres),  used  for  grms.  (grammes),  causes  an  error  of  five  per 
cent  (excess). 

A  teaspoonful  is  usually  5  grms. ;  a  tablespoonful,  20  grms. 


I^TDEX. 


Abasia,  803  (foot-note). 

Abdomen  in  typhoid  fever,  10. 

Abdominal  typhus,  1. 

Abdueens  nerve,  paralysis  of,  556. 

Abortion  in  acute  yellow  atrophy  of  the  liver,  488  ; 
in  chorea,  784  ;  in  pernicious  anaemia,  944  ;  in  ty- 
phoid fever,  18. 

Abscesses,  embolic,  in  lungs,  247 ;  in  appendicitis, 
420  ;  in  glanders,  116 ;  in  parotitis,  349  ;  in  peri- 
nephritis, 868  ;  in  perityphlitis,  420  ;  in  smallpox, 
56  ;  in  septico-pysemia,  110  ;  in  typhoid  fever,  17  ; 
of  brain,  741 ;  of  liver,  476  ;  of  mediastinum,  273  ;  of 
tonsils,  353  ;  retropharyngeal.  360  ;  sub-diaphrag- 
matic, in  peritonitis,  456. 

Absorption,  impaired,  in  chronic  gastric  catarrh,  375. 

Accentuation  of  the  aortic  second  sound  in  chronic 
nephritis,  859  ;  in  arterio-sclerosis,  333  ;  of  the  pul- 
monic second  sound  in  emphysema,  178  ;  in  mitral 
regurgitation,  285  ;  in  mitral  stenosis,  287. 

Accessorius  nerve,  spasm  of,  574  ;  position  of  head  in 
spasm  of,  574  ;  paralysis  of,  562. 

Acetonsemia  in  diabetes,  969. 

Acetone,  odor  of,  in  diabetes,  971 ;  reaction,  969. 

Achilles'  tendon  reflex,  545. 

Acholia,  489. 

Achromatopsia  in  hysteria,  801. 

Acid  dyspepsia,  382. 

Acid,  free,  in  gastric  juice,  tests  for,  378. 

Aconitine  in  neuralgia,  520  ;  in  trigeminal  neuralgia, 
523. 

Acoustic  nerve,  atrophy  of,  in  locomotor  ataxia,  643. 

Acromegaly,  589. 

Actinomycosis,  274. 

Acupuncture  in  aneurism,  338  ;  in  cardiac  dropsy,  306. 

Acute  bulbar  paralysis,  691. 

Acute  tuberculosis,  236. 

Acute  yellow  atrophy  of  the  liver,  485. 

Addison's  disease,  878. 

Adenia,  951. 

Adeno-carcinoma,  426. 

Adenoid  growths  in  pharynx,  358. 

Adherent  pericardium,  326. 

Adrenals  in  Addison's  disease,  879. 

.Egophony,  260. 

After-sensations,  509  ;  in  locomotor  ataxia,  640. 

Agaricine  in  pulmonary  tuberculosis,  235. 

Ageusia,  533. 

Agraphia,  720. 

Ague,  90. 

Air,  inspired,  as  carrier  of  infection,  209. 

Alalia,  685. 

Albumen  in  urine,  tests  for,  823. 


Albuminous  expectoration  in  pleurisy,  266. 

Albuminuria,  accidental,  821 ;  in  acute  ascending 
spinal  paralysis,  675  ;  in  acute  Bright's  disease, 
841  ;  in  anaemia,  934,  942  ;  in  bulbar  apoplexy,  692  ; 
in  chronic  Bright's  disease,  852,  859  ;  in  diabetes, 
970  ;  in  diphtheria,  70  ;  in  epilepsy,  773;  in  erysipe- 
las, 64  ;  in  fevers,  837  ;  in  gout,  987  ;  neurotic,  825  ;  in 
osteomalacia,  92"  ;  physiological,  823  ;  in  pneumo- 
nia, 197  ;  renal,  genuine,  824  ;  in  scarlet  fever,  41 ; 
in  scurvy,  959  ;  in  smallpox,  56  ;  spurious,  824  ; 
transitory,  825  ;  in  typhoid  fever,  17  ;  in  yellow 
fever,  102. 

Albuminuric  retinitis,  854,  861. 

Alcohol,  effects  of,  on  the  digestive  system,  372,  374  ; 
on  the  kidneys,  856  ;  on  the  nervous  system,  584  ; 
poisonous  effects  of,  1006. 

Alcoholic  beverages  in  aneemia,  936  ;  in  diabetes,  979  ; 
in  gout,  991  ;  in  neurasthenia,  818  ;  in  obesity,  993  ; 
in  pneumonia,  206  ;  in  tuberculosis,  232. 

Alcoholic  neuritis,  584. 

Alcoholic  poisoning,  acute,  1006. 

Alcoholism,  1006  ;  acute,  1006  ;  chronic,  1007  ;  treat- 
ment of,  1006. 

Alexia,  720. 

Alimentary  canal,  tuberculosis  of,  215,  423. 

Alkalies  in  diabetes,  981;  in  gout,  991. 

Allantiasis  (botulismus),  1009. 

Alopecia,  589. 

Altitude  in  tuberculosis,  233. 

Alum  in  intestinal  catarrh  of  children,  417. 

Amaurosis,  anaemic,  932  ;  in  gastric  ulcer,  387  ;  hys- 
terical, 802  ;  ursemic,  832. 

Amblyopia,  751 ;  in  hysteria,  802. 

Ambulatory  typhoid  fever,  18. 

Amimia,  720. 

Ammoniaemia,  883,  890,  895. 

Ammonia  in  asthma,  172  ;  in  diabetes,  981 ;  poisoning 
from,  1004. 

Amnesia,  717. 

Amoeba  coli  (amoeba  dysenteria?).  81  ;  in  liver  ab- 
scess, 81  ;  in  lungs,  81. 

Amoebic  dysentery,  81. 

Amphoric  breathing,  222,  269. 

Amyl  nitrite  in  asthma,  172 :  in  epilepsy,  778 ;  in 
hemicrania,  593  ;  in  trigeminal  neuralgia,  523  ;  in 
valvular  disease,  307. 

Amyloid  disease,  chronic  nephritis  combined  with, 
865  ;  of  kidney,  864  ;  of  liver,  498  ;  in  phthisis,  228  ; 
in  syphilis,  865. 

Amyotrophic  lateral  sclerosis,  650. 

Anaemia  in  Addison's  disease,  880;  in  anchylostomia- 
sis,  448  ;    in  articular  rheumatism,  906  ;  fever  in, 
(1013) 


1014 


INDEX. 


934  :  from  gastric  atrophy,  939  ;  in  gastric  cancer, 
391  ;  in  gastric  ulcer,  387  ;  idiopathic,  928  ;  tubercu- 
losis as  a  complication  of,  326,  424  ;  progressive 
pernicious,  938  ;  primary  or  essential,  928  ;  second- 
ary, 929  ;  toxic,  931. 

Anaemia,  pernicious,  938  ;  associated  with  atrophy  of 
gastrointestinal  walls,  939  ;  chemical  examination 
of  blood  in,  943  ;  diagnosis,  944  ;  post-mortem  le- 
sions in,  940  ;  symptoms  of,  941  ;  treatment  of, 
944. 

Anaemia,  simple  constitutional,  928  ;  diagnosis  of, 
936  ;  symptoms  of,  931  ;  treatment  of,  936. 

Anaemia,  spastic,  511  ;  splenic,  944. 

Anaemic  murmurs,  933. 

Anaesthesia,  510  ;  dolorosa,  512  ;  in  hemiplegia,  733  ; 
in  hysteria,  800  ;  in  locomotor  ataxia,  636  ;  in  Mor- 
van's  disease,  679  ;  in  myelitis,  619  ;  in  neuralgia, 
517  ;  in  neuromata,  586  ;  in  railway  spine,  820  ;  in 
unilateral  lesions  of  the  spinal  cord,  683  ;  of  the 
skin,  510  ;  of  the  trigeminus,  513. 

Analgesia,  508  ;  in  hysteria,  800  ;  in  locomotor  ataxia, 
656,  640  ;  in  Morvan's  disease,  679  ;  in  syringo-mye- 
lia,  678. 

Anarthria,  685  ;  in  bulbar  apoplexy,  692. 

Anchylostomum  duodenale,  448. 

Aneurism,  334  ;  cylindrical,  334;  dissecting,  340  ;  fusi- 
form, 334  ;  sacciform,  334  ;  of  the  abdominal  aorta, 
339  ;  of  carotid  artery,  339  ;  of  the  cerebral  arteries, 
725  ;  of  the  heart,  308,  330  ;  of  subclavian  artery, 
339  ;  of  pulmonary  artery,  218,  339. 

Aneurism  of  thoracic  aorta,  334  ;  diagnosis  of,  337  ; 
dyspnoea  in,  336  ;  haemorrhage  in,  337  ;  pain  in, 
337  ;  physical  signs  of,  335  ;  symptoms  of,  335  ; 
treatment  of,  338  ;  Tuf nell's  treatment  of,  338. 

Angina  pectoris,  397,  309,  310,  318  ;  pseudo  or  hyster- 
ical, 318. 

Angina  (see  Sore  Throat). 

Angio-neurotic  oedema,  588. 

Animal  lymph,  59. 

Animals,  lower,  diphtheria  in,  67. 

Ankle  clonus,  545  ;  in  cerebral  haemorrhage,  732  ;  in 
hysterical  paraplegia,  803 ;  in  myelitis,  620 ;  in 
spastic  paraplegia,  664  ;  in  tetanus,  792. 

Anosmia,  532. 

Anterior  crural  nerve,  paralysis  of,  568. 

Anthracosis  of  lungs,  245. 

Anthrax,  117  ;  bacillus,  117  ;  in  animals,  118. 

Antidotes  in  poisoning  from  atropine,  1008  ;  lead, 
1004  ;  mushrooms,  1009  ;  phosphorus,  1006. 

Antidotum  arsenici,  1006. 

Antimony,  arsenite  of,  in  cardiac  valvular  disease, 
303. 

Antipyrine  in  typhoid  fever,  24. 

Antiseptic  medication  in  typhoid  fever,  20. 

Antiseptics  in  pyelitis,  884. 

Anuria  in  hydronephrosis,  892;  in  nephritis,  841. 

Aorta,  aneurism  of,  334  ;  hypoplasia  of,  in  chlorosis, 
929  ;  rupture  of,  339. 

Aortic  incompetency,  287  ;  sudden  death  in,  290  : 
symptoms  of,  287. 

Aortic  orifice,  congenital  lesions  of,  294. 

Aortic  stenosis,  290. 

Apex  of  lungs,  catarrh  affecting,  222. 

Apex  pneumonia,  195,  202. 

Aphasia,  716  ;  amnesic,  717  ;  anatomical  localization 
of,  716  ;  ataxic,  717  ;  diagnosis  of,  719  ;  hemiplegia 
with,  736  ;  in  typhoid  fever,  16. 

Aphemia  (see  Aphasia),  716. 


Aphonia,  hysterical,  803  ;  in  acute  laryngitis,  130  ;  in 
adductor  paralysis,  140  ;  in  pericardial  effusion, 
325. 

Aphthae,  343. 

Aplasia  of  the  lungs,  181. 

Apoplectic  cyst,  727  ;  habit,  726  ;  scar,  727. 

Apoplexy,  728  ;  delayed.  728  ;  from  cerebral  syphilis, 
758  ;  from  haematoma  of  the  dura  mater,  697  ;  from 
haemorrhage  into  medulla  and  pons,  691  ;  from 
tumors  of  the  brain,  750 ;  ingravescent,  728  ;  in 
multiple  sclerosis,  630  ;  premonitory  symptoms  of, 
728  ;  pulmonary,  247  ;  spinal,  604. 

Appendicitis,  420. 

Appendix  vermiformis,  perforation  of,  in  typhoid 
fever,  11  ;  situation  of,  420. 

Apraxia,  720. 

Apyrexia  in  relapsing  fever,  32. 

Arachnitis  (see  Meningitis). 

Aran-Duchenne  type  of  muscular  atrophy,  653. 

Arbutine  in  cystitis,  896. 

Arch  of  aorta,  aneurism  of,  334. 

Argyll-Robertson  pupil,  642  ;  in  ataxia,  642  ;  in  pro- 
gressive general  paralysis,  763. 

Arm,  peripheral  paralysis  of,  564. 

Arhythmia,  297. 

Arsenical  neuritis,  571. 

Arsenical  poisoning,  931,  1006  ;  paralysis  in,  571. 

Arsenic  in  anaemia  and  chlorosis,  938  ;  in  asthma, 
172 ;  in  cerebral  tumor,  756  :  in  chorea,  783  ;  in 
diabetes,  981  ;  in  exophthalmic  goitre,  598 ;  in 
habitual  headache,  531  ;  in  hysteria,  813  ;  in  leu- 
kaemia, 950  ;  in  locomotor  ataxia,  648  ;  in  malaria, 
97  ;  in  neuralgia,  519  ;  in  paralysis  agitans,  787  ;  in 
pernicious  anaemia,  945  ;  in  pseudo-leukasmia,  953  ; 
in  scrofula,  1001  ;  in  spasm  of  the  muscles  of  the 
neck,  575  ;  paralysis  from,  571  ;  poisoning  from, 
931,  1006. 

Arteries,  diseases  of,  331  ;  calcification  of,  331. 

Arterio-sclerosis,  331  ;  in  diabetes,  972 ;  in  obesity, 
996  ;  symptoms  of,  332  ;  treatment  of,  334. 

Arteritis,  syphilitic,  757. 

Arthralgia  from  lead,  1005. 

Arthritis,  acute  rheumatic,  900  ;  gonorrhceal,  901  ;  in 
cerebro-spinal  meningitis,  106  ;  in  dengue,  99  ;  in 
diphtheria,  70  ;  in  dysentery,  79  ;  in  haemophilia, 
962 ;  in  purpura,  965  ;  in  scarlet  fever,  43,  901  :  in 
tabes  dorsalis,  644  ;  multiple  secondary,  901,  907  ; 
rheumatoid,  911  ;  septic,  111,  907. 

Arthritis  deformans,  911  ;  monarticular  form  of,  914  ; 
of  the  poor,  912 ;  of  the  rich,  985  ;  polyarticular 
form  of,  914  ;  sicca,  913. 

Arthrogryposis,  576. 

Arthropathies  in  tabes,  644. 

Arthrospores,  82. 

Asafoetida  in  hysteria,  813. 

Ascaris  lumbricoides,  445. 

Ascites,  460  ;  from  cancerous  peritonitis,  463  ;  in  can- 
cer of  the  liver,  493  ;  in  cancer  of  the  pancreas, 
504  ;  in  children,  459  ;  in  chronic  endocarditis,  299  : 
in  cirrhosis  of  the  liver,  480  ;  in  scarlet  fever,  42  ; 
in  suppurative  hepatitis,  477  :  in  syphilis  of  the 
liver,  491 ;  in  thrombosis  of  the  portal  vein,  502  :  in 
tuberculous  peritonitis,  459  ;  physical  signs  of,  461  ; 
treatment  of,  462. 

Ascitic  fluid,  461  ;  haemorrhagic,  461. 

Aspect,  facial,  in  paralysis  agitans,  785. 

Asphyxia,  local,  588 ;  death  by,  in  phthisis,  217  ;  in 
diphtheria,  68. 


INDEX. 


1015 


Aspiration  in  empyema,  204  :  in  pericardial  effusion, 
328  ;  in  pleuritic  effusion,  Stil. 

Aspiration  pneumonia,  185. 

Associated  movements,  541  ;  in  cerebral  haemor- 
rhage, 735  ;  in  facial  paralysis,  561  ;  in  infantile 
cerebral  paralysis,  745  ;  of  the  facial  muscles  in 
progressive  paralysis,  7(12. 

Astasia-abasia,  803. 

Asthenopia,  neurasthenic,  810. 

Asthma,  bronchial,  108  ;  cardiac,  200  ;  crystals,  109  ; 
aetiology  of,  170  ;  hay,  124  ;  humid,  152 ;  Millar's, 
142  ;  nasal  affections  in,  171  ;  nervous,  168  ;  origin 
of,  170  ;  renal,  800  ;  sputum  in,  800  ;  symptoms  of, 
108  ;  symptomatic,  170  ;  thymic,  142  ;  treatment  of, 
172 ;  uraemic,  860. 

Atavism,  in  haemophilia,  063  ;  in  gout,  985,  987. 

Ataxia,  542  ;  after  smallpox,  56  ;  cerebellar,  723  ; 
drunkard's,  584  ;  hereditary,  048  ;  in  diphtheria,  70  ; 
in  locomotor  ataxia,  630  ;  in  myelitis,  619  ;  in  pe- 
ripheral neuritis,  583  ;  in  progressive  paralysis,  764  ; 
in  typhoid  fever,  16  ;  locomotor,  632. 

Ataxic  gait,  637. 

Ataxic  paraplegia,  649. 

Atelectasis,  pulmonary,  181. 

Atheroma  of  the  arteries,  331. 

Athetosis,  541,  787  ;  congenital,  788  ;  idiopathic,  788  ; 
in  cerebral  paralysis  of  children,  745,  788  ;  move- 
ments of,  541  ;  nature  of,  789  ;  symptomatic,  788. 

Athrepsia,  414. 

Atresia  ani,  432. 

Atrophy,  414 ;  idiopathic  muscular,  658 ;  juvenile 
muscular,  658  ;  of  brain,  diffuse,  in  general  paresis, 
765 ;  of  cardiac  muscle  in  pericarditis,  323 ;  of 
muscles,  various  forms  of,  658  ;  progressive  muscu- 
lar, of  spinal  origin.  653  ;  unilateral,  of  face,  594. 

Atropine  in  asthma,  172  ;  in  epilepsy,  778  ;  in  exoph- 
thalmic goitre,  598  ;  in  neuralgia,  520  ;  in  progres- 
sive bulbar  paralysis,  690  ;  in  pulmonary  tuber- 
culosis, 235  ;  poisoning  from,  1008. 

Attitude  in  paralysis  agitans,  785  ;  in  pseudo-hyper- 
trophic  muscular  paralysis,  660. 

Auditory  center,  affections  of,  721  ;  nerve  in  facial 
palsy,  559  ;  vertigo,  769. 

Aura,  forms  of,  in  epilepsy,  771. 

Automatism  in  petit  mal,  773. 

Bacilli  of  anthrax,  117  ;  Asiatic  cholera,  82  ;  cerebro- 
spinal meningitis,  103  ;  diphtheria,  66  ;  glanders, 
116  ;  laryngeal  tuberculosis,  136  ;  pneumonia,  189  ; 
pulmonary  tuberculosis,  208  ;  tetanus.  791  ;  typhoid 
fever,  1. 

Bacteria  in  hepatitis  suppurativa,  476  ;  gangrene  of 
lungs,  241  ;  pleurisy,  253,  254,  263  ;  septico-pyaemia, 
109. 

Balanitis  in  diabetes,  972. 

Balsams  in  chronic  bronchitis,  154  ;  in  pulmonary 
emphysema,  180. 

Bandage  for  compression  in  chronic  hydrocephalus, 
769  ;  for  extension  in  pressure  paralysis  of  the 
spinal  cord,  614  ;  for  the  legs  in  locomotor  ataxia, 
648 ;  in  anaesthesia  of  the  trigeminus,  515  ;  in  neu- 
ralgia of  the  joints,  529. 

Banting's  treatment  of  obesity,  997. 

Baraesthesiometer.  507. 

Barrel-shaped  chest  in  emphysema,  177. 

Basedow's  disease  (see  Exophthalmic  Goitre),  595. 

Basilar  artery,  embolism  and  thrombosis  of,  693. 

Basilar  meningitis,  702. 


Baths  in  acute  ascending  spinal  paralysis,  67d;  in 
acute  poliomyelitis,  671  ;  in  anaa  the  la  of  the  tri- 
geminus, 515;  in  bronchitis,  150,  155 ;  in  cerebral 
haemorrhage,  737  ;  in  cerebral  hyperemia,  710 ;  in 
cholera  morbus,  413;  In  chorea,  788;  in  chronic 
spinal  leptomeningitis),  001  :  in  cutaneous  anaes- 
thesia, 515;  in  cystitis,  8!lO  ;  in  diabetes.  '.i*-f)  ;  in 
diphtheria,  78 ;  in  erysipelas,  64;  in  gout,  992;  in 
habitual  headache,  581  ;  in  hyperpyrexia  of  rheu- 
matism, 011  ;  in  hysteria,  812  ;  in  mull  i pie  sclerosis, 
681;  in  myelitis,  627;  in  nephritis,  847,  864;  in 
nephrolithiasis,  888  ;  to  neuralgia,  521  ;  to  neuras- 
thenia, 818  ;  in  neuritis,  584,  585  ;  in  obesity,  998  ;  in 
osteomalacia,  927  ;  in  pachymeningitis  cervicalis 
hypertrophica,  003  ;  in  paralysis  agitans,  787  ;  in 
paralysis  of  the  upper  limbs,  568;  to  pneumonia, 
205  ;  in  progressive  bulbar  paralysis.  690  ;  in  pro- 
gressive paralysis  of  the  insane,  767  ;  in  purulent 
meningitis,  701  ;  in  pyelitis,  884  ;  in  rachitis,  924  : 
in  railway  spine,  821' ;  in  rheumatism  (acute  artic- 
ular), 910,  911  ;  in  rheumatism  (muscular;,  919  ;  in 
scarlet  fever,  45  ;  in  smallpox,  60  ;  in  spasms  of 
the  respiratory  muscles,  577  ;  in  tetanus,  794  ;  in 
tetany,  791  ;  in  typhoid  fever,  23. 

Baths,  electric,  in  neurasthenia,  818. 

Beaded  ribs  in  rickets,  923. 

Bedsores  in  myelitis,  622. 

Beer-drinkers,  heart  disease  in,  313. 

Belladonna  in  asthma,  172  ;  in  diabetes,  981  ;  in  epi- 
lepsy, 778  ;  in  whooping-cough,  163  ;  poisoning 
from,  1008. 

Bell's  palsy,  558. 

Benzine  in  trichinosis.  124  ;  in  whooping-cough,  163. 

Beri-beri,  582  ;  in  Japan,  582  ;  in  United  States,  582. 

Biermer's  change  of  note  in  pneumothorax,  269. 

"  Big-jaw  "  in  cattle,  274. 

Bile  coloring  matter,  tests  for,  467. 

Bile-ducts,  ascarides  in,  445  ;  cancer  of,  492. 

Bile  in  intestinal  catarrh,  464  ;  in  typhoid  fever.  11. 

Biliary  abscess,  474,  476  ;  acids  in  the  blood,  466 ; 
acids  in  the  urine,  467. 

Biliary  colic,  470. 

Biliary  fistulas,  473. 

Bilious  remittent  fever,  95. 

Birth  palsies,  567. 

Bismuth,  subnitrate  of.  in  gastric  catarrh,  382  ;  in  in- 
testinal catarrh  of  children,  417.  418. 

Bitters  in  gastric  catarrh.  381  ;  in  scurvy,  960  :  in  val- 
vular cardiac  disease,  307. 

Black  expectoration,  245. 

Black  vomit,  102. 

Bladder,  cancer  of,  897  ;  care  of.  in  myelitis.  627  :  ca- 
tarrh of,  893  ;  diphtheria  of,  894  ;  "  haemorrhoids  " 
of,  429  ;  paralysis  of,  in  injuries  to  spinal  cord.  607  ; 
paralysis  of,  in  locomotor  ataxia,  643  :  paralysis  of, 
in  myelitis,  621  ;  paralysis  of,  in  pressure-paralysis 
of  the  spinal  cord,  613  ;  paralysis  of.  in  progressive 
paralysis,  764  ;  paralysis  of,  in  spinal  apoplexy.  605. 

"  Bleeders,"  963. 

Bleeding.    See  Hemorrhage. 

Bleeding  in  cerebral  haemorrhage,  736  ;  in  heart  dis- 
ease, 300  ;  in  pneumonia.  205  :  in  sunstroke.  748. 

Bleeding  (local)  for  cerebral  abscess,  743  :  for  cere- 
bral haemorrhage.  736  :  for  cerebral  hyperaemia, 
710;  for  cystitis,  896  ;  for  haematoma  of  the  dura 
mater,  698  ;  for  haemorrhage  into  the  spinal  me- 
ninges, 603  :  for  infantile  spinal  paralysis.  670  ;  for 
meningitis,  108,  701  :  for  pericarditis,  328  ;  for  peri- 


1016 


INDEX. 


touitis,  456  ;  for  pneumonia,  205  ;  for  sciatica,  527  ; 
for  typhlitis,  421. 

Blepharitis  eiliaris.  1000. 

Blepharospasm,  572. 

Blindness  from  anaemia  (amaurosis,  anaemic),  932  ; 
from  tumors  of  the  brain,  751. 

Blisters  for  neuralgia,  519  ;  for  sciatica,  527. 

Blood-casts,  826,  827. 

Blood,  changes  in  the,  924. 

Blood,  character  of,  in  anaemia,  935  ;  in  cancer  of  the 
stomach,  393  ;  in  chlorosis,  935  ;  in  cholera,  87  ;  in 
diabetes,  965,  975  ;  in  gout,  984  ;  in  hsemoglobinuria, 
953.  955  ;  in  haemophilia,  963  ;  in  leukaemia,  947  ;  in 
pernicious  anaemia,  943  ;  in  pseudo-leukaemia,  952. 

Blood,  poverty  of  the.  928. 

Blood-test,  Heller's,  828. 

Blood,  transfusion  of,  in  leukaemia,  951  ;  in  pernicious 
anaemia,  945  ;  in  poisoning  from  carbonic  oxide 
gas,  1007  ;  in  poisoning  from  nitrobenzine,  1008. 

Blood-vessels,  affections  of,  331. 

Blue  line  on  gums  in  lead  poisoning,  1005. 

Boils  after  small-pox,  56  ;  in  diabetes,  973,  976. 

Bones,  growth  of,  in  infantile  spinal  paralysis,  669  ; 
in  rachitis,  921. 

Bones,  lesions  of,  in  leukaemia,  946,  948  ;  in  rickets, 
921;  in  scrofula.  1000  ;  in  typhoid  fever,  17  ;  mar- 
row of,  in  leukaemia,  946  ;  in  osteomalacia,  926  ;  in 
pernicious  anaemia,  940,  941  ;  in  pseudo-leukaemia, 
952;  pain  in,  in  leukaemia,  948  ;  in  pernicious  anae- 
mia, 942  ;  softening  of,  in  osteomalacia,  926 ;  in 
rachitis,  921. 

Borborygmi  in  intestinal  catarrh,  405. 

Bothriocephalus  latus,  440,  442. 

Botulismus,  1009. 

Bovine  tuberculosis,  208. 

Brachial  paralysis,  564  ;  combined,  567  ;  in  acute  as- 
cending spinal  paralysis,  675;  peripheral,  prognosis 
and  treatment  of,  567. 

Brachial  spasm,  575. 

Brain,  abscess  of,  741  ;  diagnosis,  743  ;  distinguished 
from  tumor  of,  encapsulated,  743  ;  focal  symptoms, 
742 ;  idiopathic,  741  ;  metastatic,  741  ;  traumatic, 
741 ;  treatment  of,  743. 

Brain,  anaemia  of,  708  :  aetiology  of,  709  ;  symptoms 
of,  709  ;  treatment  of,  709. 

Brain  and  cord,  multiple  sclerosis  of,  627,  744.  See 
also  Multiple  Sclerosis. 

Brain,  atrophy  of,  in  progressive  general  paralysis, 
765. 

Brain,  cancer  of,  749;  congestion  of,  709;  cortical 
centers  of,  711  ;  cysts  in,  441,  756. 

Brain,  diseases  of,  remarks  in  regard  to  topical  diag- 
nosis of,  710. 

Brain,  echinococcus  of,  756;  foci  of  sclerosis  in  syph- 
ilis, 757. 

Brain,  glioma  of,  haemorrhages  into,  749  ;  situation 
of,  749. 

Brain,  hyperaemia  of,  708  ;  symptoms  of,  710  ;  treat- 
ment of,  710. 

Brain  in  cerebro-spinal  meningitis,  104  ;  inflamma- 
tion of.  741. 

Brain,  oedema  of,  in  uraemia,  831. 

Brain,  porencephalus  of,  745. 

Brain,  psammoma  of,  749  ;  sarcoma  of,  749. 

Brain,  sclerosis  of,  627. 744  ;  diffuse,  744  ;  insular,  627. 

Brain,  softening  of,  red,  yellow,  and  white,  737,  739  ; 
aetiology  of,  737  ;  diagnosis  of,  740 ;  idiopathic, 
744  ;  in  tumor  of,  752. 


Brain,  syphilis  of,  757  ;  apoplectic  symptoms  in,  758  ; 
diagnosis  of,  759  ;  disease  of  arteries  in,  757  ;  he- 
reditary, 757  ;  new  growths  in,  758  ;  symptoms  of, 
758. 

Brain,  syphiloma  of,  749  ;  situation  of.  757,  758. 

Brain,  tubercle  of,  749. 

Brain,  tumors  of,  748  ;  at  base,  752  ;  cerebral  com- 
pression caused  by,  749  ;  diagnosis  of,  754  ;  in  the 
cerebellum,  753  ;  in  the  cerebral  hemispheres,  752  ; 
in  the  cortex,  752,  754  ;  involving  nerves  at  base, 
752  ;  medical  treatment  of,  755  ;  originating  in  the 
meninges,  749,  754 ;  surgical  treatment  of,  756  ; 
symptoms,  general,  749 ;  symptoms,  localizing, 
751  ;  varieties,  748. 

Brand's  method  in  tj'phoid  fever,  22. 

Breakbone  fever,  99. 

Breathing  (see  Respiration)  ;  mouth,  356. 

Breath,  odor  of,  in  diabetic  coma,  973. 

Brickmaker's  anaemia,  448. 

Bright's  disease,  822  ;  acute,  836  ;  diagnosis  of,  845  ; 
aetiology  of,  836  ;  parenchymatous  form  of,  839  ; 
prognosis  in,  845  ;  symptoms  of,  841  ;  treatment  of, 
846. 

Bright's  disease,  chronic,  849,  856  ;  cardio-vascular 
changes  in.  853,  859  ;  causes  of,  849,  856  ;  interstitial 
form  of,  856  ;  parenchymatous  form  of,  849  ; 
symptoms  of,  852,  858  ;  treatment  of,  855, 863. 

Bromide  of  ammonium  in  epilepsy,  778. 

Bromide  of  potash  in  abscess  of  the  brain,  746  ;  in 
athetosis,  789  ;  in  bronchial  asthma,  172  ;  in  chorea, 
783  ;  in  diabetes,  981  ;  in  epilepsy,  777  ;  in  epilepti- 
form attacks  following  cerebral  paralysis  of  chil- 
dren, 746  ;  in  habitual  headache,  532  ;  in  hysteria, 
813  ;  in  infantile  convulsions,780 ;  in  neuralgia,  520  : 
in  neurasthenia,  818  ;  in  paralysis  agitans,  787  ;  in 
spasm  of  the  face,  573  ;  in  spasm  of  the  glottis,  143  ; 
in  spasm  of  the  muscles  of  mastication,  572  ;  in 
spasm  of  the  muscles  of  the  neck,  575  ;  in  tetanus, 
794  ;  in  tetany,  791  ;  in  whooping-cough,  163. 

Bromide  of  sodium  in  epilepsy,  778. 

Bromine,  poisoning  from,  1004. 

Bromism,  1004. 

Bronchi,  casts  of  the,  158  ;  dilatation  of,  164  ;  steno- 
sis of,  167. 

Bronchial  blennorrhoea,  152. 

Bronchial  catarrh  (see  Bronchitis),  146,  151. 

Bronchiectasis,  164  ;  cylindrical,  164  ;  saccular,  164  ; 
sputum  in,  165. 

Bronchiolitis,  148;  exudative,  171. 

Bronchitis,  acute,  146  ;  aetiology  of,  146  ;  symptoms 
of,  147  ;  treatment  of,  150  ;  capillary,  148  ;  after 
whooping-cough,  161  ;  asthmatic,  171. 

Bronchitis,  chronic,  151  ;  aetiology  of,  151  ;  symptoms 
of,  151  ;  treatment  of,  153. 

Bronchitis,  croupous,  158  ;  fibrinous,  158  ;  foetid,  155  ; 
hemorrhagic,  147  ;  in  children,  149  ;  in  erysipelas, 
64  ;  in  gout,  987  ;  in  malaria,  94  ;  in  measles,  47, 
49  ;  in  rachitis,  923,  924  ;  in  small-pox,  56  ;  in  ty- 
phoid fever,  12  ;  in  valvular  cardiac  disease.  296  ; 
pseudo-membranous.  158  ;  putrid,  155  ;  second- 
ary, 146  ;  symptomatic  croupous,  158  ;  tubercular, 
213. 

Bronchophony  in  pneumonia,  195. 

Broncho-pneumonia,  184. 

Bronchorrhcea,  serous,  152. 

Bronzed  skin,  878. 

Brown  induration  of  lung,  249. 

Brown-Sequard's  paralysis,  682. 


INDEX. 


1017 


Bruit.    See  Murmur. 

Bruit,  d'airain,  2(59  ;  de  cuir  neuf,  in  pericarditis. 
258  ;  dediable  in  anaemia,  933  ;  in  chlorosis,  933  ;  in 
pernicious  anaemia,  942  ;  de  pot  1'616,  222. 

Bulbar.    See  also  Medulla. 

Bulbar  myelitis,  acute,  694. 

Bulbar  paralysis,  acute,  694  ;  chronic,  685,  690  ;  in- 
flammatory, 694  ;  in  progressive  muscular  atrophy, 
652 ;  progressive,  685 ;  progressive,  aetiology  of, 
685  ;  progressive,  complications  of,  657,  689  ;  pro- 
gressive, extension  of,  to  the  nerves,  690  ;  progres- 
sive, treatment  of,  689. 

Bulbar  symptoms  in  acute  ascending  spinal  paraly- 
sis, 675  ;  in  amyotrophic  lateral  sclerosis,  652  ;  in 
compression  of  the  medulla,  695  ;  in  embolism  and 
thrombosis  of  the  basilar  artery,  094  ;  in  progres- 
sive general  paralysis,  764  ;  in  tubercular  menin- 
gitis, 704. 

"  Bulbar  pulse,"  292. 

Butyl  chloral  in  neuralgia  of  the  trigeminus,  523. 

Butyric  acid  in  gastric  juice,  379. 

Cachexia  in  cancer  of  the  stomach,  393  ;  malarial, 
95  ;  saturnine,  1005. 

Cachexie  pachydermique,  589. 

Cseeitis,  stercoral,  418. 

Caecum,  cancer  of,  426  ;  inflammation  of,  418. 

Caffeine  in  hemicrania,  593. 

Caisson  disease,  608. 

Calabar-bean  in  tetanus,  794. 

Calcaneus  in  paralysis  of  the  tibial  nerve,  569. 

Calculi,  biliary,  470  ;  pancreatic,  504  ;  renal,  884  ;  ton- 
sillar, 353  ;  urinary,  forms  of,  885. 

Calculous  pyelitis,  882. 

Calm  stage  in  yellow  fever,  101. 

Calomel  in  cholera  morbus,  413 ;  in  intestinal  catarrh 
of  children,  416  ;  in  purulent  meningitis,  702  ;  in 
relapsing  fever,  36  ;  in  tubercular  meningitis,  706  ; 
in  typhoid  fever,  21. 

Camphor  in  articular  rheumatism,  911  ;  in  erysipe- 
las, 65  ;  in  scarlet  fever,  45  ;  in  typhoid  fever,  26. 

Cancer,  colloid,  391  ;  fibroid,  391  ;  medullary,  391. 

Cancer,  metastatic,  in  cancer  of  the  oesophagus,  370; 
in  the  bones,  393  ;  in  the  pleura,  272. 

Cancer  of  the  bile-ducts,  492  ;  bowel,  426  ;  brain,  749  ; 
intestines,  426  ;  kidney,  872  ;  larynx,  145  ;  liver, 
492  ;  lungs,  250  ;  oesophagus,  369  ;  pancreas,  504  ; 
peritoneum,  463  ;  pleura,  272  ;  stomach,  391. 

Cancrum  oris,  347. 

Cannabinum  tannicum  in  neurasthenia,  819. 

Cannabis  indica  in  diabetes,  931  ;  in  hemicrania,  593  ; 
in  neurasthenia,  819. 

Cantani's  dietary  for  diabetes,  978. 

Cantharides  as  a  cause  of  cystitis,  893. 

Capillary  pulse  in  aortic  insufficiency,  289. 

Capsule,  internal,  lesions  of,  721  ;  as  a  cause  of  cere- 
bral hemianaasthesia,  721,  725  ;  as  a  cause  of  hemi- 
plegia, 721,  724  ;  as  a  cause  of  post-hemiplegic 
chorea,  721,  725  ;  involving  facial  nerve,  721. 

Caput  Medusae,  481. 

Caput  obstipum,  574. 

Caput  quadratum  in  rickets,  923. 

Carbolic  acid  in  articular  rheumatism,  910  ;  in  dia- 
betes, 981  ;  in  erysipelas,  65  ;  in  scarlet  fever,  44, 
45  ;  in  whooping-cough,  163  ;  poisoning  from,  1008. 

"  Carbolic  mask,"  157. 

Carboluria,  1008. 

Carbuncle  in  diabetes,  973. 


Carhunculus  contagiosum  117. 
Carcinoma.    Sec  Cancer. 

Carcinosis,  miliary,  of  the  lungs,  250  ;  of  the  peri- 
toneum, 463. 

Cardiac.    See  also  Heart. 

Cardiac  compensation,  rupture  of,  283. 

Cardiac  failure,  283. 

Cardiac  murmurs,  anaemic,  983  ;  En  chlorosis,  935  ;  In 
chorea,  782;  in  idiopathic  an;i;inia,  912;  in  leu 
kaemia,  949. 

Cardiac  murmurs,  organic,  in  aortic  insufficiency, 
287,  288;  in  aortic  stenosis,  290;  in  congenital 
heart  affections,  293,  294  ;  in  mitral  incompetency, 
283  ;  in  mitral  stenosis,  285  ;  in  tricuspid  valve  dis- 
ease, 292. 

Cardiac  muscle,  atrophy  of,  from  pericarditis,  326, 
327 ;  cloudy  swelling  of,  16,  298  ;  fatty  degenera- 
tion of,  315  ;  lesions  of,  298. 

Cardiac  neuroses,  318  ;  overstrain,  312. 

Cardiac  septa,  anomalies  of,  394. 

Cardialgia  in  gastric  ulcer,  385  ;  in  malaria,  95. 

Cardio-sclerosis,  307. 

Cardio- vascular  changes  in  renal  disease,  834,  858. 

Carotids,  aneurism  of,  339  ;  compression  of,  in  epilep- 
tic paroxysms,  7'78  ;  ligature  and  compression  of, 
in  cerebral  haemorrhage,  736. 

Caseation,  213. 

Castoreum  in  hysteria,  813. 

Castration  for  hysteria,  813. 

Casts  of  bronchial  tubes  in  fibrinous  bronchitis,  158. 

Casts  of  urinary  tubules,  826  ;  epithelial,  827  ;  fatty, 
827  ;  granular,  827  ;  hyaline,  826  ;  waxy,  827. 

Casts,  tube,  in  acute  BriglnVs  disease,  842  ;  in  chronic 
Bright's  disease,  852,  859. 

Catalepsy,  796  ;  hypnotic,  796  ;  hysterical,  796  ;  in 
cerebral  disease,  797  ;  in  connection  with  psychoses, 
797. 

Cataract  in  diabetes,  972. 

Catarrh,  acute  gastric,  372  ;  bronchial,  146  ;  chronic 
bronchial,  151  ;  chronic  gastric,  374  ;  chronic  laryn- 
geal, 132  ;  dry  bronchial.  152  :  gastro-duodenal, 
464  ;  nasal,  125  ;  of  the  bladder,  893  ;  simple  chrome 
(nasal),  126. 

Catarrhal  inflammation,  influence  in  tuberculosis, 
210. 

Catarrhe  pituiteux,  152  ;  sec,  152. 

Catarrhus  aestivus,  125. 

Cathartics  in  anosmia  and  chlorosis,  938  ;  in  cerebral 
haemorrhage,  736  ;  in  cerebral  hyperemia,  710  ;  in 
cirrhosis  of  the  liver,  483  ;  in  dysentery,  80  ;  in 
haematoma  of  the  dura  mater,  698  ;  in  haemophilia, 
965 ;  in  infantile  convulsions,  779  ;  in  intestinal 
catarrh,  409  ;  in  locomotor  ataxia,  648 ;  in  trichi- 
nosis, 123. 

Catheterization  in  myelitis,  627. 

Cat's  purr,  284,  286. 

Caustic  potash,  poisoning  from,  1004  ;  soda,  poisoning 
from,  1004. 

Cautery,  actual,  in  acute  ascending  spinal  paralysis, 
676  ;  in  neuralgia,  519  ;  in  pachymeningitis  cerri- 
calis  hypertrophica,  603  ;  in  pressure  paralysis  of 
the  spinal  cord,  614  ;  in  spasm  of  the  muscles  of 
the  face,  573  ;  in  spasm  of  the  muscles  of  the  neck, 
575. 

Cavities  and  fissures  in  the  spinal  cord.  677. 

Cavities,  pulmonary,  physical  signs  of.  202. 

Centrum  ovale,  lesions  of.  as  a  cause  of  ataxic  apha- 
sia, 721 ;  as  a  cause  of  hemiopia,  721 ;  as  a  cause  of 


1018 


INDEX. 


hemiplegia.  721  ;  as  a  cause  of  monoplegia,  721  ;  as 
a  cause  of  word  deafness,  721. 

Cephalaea  (see  Headache,  Habitual),  530. 

Cephalalgia  (see  Headache,  Habitual),  530. 

Cerebellar,  ataxia,  723  ;  vertigo,  723,  724. 

Cerebellum,  tumors  of,  753. 

Cerebral  arteries,  aneurism  of,  725  ;  arterio-sclerosis 
of,  725  ;  endarteritis  of,  725  ;  syphilitic  endarteritis 
of,  757  ;  syphilis  of,  757  ;  syphilis  of,  as  a  cause  of 
apoplectiform  attacks,  758  ;  syphilis  of,  as  a  cause 
of  cerebral  softening,  738, 757  ;  syphilis  of,  histology 
of,  757. 

Cerebral  embolism,  737  ;  in  gout,  988  ;  repeated  at- 
tacks caused  by,  740. 

Cerebral  haemorrhage,  725  ;  aetiology  of,  725  ;  aneu- 
risms, miliary,  in,  725  ;  as  a  cause  of  cerebral  hemi- 
plegia, 731  ;  convulsions  in,  729  ;  diagnosis  of,  736  ; 
focal  symptoms  of,  731  ;  hereditary  tendency  to, 
726 ;  in  arterio-sclerosis,  725  ;  in  gout,  726 ;  in 
tumors  of  the  brain,  750  ;  in  valvular  cardiac  dis- 
ease, 301  ;  morbid  anatomy  of,  726  ;  prognosis  in, 
736  ;  symptoms  of,  727  ;  treatment  of,  736  ;  usual 
situation  of,  726. 

Cerebral  localization,  710. 

Cerebral  meninges,  diseases  of,  696. 

"  Cerebral  rheumatism,"  905. 

Cerebral  sinuses,  thrombosis  of,  707. 

Cerebral  symptoms  in  contracted  kidney,  861,  862  ;  in 
gout,  988  ;  in  nephritis,  831,  832 ;  in  pneumonia, 
198  ;  in  pseudo-leukaemia  lymphatica,  952  :  in  pur- 
pura haemorrhagica,  962  ;  in  relapsing  fever,  32  ; 
in  scarlet  fever,  37  ;  in  septico-pyaemia,  111. 

Cerebral  tuberculosis,  749,  755  ;  symptoms  of,  749. 

Cerebro-spinal  meningitis,  epidemic  (see  also  Menin- 
gitis), 103  ;  anomalous  forms  of,  107  ;  complications 
of,  106  ;  distinguished  from  tubercular  meningitis, 
107  ;  encephalitic  foci  in,  104  ;  malignant  form,  104  ; 
sequelae  of,  107  ;  treatment  of,  108  ;  varieties  of,  105, 
107. 

Cervical  muscles,  paralysis  of,  562  ;  in  acute  ascend- 
ing spinal  paralysis,  675  ;  resulting  from  stasis, 
677. 

Cervical  muscles,  spasm  of,  574,  575  ;  in  hysteria, 
804  ;  prognosis  of,  574  ;  treatment  of,  574. 

Cervical  pachymeningitis,  602. 

Cervico-brachial  neuralgia,  524. 

Cervico-occipital  neuralgia,  523. 

Cestodes,  440. 

Chalicosis  pulmonum,  245. 

Champagne  in  yellow  fever,  103. 

Charbon,  117. 

Charcot's  crystals,  169  ;  joints,  644. 

Cheek,  gangrene  of,  347. 

Cheese,  poisoning  from,  1010. 

Cheyne-Stokes  breathing  in  tuberculous  meningitis, 
704. 

Chicken  breast,  923. 

Chicken-pox,  60. 

Children,  diabetes  in,  967  ;  pneumonia  in,  200  ;  rheu- 
matism in,  900  ;  broncho-pneumonia  in,  185  ;  tuber- 
culosis of  mesenteric  glands  in,  424  ;  typhoid 
fever  in,  4. 

Chloral  in  chorea,  783;  in  diabetes,  981 ;  in  eclampsia, 
780  ;  in  neuralgia,  520  ;  in  tetanus,  794  ;  in  trigemi- 
nal neuralgia,  523. 

Chlorine  gas,  poisoning  from,  1004. 

Chloro-anaemia  in  phthisis,  936. 

Chloroform  in  epilepsy,  778  ;  in  hepatic  colic,  475  ;  in 


hysteria,  804 ;    in    infantile   convulsions,  779  ;    in 
renal  colic,  888  ;  in  spasms  of  the  diaphragm,  577. 

Chloroform,  poisoning  from,  1007. 

Chloroform  test  for  bile,  407. 

Chlorosis,  928,  934  ;  diagnosis  of,  936  ;  distinguished 
from  gastric  diseases,  930 ;  distinguished  from 
renal  diseases,  931  ;  distinguished  from  syphilis. 
931  ;  distinguished  from  tuberculosis,  941,  936 
Egyptian,  448 ;  chlorosis,  aetiology  of,  928,  929 
fever  in,  934  ;  heart  symptoms  in,  933  ;  menstrual 
disturbance  in,  935  ;  morbid  anatomy  of,  933,  935  ; 
relapses  of,  936  ;  symptoms  of,  934  ;  treatment  of, 
936  ;  with  regard  to  sexual  disturbances,  929,  935. 

Choked  disk.    See  Neuritis,  Optic. 

Cholaemia.  468,  489. 

Cholelithiasis,  470. 

Cholera  (Asiatic),  81  ;  asphyxia  in,  84  ;  bacillus  of,  82 ; 
complications  of,  86  ;  contagiousness  of,  82  ;  dejec- 
tions in,  84  ;  diagnosis  of,  84  ;  distinguished  from 
acute  arsenical  poisoning,  87  ;  eruption  in,  86  ;  ex- 
citing causes  of,  83  ;  period  of  incubation  in,  84  ; 
post-mortem  appearances  in,  86  ;  predisposition  to, 
83  ;  prognosis  of,  88  ;  specific  poison  of,  82  ;  treat- 
ment of,  88. 

Choleraic  diarrhoea,  simple,  84  ;  premonitory,  84. 

Choleraic  nephritis,  86. 

Choleraic  typhoid,  86  ;  uraemic,  86. 

Cholera  morbus,  410  ;  diagnosis  of,  412  ;  mortality  in, 
412 ;  treatment  of,  412  ;  cholera  nostras,  410  ; 
cholera  sicca,  85  ;  cholera  typhoid,  86. 

Cholerine,  84. 

Cholesterine,  calculi  formed  of,  471. 

Cholesterine  and  pigment,  calculi  formed  of,  471. 

Chorditis  tuberosa,  133. 

Chorditis  vocalis  inferior  hypertrophica,  133. 

Chorea,  780  ;  aetiology  of,  780  ;  as  related  to  chorea 
major,  780  ;  as  related  to  embolic  processes,  783  ; 
complications  of,  780,  782  ;  diagnosis  of,  783  ;  gravi- 
darum, 781 ;  in  articular  rheumatism,  780  ;  nature 
and  situation  of  the  disease,  782  ;  predisposition  to, 
780  ;  premonitory  symptoms  of,  781  ;  prognosis  of, 
and  treatment,  783  ;  relapses  in,  782  ;  unilateral, 
781. 

Chorea,  endemic,  780 ;  major,  780 ;  rhythmic  or 
hysterical,  810  ;  Sydenham's,  780. 

Chorea,  heart  symptoms  of,  782  ;  infectious  origin  of, 
780  ;  seasonal  relations  of,  780. 

Chorea,  Huntington's  or  hereditary,  780. 

Chorea,  spasm,  573,  576,  810. 

Choroid,  tubercles  in,  240. 

Choroid,  tuberculosis  of  the,  in  meningitis,  704. 

Chyluria,  parasitic,  875. 

Cicatrices  of  the  oesophagus,  366  ;  of  the  oesophagus 
from  sulphuric  acid,  1003. 

Cicatricial  induration  caused  by  syphilis  of  the  brain, 
757. 

Cinchona,  in  purpura  haemorrhagica,  962  ;  in  scurvy, 
961. 

Circulatory  system,  diseases  of,  276. 

Circumcision,  dangerous  in  haemophilia,  964. 

Circumflex  nerve,  affections  of,  564.  574. 

Cirrhosis,  hypertrophic,  of  the  liver,  483. 

Cirrhosis  of  kidney,  856  ;  of  liver,  478  ;  of  lung,  223  ; 
of  pancreas.  504. 

"  Clap-threads  "  in  cystitis,  895. 

Clavicles,  deformed,  in  rachitis,  923. 

Claw-shaped  hand,  566. 

Climate,    change    of,    in    asthma,   172 ;    in    chronic 


INDEX. 


1010 


Bright's  disease,  855  ;  in  pulmonary  tuberculosis, 
232,  233. 

Clitoris,  cauterization  of,  in  hysteria,  813. 

Clonus,  545. 

Clownismus  in  listeria,  808. 

Club-foot  resulting  from  infantile  spinal  paralysis, 
669. 

Coagulation  necrosis,  213. 

Coccyoclynia,  528  ;  in  locomotor  ataxia,  528, 043  ;  oper- 
ative removal  of  coccyx  for,  528. 

Cod-liver  oil  in  diabetes,  979  ;  in  osteomalacia,  927  ;  in 
pulmonary  tuberculosis,  232  ;  in  rachitis,  925  ;  in 
scrofula,  1001. 

Coffee- ground  vomit,  392. 

Coin  sound,  269. 

Colchicum  in  articular  rheumatism,  910  ;  in  gout,  992. 

Cold  pack,  method  of  giving,  188. 

Colic,  biliary,  470  ;  hepatic,  470  ;  in  angio-neurotic 
oedema,  588  ;  lead,  1005  ;  renal,  884. 

Collapse  stage,  in  cholera,  85  ;  in  cholera  morbus,  411 ; 
in  hepatic  colic,  472  ;  in  peritonitis,  454  ;  in  pneu- 
monia, 196  ;  in  pneumothorax,  268  ;  in  typhoid  fever, 
8,26. 

Colloid  cancer  of  peritoneum,  463  ;  of  stomach,  391. 

Colon,  cancer  of,  426. 

Colo-typhoid,  9. 

Columns,  posterior,  gray  degeneration  of,  632. 

Coma,  diabetic,  973  ;  causes  of,  974  ;  treatment  of,  981. 

Coma,  epileptic,773  ;  from  heat  stroke,  747  ;  in  abscess 
of  the  brain,  742  ;  in  acute  yellow  atrophy,  487  ;  in 
alcoholic  poisoning,  1006  ;  in  apoplexy,  729  ;  in  cere- 
bral haemorrhage,  729  ;  in  cerebral  syphilis,  758  ;  in 
multiple  sclerosis,  630  ;  in  pernicious  malaria,  94  ;  in 
thrombosis  of  the  cerebral  sinuses,  707  ;  in  typhus 
fever,  30  ;  in  uraemia,  832,  834. 

Coma,  post-epileptic,  773. 

Coma-vigil,  in  typhoid  fever,  14. 

Comma  bacillus,  82. 

Commotio  spinalis,  819. 

Compensation  in  valve  lesions,  282. 

Complexion  in  anaemia,  931,  934,  941  ;  in  diabetic 
coma,  973  ;  in  leukaemia,  949  ;  in  pseudo-leukaemia, 
952. 

Compression  as  a  cause  of  thrombosis,  502. 

Compression  of  the  medulla  oblongata, 695  ;  diagnosis 
and  prognosis  of ,  695. 

Compression  of  the  oesophagus,  366. 

Conchinine  in  malaria,  97. 

Concretio  pericardii,  326. 

Concussion  of  spinal  cord,  819. 

Congenital  heart  affections,  293. 

Congo-red  test  for  free  acid,  378. 

Conjugate  deviation  in  hemiplegia,  729. 

Conjunctivitis  in  difficult  dentition,  351  ;  in  diphtheria, 
69  ;  in  gout,  987;  in  measles,  48  ;  in  scarlet  fever,  41 ; 
in  scrofula,  1000  ;  in  whooping-cough,  160. 

Conscience  musculaire,  509,  802. 

Constipation,  habitual,  430  ;  in  diseases  of  the  nervous 
system,  430  ;  treatment  of,  431. 

Constipation  in  anaemia  and  chlorosis,  932  ;  in  cases 
of  cerebral  tumor,  751  ;  in  cirrhosis  of  the  liver,  480  ; 
in  gastric  catarrh,  379  ;  in  intestinal  stenosis,  435  ; 
in  jaundice,  466  ;  in  locomotor  ataxia,  643  ;  in  mye- 
litis, 621  ;  in  typhlitis,  419  ;  in  typhoid  fever,  9. 

Constitutional  diseases,  928. 

Consumption.    See  Tuberculosis. 

Consumption,  galloping,  2\7. 

Contracted  kidney,  856  ;  embolic,  872  ;  genuine,  856  ; 


in  arteriosclerosis,  857  ;  in  gout,  856,  987  ;  in  obesity, 
996  ;  secondary,  849,  856. 

Contractions,  rhythmical,  540. 

Contracture  des  nourrices,  789;  hysterical,  808;  In 
hemiplegia,  734. 

Convulsions,  cataleptic,  511  ;  epileptiform,  510,  701, 
770,  778. 

Convulsions,  epileptic,  771  ;  hysterical,  806  ;  in  acute 
yellow  atrophy,  487  ;  in  alcoholism,  1006  ;  in  cere- 
bral embolism,  789 ;  in  cerebral  haemorrhage,  789  ; 
in  cerebral  hydatids,  750  ;  in  cerebral  syphilis.  758  ; 
in  cerebral  tumors,  750  ;  in  chronic  Bright's  disease, 
831  ;  in  compression  of  the  medulla,  095  ;  in  diffuse 
sclerosis  of  the  brain,  744. 

Convulsions,  infantile,  779  ;  diagnosis  of,  779  ;  aetiology 
of,  779  ;  relation  to  rickets,  779  ;  symptoms  of,  779  ; 
treatment  of,  779. 

Convulsions  in  focal  lesions  of  the  cortex,  714,  724  ;  in 
general  paralysis,  764  ;  in  haematoma  of  the  dura 
mater,  697  ;  in  hepatic  colic,  472  ;  in  hydrophobia, 
114  ;  in  hysteria,  806  ;  in  infantile  cerebral  paralysis, 
744  ;  in  infantile  spinal  paralysis,  008  ;  in  meningitis, 
700,  704 ;  in  multiple  sclerosis,  030  ;  in  sunstroke, 
747  ;  in  thermic  fever,  747  ;  in  uraemia,  831  ;  Jack- 
sonian,  714. 

Convulsive  tic,  573. 

Cb-ordination,  disturbance  of,  in  tabes,  639. 

Copaiba,  balsam  of,  in  cirrhosis  of  the  liver,  483  ;  in 
cystitis,  896. 

Copaiba,  resin  of,  in  cirrhosis  of  the  liver,  483. 

Copper,  paralysis  due  to,  571  ;  poisoning  from,  1005  ; 
sulphate  of,  in  chorea,  783  ;  test  for  sugar,  968. 

Coprolalia,  573. 

Coprostasis,  432. 

Cor  adiposum,  315. 

Cor  villosum,  322. 

Coronary  arteries,  in  angina  pectoris,  308,  318  ;  oblit- 
eration, 308. 

Corpora  quadrigemina,  lesions  of,  722  ;  as  a  cause  of 
ocular  disturbances,  722,  725  ;  tumors  in,  753. 

Corpulence,  992. 

Corrigan's  pulse,  289. 

Corset-liver,  499. 

Coryza,  125  ;  fever  caused  by,  126  ;  fcetida,  127  ;  from 
the  iodides,  125. 

Cortical  epilepsy,  714. 

Costiveness,  430. 

Cough,  during  aspiration  of  pleural  effusion.  266  ; 
hysterical,  577  ;  in  pertussis,  160  ;  paroxysmal,  in 
bronchiectasis,  164  ;  spasmodic,  577. 

Cow's  milk  as  food  for  infants,  411. 

Cow-pox,  58. 

Cracked-pot  sound,  222. 

Cramps  in  cholera,  85. 

Cramps  in  the  legs,  575  ;  after  severe  physical  exer- 
cise, 575  ;  in  hysteria,  575  ;  liability  to,  575. 

Craniometric  anomalies  in  the  epileptic,  775  ;  in  the 
rachitic,  923. 

Craniotabes,  in  rachitis,  923  ;  relation  (alleged)  to 
congenital  syphilis,  921 . 

Cranium,  in  osteomalacia,  927  ;  in  rachitis,  923. 

Creasote  in  gastric  catarrh,  381  ;  in  intestinal  catarrh 
of  children,  417  ;  in  tuberculosis  of  the  lungs.  231. 

Cremaster  reflex,  543  :  in  cerebral  haemorrhage.  732. 

Crepitant  rales  in  croupous  pneumonia.  195. 

Crepitatio  redux,  195. 

Crescents  in  blood  in  malaria,  92. 

Crises,  gastro-intestinal,  643;  in  locomotor  ataxia,  643. 


1020 


INDEX. 


Crisis,  in  pneumonia,  lf»9  ;  in  typhus  fever,  29. 

Croup.  65  ;  ascending,  08  ;  relation  to  diphtheria,  68. 

Croup,  false,  131. 

Croupous  pneumonia,  189. 

Crura  cerebri,  lesions  of,  723. 

Crural,  anterior,  paralysis  of,  508. 

Cry,  cephalic,  705. 

Crystals,  Leyden's,  169. 

Cuudurango  bark  in  cancer  of  the  stomach,  395. 

Cups,  dry,  in  acute  ascending  spinal  paralysis,  676  ; 
in  pressure  paralysis  of  the  spinal  cord,  614. 

Curare  in  paralysis  agitans,  787  ;  in  spasms  of  the 
facial  muscles,  573  ;  in  tetanus,  794  ;  in  tetany,  791. 

Curschmanu's  spirals,  169. 

Cutaneous.    See  also  Skin. 

Cutaneous  abscesses  in  erysipelas,  64. 

Cutaneous  anaesthesia,  510  ;  bilateral,  511  ;  cerebral, 
510,  512 ;  in  diseases  of  the  internal  capsule,  721, 
725  ;  in  hysteria,  512,  800  ;  in  laundresses,  511  ;  in 
locomotor  ataxia,  511  ;  painful,  512  ;  peripheral, 
510,  511  ;  spinal,  510,  511  ;  symptoms  of,  512  ;  treat- 
ment of,  514. 

Cutaneous  ecchymoses  in  articular  rheumatism,  904  ; 
in  typhoid  fever,  17. 

Cutaneous  reflexes,  543  ;  diminution  or  absence  of, 
544 ;  exaggeration  of,  544 ;  in  cerebral  haemor- 
rhage, 732 ;  in  epilepsy,  773  ;  in  infantile  spinal 
paralysis,  669  ;  in  locomotor  ataxia,  641  ;  in  mye- 
litis, 620;  in  poliomyelitis  of  adults,  672  ;  in  pressure 
paralysis  of  the  spinal  cord,  612  ;  in  tetanus,  792  ; 
in  the  extremities,  543  ;  sluggishness  of,  543. 

Cutaneous  sensibility,  electro-,  508. 

Cutaneous  sensibility,  in  locomotor  ataxia,  639 ;  in 
tubercular  meningitis,  704  ;  varieties,  and  modes 
of  testing,  505. 

Cyanosis,  in  acute  tuberculosis,  237  ;  in  congenital 
heart  disease,  293,  294  ;  in  emphysema,  176,  177  ; 
in  epileptic  paroxysms,  772  ;  in  stenosis  of  the 
pulmonary  orifice,  293. 

Cynanche  contagiosa,  65  ;  gangraenosa,  349. 

Cystic  disease,  of  kidney,  874  ;  of  liver,  494. 

Cystic  duct,  obstruction  of,  473. 

Cysticercus  cellulosae,  441  ;  in  the  brain,  756. 

Cysticercus  racemosus,  441. 

Cystine,  calculi  composed  of,  885. 

Cystitis,  893  ;  aetiology  of,  893  ;  chronic,  895  ;  compli- 
cations of,  896  ;  in  locomotor  ataxia,  643  ;  in  mye- 
litis, 621  ;  in  pressure  paralysis  of  the  spinal  cord, 
613 ;  in  spinal  apoplexy,  605 ;  symptoms,  894 ; 
treatment  of,  896  ;  tuberculous,  888  ;  varieties,  894. 

Cysts,  in  kidneys,  874  ;  of  brain,  apoplectic,  727  ;  of 
brain,  thrombotic,  739  ;  of  larynx,  144  ;  pancreatic, 
504  ;  porencephalic,  7'45. 

Dancing  mania,  780. 

Dandy  fever  (dengue),  99. 

Deaf-mutism  after  cerebro-spinal  fever,  107. 

Deafness,  in  cerebral  tumor,  753,  754  ;  embolism  and 
thrombosis  of  the  basilar  artery,  694  ;  in  epidemic 
cerebro-spinal  meningitis,  107  ;  in  epilepsy,  772  ;  in 
hysteria,  801  ;  in  lesions  of  the  centrum  ovale,  721  ; 
in  locomotor  ataxia,  643  ;  in  Meniere's  disease,  769; 
in  scarlet  fever,  40  ;  in  uraemia,  832. 

Debility,  nervous,  815. 

Decubitus,  acute  malignant,  in  hemiplegia,  735  ;  (bed- 
sores) in  transverse  myelitis,  622  (treatment)  627. 

Decubitus  laryngis  in  typhoid,  13. 

Degeneration,  fatty,  in  acute  phosphorus  poisoning, 


1006  ;  in  acute  yellow  atrophy,  486  ;  in  anaemia,  933, 
940  ;  in  typhoid  fever,  16  ;  of  the  heart,  315  ;  of  the 
liver,  486,  498. 
Degeneration,  parenchymatous,  in  typhoid  fever,  11, 

16  ;  of  the  kidney,  839. 
Degeneration,  physical  signs  of,  in  epileptics,  775. 
Degeneration,  reaction  of,  551  ;  anatomical  changes 
in  nerves  and  muscles  in,  553  ;  complete,  552 ;  in 
amyotrophic  lateral  sclerosis,  652  ;  in  infantile  spi- 
nal paralysis,  669  ;  in  lead  paralysis,  570  ;  in  myeli- 
tis, 622  ;  in  paralysis  of  the  deltoid,  564 ;  in  paral- 
ysis of  the  facial,  560  ;  in  poliomyelitis  of  adults, 
672  ;  in  progressive  bulbar  paralysis,  687  ;  in  pro- 
gressive muscular  atrophy,  656  ;  in  secondary  neu- 
ritis, 582  ;  partial,  551. 

Degeneration,  sclerotic,  of  the  heart,  307. 

Deglutition,  impairment  of,  in  acute  bulbar  myelitis, 
694  ;  in  acute  bulbar  paralysis,  692  ;  in  amyotrophic 
lateral  sclerosis,  652  ;  in  chronic  poliomyelitis,  673  ; 
in  compression  of  the  medulla,  695  ;  in  dilatation  of 
the  oesophagus,  363  ;  in  diphtheria,  70  ;  in  laryn- 
geal catarrh,  131  ;  in  pericarditis,  325  ;  in  progres- 
sive bulbar  paralysis,  686  ;  in  progressive  muscular 
atrophy,  657  ;  in  pseudo-leukaemia  lymphatica,  952  ; 
in  thoracic  aneurism,  337  ;  in  tonsillitis,  352 ;  in 
trichinosis,  122. 

Deglutition,  paralysis  of,  in  bulbar  haemorrhage,  692  ; 
in  embolism  and  thrombosis  of  the  basilar  artery, 
694  ;  in  hysteria,  803  ;  in  progressive  general  paral- 
ysis, 764. 

Deglutition  pneumonia,  185. 

Delayed  resolution  in  pneumonia,  202. 

Delayed  sensation  in  tabes,  640. 

Delirium,  acute,  in  lead  poisoning,  1005  ;  expansive, 
763  ;  in  acute  rheumatism,  905  ;  in  acute  yellow 
atrophy,  487  ;  in  cerebral  haemorrhage,  728 ;  in 
dengue,  100  ;  in  diabetes,  973  ;  in  hysteria,  807,  808  ; 
in  meningitis,  105,  700,  705  ;  in  pneumonia,  198  ;  in 
pylephlebitis  suppurativa,  501  ;  in  typhoid  fever, 
14;  in  typhus  fever,  30. 

Delirium  tremens,  1007  ;  in  croupous  pneumonia,  198. 

Delivery  paralysis,  567. 

Deltoid  paralysis,  564. 

Delusions  of  grandeur,  763. 

Dementia  from  epilepsy,  775. 

Dementia  paralytica,  760. 

Dengue,  99. 

Dentitio  difficilis,  350. 

"  Desiccation  "  in  small-pox,  54  ;  in  the  treatment  of 
obesity,  999. 

Desquamation,  in  measles,  47  ;  in  scarlet  fever,  41  ; 
in  small-pox,  54  ;  in  typhoid  fever,  17. 

Diabetes  inositus,  983. 

Diabetes  insipidus,  982  ;  heredity  in,  982,  983  ;  related 
to  diabetes  mellitus,  976,  982  ;  related  to  polyuria, 
982 

Diabetes  mellitus,  965;  "accidental,"  967;  coma  in, 
973  ;  complications  of,  967,  971,  972  ;  decipiens,  968  ; 
diagnosis  of,  977  ;  gangrene  in,  973  ;  hereditary  in- 
fluences in,  967  ;  intermittent,  976  ;  in  children,  967  ; 
in  obesity,  976  ;  pancreas  in,  966,  967  ;  related  to 
glycosuria,  976 ;  theories  of,  976 ;  treatment  of, 
978  ;  urine  in,  967. 

Diagnosis,  topical,  in  brain  diseases,  710. 

Diaphoresis  for  bronchitis,  150  ;  for  nephritis,  847. 

Diaphragm,  paralysis  of  the,  568  ;  in  acute  inflam- 
matory bulbar  paralysis,  694  ;  modifying  the  move- 
ments of  respiration,  568  ;  treatment  of  568. 


INDEX. 


1021 


Diaphragm,  spasm  of,  clonic,  577  ;  in  hysteria,  810  ; 
tonic,  576. 

Diarrhoea,  in  cholera  Asiatica,  84  ;  in  cholera  mor- 
bus, 411  ;  in  cirrhosis  of  the  liver,  480  ;  in  dysen- 
tery, 78  ;  in  exophthalmic  goitre,  597 ;  in  gastric 
catarrh,  379  ;  in  hysteria,  805  ;  in  intestinal  catarrh, 
404  ;  in  locomotor  ataxia,  043  ;  in  noma,  347  ;  in 
pneumonia,  197  ;  in  pulmonary  gangrene,  243  ;  in 
pulmonary  tuberculosis,  227  ;  in  pylephlebitis,  501  ; 
in  rachitis,  924  ;  in  septico-pyaemia,  112  ;  in  typhoid 
fever,  9  ;  in  uraemia,  832  ;  in  whooping-cough,  102. 

Diathesis,  gouty,  991. 

Diathesis,  haemorrhagic,  in  acute  articular  rheuma- 
tism, 904  ;  in  anaemia,  934  ;  in  jaundice,  406  ;  in 
scurvy,  958. 

Diazo-reaction  in  typhoid  fever,  18. 

Dicrotism  of  the  pulse  in  typhoid  fever,  16. 

Diet,  in  chronic  gastric  catarrh,  380  ;  in  constipa- 
tion, 431  ;  in  diabetes,  978  ;  in  gout,  990  ;  in  infan- 
tile diarrhoea,  415  ;  in  obesity,  997  ;  in  scurvy,  960  ; 
in  tuberculosis,  232  ;  in  typhoid  fever,  22. 

Digestive  system,  diseases  of,  341. 

"  Digitalis  eaters,"  305. 

Digitalis  in  nephritis,  848  ;  in  pericarditis,  328  ;  in 
pleurisy,  264  ;  in  pulmonary  emphysema,  180 ;  in 
typhoid  fever,  26  ;  in  valvular  cardiac  disease,  304  ; 
poisoning  from,  1008. 

Dilatation,  bronchial,  164  ;  stomachic,  396. 

Diphtheria,  65  ;  and  croup,  65,  68  ;  bacillus  of,  66  ; 
contagiousness  of,  67  ;  diagnosis  of,  70  ;  gangre- 
nous, 69 ;  in  animals,  67 ;  in  measles,  49  ;  laryngeal, 
68 ;  nephritis  in,  70  ;  neuritis  in,  70  ;  of  nares,  68  ; 
prognosis  of,  71  ;  septic,  66  ;  symptoms  of,  67  ; 
systemic  infection,  69  ;  treatment  of,  71. 

Diphtheritic  colitis,  77,  78. 

Diplegia,  facial,  690. 

Diplococcus  pneumoniae,  189. 

Diplopia,  555  ;  in  multiple  sclerosis,  630. 

Disease,  trichinatous,  121. 

Disinfection  in  infectious  diseases,  26  ;  in  typhoid  fe- 
ver, 26. 

Dislocation,  paralysis  of  the  upper  arm  following, 
564. 

Displacement,  symptoms  resulting  from,  of  other 
organs,  in  pleurisy,  260  ;  in  pneumonia  complicated 
by  pleurisy,  196  ;  in  pneumothorax,  269. 

Dissecting  aneurism,  340. 

Distoma  haematobium,  874. 

Disuse,  atrophy  from,  622. 

Dittrich's  plugs,  156. 

Diuretics  in  cirrhosis  of  the  liver,  483  ;  in  nephritis, 
848 ;  in  pleurisy,  264  ;  in  pulmonary  emphysema, 
180  ;  in  valvular  cardiac  disease,  306. 

Diverticula  of  the  oesophagus,  363. 

Dochmius  duodenalis,  448. 

Dorso-intercostal  neuralgia,  524. 

Double  vision,  555. 

Douche,  cold,  in  cutaneous  anaesthesia,  515  ;  in  dia- 
betes, 980 ;  in  hysteria,  812  ;  in  neuralgia  of  the 
joints,  529  ;  in  neurasthenia,  818 ;  in  scarlet  fever, 
45  ;  in  spasm  of  the  diaphragm,  577. 

Drainage  and  diphtheria,  67  ;  and  tonsillitis,  351 ;  and 
typhoid  fever,  3. 

Drinker's,  gin,  liver,  478. 

Drinking  water  as  a  cause  of  cholera,  83  ;  of  typhoid 
fever,  3. 

Dropsy.    See  also  CEdema. 

Dropsy,  cardiac,  treatment  of,  306  ;  in  amyloid  dis- 


ease of  the  kidney,  867  ;  in  aortic  insufficiency,  290; 
in  cancer  of  stomach,  393  ;  in  mitral  insufficiency, 
284  ;  in  mitral  stenosis,  287  ;  in  phthisis,  229  ;  in  re- 

nal  diseases,  828,  813,  853,  860;  in  scarlet  r<:v<T.  n, 
42  ;  in  typhoid  fever,  16  ;  in  valvular  cardiac  dis- 
ease, 299. 

Dropsy,  intermittent,  of  the  joints,  590. 

Dropsy  of  the  gall-bladder,  473. 

Duchenne's  paralysis,  685. 

Dullness,  movable,  in  pleural  effusion,  200  ;  in  pneu- 
mothorax, 209. 

Dumb  ague,  94,  95. 

Duodenal  ulcer,  diagnosis  of,  from  gastric,  423. 

Duodenum,  cancer  of  the,  426  ;  catarrh  of  the,  400, 
464  ;  fistula  of  the,  473,  474  ;  ulcer,  perforating,  of 
the,  423. 

Dura  mater,  diseases  of,  096  ;  haematoma  of,  090. 

Durande's  remedy  for  biliary  calculi,  475. 

Duroziez's  double  murmur,  290. 

Dust,  diseases  due  to  the  inhalation  of,  245  ;  prophy- 
laxis of,  246  ;  tubercle  bacilli  in,  246. 

Dysarthria,  685,  716. 

Dysentery,  77  ;  abscess  of  liver  in,  79  ;  acute,  78 ; 
amoeba  coli  in,  81  ;  catarrhal,  78 :  chronic,  79  ;  di- 
agnosis of,  79  ;  diphtheritic,  78  ;  gangrenous,  78  ; 
prognosis  of,  79  ;  secondary,  78  ;  treatment  of,  80  ; 
tropical  or  amoebic,  81. 

Dyspepsia,  acute,  372  ;  chronic,  374  ;  nervous,  400  ;  of 
children,  413. 

Dysphagia,  convulsive,  in  tetanus,  792  ;  hysterical, 
810  ;  in  cancer  of  the  oesophagus,  366,  369  ;  in  hy- 
drophobia, 114  ;  in  cesophagismus,  371  ;  in  oesopha- 
gitis. 362  ;  in  pericardial  effusion,  325  ;  in  thoracic 
aneurism,  337  ;  in  tuberculous  laryngitis,  137  ;  luso- 
ria,  366. 

Dyspnoea,  cardiac,  treatment  of,  306  ;  from  aneu- 
rism, 336  ;  hysterical,  807  ;  in  acute  miliary  tuber- 
culosis, 237  ;  in  anaemia,  932,  942  ;  in  anthrax,  120  ; 
in  bilateral  paralysis  of  abductors,  140  ;  in  bronchi- 
tis, 147,  152 ;  in  contracted  kidney,  860  ;  in  croup, 
68  ;  in  diabetic  coma,  973  ;  in  new  growths  of  the 
lungs,  251  ;  in  new  growths  of  the  mediastinum, 
273  ;  in  oedema  of  the  glottis,  136  ;  in  paralysis  of 
the  muscles  of  the  larynx,  140  ;  in  pleurisy,  257  ;  in 
pneumonia,  186,  193  ;  in  pneumothorax,  268 ;  in 
pulmonary  emphysema,  176  ;  in  pulmonary  tuber- 
culosis, 221  ;  in  septico-pyaemia,  112  ;  in  spasmodic 
laryngitis,  131  ;  in  stenosis  of  the  bronchi,  167 ;  in 
stenosis  of  the  trachea,  166  ;  in  trichinosis,  122  ;  in 
valvular  cardiac  disease,  296. 

Dyspnoea,  uraemic  (uraemic  asthma),  833. 

Dystrophy,  primary  muscular,  658. 

Ear,  care  of,  in  scarlet  fever,  45  ;  complications  of, 
in  scarlet  fever,  40. 

Ear,  symptoms  in  the,  in  anaemia,  932,  942  ;  in  caisson 
disease,  608  ;  in  cerebral  anaemia.  709  ;  in  compres- 
sion of  the  medulla  oblongata,  695  ;  in  facial  pa- 
ralysis, 559,  560  ;  in  haemorrhage  into  the  medulla 
oblongata,  691  ;  in  hysteria,  801  ;  in  leukaemia,  949 ; 
in  Meniere's  disease,  769  ;  in  meningitis,  cerebro- 
spinal, 105  ;  in  scarlet  fever,  40  ;  in  scrofula,  1000. 

Ebstein's  method  in  obesity,  997. 

Eburnation  of  cartilages,  913. 

Echinococcus,  494  ;  diagnosis,  495  ;  endogenous,  494, 
495 ;  exogenous,  495  ;  fluid.  496  ;  granulosus.  495  : 
hydatidosus,  495  ;  multilocularis,  495  ;  of  the  kid- 
ney, 874. 


1022 


INDEX. 


Echolalia,  573. 

Eclampsia.    See  also  Convulsions. 

Eclampsia  gravidarum  in  acute  nephritis,  845. 

Eclampsia  infantum,  779  ;  aetiology  of,  779  ;  associ- 
ated with  spasms  of  the  glottis,  142  ;  liability  of 
rachitic  children  to,  779. 

Eclampsia,  uraemic,  831,  844. 

Ectasis,  alveolar,  173. 

Ehrlich's  reaction  in  typhoid  fever,  18. 

Elastic  tissue  in  sputum,  219. 

Electrical  reactions  in  facial  palsy,  560,  561  ;  in  idio- 
pathic muscular  atrophy,  660,  662  ;  in  Landry's  pa- 
ralysis, 674  ;  in  multiple  neuritis,  583  ;  in  poliomye- 
litis anterior,  669  ;  in  Thomsen's  disease,  795. 

Electricity  in  acute  ascending  spinal  paralysis,  676  ; 
in  acute  bulbar  paralysis,  695  ;  in  amyotrophic  lat- 
eral sclerosis,  653  ;  in  anaesthesia  of  the  trigeminus, 
515  ;  in  anomalies  of  the  sense  of  smell,  533  ;  in 
anomalies  of  the  sense  of  taste,  534  ;  in  articular 
neuroses,  529  ;  in  articular  rheumatism,  911 ;  in 
asthma,  172  ;  in  athetosis,  789  ;  in  cerebral  abscess, 
743 ;  in  cerebral  haemorrhage,  737 ;  in  cerebral 
syphilis,  760  ;  in  cervico-brachial  neuralgia,  524  ;  in 
chorea,  783  ;  in  chronic  poliomyelitis,  674  ;  in  cuta- 
neous anaesthesia,  515  ;  in  diabetes,  981  ;  in  dilata- 
tion of  the  stomach,  400 ;  in  epilepsy,  778  ;  in  ex- 
ophthalmic goitre,  598  ;  in  facial  paralysis,  562  ;  in 
facial  spasm,  573  ;  in  habitual  constipation,  431 : 
in  habitual  headache,  532  ;  in  hemicrania,  593  ;  in 
hysteria,  812  ;  in  incontinence  of  urine,  898  ;  in  in- 
fantile cerebral  paralysis,  745  ;  in  intercostal  neu- 
ralgia, 525  ;  in  lead  paralysis,  570  ;  in  locomotor 
ataxia,  647  ;  in  mastodynia,  525  ;  in  multiple  sclero- 
sis, 631  ;  in  muscular  rheumatism,  919  ;  in  myelitis, 
626  ;  in  nervous  dyspepsia,  403  ;  in  neuralgia,  519  ; 
in  neurasthenia,  818  ;  in  neuritis,  584  ;  in  occipital 
neuralgia,  523  ;  in  pachymeningitis  cervicalis  hy. 
pertrophica,  603 ;  in  paralysis  of  the  diaphragm, 
568  ;  in  paralysis  of  the  motor  branch  of  the  trigem- 
inus, 558  ;  in  paralysis  of  the  ocular  muscles,  557 ; 
in  peripheral  paralysis  of  the  arm,  567  ;  in  pressure 
paralysis  of  the  spinal  cord,  614  ;  in  progressive 
muscular  atrophy,  658  ;  in  progressive  bulbar  pa- 
ralysis, 689  ;  in  progressive  general  paralysis,  767  ; 
in  pseudo-muscular  hypertrophy,  663  ;  in  railway 
spine,  821  ;  in  sciatica,  527  ;  in  spasm  of  the  dia- 
phragm, 577  ;  in  spasm  of  the  muscles  of  the  neck, 
574  ;  in  spasm  of  the  muscles  of  the  shoulder,  575 ; 
in  spasm  of  the  trigeminus,  571  ;  in  spastic  spinal 
paralysis,  666  ;  in  splenic  leukaemia,  951  :  in  tetany. 
791  ;  in  unilateral  progressive  facial  atrophy,  594  ; 
in  writer's  cramp,  579. 

Electricity  used  to  test  sensibility,  508. 

Electro-cutaneous  sensibility,  508. 

Electrolysis  in  aneurism,  338. 

Embolic  processes  in  the  lungs,  247. 

Embolism  and  thrombosis  of  the  basilar  artery,  693  ; 
a  cause  of  softening  of  the  medulla  and  pons,  693  ; 
aetiology  of,  693  ;  symptoms  of,  693  ;  treatment  of, 
694. 

Embolism  in  chorea,  783 ;  in  typhoid  fever,  16  ;  of 
cerebral  arteries,  737  ;  of  cerebral  arteries,  diagno- 
sis of,  740. 

Emetics  in  bronchitis,  151  ;  in  dysentery,  80  ;  in  in- 
fantile convulsions,  779  ;  in  pulmonary  oedema,  184. 

Emotion,  convulsive  expressions  of,  in  hysteria,  807. 

Emphysema,  173  ;  acute,  162  ;  atropine,  173  ;  com- 
pensatory, 175  ;   complementary,    175  ;    connected 


with  whooping-cough,  162,  175  ;  diagnosis  of,  179  ; 
essential,  173  ;  followed  by  pulmonary  tuberculo- 
sis, 179 ;  hypertrophic,  hereditary  character  of, 
174  ;  interlobular,  175  ;  interstitial,  175  ;  prognosis 
of,  179  ;  treatment  of,  180  ;  vesicular,  175  ;  vicarious, 
175. 

Empyema,  262 ;  necessitatis,  256 ;  perforation  of 
lung  in,  262  ;  terminations  of,  263  ;  treatment  of, 
264. 

Encephalitis,  curable  form  of.  744  ;  in  children,  744  ; 
non-purulent,  743  ;  purulent,  741. 

Encephalomalacia,  737. 

Encephalopathy,  lead,  or  saturnine,  1005  ;  syphilitic, 
758. 

Enchondroma  of  the  lungs,  250. 

Endarteritis  chronica  deformans,  331. 

Endocarditis,  acute,  276  ;  acute  recurrent,  279  ; 
chronic,  280  ;  diagnosis  of,  279  ;  diphtheritic,  277  ; 
aetiology  of,  276  ;  foetal,  277  ;  in  articular  rheuma- 
tism, 276,  903  ;  in  chorea,  782  ;  infectious,  276  ;  in 
gonorrhoea,  276  ;  in  pneumonia,  197  ;  in  septicae- 
mia, 111,  276  ;  in  tuberculosis,  228  ;  malignant,  278  ; 
prognosis  of,  280  ;  recurring,  277,  279  ;  rheumatoid, 
278  ;  ulcerative,  277  ;  verrucosa,  277. 

Endothelial  carcinoma  of  the  pleura,  272. 

Enemata  of  cold  water  in  jaundice,  469. 

"  English  disease,"  920. 

Engouement.  190. 

Enteric  fever  (see  Typhoid  Fever),  1. 

Enteritis  catarrhalis,  403  ;  in  children,  413  ;  mem- 
branous or  tubular,  408, 

Enteroliths  as  a  cause  of  appendicitis,  418,  419. 

Enuresis  nocturna,  898. 

Eosinophilous  blood-globules,  948. 

Epidemic  of  typhoid  fever  in  Plymouth,  Pa.,  4. 

Epidermis,  desquamation  of,  in  scarlet  fever,  41  ;  in 
measles,  47  ;  in  smallpox,  54  ;  in  typhoid  fever,  17. 

Epilepsy,  770  ;  aetiology  of,  770  ;  cortical,  714  ;  diag- 
nosis of,  776;  diurnal,  774;  heredity  in,  770;  in 
general  paresis,  764  ;  in  lead  poisoning,  1005  ;  in 
regard  to  cerebral  anaemia,  776 ;  in  regard  to 
sudden  somnolence,  773  ;  in  regard  to  teething 
convulsions,  774  ;  Jacksonian,  714  ;  masked,  773  ; 
nocturnal,  774  ;  occurrence  of  various  forms  of, 
771  ;  procursive,  773,  774  ;  reflex,  771  ;  seat  of  the 
disease,  775  ;  surgical  treatment  of,  777  ;  traumatic, 
771  ;  treatment,  777. 

Epileptic  paroxysm,  771  ;  aura  preceding  the,  771 ; 
convulsive  stage  of,  772 ;  frequency  of,  774  ;  in 
progressive  general  paralysis,  764  ;  rudimentary 
forms  of,  773. 

Epileptoid  confusion  of  intellect,  773  ;  sweating,  774. 

Epistaxis,  129  ;  in  haemophilia,  964  ;  in  scurvy,  129  ; 
in  typhoid  fever,  129  ;  "  renal,"  862  ;  vicarious,  129. 

Erethitic  habitus,  1000. 

Ergot  (ergotine)  in  acute  ascending  spinal  paralysis, 
676  ;  in  aneurism  of  the  thoracic  aorta,  338  ;  in 
diabetes  insipidus,  984  ;  in  exophthalmic  goitre, 
598  ;  in  habitual  headache,  532  ;  in  haemophilia, 
965  ;  in  hemicrania,  593  ;  in  locomotor  ataxia,  648  ; 
in  myelitis,  627  ;  in  neuralgia,  520  ;  in  paialysis 
agitans,  787  ;  in  poliomyelitis  of  adults,  672  ;  in 
progressive  general  paralysis,  767  ;  in  pulmonary 
tuberculosis,  235  ;  in  purpura  hemorrhagica,  962  ; 
in  spastic  spinal  paralysis.  667  ;  in  spinal  apoplexy, 
605  ;  poisoning  from,  1009  ;  psychoses  due  to,  1009. 

Ergotism,  1009  ;  convulsive,  1009  ;  gangrenous,  1009. 

Erosion,  ulcers  due  to,  in  laryngeal  catarrh,  130,  133. 


INDEX. 


1023 


Eructations  in  anaemia,  932,  942  ;  in  diabetes,  967  ;  in 
intestinal  obstruction,  435  ;  in  peritonitis,  454. 

Eruption,  acute,  in  scarlet  fever,  37  ;  hemorrhagic, 
in  small-pox,  57. 

Erysipelas,  61  ;  abscess  in,  04  ;  after  vaccination,  59  ; 
bullous,  G3  ;  complications  of,  64  ;  contagiousness  of, 
62  ;  diagnosis  of,  64  ;  facial,  61  ;  Fehleisen's  strep- 
tococcus of,  62  ;  gangrenous,  63  ;  idiopathic,  61  ; 
inoculation  of,  62  ;  in  smallpox,  56  ;  migratory,  63  ; 
of  the  new-born,  61  ;  prognosis  of,  64  ;  puerperal, 
61  ;  pustulous,  63  ;  traumatic,  61  ;  treatment  of,  64  ; 
vesicular,  63. 

Erythema  exsudativum,  962. 

Erythromelalgia,  588. 

fitat  de  mal,  774. 

Eucalyptus,  oil  of,  in  splenic  leukaemia,  950. 

Eustrongylus  gigas,  875. 

Exaltation  of  ideas  in  general  paresis,  763. 

Exophthalmic  goitre,  595  ;  acute  form,  597  ;  aetiology 
of,  595  ;  diagnosis  of,  597  ;  diminution  of  electrical 
resistance  in,  597  ;  examination  of  heart  in,  595  ; 
"  Graefe  symptom  "  in,  596  ;  nervous  symptoms  in, 
596,  597  ;  pigmentation  in,  597  ;  treatment  of,  598  ; 
tremor  in,  596  ;  urticaria  in,  597. 

Exophthalmus  in  exophthalmic  goitre,  596  ;  in  paral- 
ysis of  the  motores  oculi,  556. 

Expectorants  in  bronchitis,  151,  154  ;  in  pneumonia, 
188,  206  ;  in  pulmonary  emphysema,  180  ;  in  pul- 
monary tuberculosis,  234. 

"Expectoration  albumineuse  "  in  pleurisy,  266. 

Expectoration  in  asthma,  168, 169  ;  in  bronchiectasis, 
165 ;  in  bronchitis,  147,  151,  156  ;  in  laryngeal 
catarrh,  131,  133  ;  in  pleurisy,  257  ;  in  pneumonia, 
186,  193  ;  in  pulmonary  cancer,  251  ;  in  pulmonary 
emphysema,  176  ;  in  pulmonary  gangrene,  242  ;  in 
pulmonary  tuberculosis,  218. 

Eye,  motor  nerves  of,  paralysis  of,  555. 

Eye-strain  in  migraine,  591. 

Eyes.    See  also  Ocular  and  Ophthalmia. 

Eyes,  conjugate  deviation  of,  in  cerebral  haemor- 
rhage, 729. 

Eyes,  disorders  of,  in  acute  bulbar  paralysis,  694  ;  in 
acute  hydrocephalus.  703  ;  in  anaemia,  932,  942  ;  in 
cerebral  haemorrhage,  729  ;  in  cerebral  tumors,  751  ; 
in  chorea,  781  ;  in  chronic  hydrocephalus,  768  ;  in 
diabetes,  972  ;  in  haematoma  of  the  dura  mater, 
697  ;  in  hemicrania,  592 ;  in  hysteria,  801  ;  in  lesions 
of  the  central  ganglia,  722  ;  in  lesions  of  the  corpora 
quadrigemina  and  crura  cerebri,  722  ;  in  lesions  of 
the  occipital  cortex,  715  ;  in  leukaemia,  949  ;  in 
locomotor  ataxia,  635,  642 ;  in  measles,  48 ;  in 
meningitis,  105,  700,  704  ;  in  miliary  tuberculosis, 
■  239 ;  in  multiple  sclerosis,  630  ;  in  progressive 
bulbar  paralysis,  687  ;  in  relapsing  fever,  35  •  in 
septicopyasmia,  111  ;  in  thrombosis  of  the  cerebral 
sinuses,  707  ;  in  trichinosis,  122. 

Face-ache,  FotherghTs,  521. 

Facial  atrophy,  unilateral  progressive,  594  ;  paralysis, 
558  ;  aetiology  of,  558  ;  diagnosis  of,  561  ;  in  acute 
bulbar  paralysis,  694 ;  in  cerebral  haemorrhage, 
731  ;  in  cerebral  tumor,  752  ;  in  compression  of  the 
medulla  oblongata,  695  ;  in  haemorrhage  into  the 
medulla  oblongata,  692  ;  in  progressive  bulbar 
paralysis,  686  ;  mimetic,  558  ;  symptoms  of,  558  ; 
through  cold,  558  ;  treatment  of,  561  ;  varieties, 
559. 

Facial  spasm,  clonic,  572  ;  in  epilepsy,  772  ;  in  menin- 


gitis, 105  ;  treatment  of,  573  ;  spasm,  mimetic,  572  ; 

spasm,  tonic,  in  tetanus,  792. 
Faecal,  concretions,  418,  419 ;  vomiting,  KJ5. 
Faeces,  in  disease  of  pancreas,  604 ;    in  jaundice, 

406. 

Fainting,  709  ;  aetiology  of,  709  ;  in  anaemia,  931  ;  in 
cerebral  haemorrhage,  728  ;  in  cerebral  tumor,  750; 
in  epilepsy,  773  ;  in  insolation,  7)0  ;  in  leukaemia, 
949  ;  in  pernicious  anaemia,  941  ;  liability  to,  709  ; 
symptoms  of,  709  ;  treatment  of,  709. 

Falling  sickness,  770. 

Famine  fever,  29. 

Farcy,  116  ;  acute,  116  ;  chronic,  117. 

Farcy- buds,  116. 

Fascia  reflex,  545  ;  in  cerebral  haemorrhage,  732. 

Fat,  ingestion  of,  in  diabetes,  979. 

Fat- drops  in  urinary  casts,  827. 

Fatty  acids,  crystals  of,  in  the  sputum  of  foetid 
bronchitis,  156. 

Fatty  degeneration,  in  anaemia,  933  ;  of  heart,  315  ; 
of  kidneys,  839,  851  ;  of  liver,  485. 

Fatty  granular  globules  in  urinary  casts,  827  ;  heart, 
315  ;  kidney,  839,  851  ;  inflammatory,  839,  851  ; 
liver,  485,  489  ;  liver  in  pulmonary  tuberculosis, 
228  ;  liver  in  trichinosis,  123. 

Fatty  stools,  504. 

Febricula,  31. 

Febris  continua,  7  ;  erratica,  94  ;  gastrica,  18  ;  inter- 
mittens, 90,  92 ;  nervosa  stupida,  14 ;  nervosa 
versatilis,  14  ;  quotidiana,  93  ;  recurrens,  31. 

Feeding,  artificial,  in  progressive  bulbar  paralysis, 
690  ;  in  stenosis  of  the  oesophagus,  368  ;  in  trismus, 
572. 

Fehling's  test  for  sugar,  968. 

Fermentation  test  for  sugar,  969. 

Fever,  anaemic,  387,  934  ;  cerebro-spinal,  103  ;  "  cold," 
85  ;  enteric,  1  ;  gastric,  18  ;  hectic,  225  ;  hysterical, 
804  ;  in  acute  ascending  spinal  paralysis,  675  ;  in 
acute  miliary  tuberculosis,  238  ;  in  angina,  351  ;  in 
appendicitis,  420  ;  in  arthrogryposis,  576  ;  in  articu- 
lar rheumatism,  901  ;  in  bronchitis,  148  ;  in  cardiac 
valvular  disease,  301  ;  in  cerebral  abscess,  742  ;  in 
cholera,  85 ;  in  cirrhosis  of  the  liver,  481  ;  in 
cystitis,  895  ;  in  dengue,  99  ;  in  diabetes,  971  ;  in 
diphtheria,  68  ;  in  dysentery,  79  ;  in  endocarditis, 
278  ;  in  erysipelas,  63  ;  in  gastric  catarrh,  373  ;  in 
glanders,  117  ;  in  gout,  986  ;  in  haemoglobinaemia, 
954 ;  in  hepatitis,  suppurative,  477 ;  in  infantile 
cerebral  paralysis,  744  ;  in  infantile  spinal  paral- 
ysis, 668  ;  in  influenza,  76  ;  in  intermittent  fever, 
93  ;  in  intestinal  catarrh,  405  ;  in  measles,  48  ;  in 
meningitis,  103,  700,  704  ;  in  noma,  347  ;  in  osteo- 
malacia, 927  ;  in  parotitis,  348  ;  in  pericarditis,  323  ; 
in  perinephritis,  870  ;  in  pleurisy,  257  ;  in  pneu- 
monia, 186,  192  ;  in  poliomyelitis  of  adults,  671  ;  in 
primary  multiple  neuritis,  582  ;  in  pulmonary  em- 
physema, 179  ;  in  pulmonary  gangrene,  243  ;  in 
pulmonary  tuberculosis,  225  ;  in  purpura  haetnor- 
rhagica,  962 ;  in  purpura  rheumatica,  962 ;  in 
pyelitis,  883  ;  in  pylephlebitis,  suppurative,  501  ;  in 
rachitis,  922  ;  in  relapsing  fever,  33  :  in  remittent 
fever,  33  ;  in  scarlet  fever,  37  ;  in  septico-pyaemia, 
HI  ;  in  small-pox,  55  ;  in  sunstroke,  747  ;  in  thermic 
fever,  747  ;  in  trichinosis,  123  :  in  tuberculosis  of 
the  genitourinary  organs,  889  ;  in  typhlitis,  419, 
420  ;  in  typhoid  fever,  6  ;  in  typhus  fever,  30  ; 
in  yellow  fever,  101. 
Fever,  intermittent,  90  ;  lung.  189  ;  ship,  28  ;  splenic, 


1024 


INDEX. 


117  ;  spotted,  28  ;  swamp,  90  ;  typhoid,   1  ;  typho- 

malarial,  98  ;  yellow,  100. 
Fibrinous,  bronchitis,  158  ;  pneumonia,  189. 
Fibroid  disease  of  heart,  307. 
Fibroma  of  the  larynx,  144. 
Fifth  nerve,  paralysis  of,  557. 
Filaria  Bancroft!,  875  ;  sanguinis,  875. 
Fish,  poisoning  from  the  ingestion  of,  1010. 
Flapping  joints  in  infantile  spinal  paralysis,  669. 
Flatulence  in  hysteria,  805  ;  in  jaundice,  466. 
Flexibility,  waxy,  796. 
Floating  kidney,  876. 
Foetus,  endocarditis  in,  293. 
Follicular  catarrh  of  the  intestines,  404. 
Foot-baths  in  asthma,  172. 
Forced  attitudes,  541. 
Forced  movements,  541  ;  in  disease  of  the  crura  cere- 

belli  ad  pontem,  725  ;  in  paralysis  agitans,  785. 
Forearm,  paralysis  of,  564 ;    paralysis  of,  in  amyo- 
trophic lateral  sclerosis,  651. 
Foreign  bodies  in  the  intestinal  canal,  432. 
Fothergill's  face-ache,  521. 
Fourth  nerve,  paralysis  of,  556. 
Fowler's  solution.    See  Arsenic. 
Fowler's  solution  in  chorea,  783 ;  in  endocarditis,  280  ; 

in  valvular  cardiac  disease,  303. 
Fractures  in  rachitis,  923  ;  in  osteomalacia,  927. 
Fremitus,  hydatid,  495. 
Fresh-air  treatment  in  tuberculosis,  233. 
Friction  in  pericarditis,  324  ;  in  peritonitis,  453  ;  in 

pleurisy,  258. 
Friedreich's  ataxia,  648. 

Friedreich's  sign  in  adherent  pericardium,  326. 
Frontal  convolutions,  lesions  of  the,  715  ;  connected 

with  the  centers  of  speech,  715,  719  ;  connected  with 

the  cortical  motor  centers,  715. 
Frontal  sinuses,  catarrh  of  the,  126. 
Fuchsine  in  nephritis,  846. 
Furunculosis  in  diabetes,  972,  973,  977 ;  in  scarlet  fever, 

41  ;  in  typhoid  fever,  17  ;  in  typhus  fever,  30. 

Gait  in  amyotrophic  lateral  sclerosis,  651  ;  in  loco- 
motor ataxia,  637  ;  in  multiple  sclerosis,  629,  630  ; 
in  osteomalacia,  927  ;  in  pseudo-hypertrophic  mus- 
cular paralysis,  659  ;  in  rachitis,  923  ;  in  spastic 
spinal  paralysis,  665  ;  pseudo-tabetic,  585. 

Gall-bladder,  dilatation  of,  473  ;  forming  abdominal 
tumor,  473. 

Gall-stones,  470  ;  diagnosis  of,  474  ;  prognosis  of,  474  ; 
treatment  of,  474. 

Galloping  consumption,  217. 

Galvano-cautery  in  hypertrophic  pharyngitis,  360. 

Galvano  -  puncture  in  aneurism  of  thoracic  aorta, 
338. 

Ganglia,  basal,  tumors  of,  752. 

Ganglia,  central,  of  the  brain,  lesions  of,  721 ;  lesions 
of,  causing  hemiplegia,  721,  722  ;  lesions  of,  causing 
hemiopia,  722  ;  lesions  of,  causing  post-hemiplegic 
chorea,  722. 

Gangrene,  embolic,  242,  248,  300. 

Gangrene  in  diabetes,  971,  973  ;  in  ergotism,  1009  ;  in 
exophthalmic  goitre.  597  ;  in  pneumonia,  203  ;  in 
small-pox,  56  ;  in  typhoid  fever,  17  ;  in  typhus  fever, 
30  ;  local  or  ss'mmetrical,  588  ;  of  the  lungs,  241  ; 
of  the  mouth,  347  ;  senile,  333. 

Garrod's  thread-test  for  uric  acid,  990. 

Gastrectasis,  396. 

Gastric.    See  also  Stomach. 


Gastric  abscess,  383  ;  cancer,  391. 

Gastric  catarrh,  acute,  372  ;  absorption  impeded  by, 
375  ;  chronic,  375  ;  diagnosis  of,  379  ;  exciting  causes 
of,  372,  374  ;  gastric  juice  in,  374  ;  liability  to,  374  ; 
mucus  secreted  in,  375  ;  peristalsis  in,  375  ;  treat- 
ment of,  373,  380. 

Gastric  crises  in  locomotor  ataxia,  643  ;  fever,  373  ; 
haemorrhage,  388  ;  haemorrhage  in  cancer,  392  ; 
haemorrhage  in  ulcer,  385,  386,  388. 

Gastric  juice,  chemical  examination  of,  377  ;  hyper- 
acidity of,  382  ;  subacidity  of,  378. 

Gastric  pain  in  case  of  ulcer,  385  ;  ulcer,  384  ;  ulcer, 
clinical  forms  of,  385  ;  ulcer,  peptic,  384 ;  ulcer, 
round,  384  ;  vertigo,  401. 

Gastritis,  acute,  372  ;  acute  suppurative,  383  ;  chronic, 
375  ;  phlegmonous,  383. 

Gastrointestinal  symptoms  in  emphysema,  179. 

Gastromalacia,  384  (foot-note). 

Gastrorrhagia,  386,  388. 

Gastrotomy,  395. 

Gastroxynsis,  nervous,  401. 

Gelsemium,  tincture  of,  in  neuralgia,  520  ;  in  tri- 
geminal neuralgia,  523. 

General  paralysis,  progressive^  760  ;  aetiology  of,  761  ; 
depressive  form,  764  ;  development  of,  762  ;  diag- 
nosis of,  766  ;  hereditary  predisposition  to,  761  ; 
influence  of  syphilis  in,  761  ;  maniacal  exaltation 
in,  763  ;  symptoms  of,  761  ;  treatment  of,  766. 

Genito-urinary  organs,  tuberculosis  of,  888  ;  diagnosis 
of,  890  ;  treatment  of,  890. 

German  measles,  51. 

Giant  cells,  212.  • 

Gin-drinker's  liver,  478. 

Girdle-sensation  in  locomotor  ataxia,  640. 

Glanders,  116  ;  acute,  116  ;  chronic,  117  ;  diagnosis 
of,  117  ;  diagnosis  from  small-pox,  117  ;  period  of 
incubation  in,  116  ;  treatment  of,  117. 

Glioma  of  brain,  748,  755. 

Globus  hystericus,  810. 

Glomerulo-nephritis,  841  ;  in  scarlet  fever,  43. 

Glossitis,  acute  parenchymatous,  345  ;  treatment  of, 
346. 

Glosso-labio-laryngeal  paralysis,  685. 

Glossy  fingers  in  cervico-brachial  neuralgia,  524  ;  in 
trophic  disorders  of  the  nerves,  589. 

Glottis,  oedema  of,  135  ;  in  Bright's  disease,  136  ;  in 
nephritis,  854  ;  in  small-pox,  56  ;  in  scarlet  fever, 
40  ;  in  typhoid  fever,  14. 

Glottis,  openers  of,  paralysis  of,  140. 

Glottis,  spasm  of,  142  ;  in  hysteria,  810  ;  in  rachitis, 
142,  924  ;  in  tetanus,  793  ;  treatment  of,  794. 

Glotzaugenkrankheit,  595. 

Gluteal  paralysis,  569  ;  reflex,  543. 

Glycerine  in  diabetes,  979  ;  in  trichinosis,  123. 

Glycogenic  function  of  liver,  974. 

Glycosuria,  966  ;  aetiology  of,  966  ;  gouty,  988  ;  in 
bulbar  hemorrhage,  692  ;  in  cerebral  haemorrhage ; 
729  ;  in  tetanus,  793. 

Gmelin's  test,  467. 

Goitre,  exophthalmic,  595  ;  symptoms  of,  595. 

Goll,  columns  of,  510. 

Gonorrhoeal  rheumatism,  endocarditis  in,  276. 

Gout,  984  ;  acute,  989  ;  atypical,  987  :  chronic,  987  ; 
complications  of,  988  ;  diagnosis  of,  989  ;  aetiology 
of,  984  ;  Ebstein's  theory  of,  989  ;  geographical  dis- 
tribution, 985  ;  hereditary  influence  in,  985  ;  influ- 
ence of  alcohol  in,  985  ;  influence  of  food  in,  985  ; 
influence  of  lead  in,  985  ;   irregular,  987  ;  morbid 


INDEX. 


1025 


anatomy  of,  988  ;  nature  of,  032  ;  symptoms  of,  980  ; 
treatment  of,  990. 

Graefe's  sign,  596. 

Grande  hystörie,  808 ;  contortions  in,  808  ;  epilepti- 
form parox3'sms  in,  808 ;  statuesque  postures  and 
"  attitudes  of  passion  "  in,  808. 

Grandeur,  delusions  of,  in  progressive  general  paral- 
ysis, 763. 

Grand  mal,  771. 

Granular  kidney,  856. 

Graphospasm,  577. 

Gravel,  renal,  884. 

Graves's  disease,  595. 

Green-siekness,  934.    See  also  Chlorosis. 

Green-stick  fracture  in  rickets,  923. 

Grinder's  rot  (pneumonoconiosis),  245. 

Grippe,  la,  74. 

Guarana  in  habitual  headache,  532  ;  in  hemicrania, 
593  ;  in  intestinal  catarrh  of  children,  417. 

Gummata  in  cerebral  syphilis,  749,  757  ;  in  hepatic 
syphilis,  490  ;  of  spinal  cord,  609  ;  of  liver,  490  ;  of 
lungs,  252. 

Gums,  affections  of,  in  diabetes,  971  ;  (blue  line  on),  in 
lead  poisoning,  1005  ;  in  scurvy,  960  ;  in  stomatitis, 
341 ;  in  typhoid  fever,  12. 

Gustatory  paralysis,  533. 

Gymnastics  in  articular  rheumatism  (chronic),  916  ; 
in  diabetes,  980  ;  in  gout,  990  ;  in  infantile  spinal 
paralysis,  671  ;  in  neurasthenia,  817  ;  in  progressive 
muscular  atrophy,  658  ;  in  writer's  cramp,  579. 

Habitus,  apoplectic,  726;  emphysematous,  177  ;  erethi- 
tic,  1000  ;  phthisical,  221. 

Haematemesis,  diagnosis  from  haemoptysis,  388. 

Haematemesis,  hysterical,  804  ;  in  acute  yellow  atro- 
phy, 487  ;  in  gastric  ulcer,  386. 

Haematemesis  in  leukaemia,  949  ;  in  scurvy,  959. 

Haematidrosis,  590. 

Haemato-chyluria,  parasitic,  875. 

Haeniatogenous  jaundice,  490,  956. 

Haematoidine,  granules  of,  in  urinary  casts,  827. 

Haematoma  of  the  dura  mater,  696  ;  apoplectic  symp- 
toms in,  697  ;  diagnosis  of,  698  ;  in  chronic  alcohol- 
ism, 697  ;  in  connection  with  the  haemorrhagic  di- 
athesis, 697  ;  in  progressive  general  paralysis,  697  ; 
origin  of,  696  ;  seat  of,  696  ;  treatment  of,  698. 

Haematomyelia,  604. 

Haematorrhachis,  603. 

Haematothorax,  271. 

Haematozoa  of  malaria,  91. 

Haematuria,  828  ;  as  a  sign  of  scurvy,  959  :  endemic, 
of  Egypt,  874,  875  ;  in  acute  nephritis,  842  ;  in  chy- 
luria,  875  ;  in  renal  calculus,  886  ;  in  renal  cancer, 
873  ;  in  tuberculosis  of  kidney,  889  ;  in  tumor  of  the 
kidney,  873  ;  tropical,  875. 

Haemine  test,  392. 

Haemoglobin,  diminution  of,  in  chlorosis,  935. 

Haemoglobinaemia,  953  ;  aetiology  of,  953  :  in  connec- 
tion with  malaria,  953  ;  in  connection  with  syphilis, 
956  ;  in  poisoning  from  mushrooms,  953  ;  paroxys- 
mal, 954,  955  ;  symptoms  of,  954. 

Haemoglobin,  granules  of,  in  the  urine.  954. 

Haemoglobinuria,  953 ;  in  poisoning  from  mush- 
rooms, 953  ;  in  Raynaud's  disease,  954  ;  paroxysmal, 
954  ;  toxic,  953. 

Haemolysis,  in  pernicious  anaemia.  944  ;  in  toxic 
haemoglobinuria,  954. 

Haemopericardium,  330. 


Haemophilia,  963  ;  aetiology  of,  903  ;  complications 
of,  905  ;  connected  with  anaemia,  905  ;  prognosis 
of ,  965  ;  rudimentary  forms  of,  '.Mil  ;  treatment  of, 
(a)  prophylactic,  905  ;  un  surgical,  965. 

Ilii-moptysis,  at  onset  of  plilhisis,  >.'IO  ;  causes  of, 
218  ;  hysterical,  804  ;  in  aneurism,  887  ;  in  bron- 
chial catarrh,  117,  152  ;  in  pneumonia,  198  ;  in  pul- 
monary gangrene,  243  ;  in  pulmonary  tuberculo- 
sis, 218  ;  in  scurvy,  959  ;  periodic,  90  ;  treatment 
of,  235. 

Haemorrhage,  cerebral,  725 ;  in  acute  yellow  atro- 
phy, 487  ;  in  anaemia,  934,  939,  942  ;  in  cirrhosis  of 
the  liver,  480  ;  in  contracted  kidney,  801  ;  in  endo- 
carditis, 279 ;  in  epileptic  paroxysms,  773 ;  in 
haemophilia,  903  ;  in  hysteria,  804  ;  in  leukaemia, 
950  ;  in  malaria,  90  ;  in  malignant  pustule,  119  ;  in 
meningitis,  epidemic  cerebro-spinal,  104  ;  in  nephro- 
lithiasis, 888  ;  in  pseudo-leukaemia,  952  ;  in  pyelitis, 
833 ;  in  purpura  haemorrhagica,  963 ;  in  scarlet 
fever,  41  ;  in  scurvy,  958  ;  in  small-pox,  57  ;  into 
spinal  cord,  604  ;  into  the  spinal  meninges,  603  ;  in 
syphilis  of  the  rectum,  425 ;  into  ventricles  of 
brain,  727  ;  in  typhoid  fever,  10  ;  in  yellow  fever, 
102 ;  pulmonary,  235. 

Haemorrhagic  diathesis,  963. 

Haemorrhoids,  428;  "attacks  of,"  428;  bleeding 
from,  428  ;  treatment  of,  429. 

Hair,  loss  of,  in  typhoid  fever,  17  ;  in  unilateral  facial 
atrophy,  594. 

Hallucinations  in  hysteria,  807. 

Halo  surrounding  the  pocks  of  small-pox,  53. 

Handwriting  in  general  paresis,  763. 

Hay  fever,  125. 

Headache,  habitual,  530  ;  in  acute  ascending  spinal 
paralysis,  674  ;  in  anaemia,  932  ;  in  bronchitis,  148 ; 
in  bulbar  paralysis,  acute,  694  ;  in  cerebral  abscess, 
742  ;  in  cerebral  anaemia,  709  ;  in  cerebral  haemor- 
rhage, 728  ;  in  cerebral  syphilis,  759  ;  in  cerebral 
tumors,  750  ;  in  chlorosis,  935  ;  in  compression  of 
the  medulla  oblongata,  695  ;  in  diabetes,  967,  973  ;  in 
diseases  of  the  cerebellum,  724  ;  in  epilepsy,  773  ; 
in  exophthalmic  goitre,  596  ;  in  haematoma  of  the 
dura  mater,  697  ;  in  infantile  spinal  paralysis,  668  ; 
in  leukaemia,  949  ;  in  meningitis,  epidemic,  104  ;  in 
meningitis,  purulent.  700  ;  in  meningitis,  tubercular, 
703,  705  ;  in  nervous  dyspepsia,  401  ;  in  neurasthe- 
nia, 815  ;  in  paroxysmal  haemoglobinuria,  954  ;  in 
pernicious  anaemia,  941  ;  in  pleurisy,  257  ;  in  pneu- 
monia, 192  ;  in  poliomyelitis  of  adults,  671  ;  in  pri- 
mary multiple  neuritis,  583  :  in  railway  spine,  820  ; 
in  small-pox,  53  :  in  tetanus,  792  ;  in  thrombosis  of 
the  cerebral  sinuses,  707  ;  in  typhoid  fever,  5  ;  in 
uraemia,  831  ;  in  writer's  cramp,  578. 

Headache,  nervous.  530  ;  sick,  591. 

Head,  deviation  of,  in  cerebral  haemorrhage.  729  :  in 
progressive  general  paralysis,  761  ;  rheumatism  in, 
918  ;  sense  of  pressure  in,  in  neurasthenia,  815. 

Head,  tetanus  of  the,  792. 

Heart,  aneurism  of,  308  :  arrhythmia  of.  in  valvular 
disease,  297  ;  congenital  affections  of.  293. 

Heart,  dilatation  of,  312  ;  in  chlorosis,  935  ;  in  ma- 
laria, 94. 

Heart,  disorders  of.  in  diabetes,  972  :  in  obesity,  995  ; 
in  pneumonia.  197  ;  in  scurvy,  959. 

Heart,  displacement  in  pleuritic  effusion.  259  :  dis 
placement  in  pneumothorax,  269  :  fatty  degenera- 
tion of,  315. 

Heart,  hypertrophy  of,  312  ;  diagnosis  of,  314  ;  idio- 


1026 


INDEX. 


pathic,  312:  in  arteriosclerosis,  332;  in  obesity, 
996  ;  in  renal  disease,  834,  843,  853,  859  ;  in  scarlet 
fever.  43  ;  treatment  of,  316. 

Heart,  indurated  degeneration  of.  308  ;  in  exophthal- 
mic goitre,  595  ;  infarctions  in,  308. 

Heart,  lesions  of,  compensated,  282  ;  congenital,  293  ; 
lungs  altered  by  disease  of,  249. 

Heart,  overexertion  of,  312. 

Heart,  palpitation  of,  diagnosis  of  the  nervous  form 
of,  319  ;  in  cardiac  valvular  disease,  296  ;  in  case 
of  tapeworm,  443  ;  in  hysteria,  810  ;  in  neurasthe- 
nia, 816  :  in  obesity,  995  ;  in  pernicious  anaemia, 
941  ;  in  scurvy,  958  ;  nervous,  319  ;  treatment  of 
the  nervous  form  of,  320. 

Heart,  parenchymatous  degeneration  of.  307,  315  ; 
rupture  of.  in  cardiac  aneurism,  308  ;  sclerosis  of, 
307. 

Heart,  valvular  disease  of,  281  ;  complications  of, 
295  ;  multiple,  294 ;  prognosis  of,  301  ;  treatment 
of,  303. 

Heart,  weakened,  312. 

Heartburn  in  chronic  gastric  catarrh,  376. 

Heart  failure,  in  diphtheria.,  69  ;  treatment  of,  in 
typhoid  fever,  26. 

Heat,  exhaustion,  746  ;  stroke,  746. 

Hebrews,  prevalence  of  diabetes  among,  967. . 

Hectic  fever,  225. 

Hegar's  funnel  for  rectal  irrigation,  410. 

Heller's  test  for  blood  in  the  urine,  828. 

Helminthiasis,  440. 

Hemiansesthesia,  in  cerebral  haemorrhage,  773  ;  in 
hysteria,  801,  813  ;  in  lesions  of  the  internal  cap- 
sule, 722,  725  ;  in  tumors  of  the  cerebral  hemi- 
spheres, 752  ;  in  unilateral  cord  lesions,  683. 

Hemianopia,  in  cerebral  haemorrhage,  733  :  in  hemi- 
crania,  592  ;  in  lesions  of  the  central  ganglia,  722, 
725  ;  in  lesions  of  the  corpora  quadrigemina,  722, 
725  ;  in  lesions  of  the  occipito-cortical  region,  716, 
725  ;  in  migraine,  592  ;  in  tumors  of  the  base  of  the 
brain,  752  ;  in  tumors  of  the  cerebral  hemispheres, 
752. 

Hemiathetosis,  post-hemiplegic,  788. 

Hemiatrophy,  progressive  facial,  594  ;  loss  of  hair 
in,  594  ;  seat  of,  594  ;  treatment,  594. 

Hemichorea,  posthemiplegic,  734  ;  in  infantile  cere- 
bral paralysis,  745;  in  lesions  of  the  internal  capsule, 
721,  725  ;  in  lesions  of  the  optic  thalamus,  722,  725. 

Hemicrania,  591  (see  also  Migraine)  ;  course  of,  592  ; 
in  diabetes,  973  ;  ophthalmic,  592  ;  paralytic,  592  ; 
spastic,  592  ;  symptoms  of,  592  ;  treatment  of,  593. 

Hemiplegia,  536. 

Hemiplegia,  crossed,  692  ;  in  cerebral  hasmorrhage, 
731,  732,  735;  in  cerebral  syphilis,  758  ;  in  diffuse 
cerebral  sclerosis,  744  ;  in  hsematoma  of  the  dura 
mater,  697  ;  in  hysteria,  803  ;  in  infantile  cerebral 
paralysis,  744  ;  in  lesions  of  the  central  ganglia, 
721  ;  in  lesions  of  the  crura  cerebri,  723,  725  ;  in  le- 
sions of  the  internal  capsule  and  centrum  ovale, 
721  ;  in  lesions  of  the  motor  cortical  region,  712  ;  in 
locomotor  ataxia,  645  ;  in  multiple  sclerosis,  631  ; 
in  progressive  general  paralysis,  764  ;  in  purulent 
meningitis,  700  ;  in  tumors  of  the  cerebral  hemi- 
spheres, 752  ;  mental  defects  in,  735. 

Hepatic.    See  also  Liver. 

Hepatic  abscess,  476  ;  in  dysentery,  79  ;  in  pylephle- 
bitis, suppurative,  501. 

Hepatic  colic,  470  ;  pulse,  289  ;  vein,  affections  of, 
500,  502. 


Hepatitis,  chronic  diffuse  interstitial,  478 ;  diffuse 
syphilitic,  491  ;  suppurative,  476. 

Hepatization  of  the  lungs,  190. 

Hepatogenous  jaundice,  464. 

Heredity  in  diabetes  insipidus,  982,  983 ;  in  haemo- 
philia, 963  ;  in  idiopathic  muscular  atrophy,  659, 
661  ;  in  tuberculosis,  210. 

Herpes  in  acute  gastric  catarrh,  373 ;  in  cerebro- 
spinal meningitis,  106  ;  in  facial  paralysis,  560  ;  in 
intercostal  neuralgia,  525 ;  in  locomotor  ataxia, 
644  ;  in  malaria,  94  ;  in  neuralgia,  517  ;  in  neu- 
ritis, 582  ;  in  pressure  paralysis  of  the  spinal  cord, 
612 ;  in  sciatica,  526  ;  in  trigeminal  neuralgia, 
522. 

Herpes  labialis  in  angina,  352  :  in  intestinal  catarrh, 
406  ;  in  malaria,  94  ;  in  meningitis,  epidemic  cere- 
bro  spinal,  106  ;  in  pneumonia,  192  ;  in  relapsing 
fever,  32 ;  in  scarlet  fever,  41  ;  in  typhoid  fever, 
17  ;  in  typhus  fever,  30. 

Herpes  zoster,  525. 

Hiccough,  577  ;  hysterical,  577  ;  in  anaemia,  932  ;  in 
cholera,  85  ;  in  dysentery,  79  ;  in  hepatitis,  suppu- 
rative, 477  ;  in  uraemia,  832  ;  reflex,  577  ;  treatment 
of,  5?'7. 

Hoarseness  in  diphtheria,  68  ;  in  laryngeal  catarrh, 
132  ;  in  trichinosis,  122. 

Hodgkin's  disease,  951  ;  morbid  anatomy  of,  952  ; 
symptoms  of,  952. 

Hot  Springs  of  Arkansas,  916. 

Hyaline  casts  in  urine,  826. 

Hydatid  disease,  494. 

Hydatid  thrill,  495. 

Hydraemia,  825. 

Hydrocephaloid  symptoms,  411. 

Hydrocephalus,  acute,  702,  703  ;  aetiology  of,  702 ; 
chronic,  767  ;  chronic,  after  cerebro-spinal  menin- 
gitis, 107  ;  congenital,  767 ;  congenital,  diagnosis 
of,  768  ;  course  of,  767  ;  effect  of,  upon  shape  of 
brain,  767  ;  enlargement  of  head  caused  by,  768  ; 
following  epidemic  cerebro-spinal  meningitis,  107  ; 
of  adults,  768  ;  skull  in,  different  from  the  rachitic, 
769  ;  spurious,  411  ;  symptoms  of,  767,  768  ;  the 
fluid  of,  767  ;  treatment,  769. 

Hydrochloric  acid  in  anaemia  and  chlorosis,  938  ;  in 
gastric  catarrh,  373,  381  ;  poisoning  from,  1003  ; 
tests  for,  in  gastric  juice,  378. 

Hydrocyanic  acid,  poisoning  from,  1007. 

Hydromyelus,  677,  678. 

Hydronephrosis,  890  ;  congenital,  891  ;  intermittent, 
891. 

Hydropericardium,  329. 

Hydroperitoneum,  460. 

Hydrophobia,  113  ;  diagnosis  of,  114  ;  hydrophobic 
stage,  114  ;  maniacal  stage  of,  113  ;  paralytic  stage 
of,  113,  114  ;  period  of  incubation  in,  114  ;  quiet 
form  of,  113  ;  raving  form  of,  113  ;  treatment  of, 
114,  115. 

Hydrops  vesicae  felleae,  473. 

Hydrorrhachis,  679. 

Hydrothorax,  271  ;  in  scarlet  fever,  42  ;  in  valvular 
cardiac  disease,  299  ;  treatment  of,  271. 

Hyoscyamine  in  paralysis  agitans,  787. 

Hyperacusis  in  facial  paralysis,  559. 

Hyperaemia,  708. 

Hyperaesthesia,  505  ;  in  ataxia,  640  ;  in  hysteria,  802  ; 
in  myelitis,  619  ;  in  neuralgia,  517  ;  in  neurasthenia, 
815  ;  in  pulmonary  tuberculosis,  226  ;  in  relapsing 
fever,  32  ;  in  spinal  meningitis,  600 ;  in  typhoid 


INDEX. 


1027 


fever,  10  ;  in  unilateral  lesions  of  the  spinal  cord, 

683  ;  of  smell,  532  ;  of  taste,  588. 
Hyperidrosis,  unilateral,  590. 
Ilypcrosniia,  532. 
Hyperpyrexia,  hysterical,    80-1,  805  ;    In    rheumatic 

fever,  905  ;  in  scarlet  fever,  38  ;   in  sunstroke,  747  ; 

in  tetanus,  793. 
Hypnotism  in  hysteria,  809. 
Hypochondriasis  and  neurasthenia,  815  ;  in  gastric 

catarrh,  379  ;  in  habitual  constipation,  430;  in  nerv- 
ous dyspepsia,  401. 
Hypodermic  syringe  in  diagnosis  of  pleural  effusion, 

263,  265. 
Hypoglossal  nerve,  paralysis  of,  752  ;  spasm  of,  573. 
Hypoglossus.  paralysis  of,  in  cerebral  tumor,  752. 
Hypophysis,  tumor  of,  752,  754. 
Hypoplasia  of  aorta,  929. 
Hypostatic  congestion  in  typhoid  fever,  12. 
Hysteria,  755  ;  {etiology  of,  755  ;  artificial  production 

of  spasms  in,  802,  810  ;  contractures  and  spasms  in, 

803  ;  convulsive  forms  of,  806  ;  course  of,  810  ;  diag- 
nosis of,  811  ;  disorders  of  sensation  in,  800  ;  fever 
in,  804  ;  grand  paroxysms  of,  808  ;  haamoptysis  in, 

804  ;  in  connection  with  floating  kidney,  877  ;  joint 
affections  in,  529,  804  ;  liability  to,  799  ;  mental 
symptoms  of,  805  ;  metallotherapeutics  in,  813  ; 
paralysis  in,  803  ;  produced  by  sexual  influences, 
800 ;  special  senses  in,  800 ;  stigmata  in,  800 ; 
symptoms  of,  800  ;  traumatic,  798  ;  treatment  of, 
811  ;  visceral  manifestations  of,  805  ;  with  regard 
to  exophthalmic  goitre,  596. 

H3Tsterical  insanity  in  typhoid  fever,  15. 
Hystero-epilepsy,  106,  107. 
Hysterogenic  points,  802,  810. 

Ice  in  cerebral  haemorrhage,  736  ;  in  infantile  spinal 
paralysis,  670  ;  in  injuries  of  the  spinal  cord,  607  ; 
in  meningitis,  97,  701,  706  ;  in  spinal  apoplexy,  605  ; 
in  spinal  meningeal  haemorrhage,  603. 

Ichthyosis  linguae  et  oris,  346. 

Icteric  casts  in  the  urine,  467. 

Icterus,  acute  febrile.  469  ;  catarrhal,  464  ;  gravis, 
489 ;  neonatorum,  490. 

Idiocy  in  infantile  hemiplegia,  745. 

Idiopathic  anasmia  of  Addison,  878. 

Ileo-csecal  region,  gurgling  in,  in  typhoid  fever,  10. 

Ileo-caecal  tumor,  419. 

Ileotyphus,  1. 

Ileus  from  intestinal  obstruction,  435  ;  in  t3rphoid 
fever,  11  ;  paralytic,  432. 

Illuminating  gas,  poisoning  from,  1007. 

Imbecility  in  infantile  hemiplegia,  745  ;  in  multiple 
sclerosis,  630. 

Imitation  in  chorea,  780. 

Impotence  in  diabetes,  972  ;  in  locomotor  ataxia,  643. 

Inanition  in  nervous  dyspepsia,  401,  402. 

Incarceration,  internal,  of  the  intestines,  433  ;  symp- 
toms of,  in  case  of  floating  kidney,  877. 

Incontinence,  nocturnal,  of  urine,  898. 

Incoordination  of  arms,  542  ;  of  legs,  542. 

Indican,  test  for,  436. 

Induction  of  premature  delivery,  in  chorea  gravi- 
darum, 784. 

Induration,  brown,  of  the  lungs,  249  ;  rheumatic,  of 
the  muscles,  917. 

Infantile  convulsions,  779. 

Infantile  paralysis,  cerebral,  744  ;  acute,  744  ;  course 
of,  745  ;  pathology  of,  745  ;  treatment  of,  745. 


Infantile  paralysis,  spinal,  067.  See  Spinal  Paralysis 
of  Children. 

Infarction,  embolic,  of  the  kidneys,  871;  hemor- 
rhagic, of  the  lungs,  247. 

Influenza,  71 ;  diagnosis  of,  77  :  aetiology  of,  74  ;  symp- 
toms of,  75  ;  treatment  of,  77. 

Inhalation-pneumonia,  186,  484. 

Inhalations  in  bronchitis,  154  in  diphtheria  i  in 
laryngitis,  132;  in  pharyngitis,  859  ;  in  pulmonary 
gangrene,  244  ;  in  pulmonary  tuberculosis,  231  ;  in 
whooping-cough,  168. 

Injection,  intravenous,  of  salines  In  diabetes,  981; 
subcutaneous,  of  salines  in  cholera,  89. 

Injury,  mechanical,  due  to  chorea,  788  ;  due  to  epi- 
lepsy, 773. 

Inoculation,  against  small-pox,  52,  58  ;  protective,  in 
hydrophobia,  115. 

Insanity,  post-febrile,  15  ;  relation  of  heart  disease  to, 
301. 

Insects,  the  sting  of,  a  cause  of  malignant  pustule, 
119. 

Insolation,  740. 

Inspection  of  meat,  governmental,  to  prevent  trichi- 
nosis, 123. 

Insufficiency,  valvular,  281. 

Insufflation  of  powders  in  chronic  pharyngitis,  359. 

Insular  sclerosis,  627. 

Intention  tremor  in  multiple  sclerosis,  C29  ;  in  myeli- 
tis, 619. 

Intercostal  neuralgia,  524. 

Intermeningeal  apoplexy,  696. 

Intermittent  fever,  92  ;  hepatic,  94  ;  masked,  95  ;  per- 
nicious, 94  ;  tertian,  93. 

Internal  capsule,  lesions  of,  721. 

Intestinal  calculi,  432  ;  casts,  408. 

Intestinal  catarrh,  403  ;  acute,  408  ;  chronic,  408  ;  fol- 
licular, 404  ;  from  the  ingestion  of  poisons,  403  ;  in 
rachitis,  924  ;  of  children,  413  ;  treatment  of,  409, 
415. 

Intestinal  glands  enlarged  in  leukaemia,  948 ;  in 
pseudo-leukaemia,  952. 

Intestinal  haemorrhage  in  dysentery,  79  ;  in  intussus- 
ception, 437  ;  in  pylethrombosis,  502  ;  in  typhoid 
fever,  10  ;  in  ulcer  of  duodenum,  423  ;  in  ulcer  of 
the  stomach,  386. 

Intestinal  parasites,  440  ;  polypi,  434. 

Intestinal  symptoms  in  cholera,  84  ;  in  dysentery, 
78  ;  in  erysipelas,  63,  64  ;  in  gastric  catarrh,  373, 
379  ;  in  glanders,  116  ;  in  malignant  pustule,  119  ; 
in  measles,  49  ;  in  pulmonary  gangrene,  243  :  in 
pulmonary  tuberculosis,  227  ;  in  purpura  haemor- 
rhagica,  962  ;  in  typhoid  fever,  9,  10. 

Intestine,  cancer  of,  426  ;  diagnosis  of,  426  ;  treat- 
ment of,  427. 

Intestine,  compression  of,  from  without,  434  :  con- 
striction of,  433  :  dilatation  of,  435  :  incarceration 
of,  433  ;  intussusception  of,  433  ;  invagination  of, 
433  :  new  growths  in,  426,  432. 

Intestine,  obstruction  of,  437  :  by  enteroliths,  432  :  by 
foreign  bodies,  433  ;  by  gall-stones.  432. 

Intestine,  perforation  of.  in  typhoid  fever.  11  :  stran- 
gulation of,  433  ;  strictures  and  tumors  of,  432  ; 
twists  and  knots  of,  433  ;  ulcers  of,  432. 

Intestine,  large,  catarrh  of,  407  ;  desquamative,  408. 

Intussusception,  434. 

Inunction,  mercurial,  in  acute  ascending  spinal  pa- 
ralysis, 676  ;  in  acute  bulbar  paralysis.  695  ;  in  cere- 
bral syphilis,  759  ;  in  ha?moglobinuria,  956  ;  in  loco- 


102S 


INDEX. 


motor  ataxia,  G47  ;  in  myelitis,  626  ;  in  progressive 
general  paralysis,  767  ;  in  spastic  spinal  paralysis, 
667  ;  in  tumors  of  the  brain,  775  ;  in  tumors  of  the 
spinal  cord,  677. 

Invagination,  434. 

Iodide  of  iron  in  peritonitis,  chronic,  460  ;  in  pressure 
paralysis  of  the  spinal  cord,  614  ;  in  scrofula, 
1001. 

Iodide  of  potassium  in  acute  ascending  spinal  paraly- 
sis, 676  ;  in  aneurism  of  the  thoracic  aorta,  338  ;  in 
asthma,  172  ;  in  bronchitis,  155,  159  ;  in  cerebral 
syphilis,  759  ;  in  cerebral  tumors,  755, 756  ;  in  chronic 
hydrocephalus,  769  ;  in  gout,  992  ;  in  habitual  head- 
ache, 531  ;  in  lead  paralysis,  570  ;  in  leptomenin- 
gitis, spinal,  601  ;  in  locomotor  ataxia,  647,  648  ;  in 
meningitis,  cerebro-spinal,  108  ;  in  multiple  sclero- 
sis, 631  ;  in  myelitis,  626,  627  ;  in  neuralgia,  520  ;  in 
pachymeningitis  cervicalis  hypertrophica,  603  ;  in 
peritonitis,  chronic,  460  ;  in  sciatica,  527  :  in  spasm 
of  the  trigeminus,  572  ;  in  spastic  spinal  paralysis, 
667  ;  in  syphilitic  paralysis  of  the  motores  oculi, 
557  ;  in  tumor  of  the  spinal  cord,  677. 

Iodine  coryza,  125. 

Iodine,  poisoning  from,  1004. 

Iodine,  tincture  of,  externally,  in  articular  rheuma- 
tism, chronic,  915  ;  in  chronic  nasal  catarrh,  128  ; 
in  pharyngitis,  chronic,  359  ;  in  pleurisy,  264  ;  in 
pressure  paralysis  of  the  spinal  cord,  614  ;  in  spinal 
leptomeningitis,  601. 

Iodine,  tincture  of,  internally,  in  diabetes,  981  ;  in 
scrofula, 1001. 

Iodoform  in  diabetes,  981  ;  in  pleurisy,  264  ;  in  pseudo- 
leukemia lymphatica,  953. 

Ipecacuanha  in  dysentery,  80. 

Iritis  in  gout,  987. 

Iron  baths  in  anaemia  and  chlorosis,  938  ;  in  infantile 
spinal  paratysis,  671  ;  in  locomotor  ataxia,  647  ;  in 
railway  spine,  821. 

Iron,  chloride  of,  in  purpura  hasmorrhagica,  962  ;  re- 
action caused  by,  in  diabetic  urine,  970. 

Iron  in  anaemia  and  chlorosis,  937  ;  in  cardiac  valvu- 
lar disease,  303  ;  in  exophthalmic  goitre,  598  ;  in 
habitual  headache,  531  ;  in  hemicrania,  593 ;  in 
nephritis,  855 ;  in  neurasthenia,  818 ;  in  osteo- 
malacia, 927  ;  in  paralysis  of  the  muscles  of  the 
larynx,  143  ;  in  pernicious  anaemia,  950  ;  in  pulmo- 
nary tuberculosis,  235  ;  in  rachitis,  924  ;  in  scurvy, 
961  ;  in  scrofula,  1001. 

Irradiation,  517. 

Irrigation  in  intestinal  catarrh,  410  ;  in  the  intestinal 
catarrh  of  children,  417. 

Ischuria  in  hysteria,  805. 

Itching  in  jaundice,  465  ;  in  uraemia,  833. 

Jacksonian  epilepsy,  714. 

Japan,  beri-beri  in,  582. 

Jaundice,  catarrhal,  464  ;  choluria  in,  467  ;  diagnosis 
of.  468  ;  epidemic  form  of,  464  ;  febrile,  469  ;  from 
gall-stones,  472 ;  haematogenous,  490  ;  hepatoge- 
nous, 464  ;  in  acute  phosphorus  poisoning,  1006  ;  in 
acute  yellow  atrophy,  486,  487  ;  in  cancer  of  the 
liver,  493  ;  in  cancer  of  the  pancreas,  504  ;  in  cir- 
rhosis of  the  liver,  480,  484  ;  in  diabetes,  971  ;  in  gas- 
tric catarrh,  373 ;  in  gastro-duodenitis,  464 ;  in 
haemoglobinuria,  954  ;  in  hepatic  colic,  472 ;  in 
hepatitis,  suppurative,  477  ;  in  pneumonia.  202  ;  in 
pylephlebitis,  suppurative,  501  ;  in  syphilis  of  the 
liver,  491  ;  in  Weil's  disease,  469  ;  in  yellow  fever, 


101  ;  malignant,  489  ;  of  the  new-born,  490  ;  perni- 
cious, 489  ;  treatment  of,  468 ;  xanthelasma  in, 
465. 

Jaw.    See  Maxilla. 

Joints,  disorders  of,  in  acute  neuritis,  583  ;  in  cerebrr.l 
haemorrhage,  735  ;  in  dengue,  99  ;  in  endocarditis, 
279  ;  in  erysipelas,  64  ;  in  gout,  986,  992  ;  in  haemo- 
philia, 965  ;  in  locomotor  ataxia,  644  ;  in  meningitis, 
cerebro-spinal,  106  ;  in  pernicious  anaemia,  943  ;  in 
purpura  hsemorrhagica,  962  ;  in  scrofula,  1000  ;  in 
scurvy,  959  ;  in  septicopyemia,  111  :  in  small-pox, 
56  ;  in  typhoid  fever,  17  ;  in  valvular  cardiac  dis- 
ease, 301. 

Joints,  neuroses  of,  528. 

Joints,  sensibility  of,  509. 

Jumpers,  576. 

"June  cold,"  125  (foot-note). 

Keratitis,  in  small-pox,  56. 

Kidney,  abscess  of,  868  ;  amyloid  or  lardaceous  dis- 
ease of,  864  ;  anomalies  in  position  of,  876  ;  calculus 
of,  884  ;  cancer  of,  872  ;  circulatory  disturbances  in, 
871  ;  cirrhosis  of,  856  ;  congestion  of,  871  ;  cystic 
disease  of,  874,  890  ;  echinococcus  of,  874  ;  genuine 
contracted,  856  ;  gouty,  857,  987  ;  granular,  856  ; 
hydatids  of,  874  ;  in  diabetes,  972  ;  in  diphtheria,  70  ; 
in  haemoglobinuria,  955  ;  in  leukaemia,  947  ;  in  obe- 
sity, 996 ;  in  pneumonia,  197  ;  in  pseudo-leukaemia, 
952  ;  in  pulmonary  emphysema,  179  ;  in  pulmonary 
tuberculosis,  228  ;  in  scarlet  fever,  41  ;  in  septico- 
pyaemia,  112  ;  large  red,  850  ;  large  white,  851  ; 
movable,  876  ;  new  growths  of,  872  ;  parasites  of, 
874  ;  pelvis  of,  dilatation  of,  890  ;  pelvis  of,  inflam- 
mation of,  881  ;  sclerosis  of,  856  ;  secondary  con- 
tracted, 849. 

Kidney,  removal  of,  for  cancer,  873. 

Kidney,  rhabdo-myoma  of,  872  ;  sarcoma  of,  872  ; 
surgical  kidney,  868  ;  tuberculosis  of,  888  ;  tumors 
of,  872. 

Knee-jerk,  loss  of.  in  ataxia,  641  ;  in  diphtheria,  70. 

Knee  phenomenon,  544.  See  also  Patellar  Re- 
flex. 

Koumyss  as  a  food  in  pulmonary  tuberculosis,  232. 

Kousso  for  tape-worm,  444. 

Kyphosis  in  osteomalacia,  926  ;  in  rachitis,  923. 

Lactic  acid  in  diabetes,  981  ;  in  nephrolithiasis,  888  ; 
in  the  bones  in  osteomalacia,  926  ;  in  the  urine  in 
osteomalacia,  927. 

Laennec's  cirrhosis,  478. 

Lagophthalmus  in  facial  paralysis,  559. 

Lancinating  pains  in  locomotor  ataxia,  640. 

Landry's  paralysis,  674. 

Lardaceous  liver,  498  ;  in  pulmonary  tuberculosis, 
228. 

Lard,  inunction  of,  in  scarlet  fever,  45. 

Laryngeal  crises  in  locomotor  ataxia,  643. 

Laryngitis,  acute,  130  ;  chronic,  132  ;  hypoglottica 
acuta  gravis,  131  ;  hypoglottica  chronica  hyper- 
trophica, 133  ;  in  measles,  48. 

Laryngitis,  phlegmonous,  134  ;  treatment  of,  135. 

Larynx,  abscess  of,  134  ;  affected  by  typhoid  fever, 
13  ;  cancer  of,  145  ;  disturbances  of  sensibility  in, 
143  ;  examination  of,  130  ;  muscles  of,  paralysis  of, 
139  ;  in  acute  bulbar  paralysis,  694  ;  in  progressive 
bulbar  paralysis,  686  ;  treatment  of,  142  ;  muscles 
of,  spasm  of,  in  hysteria.  807  ;  new  growths  in,  144 ; 
treatment   of,  145 ;    polypi   of,   144 ;    stenosis   of, 


INDEX. 


1 029 


chronic,  133 ;  in  diphtheria,  68 ;  in  laryngitis, 
acute,  131  ;  tuberculosis  of,  130  ;  diagnosis  of,  187  ; 
treatment  of,  138. 

Lateral  sclerosis,  amyotrophic,  650 ;  diagnosis  of, 
653  ;  involving  the  medulla  oblongata,  652  ;  symp- 
toms and  course  of,  651  ;  treatment  of,  653. 

Laughter,  spasmodic,  577. 

Lead  colic,  1005. 

Lead  paralysis,  509 ;  bilateral,  570 ;  localization  of, 
570  ;  treatment  of,  570. 

Lead  poisoning,  chronic,  1005  ;  chronic,  related  to 
contracted  kidney,  856,  1005  ;  chronic,  related  to 
gout,  985,  1005. 

Leptomeningitis,  cerebral  purulent,  698  ;  tubercular, 
702. 

Leptomeningitis,  chronic  spinal,  601  ;  primary,  601  ; 
secondary,  601  ;  symptoms  of,  601  ;  treatment  of, 
601. 

Lesions,  cerebral,  topical  diagnosis  of,  710. 

Lethargy  in  hysteria,  809. 

Leukaemia,  945  ;  aetiology  of,  945  ;  complications, 
949  ;  diagnosis  of,  950  ;  lymphatic,  947,  950  ;  mye- 
logenous, 946  ;  splenic,  946,  950  ;  symptoms  of,  947  ; 
treatment,  950  ;  with  regard  to  anaemia,  949. 

Leukocythaeinia,  945. 

Leukocytosis,  945. 

Lids,  spasm  of,  572. 

Lime  in  osteomalacia,  927  ;  in  poisoning  from  oxalic 
acid,  1004  ;  in  rachitis,  925. 

Lingua  geographica  in  glossitis,  346. 

Lips,  atrophy  of,  in  amyotrophic  lateral  sclerosis, 
652  ;  in  progressive  bulbar  paralysis,  686. 

Lithium,  carbonate  of,  in  nephrolithiasis,  887. 

Lithium  water  in  gout,  991. 

Liver.    See  also  Hepatic. 

Liver,  anomalies  in  the  shape  and  position  of,  499  ; 
atrophy  of,  498  ;  atrophy  of,  acute  yellow,  485  ; 
atrophy  of,  acute  yellow,  diagnosis  of,  488  ;  atro- 
phy of,  acute  yellow,  treatment  of,  489. 

Liver,  cancer  of,  492  ;  diagnosis  of,  492  ;  prognosis 
of,  494  ;  secondary  to  cancer  of  stomach,  493  ;  treat- 
ment of,  494. 

Liver,  cirrhosis  of,  478  ;  biliary,  483  ;  diagnosis  of, 
482,  485 ;  hypertrophic,  483 ;  prognosis  of,  482  ; 
treatment  of,  482,  485. 

Liver,  disturbances  of  circulation  in,  496  ;  gin-drink- 
er's, 478  ;  granulated,  479  ;  hydatids  of,  494  ;  hy- 
perasmia  of,  496,  497  ;  hypertrophy  of,  498  ;  in  gout, 
987  ;  in  haemoglobinuria,  954,  956  ;  in  jaundice,  468 ; 
in  leukaemia,  847  ;  in  pseudo-leukaemia,  952  ;  in  pul- 
monary emphysema,  179  ;  in  pulmonary  tubercu- 
losis, 228  ;  in  rachitis,  924  ;  in  yellow  fever,  101  ; 
lobulated  479  ;  syphilis  of,  490. 

Lobelia,  tincture  of,  in  asthma,  173. 

Locality,  testing  the  sense  of,  506. 

Lock-jaw,  791. 

Locomotor  ataxia,  632  ;  ataxic  stage  of,  636  ;  devel- 
opment of,  632  ;  diagnosis  and  prognosis  of,  645  ; 
Friedreich's  form  of,  648;  hereditary  predisposition 
to,  632  ;  histology  of,  632  :  in  chronic  ergotism, 
633  ;  initial  stage  of,  635  ;  involving  cranial  nerves, 
642  ;  symptoms  of,  635  ;  terminal  stage  of,  636  ; 
treatment  of,  646  ;  with  regard  to  progressive  gen- 
eral paralysis,  645. 

Loins,  pains  in,  in  relapsing  fever,  32  ;  in  small-pox, 
53  ;  in  typhus  fever,  30. 

Lordosis  in  pseudo-muscular  hypertrophy,  660. 

Lower  extremities,  in  rachitis,  923  ;  spasm  of,  575  ; 


spasm  of,  in  amyotrophic   lateral  sclerosis,  652  ; 
spasm  of,  in  tetanus,  792. 

Lower  jaw.    See  Max.ii.la. 

Lumbago,  918. 

Lungs,  abscesses  of ,  in  s«'ptico  pytr-mia,  112  ;  aplasia 
of,  181 ;  aplasia  of,  in  kyphoscoliosis,  iK2;  atelectasis 
of,  181  ;  capillaries  of ,  atrophy  of,  In  emphysema, 
175  ;  cancer  of ,  360  ;  compression  of,  181,  269  :  con- 
sumption of,  207  ;  contraction  of,  161,  214,  217,  22:5  : 
disorders  of,  in  diabetes,  976;  disorders  of ,  in  leu 
kaemia,  947  ;  disorders  of,  in  progressive  bulbar 
paralysis,  687  ;  disorders  of,  in  typhoid  fever,  18  ; 
echinococcus  of,  252  ;  embolic  changes  in,  247. 

Lungs,  emphysema  of,  173  ;  caused  by  pertussis,  176  ; 
diagnosis  of,  179  ;  followed  by  pulmonary  tubercu- 
losis, 179  ;  prognosis  of,  179  ;  treatment  of,  180. 

Lungs,  gangrene  of,  241  ;  circumscribed,  242  ;  devel- 
opment of,  241  ;  diagnosis  of,  244  ;  diffuse.  242 ;  in 
cancer  of  oesophagus,  370  ;  liability  to,  in  diabetes, 
241 ;  prognosis  of.  244  ;  treatment  of,  244. 

Lungs,  haemorrhage  from,  218  ;  increased  volume  of, 
173  ;  induration  of,  brown,  249 ;  infarctions  in, 
haemorrhagic,  247  ;  infarctions  in,  haemorrhagic, 
diagnosis  and  prognosis  of,  249  ;  infarctions  in, 
haemorrhagic,  symptoms  of,  248  ;  infarctions  in, 
haemorrhagic,  treatment  of,  249  ;  inflammation  of, 
189  (see  also  Pneumonia)  ;  oedema  of,  inflamma- 
tory, 183  ;  oedema  of,  influencing  respiration,  183  ; 
oedema  of,  treatment  of,  184 ;  pigmentation  of, 
245  ;  syphilis  of,  252  ;  tuberculosis  of,  207  ;  tumors 
of,  250  ;  tumors  of,  causing  symptoms  of  compres- 
sion, 251  ;  tumors  of,  prognosis  of,  252  ;  tumors  of, 
treatment  of,  252. 

Lymph,  animal,  for  vaccination,  59. 

Lymph-glands,  extirpation  of,  in  pseudo-leukaemia, 
953  ;  progressive  multiple  hypertrophy  of,  951. 

Lymph-glands,  swollen,  in  dengue,  100  ;  in  diphthe- 
ria, 67  ;  in  erysipelas,  64  ;  in  leukaemia,  947,  948, 
949,  950  ;  in  malignant  pustule,  119  ;  in  pseudo- 
leukaemia,  952 ;  in  pulmonary  cancer,  251  ;  in  pul- 
monary tuberculosis,  228  ;  in  scarlet  fever,  40 ;  in 
scrofula,  999,  1001  ;  in  typhoid  fever,  11. 

Lympho-sarcoma,  malignant,  951. 

Magnesia  in  gastric  catarrh,  374  ;  in  sulphuric-acid 
poisoning,  1003. 

Magnet,  application  of,  in  hysteria,  814. 

Main  en  griffe,  566. 

Maladie  des  tics  convulsifs,  573. 

Malaria,  90  ;  diagnosis  of,  96  ;  distribution  of,  90 ; 
germs  of,  91  ;  liability  to,  92  ;  period  of  incuba- 
tion of,  92  ;  treatment  of,  96. 

Malarial  cachexia,  95. 

Malarial  fever,  remittent  and  continuous,  95. 

Malarial  neuralgia,  516,  518. 

Malarial  poison,  90. 

Male  fern,  ethereal  extract  of.  for  tape-worm,  444. 

Malignant  pustule,  117,  119  ;  in  animals.  117  :  bacilli 
of,  117  ;  diagnosis  of,  120  ;  prophylactic  inoculation 
of,  120 ;  spores  of,  118  ;  transmission  to  man,  118  ; 
treatment  of,  121. 

Mal  perforant  du  pied  in  diabetes,  973  ;  in  tabes.  645. 

Malum  Cotunnii,  526.     See  Sciatica. 

Mammillary  reflex,  544. 

Marasmus  in  diabetes,  971. 

Massage  in  articular  neuralgia.  529  ;  in  articular 
rheumatism,  910,  916  ;  in  brachial  paralysis,  568  ; 
after  cerebral  haemorrhage,  737  ;  in  facial  paraly- 


1030 


INDEX. 


sis,  562  ;  in  gout,  092  ;  in  hysteria,  812  ;  in  infantile 
paralysis  (cerebral),  745  ;  in  infantile  paralysis  (spi- 
nal), 071  ;  in  migraine,  598  ;  in  muscular  rheuma- 
tism, 919  ;  in  neuralgia,  521  ;  in  neurasthenia,  817, 
S18  ;  in  paralysis  agitans,  787  ;  in  progressive  mus- 
cular atrophy,  658;  in  pseudo-hypertrophic  mus- 
cular paralysis,  003  ;  in  sciatica,  527  ;  in  scorbutic 
ecchymoses,  901  ;  in  writer's  cramp,  579. 

Mastication,  disturbances  of,  in  progressive  bulbar 
paralysis,  080,  087. 

Mastication,  muscles  of,  paralysis  of,  557  ;  in  general 
paralysis  of  the  insane,  704  ;  in  tumors  at  the  base 
of  the  brain,  752  ;  spasm  of,  clonic,  571  ;  tonic,  571. 

Mastodynia,  525  ;  treatment  of,  525. 

Measles,  40  ;  black,  48  ;  catarrh  in.  48  ;  complications 
of,  48  ;  contagiousness  of,  40  ;  diagnosis  of,  50  ; 
diphtheria  in,  49  ;  inoculation  of,  47  ;  period  of  in- 
cubation in,  47  ;  prognosis  of,  50  ;  prophylaxis  of, 
50  ;  relation  of,  to  pulmonary  tuberculosis,  49  ;  re- 
lation of,  to  whooping-cough,  49  ;  treatment  of,  50  ; 
typhoid,  49. 

Measles,  German,  51.    See  Rötheln. 

Measles  in  pork,  441.    See  T^nia. 

Meat,  compulsory  inspection  of,  in  trichinosis,  123  ; 
poisoning  from,  1010. 

Meckel's  diverticulum  in  obstruction  of  the  intestine, 
433. 

Median  paralysis,  566  ;  disturbances  of  the  functions 
of  the  forearm  and  hand  in,  560  ;  traumatic,  506. 

Mediastinal  tumors,  273  ;  diagnosis  of,  273  ;  prognosis 
of.  274  ;  treatment  of,  274. 

Mediastino-pericarditis,  325. 

Medulla  oblongata,  acute  apoplectiform  paralysis  of, 
091  ;  compression  of ,  695  ;  diseases  of,  685;  progress- 
ive paralysis  of,  685. 

Medulla  oblongata  and  pons,  haemorrhages  into,  691  ; 
apoplexy  from,  691  ;  cysts  and  scars  from,  691 ; 
seat  and  extent  of,  691  ;  treatment  of,  693. 

Melaena  neonatorum,  390. 

Mellituria,  966.    See  Glycosuria. 

Memory,  weakness  of,  in  exophthalmic  goitre,  596. 

Meniere's  disease,  769  ;  implication  of  the  semicir- 
cular canals  in,  769  ;  in  tabes,  643  ;  treatment  of, 
769. 

Meningeal  apoplexy,  603. 

Meningeal  haemorrhage,  603. 

Meningeal  tumors,  676  ;  different  forms  of,  676 :  prog- 
nosis and  treatment  of,  677  ;  symptoms  of,  677. 

Meningitis,  basilar,  702. 

Meningitis  of  the  convexity,  698. 

Meningitis,  epidemic  cerebrospinal,  103,  698,  701  (see 
also  Cerebro-spinal  Meningitis)  ;  diagnosis  of, 
107  ;  in  pneumonia,  107  ;  prognosis  of.  107  ;  second- 
ary, 107,  698  ;  sequelae  of,  107  ;  siderans,  104  ;  treat- 
ment of,  108. 

Meningitis,  purulent.  698  ;  aetiological  factors  in,  698  ; 
complications  of,  699  ;  diagnosis  of,  701  ;  localiza- 
tion of  the  morbid  process  in,  699  ;  metastatic,  699  ; 
primary,  698  ;  symptoms  of,  700  ;  treatment  of,  701. 

Meningitis,  tubercular,  702  ;  causes  of,  702  ;  duration 
of,  705  ;  haemorrhages  into  the  pia  mater  in,  703  ; 
hydrocephalic  effusion  into  the  ventricles  in,  703  ; 
implication  of  the  spinal  cord  in,  703  ;  inflamma- 
tory changes  in.  703  ;  seat  of  miliary  tubercles  in, 
703  :  symptoms  of,  703. 

Meningitis,  tubercular,  in  children,  705  ;  diagnosis  of, 
706  ;  loud  outcry  of  child  in,  705  ;  treatment  of,  706. 

Meningocele,  679. 


Menstruation  in  chlorosis,  935  ;  influence  of,  on  epi- 
lepsj%  774  ;  vicarious,  129. 

Mental  disturbances  in  acute  general  miliary  tuber- 
culosis. 239  ;  in  anaemia,  931  ;  in  articular  rheuma- 
tism, 906 ;  in  athetosis,  789 ;  in  bulbar  haemor- 
rhage, 091  ;  in  cerebral  abscess,  742  ;  in  cerebral 
anaemia,  709  ;  in  cerebral  embolism,  740  ;  in  cere- 
bral haemorrhage,  728,  730, 735  ;  in  cerebral  hyperae- 
mia,  710  ;  in  cerebral  syphilis,  759  ;  in  cerebral  tu- 
mor, 750 ;  in  cerebro-spinal  meningitis,  105  ;  m 
cholera,  Asiatic,  85  ;  in  cholera  morbus,  411  ;  in 
chorea,  780,  782  ;  in  convulsions,  541  ;  in  cutaneous 
anaesthesia,  513. 

Mental  disturbances  in  diabetic  coma,  973  ;  in  epi- 
lepsy, 770,  772,  773,  775,  777  ;  in  fainting  attacks, 
709  ;  in  general  paralysis  of  the  insane,  761  ;  in 
habitual  constipation,  430 ;  in  haematoma  of  the 
dura  mater,  697  ;  in  hydrocephalus,  768  ;  in  hyste- 
ria, 805,  808  ;  in  infantile  paralysis  (cerebral),  745  ; 
(spinal),  668  ;  in  jaundice,  466  ;  in  meningitis,  700, 
703  ;  in  multiple  sclerosis,  630,  631 ;  in  neuralgia, 
518  ;  in  neurasthenia,  815  ;  in  peritonitis,  454  ;  in 
poliomyelitis  of  adults,  671 ;  in  pseudo-hypertrophic 
muscular  paralysis,  660  ;  in  pulmonary  tuberculosis, 
226  ;  in  pylephlebitis,  501  ;  in  sinus  thrombosis,  707; 
in  typhoid  fever,  14,  15  ;  in  typhus  fever,  30  ;  in 
uraemia,  831  ;  in  valvular  heart  disease,  301  ;  in 
writer's  cramp,  578. 

Mercurialism,  chronic,  1005. 

Mercurial  poisoning,  1005. 

Metabolism,  defective,  in  neurasthenia,  816. 

Metallic  tinkling,  269,  270. 

Metalloscopy  in  hysteria,  813. 

Meteorism  in  hysteria,  805  ;  in  intestinal  obstruction, 
437  ;  in  intestinal  tuberculosis,  424  ;  in  peritonil  is, 
453  ;  in  pulmonary  tuberculosis,  227  ;  in  typhlitis, 
419  ;  in  typhoid  fever,  9. 

Micrococci  in  cystitis,  894  ;  in  endocarditis,  277  ;  in 
erysipelas,  61,  62 ;  in  pneumonia,  189  ;  in  septico- 
pyaemia,  109,  110. 

Migraine,  591  (see  Hemicrania);  duration  of  the  at- 
tacks of,  592  ;  in  general  paralysis  of  the  insane, 
703  ;  treatment  of,  593. 

Miliary  tuberculosis,  acute  general,  236 ;  cerebral 
symptoms  in,  238  ;  causes  of,  236  ;  diagnosis  of, 
240  ;  intermittent  form  of,  238  ;  prognosis  of,  240  : 
relation  of,  to  tubercular  meningitis,  238  ;  symp- 
toms of,  237  ;  treatment  of,  240  ;  typhoid  form  of, 
237. 

Milk-cure  in  anaemia,  936  ;  in  nephritis,  846  ;  in  pul- 
monary tuberculosis,  232  ;  in  pyelitis,  884. 

Milker's  cramp,  579. 

Millar's  asthma,  142.    See  Glottis,  Spasm  of. 

Mimetic  expression  in  lesions  of  optic  thalamus,  722. 

Mineral  acids  in  scurvy,  961. 

Mineral  springs  in  anaemia  and  chlorosis,  938 ;  in 
bronchitis,  154  ;  in  cholelithiasis,  475  ;  in  diabetes, 
981  ;  in  exophthalmic  goitre,  598 ;  in  gastric  ca- 
tarrh, 381  ;  in  gout,  991  ;  in  habitual  headache.  531 ; 
in  intestinal  catarrh,  410  ;  in  laryngeal  catarrh, 
134  ;  in  nephrolithiasis,  888  ;  in  neuritis,  584  ;  in 
obesity,  999  ;  in  pulmonary  emphysema,  180  ;  in 
pyelitis,  884. 

Miserere  in  intestinal  obstruction,  435. 

Mitral  insufficiency,  283. 

Mitral  stenosis.  285. 

Mogigraphia.  577.    See  Writer's  Cramp. 

Monophasia,  718. 


INDEX. 


L031 


Monoplegia,  530 ;  in  focal  diseases  of  the  centrum 
ovale,  721 ;  in  focal  diseases  of  the  motor  cortex, 
713,  724  ;  in  general  paralysis  of  the  insane,  701  ;  in 
meningitis,  700,  704. 

Morbilli,  46.    See  Measles. 

Morbus  Addisonii,  878.    See  Addison's  Disease. 

Morbus  Basedowii,  595.    See  Exophthalmic  GIoItre. 

Morbus  Brightii,  836.    See  Nephritis. 

Morbus  Gravesii,  595.    See  Exophthalmic  GoItue. 

Morbus  maculosus  Werlhofii,  961.    See  Purpura. 

Morbus  sacer,  770.    See  Epilepsy. 

Morphine  in  angina  pectoris,  319  ;  in  cholelithiasis, 
474  ;  in  endocarditis,  280  ;  in  gastric  ulcer,  390  ;  in 
intercostal  neuralgia,  525  ;  in  intestinal  obstruction, 
439  ;  in  tabes,  648  ;  in  myelitis,  627  ;  in  myocarditis, 
312  ;  in  nephritis,  849  ;  in  neuralgia,  520  ;  in  occip- 
ital neuralgia,  523  :  in  peritonitis,  457  ;  in  pleurisy, 
264  ;  in  pneumothorax,  270  ;  in  sciatica,  527  ;  in 
spasm  of  the  diaphragm,  577.    See  also  Opium. 

Morphine,  poisoning  from,  1008. 

Morphinism,  chronic,  1008. 

Morvan's  disease,  679. 

Mosquitoes,  relation  of,  to  chyluria,  876. 

Mothers1  milk,  substitutes  for,  in  feeding  children, 
416. 

Motility,  disturbances  of,  534  ;  in  caisson  disease,  608  ; 
in  chronic  hydrocephalus,  768  ;  in  tabes,  636 ;  in 
pressure  paralysis  of  the  spinal  cord,  611. 

Motion,  sensations  of,  507. 

Motor  nerves,  diseases  of,  534  ;  changes  of  electrical 
excitability  in,  546. 

Motor  region  of  the  cortex  and  its  focal  diseases,  711, 
742  ;  centers  of  different  muscular  territories  in, 
711  ;  diagnosis  of  focal  lesions  of,  712  ;  relation  of 
hemiplegia  to,  712,  725  ;  relation  of  monoplegia  to, 
712,  724  ;  relation  of  symptoms  of  irritation  in  dif- 
ferent muscular  territories  to,  713,  714,  724  ;  rela- 
tion of  tonic-clonic  spasms  to,  713,  714. 

Mouth,  cavity  of,  inflammation  of.  341  ;  in  pulmonary 
tuberculosis,  227  ;  in  typhoid  fever,  12. 

Mucous  haemorrhoids,  428. 

Mucous  polypi  in  the  larynx,  144. 

Mud-baths  in  muscular  rheumatism,  919  ;.  in  myelitis, 
627  ;  in  tabes,  047. 

Muguet,  344.    See  Thrush. 

Mulberry  calculi  in  nephrolithiasis,  885. 

Mumps,  348.    See  Parotitis. 

Muscles,  abscess  of,  in  septico-pyaemia,  108  :  regen- 
eration of,  554  ;  sensory  nerves  to,  511  ;  stretching 
of,  in  facial  paralysis,  562  ;  trichinae  in,  121. 

Muscular  atrophy  in  amyotrophic  lateral  sclerosis, 
650,  652,  653  ;  in  articular  rheumatism,  905  ;  in  cere- 
bral haemorrhage,  735  ;  degenerative,  553,  655  ;  in 
deltoid  paralysis,  564  ;  in  infantile  paralysis  (cere- 
bral), 745  ;  (spinal),  668,  669  ;  in  lead  paralysis,  570  ; 
in  myelitis,  622  ;  in  neuritis,  583,  584  ;  in  pachymen- 
ingitis cervicalis  hypertrophica,  602  ;  in  paralysis, 
538  ;  in  poliomyelitis  in  adults,  672,  673  ;  in  pressure 
paralysis  of  the  spinal  cord,  612  ;  in  progressive 
bulbar  paralysis,  6S5,  687  ;  in  radial  paralysis,  565  ; 
in  syringomyelia,  678  ;  in  tabes,  644,  649  ;  in  ulnar 
paralysis,  566  ;  in  unilateral  lesion  of  the  spinal 
cord,  684. 

Muscular  atrophy,  progressive,  655 ;  beginning  of,  655 ; 
causes  of,  655  ;  complication  of,  with  progressive 
bulbar  paralysis.  657  ;  diagnosis  of,  657  ;  hereditary, 
655,  658,  661  ;  juvenile  form  of.  661  ;  pathological 
lesion  in,  655  ;  symptoms  of,  655  ;  treatment  of,  058. 


Muscular  contractures  in  amyotrophic  lateral  sclero- 
sis, 652;  in  cerebral  hemorrhage,  784  ;  In  cholera, 
85 ;  in  Friedreich's  ataxia,  649;  in  hysteria, 
8(i9;  In  infantile  paralysis  (cerebral),  74B  ;  'spinal.», 
669  ;  in  paralysis  agitans,  784  ;  in  secondary  degen- 
eration of  the  spinal  cord,  882. 

Muscular  degeneration,  558. 

Muscular  excitability  in  acute  ascending  spinal  pa 
ralysis,  671 ;  in  amyotrophic  lateral  sclerosis,  652  ; 
in  cerebral  haemorrhage,  782,  785 ;  electrical,  546 ; 
in  facial  paralysis,  560  ;  in  hysteria,  809  ;  mechan- 
ical, 546  ;  in  myelitis,  622  :  in  neuritis,  585  :  in  pro- 
gressive muscular  atrophy,  056  ;  in  pseudo-hyper- 
trophic  muscular  paralysis.  660  ;  in  radial  paraly- 
sis, 505  ;  in  spinal  infantile  paralysis,  669  ;  in  tabes, 
042  ;  in  unilateral  lesion  of  the  spinal  cord,  684. 

Muscular  hypertrophy  in  congenital  myotonia,  795. 

Muscular  pains  in  cholera  morbus,  411  ;  in  intestinal 
catarrh,  406  ;  in  muscular  rheumatism,  917  ;  in 
scarlet  fever,  43  ;  in  typhoid  fever,  17. 

Muscular  rheumatism,  9)6  ;  acute,  910  ;  chronic,  916  ; 
diagnosis  of,  918  ;  in  haemophilia,  965  ;  treatment 
of,  918. 

Muscular  rigidity  in  congenital  myotonia,  795  ;  in 
paralysis  agitans,  785,  786  ;  in  tetanus,  792. 

Muscular  sense,  509. 

Muscular  sensibility,  abnormal,  510  ;  electro-muscu- 
lar, 510  ;  in  tabes,  636,  639,  641  ;  test  of,  509. 

Muscular  stiffness  after  cerebral  haäinorrhage,  729  ; 
in  cholera,  87. 

Muscular  tonus,  in  spastic  spinal  paralysis,  664  ;  in 
tabes,  639. 

Mushroom  poisoning,  1009. 

Musk  in  spasm  of  the  glottis,  143. 

Mussels,  poisoning  from,  1010. 

Mustard  in  asthma,  172  ;  in  pleurisy,  264. 

Mutism,  hysterical,  803. 

Myalgia,  cervical,  918  ;  lumbar,  918  ;  rheumatic,  916. 

Mycoderma  vini  in  relation  to  thrush-formation.  344. 

Mycosis,  intestinal,  119.    See  Malignant  Pustule. 

Mydriasis  in  oculo-motor  paralysis,  556. 

Myelitis,  015  ;  acute  bulbar,  694  ;  cervical,  623  ;  diag- 
nosis of  diffuse  transverse,  625  ;  diffuse,  015,  610  ; 
dorsal,  023  ;  lumbar.  623  ;  pathological  changes  in 
the  spinal  cord  in,  616  ;  symptoms  of.  618  ;  trans 
verse,  615  ;  treatment  of,  antisyphilitic,  626  ;  by 
baths,  626  ;  electrical,  626  ;  hygienic  and  symp- 
tomatic, 627. 

Myelocele,  679. 

Myocarditis,  307  ;  diagnosis  of,  311  ;  prognosis  of,  311  ; 
treatment  of,  311. 

Myoclonia,  810.    See  Paramyoclonus  Multiplex. 

Myodegeneration  of  the  heart,  307. 

Myopathy,  603. 

Myositis,  rheumatic,  910. 

Myotonia,  congenital,  795 ;  congenital  muscular 
anomalies  in,  795. 

Myriachit.  570. 

Myxoedema,  589  ;  atrophy  of  thyroid  in,  589. 

Nails  in  typhoid  fever,  17. 

Narcotics  in  acute  bulbar  paralysis.  095  :  in  asthma. 
172  ;  in  bronchitis,  155  ;  in  cerebral  abscess,  743  :  in 
cerebral  syphilis,  700  ;  in  cystitis.  896  :  in  diabetes. 
980  ;  in  epilepsy,  778  :  in  habitual  headache,  532  ;  in 
hemicrania,  593  :  in  hiccough,  577  :  in  hysteria, 
813  ;  in  mastodynia,  525  ;  in  meningitis,  10S.  702.  706  ; 
in  nephrolithiasis,  S83  ;  in  neuralgia,  520  ;  in  neu- 


1032 


INDEX. 


rasthenia,  818  ;  in  neuritis,  584  ;  in  osteomalacia, 
927  ;  in  palpitation  of  the  heart,  320  ;  in  pneumonia, 
205,  207  ;  in  progressive  bulbar  paralysis,  690  ;  in 
pulmonary  emphysema,  180  ;  in  pulmonary  tuber- 
culosis, 231  ;  in  pyelitis,  884  ;  in  spasm  of  the  cervi- 
cal muscles,  575  ;  iu  spasm  of  the  glottis,  143  ;  in 
spasm  of  the  trigeminus,  572  ;  in  spermatic  neu- 
ralgia, 528  ;  in  tetanus,  794  ;  in  trigeminal  neural- 
gia, 523  ;  in  valvular  disease  of  the  heart,  307  ;  in 
whoopiug-cough,  163.  ' 

Nasal  catarrh,  chronic  126  ;  diagnosis  of,  127  ;  treat- 
ment of,  127. 

Nasal  catarrh  in  typhus  fever,  30. 

Nasal  douche  in  diphtheria,  72  ;  in  nasal  catarrh,  128  ; 
in  pharyngeal  catarrh,  359. 

Naso-pharyngeal  catarrh,  357. 

National^  in  relation  to  hysteria,  799  ;  to  neuras- 
thenia, 815. 

Nephritis,  acute,  836,  839  ;  acute  hemorrhagic,  840  ; 
acute  infectious,  836  ;  in  articular  rheumatism,  837, 
906 ;  in  cholera,  86,  837 ;  chronic,  849  ;  chronic 
hemorrhagic,  849;  chronic  interstitial,  856  ;  chronic 
parenchymatous,  849  ;  in  diabetes,  972  ;  diagnosis 
of,  845,  855,  870  ;  in  diphtheria,  70,  836  ;  in  endocar- 
ditis, 279,  837  ;  in  epidemic  meningitis,  106,  837  ; 
gravidarum,  838  ;  in  intestinal  affections,  837  ;  in 
measles,  49,  837  ;  in  pneumonia,  197,  837  ;  primary 
idiopathic  acute,  838,  844  ;  prognosis  of,  845,  855  ; 
in  pulmonary  tuberculosis,  228,  837  ;  in  purpura 
hsemorrhagica,  962  ;  purulent,  868 ;  in  relapsing 
fever,  35,  837  ;  in  rötheln,  837  ;  in  scarlet  fever,  41, 
837  ;  in  scurvy,  959  ;  in  septico-pyaemia,  112  ;  septic, 
837  ;  in  small-pox,  837  ;  in  sore  throat,  837  ;  in  syphi- 
lis, 837  ;  in  tetanus,  792,  837  ;  toxic,  837  ;  treatment 
of,  846,  855,  871  ;  in  typhoid  fever,  17,  837. 

Nephritis,  chronic  and  subchronic.  849  ;  diagnosis  of, 
855  ;  prognosis  of,  855  ;  treatment  of,  855. 

Nephrolithiasis,  884  ;  diagnosis  of,  887  ;  heredity  of, 
885  ;  origin  of,  885  ;  treatment  of,  887. 

Nephrophthisis,  888.  See  Tuberculosis,  Genito-uri- 

NARY. 

Nerves,  atrophy  of,  in  amyotrophic  lateral  sclerosis, 
651  ;  degenerative,  553,  589  ;  in  lead  paralysis, 
570  ;  in  locomotor  ataxia,  633,  634  ;  in  paralysis, 
539. 

Nerves,  degeneration  of,  533  ;  in  amyotrophic  lateral 
sclerosis,  051  ;  in  the  lumbar  cord  in  tabes,  639  ;  in 
spinal  paralysis  of  children,  668. 

Nerves,  excitability  of,  changes  of  electrical,  546  ;  in 
facial  paralysis,  560  ;  in  hysteria.  809  :  in  neuritis, 
583  ;  in  spinal  paralysis  of  children,  669  ;  in  tabes, 
639  ;  in  tetany,  790. 

Nerves,  regeneration  of,  533. 

Nerve-stretching  in  cervico-brachial  neuralgia,  524  ; 
in  facial  spasm,  573  ;  ataxia,  648  ;  in  neuralgia,  521  ; 
in  paralysis  agitans,  787  ;  in  sciatica,  527  ;  in  spasm 
of  the  cervical  muscles,  575  ;  in  tabes,  648  ;  in  tri- 
geminal neuralgia,  523. 

Nervines  in  palpitation  of  the  heart,  320. 

Nervous  fever,  14. 

Neuralgia,  515  ;  in  the  anaemic,  516  ;  in  aneurism  of 
the  thoracic  aorta,  337  ;  brachial,  524  ;  causes  of, 
516  ;  cervico-brachial,  524  ;  in  diabetes  mellitus, 
517,  973  ;  dorso-intercostal,  524  ;  epileptiform,  522  ; 
in  general  paralysis  of  the  insane,  763  ;  of  the  geni. 
tals  and  rectal  region,  528  ;  in  gout,  517  ;  in  haemo- 
philia, 965  ;  hereditary  predisposition  to,  516  ;  idio- 
pathic, 517  ;  intercostal,  524  ;  ischiatic,  526  ;  lum- 


bar, 526  ;  in  malaria,  95,  516  ;  in  neuromata,  586  ; 
occipital,  523  ;  phrenic,  524  ;  reflex,  517  ;  rheumatic, 
516;  sciatic,  526  ;  spermatic,  528  ;  symptomatic,  517  ; 
syphilitic,  516,  523  ;  treatment  of,  518  ;  trigeminal, 
521  ;  in  typhoid  fever,  16. 
Neurasthenia,  815  ;  causes  of,  815  ;  course  of,  816  ; 
and  diabetes,  976  ;  diagnosis  and  prognosis  of,  816  ; 
disposition  to,  817  ;  sj'mptoms  of,  815  ;  traumatic, 
821 ;  treatment  of,  817. 
Neurectomy  in  neuralgia,  520. 

Neuritis,  579  ;  of  alcoholic  subjects,  584  ;  ascending, 
581,616;  causes  of,  580;  chronic,  579,  584;  diag- 
nosis and  prognosis  of  multiple,  584  ;  epidemic, 
582,  hypertrophic,  after  cerebral  haemorrhage,  735  ; 
mental  symptoms  in,  585  ;  multiple,  582  ;  new  for- 
mation of  connective  tissue  in,  580  ;  nodosa,  580  ; 
primary  simple,  582  ;  purulent,  580  ;  in  relation  to 
primary  degenerative  atrophy  of  the  nerves,  580  ; 
secondary,  581  ;  spontaneous,  581  ;  symptoms  and 
cause  of,  581  ;  traumatic,  580  ;  treatment  of,  584, 
585. 

Neuritis,  optic,  in  acute  general  miliary  tuberculo- 
sis, 240  ;  in  cerebral  tumor,  751  ;  in  chronic  hydro- 
cephalus, 768  ;  in  haematoma  of  the  dura  mater, 
697  ;  in  meningitis,  700,  704  ;  in  myelitis,  623. 

Neuroma,  585  ;  amputation,  586  ;  diagnosis  of,  586  ; 
extirpation  of,  586  ;  false,  585  ;  hereditary  predis- 
position to,  586  ;  after  injuries  of  the  nerves,  586  ; 
multiple  occurrence  of.  586  ;  symptoms  of,  586  ; 
treatment  of,  586  ;  true,  585. 

Neuroses,  articular,  528  ;  of  the  heart,  318 ;  of  the 
vagus,  319. 

Neurotomy  in  neuralgia,  520. 

Nicotine  poisoning,  1008. 

Night-sweats  in  phthisis,  216. 

Nitric  acid  in  diabetes  insipidus,  984  ;  in  nephritis, 
846  ;  poisoning  from,  1003. 

Nitrites  in  contracted  kidney,  864. 

Nitro-benzene  poisoning,  1007. 

Nitro-glycerine,  in  contracted  kidney,  864  ;  in  hemi- 
crania,  593. 

Nitrous-acid  fumes,  poisoning  from,  1003. 

Nocturnal  incontinence  of  urine,  898.    See  Enuresis. 

Nodding  spasm,  574. 

Nodules,  myocarditic,  in  valvular  disease  of  the 
heart,  298. 

Noma,  347  ;  in  measles,  49  ;  treatment  of,  347. 

Nose,  affections  of.  in  diphtheria,  68 ;  in  glanders, 
116  ;  in  measles,  48 ;  in  scarlet  fever,  39,  40 ;  in 
typhoid  fever,  14. 

Nose-bleed,  129  ;  in  contracted  kidney,  860,  862 ;  ha- 
bitual, 129  ;  in  nephritis,  843  ;  in  relapsing  fever, 
35  ;  in  typhoid  fever,  14  ;  as  vicarious  menstrua- 
tion, 129. 

Nutmeg  liver,  497. 

Nux  vomica  in  dilatation  of  the  stomach,  400. 

Nystagmus  in  hereditary  ataxia,  649  ;  in  lesions  of 
the  corpora  quadrigemina,  722  ;  in  multiple  sclero- 
sis, 629 ;  in  purulent  meningitis,  700 ;  in  sinus  throm- 
bosis, 707. 

Obesity,  992  ;  causes  of,  992  ;  complications  of,  995  ; 

treatment  of,  996. 
Obstruction,  intestinal,  432,  474  ;  tables  for  diagnosis 

of,  437. 
Obturator  paralysis,  569  ;  symptoms  of,  569. 
Occipital  lobes,  focal  diseases  of  their  cortex,  715, 

743  ;  relation  of,  to  hemiopia,  716,  725  ;  relation  of, 


INDEX. 


1033 


to  soul-blindness,  710  ;  seat  of  the  visual  sense  in 
the  cortex  of,  715. 

Occipital  neuralgia,  523 ;  bilateral,  523;  painful  points 
in,  523. 

Ocular  nerves  in  meningitis,  700. 

Oculo-motor  paralysis,  555  ;  in  diphtheria,  70  ;  diplo- 
pia in,  555  ;  in  lesions  of  the  corpora  quadrigemina, 
722  ;  in  lesions  of  the  crura  cerebri,  723, 725  ;  partial, 
556  ;  periodical,  557  ;  in  purulent  meningitis,  700  ;  in 
tabes,  642  ;  in  tumor  of  the  brain,  752. 

CEdema,  828. 

CEdema,  acute  angioneurotic,  588  ;  in  acute  ascend- 
ing spinal  paralysis,  674  ;  in  anaemia,  934  ;  in  can- 
cer of  the  stomach,  393  ;  in  contracted  kidney,  860  ; 
in  diabetes,  973. 

CEdema  in  leukaemia,  949  ;  in  myelitis,  622  ;  in  ne- 
phritis, 842,  852  ;  in  neuritis,  583  ;  in  scarlet  fever. 
42  ;  in  tetany,  790  :  in  trichinosis,  123  ;  in  typhoid 
fever,  16  ;  in  valvular  disease  of  the  heart,  299. 

Oesophagitis,  361  ;  catarrhal,  361  ;  corrosive,  362  ; 
croupous-diphtheritic,  362  ;  purulent,  362  ;  treat- 
ment of,  362. 

CEsophagomalacia,  371. 

Oesophagus,  cancer  of,  369  ;  complications  of,  369  ; 
metastases  of,  370 ;  symptoms  of,  369  ;  treatment 
of,  370. 

GEsophagus,  diffuse  dilatation  of,  363  ;  after  stenosis 
of  the  cardiac  orifice,  363  ;  symptoms  of,  363  ;  treat- 
ment of,  363. 

Oesophagus,  dilatation  of,  363  ;  diseases  of,  361. 

Oesophagus,  diverticula  of,  363  ;  causes  of,  364  ;  com- 
plications of,  365  ;  pressure,  363  ;  symptoms  of,  364  ; 
symptoms  of  compression  in,  364  ;  traction,  365  ; 
treatment  of,  365. 

Oesophagus,  paralysis  of,  371  ;  rupture  of,  371  ;  spasm 
of,  371 ;  stenosis  of,  366 ;  auscultation  of,  367  ;  causes 
of,  366  ;  examination  of,  by  the  sound,  367  ;  prog- 
nosis and  treatment  of,  368  ;  symptoms  of,  366. 

Oidium  albicans,  344. 

Oligocythemia,  928. 

Omalgia,  917,  918. 

Ophthalmia  in  diphtheria,  69  ;  in  exophthalmic  goi- 
tre, 596  ;  neuroparalytic,  in  anaesthesia  of  the  tri- 
geminus, 513  ;  in  scrofula,  1000. 

Ophthalmoplegia,  progressive,  690. 

Opisthotonos,  541  ;  in  epilepsy,  772  ;  in  tetanus,  792. 

Opium  in  Asiatic  cholera,  89  ;  in  cholera  morbus,  412  ; 
in  diabetes,  980  ;  in  gastric  ulcer,  396  ;  in  intestinal 
catarrh,  409  ;  in  intestinal  catarrh  of  children,  416  ; 
in  intestinal  obstruction,  439  ;  in  nephritis,  849  ;  in 
neuralgia,  520  ;  in  peritonitis,  456,  457  ;  in  tetanus, 
794  ;  in  trigeminal  neuralgia,  523  ;  in  typhlitis,  421  ; 
in  typhoid  fever,  25. 

Opium  habit,  1008  ;  poisoning,  1008. 

Optic  atrophy  in  chronic  hydrocephalus,  768  ;  in  dia- 
betes, 972  ;  in  general  paralysis  of  the  insane,  763  ; 
in  multiple  sclerosis,  630  ;  in  tabes,  642. 

Optic  neuritis.    See  Neuritis. 

Orchitis  in  typhoid  fever,  18. 

Orthopaedics  in  pressure  paralysis  of  the  spinal  cord, 
614  ;  in  rachitis,  925  ;  in  spasm  of  the  cervical  mus- 
cles, 575  ;  in  spinal  paralysis  of  children,  671. 

Osmic  acid  in  neuralgia,  520. 

Osteomalacia,  925  ;  diagnosis  of,  927  ;  examination  of 
the  bones  in,  926  ;  symptoms  of,  926  ;  treatment  of, 
927. 

Osteomyelitis  in  septico-pyaevnia,  112. 

Ovarian  neuralgia,  528. 


Ovarie  in  hysteria,  802,  810. 
Oxalic-acid  poisoning,  1008, 

Oxygen  inhalations  in  anaemia,  915  ;  in  diabetes,  980  ; 
in  leukaemia,  951. 

Oxyuris  vermicularis,  446;  diagnosis  of,  117;  treat 

ment  of,  447. 
Ozaena,  126  ;  in  scrofula,  1000. 

Pachymeningitis  cervicalis  hypertrophica,  603  ;  com- 
pression of  the  spinal  cord  in,  602  ;  development  of, 
602  ;  diagnosis  of,  602  ;  treatment  'if,  on:;. 

Pachymeningitis  haemorrhagica,  603,  096  ;  develop- 
ment of,  603  ;  interna,  603.  696  ;  spinalis,  608  ;  symp- 
toms of,  603  ;  treatment  of,  603. 

Pain,  sensations  of,  in  chorea,  781  ;  in  chronic  hydro- 
cephalus, 768  ;  conduction  of,  619  ;  in  cramps,  542  ; 
in  hysteria,  802,  810  ;  in  paralysis  agitans,  780  ;  pro- 
longed, 509  ;  rheumatoid,  in  general  paralysis,  762  : 
in  tabes,  659  ;  test  of,  508. 

Palate,  inflammation  of,  351,  357. 

Palate,  paralysis  of,  in  compression  of  the  medulla, 
695  ;  after  diphtheria,  70  ;  (unilateral;  in  cerebral 
haemorrhage,  732. 

Palisade-worm,  875. 

Palpitation  of  the  heart,  diagnosis  of  nervous,  319  ; 
in  hysteria,  806  ;  nervous,  319  ;  in  neurasthenia, 
816  ;  in  obesity,  995  ;  in  pernicious  anaemia,  941  ; 
in  scurvy,  958 ;  in  tape- worm,  443 ;  treatment  of 
nervous,  320  ;  in  valvular  disease  of  the  heart,  296. 

Palsy,  shaking,  784.    See  Paralysis  Agitans. 

Pancreas,  atrophy  of,  503  ;  in  diabetes,  966,  975. 

Pancreas,  cancer  of,  504  ;  diagnosis  of,  504  ;  symp- 
toms of,  504  :  treatment  of,  504. 

Pancreas,  haemorrhage  of,  503. 

Pancreatitis,  acute,  503  ;  chronic  indurated.  504. 

Pancreatized  meat,  enemata  of,  in  stenosis  of  the 
oesophagus,  369. 

Papilloma  of  the  larynx,  144. 

Paquelin's  thermo-cautery  in  noma,  347. 

Para-anaesthesia,  512. 

Paradoxical  contraction,  546. 

Paraesthesia,  505  ;  in  cerebral  haemorrhage,  733  ;  in 
epilepsy,  772  ;  in  injuries  of  the  spinal  cord,  607  ; 
in  neurasthenia,  816  ;  iD  pressure  paralysis  of  the 
spinal  cord,  611  ;  in  spinal  neurasthenia,  606  ;  in 
subacute  poliomyelitis,  673  ;  in  tabes.  639  ;  of  taste, 
533  ;  in  tumors  of  the  spinal  cord,  677. 

Paragraphia,  720. 

Paraldehyde  in  neuralgia.  520  :  in  neurasthenia.  819. 

Paralysie  ascendante  aigue,  674.  See  Spinal  Paral- 
ysis. 

Paralysie  gön£rale  spinale  antärieure  subaigue,  673. 
See  Spinal  Paralysis. 

Paralysis,  534:  acute  ascending  spinal.  674,  675:  arsen- 
ical, 571  ;  in  articular  rheumatism,  905  :  atrophic, 
538,  669;  bilateral,  536;  bulbar. 685:  in  bulbar  haemor- 
rhage, 691  :  central,  534  ;  cerebral.  536  :  in  cerebral 
haemorrhage,  729,  731,  732,  733,  734  :  in  cerebral 
syphilis,  758  ;  in  cerebral  tumor.  752,  753:  in  chronic 
hydrocephalus,  768  ;  combined,  of  the  upper  ex- 
tremity, 567  ;  condition  of  the  paralyzed  muscles 
in,  539  :  in  compression  of  the  medulla.  695  :  cor- 
tical, 536  ;  of  the  diaphragm.  568  :  diphtheritic.  70. 
537 ;  in  embolism  and  thrombosis  of  the  basilar 
artery,  693  :  of  the  facial  muscles  in  facial  paral- 
ysis. 558  ;  flaccid,  539  :  forms  of  peripheral.  555  ; 
general,  760  ;  in  general  paralysis  of  the  insane, 
764  ;  glosso-labio-laryngeal,  6S5  ;  in  hydrophobia, 


1031 


INDEX. 


114  ;  hysterical.  537,  803,  810,  811,  812  ;  after  infec- 
tious diseases,  537  ;  after  injury  to  the  spinal  cord, 
607  ;  of  the  laryngeal  muscles,  139  ;  lead,  509  ;  in 
tahes,  636,  639, 641, 643,  649  ;  of  the  lower  extremity, 
568  :  median,  566  ;  in  meningeal  haemorrhage,  603  ; 
in  multiple  sclerosis,  629  ;  of  the  muscles  of  the 
back.  564  ;  in  myelitis,  618  ;  myopathic,  534 ;  in 
neuralgia,  517  ;  in  neuritis,  582,  583,  585  ;  oculo- 
motor, 555,  £56  ;  of  the  oesophagus,  371  ;  in  pachy- 
meningitis cerviealis  hypertrophica,  602;  periph- 
eral, 536 ;  in  poliomyelitis  of  adults,  671,  673  ;  in 
pressure  paralysis  of  the  spinal  cord,  612,  613  ;  in 
progressive  bulbar  paralysis,  685,  686 ;  pseudo- 
hypertrophic muscular,  058;  from  psychical  causes, 
537  ;  from  ptomaines,  537  ;  in  purulent  meningitis, 
700 ;  radial,  564  ;  reflex,  537  ;  refrigeratory,  537  ; 
rheumatic,  537 ;  of  the  shoulder-muscles,  562 ; 
spastic,  539  ;  in  spina  bifida,  680  ;  spinal,  536,  600, 
667,  671  ;  in  spinal  apoplexy,  604  ;  in  spinal  menin- 
gitis, 600 ;  spinal  atrophic  of  adults,  671  ;  spinal, 
of  children,  667  ;  in  spinal  paralysis  of  children, 
668 ;  of  the  stapedius  in  facial  paralysis,  559 ; 
symptomatology  of,  538 ;  after  syphilis,  537 ;  in 
syringom3relia,  678  ;  after  tuberculosis,  537  ;  toxic, 
537,  569  ;  traumatic,  537  ;  in  tumor  of  the  spinal 
cord,  077;  in  typhoid  fever,  16  ;  ulnar,  566  ;  unilat- 
eral, 536  ;  in  unilateral  lesion  of  the  spinal  cord, 
683  ;  of  the  upper  extremity,  564  :  vaso-motor,  587. 

Paralysis  agitaus,  784  ;  development  of,  784  ;  diag- 
nosis of,  786  ;  displacement  of  the  center  of  grav- 
ity in,  785  ;  distinction  of,  from  multiple  sclerosis. 
787 ;  excretion  in,  786 ;  hereditary  predisposition 
to,  784  ;  pathology  of,  786  ;  symptoms  of,  784  ; 
treatment  of,  787  ;  voice  in,  786. 

Paramyoclonus  multiplex,  576,  810. 

Paramyotone,  ataxic,  796  ;  congenital,  796. 

Paraphasia,  718  ;  association  in,  718. 

Paraplegia,  536 ;  ataxic,  649 ;  in  acute  ascending 
spinal  paralysis,  674  ;  in  chronic  hydrocephalus, 
768  ;  dolorosa,  614  ;  in  myelitis,  619  ;  in  tabes,  639. 

Parietal  convolutions,  focal  diseases  of,  715  ;  relation 
of,  to  cutaneous  and  muscular  sensibility,  715. 

Parkinson's  disease,  784.    See  Paralysis  Agitans. 

Parotitis,  348  ;  contagiousness  of,  348  ;  diagnosis  of, 

348  ;  duration  of  stage  of  incubation  of,  348  ;  meta- 
static, 349  ;  primary,  348  ;  in  scarlet  fever,  40  ;  sec- 
ondary, 349  ;  in  small-pox,  56  ;  treatment  of,  348, 

349  ;  in  typhoid  fever,  12. 

Partial  paralysis  of  sensation,  508  ;  in  tabes,  611  ;  in 
syringomyelia,  678. 

Passive  congestion  of  kidney,  871  ;  in  pulmonary  em- 
physema. 179  :  in  valvular  disease  of  the  heart.  300. 

Passive  congestion  of  liver,  496  :  in  pneumonia,  197  ; 
in  pulmonary  emphysema,  179  ;  in  valvular  disease 
of  the  heart,  299. 

Passive  congestion  of  spleen,  in  cirrhosis  of  the  liver, 
480 ;  in  pulmonary  emphysema,  179  ;  in  valvular 
disease  of  the  heart,  300. 

Passive  motion,  sense  of,  510  ;  of  the  extremities  in 
hemiplegia,  737  ;  in  hysteria,  812 ;  in  spinal  paral- 
ysis of  children,  671. 

Patellar  reflex.  544  ;  absence  of,  641  ;  in  general  pa- 
ralysis of  the  insane,  763  ;  in  myelitis,  621  ;  in  neu- 
ritis. 585  :  in  pressure  paralysis  of  the  spinal  cord, 
612 :  in  pseudo-hypertrophic  muscular  paralysis, 
660  ;  in  tabes.  644  ;  in  tetanus,  792. 

Pavement  epithelium  in  cancer  of  the  oesophagus. 
369. 


Pearly  distemper  in  cattle  in  relation  to  tuberculosis 
in  man,  208,  209. 

Pelioma  typhosum,  17. 

Peliosis,  961  ;  rheumatica,  962  ;  senile,  961. 

Pelvis  in  osteomalacia,  926,  927  ;  rachitic,  924. 

Pelvis  of  the  kidney,  dilatation  of.  See  Hydrone- 
phrosis. 

Pelvis  of  the  kidney,  inflammation  of.    See  Pyelitis. 

Pepsine  in  gastric  catarrh,  381. 

Percussion,  change  of  pitch  on,  over  cavities,  223. 

Perforation,  peritonitis  from,  449  ;  in  purpura  haem- 
orrhagica,  962. 

Peribronchitis,  tubercular,  213. 

Pericardial  surfaces,  adhesion  of,  326. 

Pericarditis,  321  ;  adhesive,  326  ;  in  articular  rheuma- 
tism, 904  ;  chronic,  323  ;  diagnosis  of,  327  ;  externa, 
322,  325  ;  fibrinous,  322  ;  haemorrhagic,  322 ;  in 
pneumonia,  197  ;  prognosis  of,  328  ;  in  pulmonary 
tuberculosis,  228;  purulent,  322;  sero-fibrinous,  322; 
treatment  of,  328;  tubercular,  322,  327  ;  in  valvular 
disease  of  the  heart,  298. 

Pericardium,  air  in  the,  330;  blood  in  the,  330;  dropsy 
of  the,  329  ;  inflammation  of  the,  321  ;  obliteration 
of  the,  326. 

Perichondritis,  laryngeal.  134  ;  diagnosis  of,  135  ;  ex- 
ternal, 134  ;  internal,  134  ;  secondary,  135  ;  treat- 
ment of,  135. 

Perinephritic  abscess,  870  ;  causes  of,  870  ;  symptoms 
of,  870  ;  treatment  of,  871. 

Perinephritis,  purulent,  870. 

Periosteal  reflex,  545  ;  in  cerebral  haemorrhage.  732. 

Periostitis  ossificans  in  articular  rheumatism,  913. 

Peripheral  nerves,  diseases  of,  505  ;  forms  of  paraly- 
sis of,  555  ;  inflammation  of,  579  ;  new  growths  in, 
585. 

Peripleuritis,  267  ;  diagnosis  of,  267  ;  prognosis  of, 
267. 

Periproctitis,  408. 

Peritoneal  cancer,  463  ;  diagnosis  of,  463  ;  treatment 
of.  463. 

Peritoneal  dropsy,  460. 

Peritonitis,  acute,  449  ;  acute  circumscribed,  451,  455 
adhesive,  451  ;  in  articular  rheumatism,  450,  464 
cancerous,  463  ;  in  children,  459  ;  in  cholelithiasis 
473  ;  chronic,  457  ;  circumscribed,  451  ;  deformans 
458 ;  diagnosis  of,  456,  458  ;  diffuse  general,  450 
fibrino-purulent,  450 ;  haemorrhagic,  with  forma- 
tion of  hasmatoma,  458  ;  in  nephritis,  450  ;  in  pleu- 
risy, 450  ;  prognosis  of,  456  ;  in  pulmonary  tuber- 
culosis, 227  :  sacculated,  451  ;  septic,  451  ;  treatment 
of,  456,  460 ;  tubercular,  457 ;  in  typhoid  fever,  10, 
11. 

Peritonsillar  abscess,  354. 

Perityphlitis,  418.    See  also  Typhlitis. 

Peroneal  paralysis,  569. 

Pertussis,  160.    See  Whooping-cough. 

Petechial  typhus,  28.    See  Typhus. 

Peyer's  patches  in  typhoid  fever,  9. 

Pharyngeal  catarrh,  chronic,  357  ;  hypertrophic,  358  ; 
prognosis  of,  359  ;  treatment  of,  359. 

Pharyngitis,  chronic,  357 ;  granular,  357  ;  sicca,  358. 

Pharynx  in  measles,  47  ;  in  scarlet  fever,  38  ;  tuber- 
culosis of,  226  ;  in  typhoid  fever,  12. 

Phenacetine.  in  chorea,  783  ;  in  headache,  532  ;  in  mi- 
graine, 593  ;  in  neuralgia,  520  ;  in  neurasthenia,  818. 

Phlebitis,  purulent,  in  septico-pysemia,  110. 

Phloridzine  as  cause  of  glycosuria,  966. 

Phosphate  calculi  in  nephrolithiasis,  885. 


INDEX. 


L03 


.) 


Phosphorus,  048  ;  in  pernicious  anosmia,  945  ;  in  neu- 
ralgia, 520  ;  in  osteomalacia,  937  ;  in  rachitis,  925  ; 
in  tabes,  018. 

Phosphorus  necrosis,  1000. 

Phosphorus  poisoning,  1000  ;  acute,  1000  ;  chronic, 
1000. 

Phrenic  nerve,  paralysis  of,  508. 

Phthisis,  fibroid,  223. 

Phthisis,  laryngeal,  136.    See  Tuderculosis. 

Phthisis  puhnonalis,  207.    See  Tuberculosis. 

Physostigmine,  in  chorea,  783. 

Piano-player's  cramp,  579. 

Picric  acid  in  trichinosis,  124. 

Pigeon-breast,  rachitic,  923. 

Pigment  calculi  in  cholelithiasis,  471. 

Pigment  induration  in  pulmonary  tuberculosis,  214. 

Pilocarpine  in  diphtheria,  72  ;  in  nephritis,  847. 

Pine-needle  baths  in  muscular  rheumatism,  919. 

Pin-worms,  446. 

Piperin  in  leukaemia,  950. 

Pitch,  change  of.  on  percussion  over  cavities,  222. 

Pityriasis  versicolor  in  pulmonary  tuberculosis,  239. 

Plethora,  709. 
.  Pleura,  cicatricial  contraction  of,  in  pleurisy,  258, 
260  ;  fistulas  of,  after  empyema,  204  ;  new  growths 
of,  272. 

Pleura  in  leukaemia,  947  ;  in  pneumothorax,  268  ;  in 
pulmonary  tuberculosis,  226. 

Pleurisy.  253  ;  adhesive,  255  ;  in  articular  rheuma- 
tism, 904  ;  complications  of,  261  ;  diagnosis  of,  202  ; 
with  effusion,  258  ;  fibrinous,  254,  257,  261  ;  in  pneu- 
monia, 193  ;  primary,  253  ;  prognosis  of,  203  ;  puru- 
lent, 262 ;  secondary,  253  ;  in  septico-pyaemia,  112  ; 
in  small-pox,  50  ;  tapping  in,  264  ;  treatment  of, 
264  ;  tubercular,  254,  261  ;  in  typhoid  fever,  13. 

Pleuritic  effusions,  258  ;  ossification,  255  ;  thickening, 
255,  260. 

Pleuritis,  253  ;  sicca,  254,  257. 

Pleuro-pericarditis,  325. 

Pleuro-pneumonia,  189. 

Plexus  paralysis  of  the  brachial  plexus,  567. 

Pneumatic  treatment  in  bronchitis,  154  ;  in  emphy- 
sema, 181. 

Pneumatometer,  178. 

Pneumonia  alba  in  pulmonary  syphilis  of  the  new- 
born, 255  ;  anomalies  in  course  of,  200  ;  asthenic, 
201  ;  in  articular  rheumatism,  906  ;  bilious,  197  ; 
catarrhal,  184  ;  central,  201  ;  cheesy,  187,  213  ;  in 
children,  200  ;  chronic  interstitial,  165  ;  complica- 
tions of  croupous,  193  ;  crossed,  191  ;  croupous,  189  ; 
delayed  resolution  of  croupous,  202 ;  diagnosis  of 
croupous,  203  ;  in  diphtheria,  69  ;  disposition  to 
croupous,  189 ;  endemic  occurrence  of  croupous, 
190  ;  erysipelatous,  196  ;  fibrinous,  190  ;  genuine, 
189  ;  infectious  nature  of  croupous,  189  ;  intermit- 
ting, 199  ;  lobar,  189  ;  lobular,  184,  213  ;  in  measles, 

49  ;  migrans,  190  ;  in  nephritis,  843  ;  in  old  people, 
200  ;  pathological  lesion  of  catarrhal,  185  ;  of  croup- 
ous, 190  ;  primary,  189  ;  prognosis  of  croupous, 
204  ;  in  rachitis,  923  ;  in  scurvy,  959  ;  in  small-pox, 

50  :  symptoms  of  catarrhal,  180  ;  of  croupous,  193  ; 
in  tetanus,  792  ;  traumatic,  189  ;  treatment  of  ca- 
tarrhal, 188  ;  of  croupous,  204  ;  typhoid,  201  ;  wan- 
dering, 196. 

Pneumonoconiosis,  245. 
Pneumopericardium,  330. 

Pneumothorax,  207  ;  circumscribed,  208  ;  closed,  209  ; 
diagnosis  of,  270  ;  open,  209  ;  in  pulmonary  tuber- 


culosis, 226  ;  sacculated,  208  ;  treatment  of,  270  ;  in 
typhoid  fever,  18  ;  valvular,  270. 

Pneumo-typhoid,  18,  202. 

Podagra,  984.    See  Qo\  x. 

Points  douloureux  in  neuralgia,  517. 

Poisoning,  1003. 

Polioencephalitis,  745. 

Poliomyelitis,  acute,  of  adults,  671 ;  diagnosis  <>f.  672  ; 
relation  of,  to  neuritis,  072;  symptoms  of,  071  ; 
i  real  ment  of,  073. 

Poliomyelitis,  acute,  in  children  007.  See  SPINAL  I'a 
ralysis  op  Children. 

Poliomyelitis,  subacute  and  chronic,  678;  treatment 
of,  674. 

Polyaesthesia,  507  ;  in  tabes,  640. 

Polyarthritis,  chronic,  911. 

Polydipsia  in  diabetes,  967,  971,  983  ;  in  hysteria,  805. 

Polymyositis,  acute,  919. 

Polypi  in  the  oesophagus,  366. 

Polysarcia  adiposa,  992. 

Polyuria  in  anasmia,  934  ;  in  cerebro-spinal  menin- 
gitis, 106  ;  in  contracted  kidney,  859  ;  in  diabetes 
insipidus,  982-984  ;  in  diabetes  mellitus,  907,  971, 
976  ;  in  epilepsy,  773  ;  in  hysteria,  805. 

Pomegranate  in  tape-worm,  444. 

Pons,  haemorrhages  into,  691.    See  also  Medulla. 

Pork  in  relation  to  trichinosis,  122. 

Portal  vein,  purulent  inflammation  of,  500  (see  Pyle- 
phlebitis) ;  thrombosis  of,  502.  See  Pylethroji- 
bosis. 

Post-epileptic  insanity,  774. 

Posterior  nasal  catarrh,  chronic,  126. 

Potassium,  acetate  of,  in  nephritis.  848  ;  chlorate  of, 
in  cystitis,  896  ;  nitrate  of,  poisoning  from,  1004  ; 
picro-nitrate  of,  in  chyluria,  876  ;  salts,  in  scurvy, 
960. 

Pott's  boss  on  the  vertebral  column,  609. 

Power,  sense  of,  510. 

Pregnancy  in  epilepsy,  774  ;  nephritis  of,  845. 

Premature  delivery  in  chorea  gravidarum,  784. 

Pressure  diverticula,  303. 

Pressure  paralysis  of  the  spinal  cord,  008  ;  bending  of 
the  cord  in,  010  ;  causes  of,  008  ;  complications  of, 
613  ;  diagnosis  of,  613  ;  pathological  lesion  of  the 
vertebras  and  of  the  cord  in,  609  ;  place  of  compres- 
sion in,  609  ;  treatment  of,  614  ;  trephining  for,  614. 

Pressure  points  in  facial  spasm,  572. 

Pressure,  sense  of,  disturbances  of,  in  tabes,  641  ; 
partial  paralysis  of,  507  ;  test  of,  507. 

Proctitis,  407. 

Professional  diseases,  245. 

Professional  neuroses  of  co-ordination,  577. 

Proglottides  of  tape-worm,  440. 

Propulsion  in  paralysis  agitans,  785. 

Prosopalgia,  521.    See  Trigeminus,  Neuralgia  of. 

Prostate  in  genito-urinary  tuberculosis.  88S. 

Pseudo-crises  in  croupous  pneumonia,  199  ;  in  relaps- 
ing fever,  33. 

Pseudo-croup,  131. 

Pseudo-hypertrophy  of  the  muscles.  659  :  beginning 
of.  059  ;  increase  of  volume  of  different  muscles  in, 
000  ;  symptoms  of,  659. 

Pseudo-leucocythasmia,  951. 

Pseudo-leukaemia,  951  ;  diagnosis  of,  953  :  examina- 
tion of  the  blood  in,  952  ;  lymphatic.  952  ;  relation 
of,  to  anaemia,  951  ;  to  infectious  tumors,  951  ; 
symptoms  of,  952  ;  treatment  of,  953. 

Pseudo-paralysis,  spastic,  664. 


1036 


INDEX. 


Pseudo-relapse  in  scarlet  fever,  44. 

Pseudo-sclerosis,  631. 

Pseudo-tabes  of  alcoholic  subjects,  584. 

Psoriasis  of  the  tongue,  346. 

Psychical  equivalent  of  epilepsy,  774. 

Ptosis  in  oculo-motor  paralysis,  556. 

Pulmonary  valve,  insufficiency  of,  293  ;  stenosis  of, 
293. 

Pulsation,  epigastric,  in  valvular  disease  of  the  heart, 
284. 

Pulsus  bigeminus,  298  ;  celer,  289  ;  inequalis,  297  ;  ir- 
regularis, 297  ;  paradoxus,  107,  324,  326  ;  tardus, 
333. 

Puncture  in  ascites,  462  ;  in  chronic  hydrocephalus, 
769  ;  in  cirrhosis  of  the  liver,  483  ;  in  hydronephro- 
sis. 892  ;  in  nephritis,  849  ;  in  pericarditis,  329  ;  in 
pleurisy,  264  ;  in  pneumonia,  100  ;  in  pneumotho- 
rax, 271 ;  in  valvular  disease  of  the  heart,  306. 

Pupils  in  epilepsy,  773,  777  ;  in  general  paralysis  of 
the  insane,  703  ;  in  haematoma  of  the  dura,  697,  098; 
in  meningitis,  700,  704  ;  in  pernicious  anemia,  942  ; 
in  tetanus,  792  :  in  thermic  fever,  747. 

Pupils,  immobility  of,  in  eclampsia  of  children,  779  ; 
in  epilepsy,  773,  777  ;  in  general  paralysis  of  the  in- 
sane, 763  ;  in  lesions  of  the  corpora  quadrigemina, 
722  ;  in  tabes  dorsalis,  636. 

Purpura,  961  ;  hemorrhagica,  962  ;  hemorrhagica, 
prognosis  and  treatment  of,  962  ;  rheumatica,  962  ; 
simplex,  962  ;  urticans,  962  ;  variolosa,  57. 

Pus,  collections  of,  as  a  cause  of  septicopyemia,  109. 

Pustule,  malignant,  117.    See  Malignant  Pustule. 

Pustules  in  glanders,  116  ;  in  small-pox,  53. 

Putrefaction,  abnormal  intestinal,  as  cause  of  con- 
vulsions, 771. 

Pyemic  symptoms  in  sinus  thrombosis,  708  ;  in  sup- 
purative pylephlebitis,  501. 

Pyelitis,  881  ;  calculosa,  881,  884  ;  in  tabes,  643 ;  in 
myelitis,  621  ;  origin  of,  881  ;  symptoms  of,  882  ; 
treatment  of,  884. 

Pyelocystitis,  881. 

Pyelonephritis,  869,  882. 

Pylephlebitis,  chronic  adhesive,  502. 

Pylephlebitis,  suppurative,  500 ;   diagnosis  of,  500  ; 

of  the  newborn,  500  ;  symptoms  of,  500. 
Pylethrombosis,  502  ;   symptoms  of,  502  ;  treatment 

of,  503. 
Pyonephrosis,  882. 
Pyopneumothorax,  268. 

Quicksilver  in  intestinal  obstruction,  439. 

Quincke's  capillary  pulse,  289. 

Quinine  in  asthma,  172  ;  in  diabetes,  981  ;  in  habitual 
headache,  532  ;  in  hemoglobinuria,  956  ;  in  leuke- 
mia, 950  :  in  malaria,  96  ;  in  Meniere's  disease,  769  ; 
in  neuralgia,  519  :  in  neurasthenia,  818  ;  in  neu- 
roses of  the  heart,  319  ;  in  pulmonary  tuberculosis, 
235 ;  in  sciatica,  520,  527 ;  after  scurvy,  901  ;  in 
trigeminal  neuralgia,  520,  523  ;  in  trophic  disturb- 
ances. 590  ;  in  typhoid  fever,  20,  24,  25  ;  in  whoop- 
ing-cough, 163. 

Rabies,  113.    See  Hydrophobia. 

Race,  influence  of,  on  diabetes  mellitus,  967 ;  on 
hemophilia,  963  ;  on  hysteria,  799  ;  on  yellow  fe- 
ver, 101. 

Rachitis,  920 ;  acute,  924  ;  chemical  examination  of 
the  bones  in,  921  ;  chronic,  924  :  diagnosis  and  prog- 
nosis of,  924 ;  fcetal,  921  ;   origin  of,  920 ;  relation 


of,  to  spasm  of  the  glottis,  142  ;  symptoms  of,  922  ; 
tarda,  921  ;  treatment  of,  924. 

Radial  paralysis,  564  ;  chronic  thickening  of  the  ex- 
tensor tendons  in,  565  ;  disturbances  of  function 
in,  505  ;  in  lead  paralysis,  570 ;  rheumatic,  565  ; 
traumatic,  564. 

Radiating  fungus,  274. 

Rag-picker's  disease,  119.    See  Malignant  Pustule. 

Railway-spine,  572.    See  Traumatic  Neuroses. 

Raynaud's  disease,  588  ;  with  hemoglobinuria,  S54. 

Rectal  speculum  in  cancer  of  the  rectum,  426. 

Rectum,  cancer  of,  426  ;  inflammation  of,  407  ;  neu 
ralgia  of,  528  ;  paralysis  of,  in  injury  of  the  spinal 
cord,  607 ;  paralysis  of,  in  myelitis,  621  ;  syphilis 
of,  425  ;  symptoms  of,  425  ;  treatment  of,  425. 

Recurrent  fever.    See  Relapsing  Fevek. 

Recurrent  nerve,  paralysis  of,  139. 

Re-enforcement  of  patellar  reflex,  544. 

Reflex  centers,  vaso-motor,  587. 

Reflexes,  543 ;  in  acute  ascending  spinal  paralysis, 
674  ;  after  cerebral  hemorrhage,  729,  732  ;  in  cho- 
rea, 782  ;  in  facial  paralysis,  561  ;  in  injury  of  the 
spinal  cord,  607  ;  in  tabes,  641 ;  in  myelitis,  620  ;  in 
neuralgia,  570  ;  in  neuritis,  583,  584 ;  in  paralysis, 
540  ;  in  pressure  paralysis  of  the  spinal  cord,  612  ; 
in  progressive  bulbar  paralysis,  687  ;  in  progressive 
muscular  atrophy,  657  ;  in  sciatica,  526  ;  in  spinal 
apoplexy,  605  ;  in  spinal  meningitis,  600  ;  tests  and 
condition  of,  543  ;  in  tetanus,  792  ;  in  trigeminal 
neuralgia,  531  ;  in  tubercular  meningitis,  704  ;  in 
unilateral  lesion  of  the  spinal  cord,  684. 

Reflex  epilepsy,  771  ;  neuralgia,  517  ;  paralyses,  537  ; 
spasm,  saltatory.  575. 

Refraction,  errors  of,  as  a  cause  of  headache,  530  ; 
migraine,  591. 

Rehme  bath,  artificial,  in  myelitis,  627. 

Relapses  of  cholera,  86  :  of  erysipelas,  64  ;  of  lead 
paralysis,  570 ;  of  scarlet  fever,  44  ;  of  sciatica, 
527  ;  of  typhlitis,  492  ;  of  typhoid  fever,  19  ;  of  ty- 
phus fever,  30. 

Relapsing  fever,  31  ;  complications  of,  35  ;  conta- 
giousness of,  32  ;  epidemic  occurrence  of,  in  Ger- 
many, 31  ;  inoculation  of,  32  ;  period  of  incubation 
of,  32  ;  prognosis  of,  35 ;  spirilli  in,  34  ;  treatment 
of,  35. 

Renal  crises  in  tabes,  643. 

Ren  mobilis,  876. 

Resonance,  thoracic,  in  pleurisy,  259. 

Respiration  in  acute  ascending  spinal  paralysis,  675  ; 
in  acute  bulbar  paralysis,  094  ;  amphoric,  269  ;  in 
amyotrophic  lateral  sclerosis,  652  ;  in  anemia,  932, 
942  ;  in  asthma,  168  ;  bronchial,  223  ;  in  bronchitis, 
148,  152  ;  in  bulbar  hemorrhage,  692  ;  in  cancer  of 
the  lungs,  251  ;  in  cerebral  hemorrhage,  729,  732  ; 
in  chronic  poliomyelitis,  673  ;  in  cirrhosis  of  the 
liver,  481  :  in  diabetic  coma,  973  ;  in  embolism  and 
thrombosis  of  the  basilar  artery,  694  ;  in  epilepsy, 
773  ;  in  exophthalmic  goitre,  597  ;  in  hepatitis.  477  ; 
in  hysteria,  803  ;  interrupted,  222  ;  in  tabes,  643  ; 
metallic,  269  ;  metamorphosing,  222 ;  in  miliary 
tuberculosis,  237,  239  ;  in  obesity,  995  ;  in  osteoma- 
lacia, 927  ;  in  phthisis,  222  ;  in  pneumonia,  186,  194  ; 
in  progressive  bulbar  paralysis,  686  ;  in  progressive 
muscular  atrophy,  656,  657,  658 ;  in  pseudo-leu- 
kemia lymphatica,  952  ;  in  scurvy,  958  ;  in  tetanus, 
793  ;  in  thermic  fever,  747  ;  in  trichinosis,  122 ;  in 
tubercular  meningitis,  704,  705  ;  in  uremia,  832. 
Respiratory  spasms,  576  ;  complicated,  577. 


INDEX. 


1037 


Retina  in  chronic  nephritis,  854  ;  in  contracted  kid- 
ney, 861  ;  in  diabetes,  973  ;  in  leukaemia,  947. 

Retinal  haemorrhages  in  septico-pyajmia,  111. 

Retropharyngeal  abscess,  360. 

Retropulsion  in  paralysis  agitans,  785. 

Retro-tonsillar  abscess,  354. 

Revaccination,  59. 

Rhabdomyoma,  872. 

Rheumatism,  acute  articular,  900  ;  alkaline  treatment 
of,  910  ;  cerebral,  905  ;  in  chorea,  780  ;  chronic,  911  ; 
diagnosis  of,  907  ;  endocarditis  in,  903  ;  hyperpy- 
retic,  905  ;  prognosis  of,  906  ;  prophylaxis  of,  911  ; 
scarlatinal,  43 ;  symptoms,  901  ;  treatment  of,  907, 
910. 

Rhinitis,  125  ;  chronic,  120  ;  in  scrofula,  1000. 

Rickets,  920.    See  Rachitis. 

Röthein,  51  ;  period  of  incubation  of,  51  ;  prognosis 
of,  51  ;  relation  of,  to  measles,  51. 

Romberg's  symptom  in  locomotor  ataxia,  636. 

Root-zones,  510. 

Rosary,  rachitic,  923. 

Rosenthal-Leube  meat  solution,  389. 

Roseola  in  typhoid  fever,  16  ;  in  typhus  fever,  30. 

Round-worms,  445. 

Sac,  pericardial,  air  in,  330  ;  blood  in,  330. 

Saccharine  in  diabetes,  980. 

Sage-tea  in  phthisis,  235. 

St.  Anthony's  fire,  61. 

St.  Vitus's  dance,  780. 

Salaam  convulsions,  574. 

Salicylate  of  sodium  in  articular  rheumatism,  908  ; 
in  diabetes,  981  ;  iu  gout,  992  ;  in  habitual  headache, 
532  ;  in  hemicrania,  593  ;  in  neuralgia,  520  ;  in  ty- 
phoid fever,  24. 

Salicylic  acid  in  articular  rheumatism,  907  ;  in  dis- 
eases of  the  trophic  nerves,  590  ;  in  gastric  catarrh, 
381  ;  in  gout,  992  ;  in  muscular  rheumatism,  919  ;  in 
neuritis,  584 ;  in  purpura  haemorrhagica,  963  ;  in 
tabes,  648  ;  in  tetanus,  784. 

Salicylic  delirium,  90S  ;  dyspnoea,  908  ;  powder  in 
phthisis,  235. 

Salivation  in  diabetes  insipidus,  983  ;  in  hydrophobia, 
114  ;  in  stomatitis,  341  ;  in  ulcerative  stomatitis,  342. 

Salol  in  rheumatism,  910. 

Salt  in  epilepsy,  778  ;  in  haemoptysis,  235. 

Salt-baths  in  gout,  991  ;  in  scrofula,  1001. 

Saltpeter-paper  in  asthma,  172. 

Sand-baths  in  articular  rheumatism,  916. 

Santonica  in  ascarides,  446. 

Santonin  in  ascarides,  446. 

Sarcina  ventriculi,  376. 

Sarcoma,  alveolar,  of  the  lungs,  250  ;  of  the  kidneys, 
872. 

Scarification  of  the  skin  in  dropsy,  306. 

Scarlatina,  36. 

Scarlatinal  diphtheria,  40  ;  eruption,  41  ;  nephritis, 
42,  43  ;  poison,  36. 

Scarlet  fever,  36  ;  contagiousness  of,  36  ;  diagnosis  of, 
44  ;  disposition  to,  36  ;  epidemic  occurrence  of,  37  ; 
haemorrhagic,  41  ;  inoculation  of,  36  ;  miliary,  41 ; 
papular,  41  ;  period  of  incubation  of,  37  ;  prognosis 
of,  44  ;  rudimentary  forms  of,  43  ;  tenacity  of  the 
contagium  of,  36  ;  treatment  of,  44  ;  typhoid  form 
of,  44  ;  variegated,  41. 

Sciatica  in  diabetes,  973  ;  diagnosis  of,  527  ;  relapses 
of,  527  ;  symptoms  and  cause  of,  526  ;  treatment 
of,  527. 


Sciatic  paralysis,  509  ;  treatment  of,  569. 

Scirrhus  cancer  of  the  oesophagus,  869  ;  <>f  the  stom- 
ach, 391. 

Sclerose  en  plaques,  627.     See  SCLEROSIS,  MULTIPLE. 

Sclerosis,  amyotrophic  lateral,  650  ;  diagnosis  of,  668  : 
implication  of  the  medulla  in,  651  ;  Symptome  and 
course  of,  651  ;  treatment  of,  653. 

Sclerosis,  disseminated,  627.  See  SCLEROSIS,  Mul- 
tiple. 

Sclerosis,  multiple,  of  the  brain  and  cord,  627  ;  dis- 
tinction of,  from  paralysis  agitans,  631  ;  hereditary 
predisposition  to,  628  ;  relation  of,  to  chronic  bul- 
bar paralysis,  631  ;  to  chronic  myelitis,  630  ;  to  gen- 
eral paralysis  of  the  insane,  631  ;  to  spastic  spinal 
paralysis,  631  ;  seat  of  the  sclerotic  nodules  in,  627  ; 
symptoms  of,  629  ;  treatment  of,  031. 

Sclerosis,  postero-lateral,  649. 

Sclerosis,  primary  lateral,  663. 

Sclerosis,  renal,  856. 

Sclerotinic  acid  in  phthisis,  235. 

Scolex,  441. 

Scoliosis,  rachitic,  923. 

Scorbutic  anaemia,  959  ;  ulcers,  959. 

Scorbutus,  956.    See  Scurvy. 

Scrofula,  999  ;  relation  of,  to  tuberculosis,  216,  1000  ; 
treatment  of,  1000. 

Scurvy,  956  ;  causes  of,  957  ;  contagiousness  of,  957  ; 
distinction  of,  from  peliosis  and  stomatitis,  960  ; 
epidemic  occurrence  of,  957  ;  forms  of,  960  ;  symp- 
toms of,  958  ;  treatment  of,  960. 

Season  and  chorea,  780. 

Seat-worms,  446. 

Secondary  degeneration.  See  Spinal  Cord  (second- 
ary degeneration). 

Secretion,  disturbances  of,  590  ;  in  acute  ascending 
spinal  paralysis,  674  ;  in  anaemia,  932  ;  in  cerebral 
haemorrhage,  723  ;  in  diabetes  insipidus,  982  ;  in  ex- 
ophthalmic goitre,  597  ;  in  hemoglobinuria,  954  ;  in 
hysteria,  805;  in  myelitis,  622;  in  neurasthenia,  816  ; 
in  progressive  bulbar  paralysis,  687  ;  in  subacute 
poliomyelitis,  673  ;  in  tetanus.  793  ;  in  tetany,  790  ; 

Secretions  in  diabetes,  975,  982,  983. 

Semilunar  valves,  insufficiency  of,  287. 

Senile  emphysema,  173. 

Senile  kidney,  333,  857. 

Sensation,  conduction  of,  in  acute  ascending  spinal 
paralysis,  674  ;  delayed,  509. 

Sensation,  paralysis  of,  in  tabes,  640  ;  partial,  505. 

Sensibility,  disturbances  of ,  in  acute  ascending  spinal 
paralysis,  675  ;  in  arsenical  paralysis,  571  ;  in  bul- 
bar hasmorrhage,  692  :  in  caisson  disease,  608 ;  in 
cerebral  haemorrhage,  733  ;  in  compression  of  the 
medulla,  695  ;  in  crural  paralysis,  568  ;  in  epilepsy, 
772  ;  in  focal  diseases  of  the  eras,  723  ;  of  the  inter- 
nal capsule,  721  ;  general  consideration  of,  505  ;  in 
general  paralysis  of  the  insane,  763  ;  in  injury  of 
the  spinal  cord,  607  ;  in  the  larynx,  143  ;  in  median 
paralysis,  566  ;  in  multiple  sclerosis,  630  ;  in  mye- 
litis, 619  ;  in  neuralgia,  511  ;  in  neuritis,  584,  585  ;  in 
obturator  paralysis,  569  ;  in  paralysis,  539  ;  in  pres- 
sure paralysis  of  the  spinal  cord,  612  ;  in  radial  pa- 
ralysis. 565  ;  in  sciatica,  526  :  in  sciatic  paralysis, 
569  ;  in  syringomyelia,  678  :  in  tabes,  639  ;  in  teta- 
nus, 792  ;  in  tumors  of  the  base  of  the  brain.  752  :  in 
ulnar  paralysis,  566  ;  in  unilateral  lesion  of  the  spi- 
nal cord,  683  ;  in  writer's  cramp,  578. 
Sensory  centers.  715. 
Sensory  nerves,  diseases  of,  505. 


103S 


INDEX. 


Septico-pyaemia,  108;  circulatory  apparatus  in,  111  ; 
cryptogenetic  or  spontaneous,  109  ;  diagnosis  of, 
112  ;  jaundice  of  the  skin  in,  112  ;  prognosis  of,  112  ; 
treatment  of,  113. 

Sero-pneumothorax,  267. 

Serous  membranes  in  articular  rheumatism,  904. 

Serratus  paralysis,  563  ;  course  of,  504  ;  rheumatic, 
563  ;  traumatic,  563  ;  treatment  of,  564  ;  wing-like 
position  of  the  scapula  in,  564. 

Serum  albumen  in  albuminuria,  823. 

Sewing-machine  girls,  affection  of,  579. 

Sex,  influence  of,  in  acute  ascending  spinal  paralysis, 
674  ;  in  acute  yellow  atrophy  of  the  liver,  485  ;  in 
autotrophic  lateral  sclerosis,  650  ;  in  anaemia,  929, 
934,  940  ;  in  cerebral  haemorrhage,  720  ;  in  cerebral 
syphilis,  757  ;  in  cerebral  tumor,  748  ;  in  cholera, 
83  ;  in  chorea,  781  ;  in  congenital  myotonia,  795  ; 
in  diabetes,  967  ;  in  exophthalmic  goitre,  595  ;  in 
Friedreich's  ataxia,  648  ;  in  general  paralysis  of  the 
insane,  761  ;  in  gout.  985  ;  in  haematoma  of  the  dura 
mater,  697  ;  in  haemophilia,  963  ;  in  hepatic  colic, 
470  ;  in  hemicrania,  591  ;  in  hysteria,  799  ;  in  leukae- 
mia, 946  ;  in  multiple  sclerosis,  628  ;  in  neuralgia, 
516  ;  in  obesity,  994  ;  in  osteomalacia,  925  ;  in  pa- 
ralysis agitans,  784  ;  in  phthisis,  211  ;  in  poliomye- 
litis, acute,  of  adults,  671 ;  in  pseudo-hypertrophic 
muscular  paralysis,  659  ;  in  pseudo-leukaemia,  952  ; 
in  rachitis,  921  ;  in  tabes,  633  ;  in  tetany,  789  ;  in  uni- 
lateral facial  atrophy,  594. 

Sexual  excess,  as  cause  of  myelitis,  616. 

Sexual  functions  in  diabetes,  972  ;  in  functional  dis- 
turbances of  the  spinal  cord,  606  ;  in  injuries  of  the 
spinal  cord,  607  ;  in  myelitis,  621  ;  in  tabes,  643. 

Sexual  organs  in  chlorosis,  929  ;  in  diabetes,  972  ; 
diphtheria  of,  69  ;  in  exophthalmic  goitre,  595  ;  in 
gout,  987  ;  in  hysteria,  800  ;  neuralgia  of,  528 ;  in 
neurasthenia,  816  ;  (female)  in  peritontis,  450. 

Shadows  of  red  blood-corpuscles  in  haemoglobinuria, 
955. 

Shaking,  540. 

Shaking  palsy,  784. 

Ship  fever,  28.    See  Typhus  Fever. 

Shoulder,  muscles  of,  paralysis  of,  562  ;  paralysis  of, 
unilateral,  in  cerebral  haemorrhage,  732  ;  spasm  of, 
575. 

Siderosis  pulmonum,  245. 

Silver,  nitrate  of,  in  chorea,  783  ;  in  dysentery,  80  ;  in 
intestinal  catarrh  of  children,  417  ;  in  tabes,  648  ;  in 
myelitis,  627  ;  in  spastic  spinal  paralysis,  667  ;  in 
valvular  disease  of  the  heart,  303. 

Singultus,  577.    See  Hiccough. 

Siphon,  in  washing  out  the  stomach,  399. 

Skin,  care  of,  in  diabetes,  980  ;  character  of,  in  ar- 
thritis deformans,  915  ;  itching  of,  in  uraemia,  833. 

Skin,  diseases  of.  in  articular  rheumatism,  904 ;  in 
dengue,  99  ;  in  diabetes,  972  :  in  gout,  987  ;  in  pneu- 
monia, 198  ;  in  scarlet  fever,  41  ;  in  scrofula,  999  ; 
in  scurvy,  958  ;  in  small-pox,  55  ;  in  trichinosis,  123  ; 
in  typhoid  fever,  16. 

Skoda's  resonance  in  pleuritic  effusion,  259. 

Sleeplessness  in  neurasthenia,  816. 

Small-pox,  52  ;  confluent,  53  ;  contagiousness  of,  52  ; 
diagnosis  of,  57  ;  haemorrhagic,  57  ;  mortality  in, 
57  ;  period  of  incubation  in,  53  ;  prognosis  of,  57  ; 
treatment  of,  58. 

Smell,  sense  of.  anaesthesia  of,  532  ;  anomalies  of, 
532  ;  in  epilepsy,  772  ;  hyperaesthesia  of,  532  ;  in 
hysteria,  801  ;  relation  of,  to  anomalies  of  taste, 


53.3  ;  subjective  sensations  of,  532  ;  test  of,  532  ; 
treatment  of  anomalies  of,  533. 

Sneezing  spasm,  577. 

Sodic  bicarbonate  in  diabetic  coma.  9S1  ;  bicarbonate 
in  gastric  catarrh,  382  ;  carbonate  in  nephrolithia- 
sis, 887  ;  hydrate  in  sulphuric-acid  poisoning,  1003  ; 
phosphate  in  nephrolithiasis,  887  ;  sulphate  in  car- 
bolic-acid poisoning,  1008. 

Soil  theory  in  relation  to  typhoid  fever,  2. 

Soil  water  in  relation  to  cholera,  83  ;  in  relation  to 
typhoid  fever,  2.  3. 

Somnambulism  in  hysteria,  809. 

Soor,  344. 

Sore  throat,  351  (see  Tonsillitis)  :  catarrhal,  352  ;  fol- 
licular, 353  ;  haemorrhagic,  354  ;  necrotic,  354  ;  par- 
enchymatous, 353  ;  phlegmonous,  354  ;  in  scarlet 
fever,  38  ;  in  small-pox,  56  ;  in  typhoid  fever,  12. 

Soul-blindness,  716. 

Soul-deafness,  716. 

Southey's  trocar  ip  dropsy,  306. 

Spasm,  539  (see  Convulsions)  ;  of  the  cervical  mus- 
cles, 573  ;  clonic,  540  ;  co-ordinated,  541 ;  of  the  fa- 
cial nerves,  572 ;  forms  of  localized,  540  ;  of  the 
muscles  of  the  lower  extremity,  575  :  of  the  oesoph- 
agus, 371  ;  of  the  respiratory  muscles,  576  ;  tonic, 
540,  541  ;  tonic-clonic,  540. 

Spasm  of  the  glottis,  142.    See  Glottis,  Spasm  op. 

Spastic-paretic  gait  in  multiple  sclerosis,  630 ;  in 
spastic  spinal  paralysis,  664 ;  in  syringomyelia, 
678. 

Speech,  disturbances  of,  716  ;  in  acute  bulbar  myeli- 
tis, 694  ;  in  amyotrophic  lateral  sclerosis,  652  ;  in 
athetosis,  787  ;  in  bulbar  haemorrhage,  692  ;  in 
cerebral  embolism,  740  ;  in  cerebral  haemorrhage, 
728,  736 ;  in  cerebral  syphilis,  759 ;  in  cerebral 
tumors,  750,  752  ;  in  chorea,  781  ;  in  compression  of 
the  medulla,  695  ;  in  embolism  and  thrombosis  of 
the  basilar  artery,  694  ;  in  epilepsy,  772  ;  in  focal 
diseases  of  the  centrum  ovale,  720  ;  in  general 
paralysis  of  the  insane,  762,  766  ;  in  haematoma  of 
the  dura,  697  ;  in  hereditary  ataxia,  649  ;  in  menin- 
gitis, 704  ;  in  multiple  sclerosis,  629  ;  in  progressive 
bulbar  paralysis,  685,  687. 

Sphincter,  reflex  spasm  of,  in  cystitis,  894. 

Spina  bifida,  679  ;  complication  of,  with  purulent 
meningitis,  680  ;  seat  of,  679  ;  surgical  treatment 
of,  680  ;  tumor  formation  in,  680. 

Spinal  apoplexy,  604  ;  symptoms  of,  605  ;  treatment 
of,  605. 

Spinal  cord,  anaemia  of,  604. 

Spinal  cord,  cavity  and  fissure  formation  in.  677  ;  in 
cerebro-spinal  meningitis,  104,  105  ;  circulatory 
disturbances  of,  604  ;  consumption  of,  632  ;  diffuse 
diseases  of,  615  ;  diseases  of,  599  ;  functional  dis- 
turbances of,  605  ;  functions  of,  624  ;  in  gout,  988  ; 
haemorrhages  into,  604  ;  new  growths  of,  676  ;  S3_s- 
temic  diseases  of,  615  ;  traumatic  lesions  of,  606. 

Spinal  cord,  compression  of,  608  ;  origin  of,  608  ;  seat 
of,  609  ;  in  spina  bifida.  680. 

Spinal  cord,  concussion  of.  See  Traumatic  Neuroses. 

Spinal  cord,  degeneration  of,  in  amyotrophic  lateral 
sclerosis,  650. 

Spinal  cord,  disease  of,  after  sudden  lowering  of  at- 
mospheric pressure,  608. 

Spinal  cord,  hyperaemia  of,  604. 

Spinal  cord,  injuries  of,  606  ;  complication  of,  with 
secondary  inflammation,  607  ;  symptoms  of,  607  ; 
treatment  of,  607. 


INDEX. 


1039 


Spinal  cord,  membranes  of,  acute  inflammation  of, 
599  ;  haemorrhages  of,  003  ;  new  growths  of,  676. 

Spinal  cord,  secondary  degeneration  of,  080  ;  after 
cerebral  haemorrhage,  732,  734  ;  after  cerebral  le- 
sions, 080  ;  in  compression  of  the  cord,  610  ;  in 
multiple  sclerosis,  028  ;  in  transverse  affections  of 
the  cord,  081  ;  in  tumors  of  the  cord,  077. 

Spinal  cord,  softening  of,  018. 

Spinal  cord,  tumors  of,  070  ;  differential  diagnosis  of, 
from  transverse  myelitis,  077  ;  forms  of,  070  ;  ori- 
gin of,  076  ;  prognosis  and  treatment  of,  677  ;  rela- 
tion of,  to  unilateral  lesion  of  the  spinal  cord,  077. 

Spinal  irritation,  000  ;  in  hysteria,  802  ;  in  neurasthe- 
nia, 815. 

Spinal  meningitis,  599,  001  ;  origin  of,  599.  001  ;  prog- 
nosis of,  000  ;  symptoms  of,  000,  001  ;  treatment  of, 
001. 

Spinal  muscles,  paralysis  of,  504 ;  in  pseudo-hyper- 
trophic  spinal  paralysis,  504,  660. 

Spinal  neurasthenia,  605  ;  diagnosis  of,  606  ;  sensi- 
tiveness of  the  vertebrae  in,  006  ;  symptoms  of,  006. 

Spinal  paralysis,  acute  ascending,  074  ;  acute  infec- 
tion in,  075  ;  diagnosis  and  prognosis  of,  676;  symp- 
toms of,  674  ;  treatment  of,  676. 

Spinal  paralysis,  atrophic,  671. 

Spinal  paralysis  of  children,  667  (see  Infantile 
Paralysis)  ;  from  acute  infection,  667  ;  diagnosis 
and  prognosis  of,  670  ;  relation  of,  to  primary  neu- 
ritis, 668  ;  spinal  cord  in,  667  ;  symptoms  of,  668  ; 
treatment  of,  670. 

Spinal  paralysis,  spastic,  663 ;  diagnosis  of,  666  ; 
pathological  lesion  in  the  cord  in,  665  ;  relation  of, 
to  chronic  hydrocephalus,  665  ;  treatment  of,  666. 

Spine,  stiffness  of,  in  sinus  thrombosis,  707  ;  (tonic) 
in  tetanus,  792  ;  in  tubercular  meningitis,  703. 

Spirilli  in  relapsing  fever,  34. 

Spirometer  in  pulmonary  emphysema,  178. 

Spleen  in  acute  ascending  spinal  paralysis,  675  ;  in 
acute  yellow  atrophy  of  the  liver,  486  ;  in  Addi- 
son's disease,  879  ;  in  articular  rheumatism,  906  ; 
in  cerebro-spinal  meningitis,  106  ;  in  cirrhosis  of 
the  liver,  480  ;  in  erysipelas,  64  ;  in  hsemoglobinu- 
ria,  956  ;  in  hepatic  syphilis,  491  ;  in  leukaemia,  946; 
in  malaria,  94,  95,  96  ;  in  miliary  tuberculosis,  239  ; 
in  pernicious  anaemia,  940  ;  in  phthisis,  228 ;  in 
pneumonia,  197  ;  in  pseudo-leuksemia,  952  ;  in  pyle- 
phlebitis, 501  ;  in  rachitis,  922  ;  in  relapsing  fever, 
32  ;  in  scarlet  fever,  37,  43  ;  in  scurvy,  959  ;  in  sep- 
tico-pyaemia,  109,  112  ;  in  tubercular  meningitis, 
705  ;  in  typhoid  fever,  11  ;  in  typhus  fever,  30  ;  in 
yellow  fever,  101. 

Spleen,  extirpation  of,  in  leukaemia,  951. 

Splenic  fever,  117. 

Splenization  of  the  lung  in  atelectasis,  181. 

Splint-rest  in  sciatica,  528. 

Spondylitis  deformans  in  chronic  articular  rheuma- 
tism, 914. 

Spoonwort  in  scurvy,  960. 

Spotted  fever,  28.  103.  See  Typhus  Fever  and  Cere- 
bro-spinal Meningitis. 

Stasis,  oedema  from,  in  renal  diseases,  829. 

Status  epilepticus,  774,  775. 

Stenocardia  in  hysteria,  761  ;  in  valvular  disease  of 
the  heart,  297. 

Stenson's  experiment  in  spinal  anaemia,  604. 

Stimulants  in  cholera  morbus,  412  ;  in  pneumonia, 
206  ;  in  tetanus,  794. 

Stitch  in  the  side  in  pleurisy,  256  ;  in  pneumonia,  192. 


Stomacace,  312.    See  Stomatitis. 

Stomach.    See  also  Q-astkio. 

Stomach,  adhesions  of,  387;  in  chlorosis,  985;  in 
dysentery,  79;  in  erysipelas,  68;  perforation  of, 
387,  394  ;  in  phthisis,  227  ;  in  pulmonary  gangrene, 
243;  in  purpura  (Hemorrhagica,  062 ;  purulent  In- 
flammation of,  388  ;  hi  yellow  lover,  101. 

Stomach,  abscess  of,  888. 

Stomach-bougie  in  dilatation,  398. 

Stomach,  cancer  of,  391. 

Stomach,  dilatation  of,  390. 

Stomach,  haemorrhage  from,  374  ;  in  gastric  cancer, 
392  ;  in  gastric  ulcer,  380. 

Stomach,  nervous  affections  of,  400  ;  diagnosis  of, 
402  ;  in  hysteria,  805  ;  nervous  complications  of. 
400  ;  peristaltic  disturbance  of  the  stomach  in,  400  ; 
prognosis  and  treatment  of,  402. 

Stomach-pump  in  chronic  gastric  catarrh,  377  ;  in 
dilatation  of  the  stomach,  399. 

Stomach,  softening  of,  358. 

Stomach,  ulcer  of,  384. 

Stomachics  in  gastric  catarrh,  382  ;  in  jaundice,  468  ; 
in  neurasthenia,  818. 

Stomatitis,  341  ;  acute,  342  ;  aphthous,  343  ;  chronic, 
342  ;  in  diabetes,  971  ;  mercurial,  341  ;  in  scarlet 
fever,  39;  scorbutic,  958;  treatment  of,  342,  343, 
344  ;  in  typhoid  fever,  12  ;  ulcerative,  342. 

Stonecutters1  lung,  245. 

Strabismus  convergens  in  abducens  paralysis,  556  ; 
in  sinus  thrombosis,  707. 

Stramonium  cigarettes  in  asthma,  172. 

Strangulation,  internal,  433. 

Stricture  of  the  intestine,  cicatricial,  432. 

Stripe-pneumonia,  189. 

Stroke,  apoplectic,  728. 

Strongylus  duodenalis,  448. 

Strongylus  gigas,  875. 

Strophanthus  in  contracted  kidney,  864. 

Struma  in  exophthalmic  goitre,  596  ;  extirpation  of, 
598  ;  of  the  supra-renal  capsules,  879. 

Strychnine  in  acute  bulbar  paralysis,  695  ;  in  cere- 
bral haemorrhage,  737  ;  in  diphtheria,  73  ;  in  facial 
paralysis,  562  ;  in  laryngeal  paralysis,  142  ;  in  mye- 
litis, 627  ;  in  neuritis,  585  ;  in  oculo-motor  paralysis, 
557  ;  in  progressive  muscular  atrophy,  658  ;  in  spi- 
nal paralysis  of  children,  671. 

Strychnine  poisoning,  1008. 

Subsultus  tendinum  in  typhoid  fever,  14. 

Succussion  of  Hippocrates  in  pyopneumothorax,  269. 

Sudamina  in  articular  rheumatism,  904. 

Sugar  formation  in  diabetes,  970  ;  influence  of  febrile 
diseases  on,  971  ; ,  influence  of  mental  excitement  on, 
970  ;  influence  of  physical  exertion  on.  970. 

Suggestion  in  catalepsy.  797  ;  in  hysteria,  808. 

Sulphonal  in  chorea.  783  ;  in  neurasthenia,  819. 

Sulphur  in  anaemia,  938  ;  in  haemorrhoids,  429. 

Sulphur  baths  in  lead  paralysis,  570. 

Sulphuretted  hydrogen  poisoning,  1007. 

Sulphuric  acid  in  purpura  haemorrhagica,  962. 

Sulphuric-acid  poisoning,  1003. 

Sulphurous-acid  poisoning,  1003. 

Sunstroke,  746  ;  causes  of,  746  ;  symptoms  of,  746  ; 
treatment  of,  747. 

Support,  mechanical,  in  spasm  of  the  cervical  mus- 
cles, 575  ;  for  the  vertebral  column  in  pressure 
paralysis  of  the  spinal  cord,  614. 

Suppositories  in  dysentery,  80. 

Suppuration  as  a  cause  of  arthritis,  912. 


1040 


INDEX. 


Suppurative  fever  iu  small-pox,  55. 

Supra-renal  capsules,  diseases  of,  878. 

Suspension  in  tabes,  648. 

Swamp  fever,  90.    See  Malaria. 

Sweat-glands  iu  jaundice.  407  ;  iu  typhoid  fever,  17  ; 
iu  uraemia,  832. 

Sweating  in  articular  rheumatism,  904  ;  in  diabetes, 
972 ;  in  haemoglobinaemia,  954  ;  in  phthisis,  226, 
229  ;  in  trichinosis,  123. 

Sympathetic,  irritation  of,  591  ;  in  exophthalmic 
goitre,  597  ;  trophic  disturbances  in,  591  ;  paralysis 
of,  591  ;  contraction  of  the  pupils  in,  591  ;  in  ex- 
ophthalmic goitre,  597  ;  in  hemicrania,  591  ;  vaso- 
motor disturbances  in,  590. 

Synovitis  iu  articular  rheumatism,  902  ;  scarlatinal, 
43. 

Syphilis  as  cause  of  tabes,  632. 

Syphilis  of  the  rectum,  425. 

Syphiloma,  formation  of,  in  syphilis  of  the  liver,  490. 

Syringomyelia,  677  ;  extent  of,  678  ;  origin  of,  678. 

Tabes  dorsalis,  632 ;  ataxic  stage  of,  636  ;  cause  of 
anaesthesia  in,  641  ;  development  of,  632 ;  diagno- 
sis and  prognosis  of,  645  ;  Friedreich's  form  of,  648  ; 
hereditary  predisposition  to,  632  ;  histology  of,  633  ; 
in  chronic  ergotism,  633  ;  initial  stage  of,  635  ;  in- 
volving cranial  nerves,  642  ;  partial  pararysis  of 
sensation  in,  641  ;  peripheral  degeneration  in,  634  ; 
peripheral  paralysis  in,  639  ;  persistence  of  patellar 
reflex  in,  641 ;  pupillary  changes  in,  642 ;  suspen- 
sion in,  648  ;  symptoms  of,  636  ;  syphilis  as  cause 
of,  632  ;  terminal  stage  of,  636  ;  treatment  of,  646  ; 
trophic  disturbances  in,  644  ;  with  regard  to  pro- 
gressive general  paralysis,  645. 

Tabes  mesenterica,  459. 

Tabes,  motor,  654.  See  Progressive  Muscular 
Atrophy. 

Tabes  spastica,  663.    See  Lateral  Sclerosis. 

Taches  bleuätres,  17. 

Taches  cerebrales,  705. 

Tachycardia,  320. 

Tactile  circles,  506. 

Tactile  compasses,  506. 

Taenia  echinococcus,  494  ;  medio-canellata,  441 ;  sagi- 
nata,  441  ;  solium,  440. 

Tailor's  cramp,  579. 

Tampons  in  nasal  catarrh,  128. 

Tannin  in  chronic  pharyngeal  catarrh,  359 ;  in  ne- 
phritis, 846. 

Tape-worms,  440  ;  cures  for,  443. 

Taste,  disturbances  of,  533  ;  central,  533 ;  diagnosis 
of,  534  :  in  epilepsy,  772 ;  in  facial  paralysis,  559  ; 
in  hysteria,  801  ;  partial,  533  ;  test  of,  533  ;  treat- 
ment of,  534. 

Teeth,  anomalies  of,  in  diabetes,  971  ;  in  rachitis,  923. 

Teething,  350  ;  convulsions  in,  351. 

Telegrapher's  cramp,  579. 

Temperature,  sense  of,  in  paralysis  agitans,  786  ;  par- 
tial paralysis  of,  508  ;  perverse,  508  ;  in  syringomye- 
lia, 678  ;  in  tabes,  641  ;  test  of,  508. 

Temporal  convolutions,  focal  diseases  of,  716  ;  rela- 
tion of,  to  deafness,  716  ;  relation  of,  to  word-deaf- 
ness, 716,  719  ;  seat  of  the  cortical  center  for  hear- 
ing in,  716. 

Tendinous  spots  on  the  pericardium,  323. 

Tendon  reflexes,  544 ;  absence  of,  545  ;  in  amyotro- 
phic lateral  sclerosis,  652  ;  in  cerebral  haemorrhage, 
732  ;    in   cerebral  paralysis  of  children,  745  ;    in 


chronic  hydrocephalus,  768  ;  in  epilepsy,  773  ;  in- 
crease of,  545  ;  in  the  lower  extremities,  544  ;  in 
multiple  sclerosis,  629  ;  in  myelitis,  620 ;  in  polio- 
myelitis of  adults,  672  ;  in  pressure  paralysis  of  the 
spinal  cord,  612  ;  in  progressive  bulbar  paralysis, 
687  ;  in  secondary  degeneration  of  the  spinal  cord, 
682  ;  in  spastic  spinal  paralysis,  663,  665  ;  in  spinal 
paralysis  of  children,  669  ;  in  tabes,  641  ;  in  unilat- 
eral lesion  of  the  spinal  cord,  684  ;  in  the  upper  ex- 
tremities, 545. 

Tendous,  sheaths  of,  in  articular  rheumatism,  902  ; 
thickening  of,  in  radial  paralysis,  565. 

Tenesmus  in  dysentery,  78  ;  in  intestinal  catarrh,  407. 

Terminal  phalanges,  thickening  of,  in  pulmonary 
stenosis,  293. 

Testicles  in  genito-urinary  tuberculosis,  889. 

Tetanilla.    See  Tetany. 

Tetanus,  791  ;  bacilli  of,  791  ;  diagnosis  of,  793  ;  dis- 
tinction of,  from  hydrophobia,  794  ;  from  menin- 
gitis, 794 ;  from  strychnine  poisoning,  794  ;  en- 
demic and  epidemic,  791  ;  hydrophobic,  792  ;  idio- 
pathic, 791  ;  influence  of  external  conditions  on, 
791  ;  intermittent  (see  Tetany),  789  ;  neonatorum, 
791  ;  paroxysms  of,  792  ;  prodromal  symptoms  of, 
791  ;  rheumatic,  791  ;  symptoms  of,  792  ;  toxiues  of 
traumatic,  791  ;  treatment  of,  794. 

Tetany,  789  ;  diagnosis  of,  790  ;  distinction  of,  from 
ergotism,  790  ;  from  professional  neuroses,  790 ; 
epidemic,  789  ;  origin  of,  789  ;  symptoms  of,  789  ; 
treatment  of,  791. 

Thermsesthesiometer,  508. 

Thermic  fever,  740  ;  pathology  of,  746  ;  symptoms  of, 
746  ;  treatment  of,  747. 

Thermo-cautery  in  noma,  347  ;  in  pressure  paralysis 
of  the  spinal  cord,  614. 

Thomsen's  disease,  795.    See  BIyotonia. 

Thoracic  aorta,  aneurism  of,  334 ;  causes  of,  334 ; 
diagnosis  of,  337  ;  prognosis  of,  337  ;  symptoms  of, 
335  ;  treatment  of,  338. 

Thoracotomy,  266. 

Thorax,  barrel-shaped,  177  ;  compression  of,  in  pul- 
monary emphysema,  180  ;  deformity  of,  in  osteo- 
malacia, 926  ;  in  rachitis,  923  ;  phthisical,  221  ;  in 
pleurisy,  258  ;  rigid  dilatation  of,  175. 

Thrombi  in  typhoid  fever,  16  ;  in  valvular  disease  of 
the  heart,  300. 

Thrombosis  of  the  portal  vein,  502. 

Thrush,  344. 

Thyroid  gland,  atrophy  of,  in  myxcedema,  589  ;  ex- 
tirpation of,  for  exophthalmic  goitre,  598  ;  relation 
of,  to  exophthalmic  goitre,  597. 

Tibialis  paralysis,  569. 

Tic  convulsif,  572,  573  (see  Spasm,  Facial)  ;  doulou- 
reux, 521  (see  Trigeminus,  Neuralgia  of)  ;  rota- 
toire,  574  (see  Spasm  of  the  Cervical  Muscles). 

Tissue  metamorphosis,  anomalies  of,  928  ;  in  anaemia, 
933  ;  in  diabetes  mellitus,  970. 

Tissue,  necrosis  of,  in  gout,  988. 

Toe-drop  in  peroneal  paralysis,  569.    , 

Tongue,  atrophy  of,  in  amyotrophic  lateral  sclerosis, 
652  ;  in  progressive  bulbar  paralysis,  685  ;  in  pro- 
gressive muscular  atrophy,  657. 

Tongue,  injuries  to,  in  epilepsy,  773. 

Tongue,  paralysis  of.  in  acute  bulbar  paralysis,  694  ; 
in  bulbar  haemorrhage,  692  ;  (unilateral)  in  cerebral 
haemorrhage,  731  ;  in  compression  of  the  medulla, 
695  ;  in  embolism  and  thrombosis  of  the  basilar 
artery,  694. 


INDEX. 


1041 


Tongue,  spasm  of.  573. 

Tongue,  ulcer  on  the  fraenum  of,  in  whooping-cough, 
161. 

Tonics  in  scurvy,  960. 

Tonsillitis,  351  (see  Sore  Throat)  ;  diagnosis  of,  355  ; 
follicular,  353  ;  necrotic,  354  ;  parenchymatous,  353  ; 
treatment  of,  356. 

Tonsils,  abscess  of,  353  ;  chronic  hypertrophy  of,  356  ; 
treatment  of,  356  ;  extirpation  of,  356  ;  in  leukaemia, 
947  ;  in  pseudo-leukaemia,  952. 

Torpid  habitus,  1000. 

Torticollis,  rheumatic,  574  ;  spastic,  574. 

Touch,  sense  of,  506  ;  condition  of,  619  ;  diminished 
in  the  tongue  in  facial  paralysis,  £59  ;  in  tabes, 
640  ;  test  of,  506. 

Tracheal  catarrh,  146  ;  stenosis,  166. 

Tracheitis,  146. 

Tracheotomy  in  diphtheria,  72  ;  in  oedema  of  the  glot- 
tis, 136  ;  in  perichondritis,  135. 

Traction  diverticula  in  the  oesophagus,  364. 

Transfer  in  hysteria.  814. 

Transudation  in  diabetes,  974  ;  in  leukaemia,  949. 

Transverse  myelitis,  615.    See  Myelitis. 

Traube's  double  sound  in  aortic  insufficiency,  289. 

Traumatic  hysteria,  820. 

Traumatic  lumbago,  821,  918. 

Traumatic  neurasthenia,  821. 

Traumatic  neuroses,  819  ;  cause  of,  821  ;  implication 
of  brain  in,  820  ;  local,  820  ;  origin  of,  after  railway 
accidents,  819  ;  relation  of,  to  hysteria,  821  ;  symp- 
toms of,  819  ;  treatment  of,  820. 

Tremor,  540  ;  alcoholic,  540  ;  in  amyotrophic  lateral 
sclerosis,  651 ;  in  epilepsy,  775  ;  essential,  540  ;  in 
exophthalmic  goitre,  596  ;  hysterical,  541  ;  inten- 
tion, 540  ;  mercurial,  1005  ;  in  multiple  sclerosis, 
629  ;  in  osteomalacia,  927  ;  in  paralysis  agitans,  784  ; 
senile,  540  ;  in  typhoid  fever,  14. 

Trephining  the  skull  in  cerebral  abscess,  743  ;  in  cere- 
bral tumor,  756  ;  in  hydatids,  756  ;  in  meningeal 
haemorrhage,  603 ;  in  pressure  paralysis,  614  ;  in 
traumatic  epilepsy,  777  ;  in  tumors  of  the  cord,  677  ; 
the  vertebral  column  in  injuries  to  the  cord,  607. 

Triceps  paralysis,  565. 

Trichina  spiralis,  121. 

Trichinosis,  121  ;  treatment  of,  123. 

Tricocephalus  dispar,  449. 

Tricuspid  insufficiency,  291 

Trigeminus,  anaesthesia  of,  513  ;  neuroparalytic  oph- 
thalmia in,  513  ;  occlusive  bandage  in,  515  ;  skin  of 
the  face  in,  514  ;  in  tabes,  641. 

Trigeminus,  neuralgia  of,  521  ;  in  compression  of  the 
medulla,  695  ;  in  diabetes,  973  ;  diagnosis  of,  522 ; 
epileptiform,  522  ;  infra-maxillary,  522  ;  infra-orbi- 
tal, 522  ;  ligature  of  the  carotid  for,  523  ;  operative 
treatment  of,  523  :  prognosis  of,  522  ;  supra-orbital, 
522  ;  symptoms  and  course  of,  521  ;  treatment  of, 
522. 

Trigeminus,  paralysis  of,  557  ;  in  bulbar  haemorrhage, 
692  ;  in  progressive  bulbar  paralysis,  687. 

Trigeminus,  spasm  of,  571  ;  treatment  of,  571. 

Trismus,  571  ;  artificial  feeding  in,  572  ;  in  cerebro- 
spinal meningitis,  105  :  in  tetanus,  792  ;  in  tubercu- 
lar meningitis,  705. 

Trochlear  paralysis,  556. 

Trophic    disturbances.  587 ;    in  arsenical  paralysis, 

571  ;    of  the  bones   and   joints,    589 ;  in    cerebral 

haemorrhage,  735  ;  in  cervico-brachial  neuralgia, 

524  ;  in  cutaneous  anaesthesia,  512  ;  in  facial  hemi- 

66 


atrophy,  594  ;  of  the  hair  and  nails,  589  ;  in  inter- 
costal neuralgia,  525  ;  in  median  paralysis.  500  :  in 
myelitis,  022  ;  in  neuralgia,  517  ;  in  neuritis,  588  ;  iu 
occipital  neuralgia,  538  ;  in  paralysis,  588  ;  in  pres- 
sure paralysis  of  the  spinal  cord,  612  ;  in  progressive 
muscular  atrophy,  055;  in  pseudo- hypertrophic 
muscular  paralysis,  059  ;  in  sciatic  paralysis,  509  ; 
of  the  skin,  588 ;  in  spinal  paralysis  of  children, 
669  ;  in  syringomyelia,  678  ;  in  tabes,  644  ;  treatment 
of,  590;  in  trigeminal  anaesthesia,  514  ;  in  trigeml 
nal  neuralgia,  522. 

Trousseau's  phenomenon  in  tetany,  790. 

Trousseau's  spots  in  tubercular  meningitis,  705. 

Tubercle  bacilli,  208  ;  detection  of,  220. 

Tubercula  dolorosa  of  the  peripheral  nerves,  586. 

Tuberculosis,  207.    See  also  Miliary  Tuberculosis. 

Tuberculosis  of  the  genito-urinary  apparatus,  888  ; 
diagnosis  of,  890  ;  prognosis  and  treatment  of,  H'MK 

Tuberculosis  of  the  intestines,  423  ;  treatment  of,  424. 

Tuberculosis  of  the  larynx,  136  ;  diagnosis  of,  137  ; 
treatment  of,  138. 

Tuberculosis  of  the  lungs,  207  ;  causes  of,  208  ;  com- 
plications of,  218  ;  diagnosis  of,  229  ;  heredity  of, 
211  ;  infectiousness  of,  209  ;  local,  212  ;  physical  ex- 
amination in,  221  ;  predisposition  to,  210  ;  prognosis 
of,  230 ;  prophylaxis  of,  231  ;  symptoms  of,  218  ; 
treatment  of,  231. 

Tuberculosis  of  the  peritoneum,  457  ;  of  the  pharynx, 
226  ;  of  the  serous  membranes,  261,  327,  457  ;  of  the 
supra-renal  capsules,  879. 

Turpentine,  inhalations  of,  in  asthma,  172  ;  in  whoop- 
ing-cough, 163. 

Turpentine,  oil  of,  in  acute  phosphorus  poisoning, 
1006  ;  in  cystitis,  896  ;  in  foetid  bronchitis,  15S  ;  in 
genito-urinary  tuberculosis,  890  ;  in  sciatica,  527  ; 
in  tape -worm,  444. 

Turpentine  pipes  in  bronchitis,  154. 

Tussis  convulsiva,  160.    See  "Whooping-cough. 

Tylosis  of  the  tongue,  346. 

Typhlitis,  418  ;  diagnosis  of,  420  ;  prognosis  of,  421  : 
treatment  of,  421. 

Typhoid,  bilious,  35.    See  also  Relapsing  Fever. 

Typhoid  fever.  1  ;  abortive,  18  ;  bacilli  of,  1  ;  baths 
in,  22  ;  in  children,  19  ;  contagiousness  of,  2  ;  in  the 
corpulent,  19  ;  diagnosis  of,  20  ;  disinfection  in,  26  : 
disposition  to,  4 ;  in  drunkards,  19 :  immunity 
toward,  4  :  influence  of  age  upon,  4  ;  influence  of 
season  upon,  5  ;  in  old  people,  19  ;  outcry  of  chil- 
dren in,  19  ;  peculiarities  in  the  course  of.  18  ;  period 
of  incubation  of,  5  ;  prodromal  symptoms  of,  5  ; 
prognosis  of,  20  ;  prophylaxis  of,  26  ;  recurrent 
fever-attack  in,  8  :  relapses  of,  19  ;  relapses  of,  du- 
ration of,  19  :  relapses  of,  frequency  of,  20  :  sopor 
in  children  in,  19  :  temperature  curve  in,  6  ;  treat- 
ment of,  20  ;  walking,  13. 

Typho-malarial  fever,  98. 

Typhus  abdominalis,  1  (see  Typhoid  Fever);  levissi- 
mus,  18. 

Typhus  exanthematicus,  28  (see  Typhus  Fever)  :  le- 
vissimus,  31. 

Typhus  fever,  28  ;  contagiousness  of,  29  ;  diagnosis 
of.  31  ;  distinction  of,  from  typhoid  fever,  31  ;  epi- 
demic occurrence  of,  29  ;  immunity  toward.  29  : 
period  of  incubation  of,  29  ;  prodromal  symptoms 
of.  29  ;  prognosis  of,  31  ;  treatment  of.  31. 

Typhus  recurrens,  31.    See  Relapsing  Fever. 

Tyrosine  crystals  in  acute  yellow  atrophy  of  the  liver, 


1042 


INDEX. 


Ulcers,  atheromatous,  333  ;  in  laryngeal  tuberculosis, 
137  ;  tubercular,  213  ;  typhoid,  9. 

Ulnar  paralysis,  506  ;  disturbance  of  function  in,  506; 
traumatic,  566. 

Umbilical  hemorrhage  in  relation  to  haemophilia,  964. 

Umbilical  vein,  inflammation  of,  in  the  new-born,  500. 

Unilateral  lesion  of  the  spinal  cord,  682. 

Upper  extremities,  thickening  and  deformity  of,  in 
rachitis,  923. 

Uraemia,  829  ;  chronic,  831  ;  in  contracted  kidney, 
861  ;  duration  of,  833  ;  in  gout,  988  ;  origin  of,  830  ; 
in  scarlet  fever,  42  ;  termination  of,  834  ;  in  yellow 
fever,  102. 

Urates  in  gout,  988. 

Urea,  deposit  of,  on  the  skin  in  uraemia,  832  ;  in  dia- 
betes insipidus,  983  ;  in  diabetes  mellitus,  969. 

Ureter,  obstruction  of,  in  relation  to  hydronephrosis, 
890. 

Ureteritis,  881. 

Urethan  in  neurasthenia,  819. 

Urethra,  stricture  of,  in  hydronephrosis,  891. 

Urethral  crises  in  tabes,  644. 

Uric  acid,  in  chorea,  780  :  in  diabetes,  969  ;  in  gout, 
988  ;  in  relation  to  contracted  kidney,  858. 

Urinary  casts  in  renal  disease,  828. 

Urinary  passages,  parasites  of,  874. 

Urinary  tests,  Böttger's,  968  ;  with  chloroform,  467  ; 
in  diabetes  mellitus,  968  ;  Fehling's,  968  ;  with  fer- 
ric chloride,  for  acetone,  970  ;  Gmelin's,  467  ;  heat, 
824  ;  Moore's,  968  ;  with  thread  in  gout,  990  ;  Trom- 
mer's,  968. 

Urine,  in  acute  yellow  atrophy  of  the  liver,  487  ; 
amount  of,  in  diabetes  insipidus,  982  ;  amount  of, 
in  diabetes  mellitus,  967  ;  in  amyloid  kidney,  866  ; 
in  anaemia,  934  ;  in  cancer  of  the  stomach,  394  ;  in 
cerebral  haemorrhage,  729  ;  in  chlorosis,  935  ;  in 
chorea,  782 ;  in  chyluria,  875  ;  in  cirrhosis  of  the 
liver,  481  ;  in  contracted  kidney,  858  ;  in  cystitis, 
894;  in  diabetes  insipidus,  982;  in  diabetes  mellitus, 
966  ;  in  diphtheria,  70  ;  in  epilepsy,  773  ;  in  erysipe- 
las, 64 ;  in  functional  diseases  of  the  spinal  cord, 
606  ;  in  gastric  catarrh,  379  ;  in  genito-urinary  tu- 
berculosis, 889  ;  in  gout,  986  :  in  haemoglobinaemia, 
954;  in  hydronephrosis,  893 ;  in  injuries  of  the 
spinal  cord,  607  ;  in  jaundice,  467 ;  in  leukaemia, 
949  ;  in  malaria,  94 ;  In  meningeal  haemorrhage, 
603  ;  in  meningitis,  701,  705  ;  in  myelitis,  621  ;  in 
nephritis,  841,  852  ;  in  osteomalacia,  972  ;  in  passive 
congestion  of  the  kidney,  871  ;  in  pernicious  anae- 
mia, 942  ;  in  pneumonia,  197  ;  in  pressure  paralysis 
of  the  spinal  cord,  613  ;  in  pseudo-leukaemia,  952  ; 
in  pyelitis,  882 ;  in  pylephlebitis,  501 ;  in  rachitis, 
924  ;  in  renal  diseases,  823  ;  in  renal  tumors,  873  ;  in 
scarlet  fever,  41  ;  in  small-pox,  56  ;  in  spinal  men- 
ingitis, 600  ;  in  spinal  paralysis  of  children,  669  ;  in 
tabes,  643  ;  in  tetanus,  793  ;  in  typhoid  fever,  17  ;  in 
typhus  fever,  30  ;  in  ulcer  of  the  stomach,  387  ;  in 
unilateral  lesion  of  the  spinal  cord,  684  ;  in  whoop- 
ing-cough, 161  ;  in  yellow  fever,  102. 

Urticaria  in  articular  rheumatism,  904;  in  erysipelas, 
64  ;  in  exophthalmic  goitre,  597  ;  in  haemoglobinae- 
mia, 954 ;  in  jaundice,  465  :  in  neuralgia,  517  ;  in 
pneumonia,  198  ;  in  scarlet  fever,  41. 

Uterine  neuralgia,  528. 

Uva  ursa  in  nephritis,  848. 

Vaccination,  58. 

Vagus  paralysis  in  relation  to  tachycardia,  321. 


Valerian  in  diabetes  insipidus,  984  ;  in  epilepsy,  778  ; 
in  hysteria,  813. 

Valvular  disease  of  the  heart,  280. 

Varicella,  60  ;  period  of  incubation  of,  60  ;  prognosis 
of,  61  ;  treatment  of,  61. 

Variola,  52  (see  Small-pox)  ;  hemorrhagica  pustulo- 
sa, 57  ;  vaccina,  58  ;  vera,  53. 

Varioloid,  54.    See  Small-pox. 

Variolois  miliaris,  55  ;  verrucosa,  55. 

Vaso-motor  disturbances,  587  ;  in  bulbar  haemor- 
rhage, 692  ;  in  cerebral  haemorrhage,  735  ;  in  cere- 
bral hyperaemia,  710;  in  cervico-brachial  neuralgia, 
525  ;  in  epilepsy,  772  ;  iD  exophthalmic  goitre,  596  ; 
in  hemicrania,  592  ;  in  hysteria,  804  ;  in  intercostal 
neuralgia,  525  ;  in  myelitis,  622  ;  in  neuralgia,  517  ; 
in  neuritis,  583  ;  in  occipital  neuralgia,  523  ;  in  pa- 
ralysis, 539  ;  in  progressive  bulbar  paralysis,  687  ; 
in  progressive  muscular  atrophy,  657  ;  in  sciatic 
paralysis,  569  ;  in  spinal  neurasthenia.  606  ;  symp- 
toms of,  587  ;  in  trigeminal  neuralgia,  521. 

Vaso-motor  paralysis,  587  ;  redness  of  the  skin  with 
heightened  temperature  in,  587;  in  unilateral  lesion 
of  the  spinal  cord,  684. 

Vaso-motor  spasm,  588  ;  relation  of,  to  spontaneous 
symmetrical  gangrene,  588  ;  relation  of,  to  sclero  ■ 
derma,  588  ;  symptoms  of,  588. 

Veal,  diseased,  as  a  cause  of  typhoid  fever,  3. 

Vegetable  acids  in  scurvy,  960. 

Veins,  diastolic  collapse  of,  in  obliteration  of  the 
pericardial  cavity,  326. 

Venesection.    See  Blood-letting. 

Venous  murmurs,  anaemic,  933,  935  ;  in  leukaemia, 
949. 

Venous  pulse,  272. 

Venous  stasis,  299. 

Veratrine  in  pneumonia,  205. 

Vermiform  process  in  relation  to  intestinal  obstruc- 
tion, 433. 

Vertebral  column  in  arthritis  deformans,  914  ;  in 
cerebro-spinal  meningitis,  105;  in  osteomalacia, 
926  ;  in  rachitis,  923. 

Vertigo  ab  aure  lsesa,  769  ;  a  stomacho  laeso,  379. 

Vertigo  in  anaemia,  932  ;  in  bulbar  haemorrhage,  691  ; 
in  cerebellar  disease,  723  ;  in  cerebellar  tumor, 
753  ;  in  cerebral  abscess,  742  ;  in  cerebral  haemor- 
rhage, 728  ;  in  cerebral  tumor,  750  ;  in  chlorosis, 
935  ;  in  compression  of  the  medulla,  695  ;  in  epilep- 
sy, 772 ;  in  insolation,  746  ;  in  leukaemia,  949  ;  in 
Meniere's  disease,  769  ;  in  multiple  sclerosis,  630  ; 
in  neurasthenia,  816  ;  in  oculo-motor  paralysis,  556 ; 
in  pernicious  anaemia,  941 ;  in  purulent  meningitis, 
700. 

Vesical.    See  Bladder. 

Vesicatory.    See  Blister. 

Villous  cancer  in  the  bladder,  897. 

Violin-player's  cramp,  579. 

Vision,  field  of,  in  hysteria,  801. 

Vocal  cords,  paralysis  of,  in  diphtheria,  70  ;  in  hyste- 
ria, 803  ;  in  mediastinal  tumor,  273  ;  in  pericarditis, 
325. 

Vocal  fremitus  in  pleurisy,  260,  263  ;  in  pneumonia, 
195  ;  in  pneumothorax,  269. 

Volume,  increased,  of  the  lungs,  175. 

Vomiting  in  acute  yellow  atrophy  of  the  liver,  486  ; 
in  Addison's  disease,  880  ;  in  anaemia,  932  ;  in  can- 
cer of  the  stomach,  392  ;  in  cerebellar  disease,  724  ; 
in  cerebral  abscess,  742  ;  in  cerebral  anaemia,  709  ; 
in  cerebral  haemorrhage,  730  ;  in  cerebral  tumor, 


INDEX. 


1043 


750  ;  in  cholera,  85  ;  in  cholera  morbus,  411  ;  in 
compression  of  the  medulla,  695  ;  in  dilatation  of 
the  stomach,  397  ;  in  dysentery,  79  ;  in  erysipelas, 
64  ;  in  exophthalmic  goitre,  597 ;  in  gastric  catarrh, 
376  ;  in  hsematoma  of  the  dura,  697  ;  in  hoemoglo- 
binsemia,  954  ;  in  hemicrauia,  592  ;  in  hepatic  colic, 
472 ;  in  hepatitis,  447  ;  in  intestinal  obstruction, 
435  ;  in  Meniere's  disease,  769  ;  in  meningitis,  104, 
701,  705  ;  in  miliary  tuberculosis,  239  ;  morning,  of 
drunkards,  376  ;  in  nephritis,  843,  854  ;  in  nephro- 
lithiasis, 886  ;  in  nervous  affections  of  the  stomach, 
400  ;  in  peritonitis,  454,  455  ;  in  pleurisy,  257  ;  in 
pneumonia,  197  ;  in  phthisis,  227  ;  in  pulmonary 
gangrene,  243  ;  in  pylephlebitis,  501  ;  in  scarlet 
fever,  37  ;  in  small-pox,  58  ;  in  tape-worm,  443  ;  in 
thermic  fever,  747  ;  in  typhlitis,  419  ;  in  typhoid 
fever,  10,  11  ;  in  typhus  fever,  29  ;  in  ulcer  of  the 
stomach,  386  ;  in  uraemia,  832  ;  in  whooping-cough, 
161  ;  in  yellow  fever,  102. 

"Voracity  in  tape-worm,  443. 

Vox  choleraica,  85. 

Warmth,  feeling  of,  increased  in  paralysis  agitans, 

786. 
"Water  cancer,  347. 
Water  cushions  in  myelitis,  627. 
Water-pipe  sound  in  open  pneumothorax,  270. 
Waxy  kidney,  864.    See  Amyloid. 
Weakened  heart,  312. 
Weeping  spasms,  577  ;  in  hysteria,  807. 
Wet-nurse,  milk  of,  415. 
Whip-worm,  449. 
Whooping-cough,  160;  catarrhal  stage  in,  160;  con- 


tagiousness of,  160;  convulsive  stage  in,  1C0;  diag- 
nosis of,  162  ;  prognosis  of,  l(J2  ;  sequelaa  of,  162  ; 
treatment  of,  162. 

Williams's  tracheal  tone  in  pleuritic  effusion,  259. 

Wine  in  cholera  morbus,  412  ;  in  typhoid  fever,  »i. 

Word-deafness,  718  ;  in  abscesses  of  the  temporal 
lobes,  743. 

Worm  abscess,  446. 

Worms,  intestinal,  440. 

Writer's  cramp,  577  ;  diagnosis  of,  578;  Nussbaum's 
bracelet  for,  579  ;  origin  of,  578  ;  paralytic,  578  ; 
prognosis  of,  578  ;•  spastic,  578  ;  symptoms  of,  578  ; 
treatment  of,  578  ;  tremulous,  578. 

Xanthelasma  in  jaundice,  465. 
Xanthine  calculi  in  nephrolithiasis,  885. 

Yawning  in  paroxysmal  hsemoglobinaimia,  954. 

Yawning  spasm,  577. 

Yellow  fever,  100  ;  black  vomit  in,  102  ;  causes  of, 
100  ;  contagiousness  of,  101  ;  diagnosis  of,  102  ;  epi- 
demic character  of,  100  ;  pathology  of,  101  ;  prog- 
nosis of,  102  ;  symptoms  and  cause  of,  101  ;  treat- 
ment of,  102. 

Zinc,  oxide  of,  in  chorea,  783  ;  in  epilepsy,  778 ;  in 

facial  spasm,  573. 
Zinc  paralysis,  571. 
Zinc,  poisoning  from,  1005. 
Zinc,  sulphate  of,  in  angina  pectoris,  319  ;  in  gastric 

catarrh,  382. 
Zinc,  valerianate  of,  in  chorea,  783  ;  in  hiccough,  577  ; 

in  spasm  of  the  cervical  muscles,  575  ;  in  trigeminal 

spasm,  572. 


THE    END. 


THE  DISEASES  OF  THE 
STOMACH. 

By  De.   C.   A.   EWALD, 

EXTRAORDINARY   PROFESSOR    OF   MEDICINE   AT   THE  UNIVERSITY  OF   BERLIN; 
DIRECTOR   OF   THE   AUGUSTA   HOSPITAL,    ETC. 


A  UTIIORIZED    TRANSLA  TION 

FROM   THE  SECOND   GERMAN  EDITION,  WITH  SPECIAL  ADDITIONS 

BY  THE  AUTHOR, 

By  MORRIS  MANGES,  A.M.,  M.  D., 

ATTENDING  PHYSICIAN  TO   OUTDOOR  DEPARTMENT,  MOUNT  SINAI  HOSPITAL, 
NEW  YORK  CITY,  ETC. 


WITH    THIRTY    ILLUSTRATIONS. 


8vo,  497  pages.     Cloth,  $5.00  ;   Sheep,  $6.00. 


SOLD    ONLY  BY   SUBSCRIPTION. 


The  following  are  extracts  from  a  few  of  the  notices  that  have  appeared  in  the 
medical  press : 

"...  "We  can  recall  no  work  on  this  special  subject  published  in  late  years  which  is 
so  thoroughly  well  written  and  useful  as  this  of  Ewald' s.  .  .  .  Kecent  therapeutics  of  dis- 
eases of  the  stomach  are  discussed  with  candor  and  justice,  yet  critically.  The  author  is  an 
authority  on  what  he  writes.  We  believe  him  to  be  the  best  authority.  .  .  .  Some  of  his 
suggestions  we  have  utilized  and  find  them  excellent." — Texas  Courier- Record  of  Medicine. 

"  The  profession  are  deeply  indebted  to  Dr.  Manges  for  this  excellent  translation  of  Dr. 
Ewald's  lectures  on  diseases  of  the  stomach,  enriched  by  notes  of  the  translator,  revised  by 
the  author,  which  renders  the  work  still  more  acceptable  to  the  American  reader.  .  .  .  The 
various  diseases  of  the  stomach  are  discussed  with  the  detail  and  scientific  accuracy  for  which 
the  author  is  noted,  and  the  work  forms  a  very  valuable  addition  to  the  library."— JYew  York 
Medical  Times. 

".  .  .  There  is  no  question  but  that  Dr.  Ewald  has  given  us  a  work  of  great  scientific  value, 
and  up  to  date  in  every  particular.  This  is  a  book  quite  as  valuable  to  the  surgeon  as  to  the 
physician,  and  no  progressive  medical  man  can  afford  to  be  without  it." — Omaha  Clinic. 

"...  The  whole  of  this  very  important  and  difficult  field  is  covered  in  a  way  that  can 
not  fail  to  commend  itself  to  all  physicians  who  desire  to  enlarge  their  sphere  of  professional 
knowledge  and  utility." — Denver  Medical  Times. 

"  The  purchaser  is  impressed  by  the  elegance  of  publication  on  opening  this  book,  and 
such  excellence  is  well  fitted  to  such  a  work  as  this  one  is.  .  .  .  The  work  is  thoroughly 
practical,  and  the  physician  who  does  not  secure  and  carefully  read  it  will  deprive  himself 
of  a  most  important  help  in  the  treatment  of  diseases  of  the  stomach."—  Virginia  Medical 
Monthly. 

New  York:  D.  APPLETON  &  CO.,  1,  3,  &  5  Bond  Street. 


TEXT-BOOK  OF  HUMAN 
PHYSIOLOGY, 

For  the  Use  of  Students  and  Practitioners  of  Medicine. 
By  AUSTIN    FLINT,  M.  D.,   LL.  D., 

Professor  of  Physiology  and  Physiological  Anatomy  in  the  Bellevue  Hospital  Medical  Col- 
lege, New  York;  Fellow  of  the  New  York  State  Medical  Association,  etc. 

FOURTH    EDITION.      ENTIRELY   REWRITTEN. 

Large  8vo.     872  pages,  with  Two  Lithographic  Plates  and 
S16    Engravings  on   Wood. 


Cloth,  $6.00;   sheep,  $7.00. 


"  During  the  short  time  that  has  elapsed  since  the  publication  of  the  third  edition  of 
this  work  the  advance  in  physiological  knowledge  has  been  so  great  that  the  author  found 
it  impossible  to  make  the  necessary  corrections,  and  bring  the  text  up  to  the  present 
without  entirely  rewriting  the  work.  Thus,  while  it  is  a  descendent  from  former 
editions,  the  work  is  new  in  all  its  features.  The  form  and  typography  have  been 
changed.  Many  old  figures  have  been  expunged,  and  numerous  new  ones  have  been  in- 
troduced. Most  of  the  figures  that  have  been  retained  are  of  cuts  that  have  been 
re-engraved.  Historical  references  contained  in  former  editions  have  been  greatly  cur- 
tailed ;  unprofitable  discussion  of  disputed  questions  and  theories  have  been  avoided ; 
physiological  chemistry  has  been  omitted  as  far  as  practicable.  The  new  book  is  there- 
fore trirnmed  of  all  incidental  subjects  and  topics,  and  the  text  confined  to  the  statement 
of  established  facts." — Physician  and  Surgeon. 

"  This  is  the  fourth  edition  of  Flint's  popular  text-book  on  physiology,  entirely  re- 
written, and  so  great  have  been  the  advances  in  our  knowledge  of  this  branch  of  medical 
science. that  little  remains  of  the  original  text;  even  the  defects,  or  rather  deficiencies, 
of  the  edition  of  1880  have  rendered  it  imperative,  in  the  light  of  recent  progress,  that 
a  new  edition  be  issued.  The  same  general  arrangement  is  preserved,  and  with  reason. 
The  beauty  of  Flint's  Physiology  consists  in  the  exactness  with  which  the  author  has 
carried  out  his  intentions  as  expressed  in  the  preface  :  '  I  shall  be  more  than  satisfied  if 
I  have  been  able  to  give  concise  and  connected  statements  of  well-established  facts,  in 
such  form  that  they  can  not  be  misunderstood.  Peculiar  views  and  theories,  whether  of 
the  author  or  of  others,  have  no  proper  place  in  a  text-book  which  should  represent  facts 
generally  recognized  and  accepted,  and  not  the  ideas  of  any  one  individual.'  For  a  text- 
book containing  the  results  of  the  most  recent  investigations  in  minute  anatomy  and 
physiology — one  that  studiously  avoids  profitless  discussions  of  unsettled  and  disputed 
questions— one  that  is  as  exact  and  reliable  as  the  present  state  of  knowledge  will  per- 
mit, Flint's  treatise  can  not  be  excelled." — Kansas  City  Medical  Index. 


New  York  :   D.  APPLETON  &  CO.,  1,  3,  &  5  Bond  Street. 


TEXT-BOOK 
OF    OPHTHALMOLOGY. 


By  Dr.  ERNEST  FUCHS, 

PROFESSOR   OF   OPHTHALMOLOGY   IN  THE    UNIVERSITY   OF   VIENNA. 


AUTHORIZED   TRANSLATION 
FROM  THE  SECOND  ENLARGED  AND  IMPROVED  GERMAN  EDITION, 

By  A.  DUANE,  M.  D., 

ASSISTANT   SURGEON,   OPHTHALMIC  AND  AURAL  INSTITUTE,  NEW  YORK. 


With  One  Hundred  and  Seventy-eight  Illustrations,  and  an  Appendix 

devoted  to  Instruments  used  in  Ophthalmic  Surgery 

and  Examination  of  the  Eye. 

8vo,  788  pages.     Cloth,  $5.00  ;  Sheep,  $6.00. 


SOLD   ONLY  BY  SUBSCRIPTION. 


n^HIS  translation,  made  from  advance  sheets  of  the  second  German  edition,  will 
-*-  introduce  to  the  English-speaking  public  of  this  country  a  book  the  high  quali- 
ties of  which  have  won  for  it  the  first  place  among  works  of  its  class  in  Europe. 
Dr.  Fuchs's  great  opportunities  for  clinical  observation,  combined  with  his  thorough 
practical  knowledge  of  anatomical  and  pathological  science,  have  enabled  him  to 
write  a  treatise  which,  for  scientific  accuracy  and  all-round  completeness,  will  com- 
pare favorably  with  any  work  of  its  character ;  and  his  experience  as  a  teacher  and 
lecturer  has  enabled  him  to  present  the  matter  in  a  form  eminently  suited  to  the 
needs  of  the  medical  student  and  the  general  practitioner.  Thus  the  work,  while 
full,  methodical,  and  in  all  respects  brought  down  to  the  latest  point  of  ophthalmo- 
logical  science,  is  couched  in  a  clear  and  attractive  style,  which  renders  the  book 
very  easy  reading ;  and  great  judgment  has  been  shown  in  the  amount  of  space 
allotted  to  the  various  subjects,  those  that  are  important  receiving  full  attention, 
while  matters  of  a  merely  scientific  interest  or  dubious  points  are  either  briefly 
touched  upon  or  are  relegated  to  the  fine  print,  where  those  who  are  curious  in  such 
matters  can  find  them,  but  where  they  do  not  interfere  with  the  continuity  of  the 
rest  of  the  text. 

New  York :  D.  APPLETON"  &  CO.,  1,  3,  &  5  Bond  Street. 


THE  PRINCIPLES  AND  PRACTICE 
OF  MEDICINE. 

Designed  for  the  Use  of  Practitioners  and  Students  of  Medicine. 
By  WILLIAM   OSLER,  M.  D., 

Fellow  of  the  Eoyal  College  of  Physicians,  London ;   Professor  of  Medicine  iD  the  Johns 

Hopkins  University,  and  Physician-m-Chief  of  the  Johns 

Hopkins  Hospital,  Baltimore. 

SOLD     ONLY     BY     SUBSCRIPTION. 


8vo.      Cloth,  $5.50;  sheep,  $6.50;  half  morocco,  $7.00. 


"  By  reason  of  extensive  clinical,  pathologic,  and  teaching  experience,  of  exceptional 
opportunity  and  broad  training,  and  of  rare  scientific  attainments,  there  are  few  pen  better 
qualified  than  Dr.  Osier  to  write  a  work  on  the  Practice  of  Medicine.  Here  m  Philadelphia, 
where  Dr  Osier  spent  but  too  few  busy  years,  he  will  not  soon  be  torgotten  ;  the  impress  ot 
his  work  and  character  will  long  remain,  and  the  impetus  given  to  careful  pathologic  study 
and  observation  will  be  transmitted  through  his  colleagues,  his  assistants,  and  his  pupi  s. 
To  say  that  Dr.  Osier  has  performed  his  task  well,  is  but  to  echo  the  verdict  concerning  the 
work  he  has  done  in  the  past.  If  there  were  one  fault  of  which  we  would  complain,  it  is 
expressed  in  the  wish  that  be  bad  said  more  than  he  has.  Everywhere  throughout  the  work 
one  feels  the  delightful  personality  of  the  man.  Every  page  contains  evidences  of  original 
observation  and  is  marked  by  an  enlightened  conservatism.  It  would  be  difficult  to  select 
any  one  section  and  say  that  it  is  much  better  than  the  others.  All  are  conspicuous  for  their 
comprehensiveness.  The  descriptions  are  in  places  concise,  but  there  are  no  important 
omissions.  Dr.  Osier's  work  needs  no  special  laudation.  It  speaks  for  itself.  We  most 
heartily  commend  his  '  Practice  of  Medicine '  to  those  who  desire  to  be  in  possession  ot  tne 
most  recent  and  best  knowledge  on  the  subject  with  which  it  has  to  deal."— Medical  Newt. 

"  This  volume  exhibits  originality  at  the  very  beginning,  inasmuch  as  there  is  no  preface. 
The  author  does  not  take  us  into  his  confidence  as  to  his  motive  for  adding  another  book  on 
the  '  Principles  and  Practice  of  Medicine '  to  those  which  have  preceded  his.  He  does  not 
tell  us  whether  it  is  because  there  were  too  many  good  ones  or  too  many  bad  ones;  whether 
the  publisher  tempted  him,  or  his  university  demanded  it;  or  whether  it  was  simply  that  he 
had  noticed  that '  they  all  do  it.'  He  skips  into  the  public  presence  without  a  word,  but 
with  a  sort  of  air  which  suggests  :  '  Here  I  am  !  Take  me,  or  leave  me,  but  you  had  better 
do  the  former ! '  He  had  probably  heard  that  good  wine  needs  no  bush  ;  and  as  he  has  written 
a  good  book,  with  an  excellent  dedication  and  some  sound  aphorisms  from  the  Greek  on  the 
first  sheet,  it  mattered  less  about  his  motives.  At  any  rate,  after  the  table  of  contents  and  a 
list  of  charts  and  illustrations,  we  find  ourselves  plunging  immediately  into  typhoid  fever, 
•which  heads  Section  I  (on  'Specific  Infectious  Diseases')  of  this  royal  octavo  volume  of 
1,080  pages.  No  preliminaries  are  devoted  to  such  abstract  subjects  as  nosology, 
symptomatology,  etiology,  inflammation,  fever,  etc.  In  this  respect  Osier's  book  resembles 
Strümpells.  The  style  in  which  Dr.  Osier's  book  is  written  is  clear,  concise,  and  at  the 
same  time  animated.  The  type  is  very  good.  The  finish  of  the  paper  is  excellent,  but  the 
texture  is  not  strong,  and  we  doubt  whether  it  stands  well  the  strain  of  the  eager  student 
who  will  certainly  want  to  use  it  often  and  much,  or  the  inadvertence  of  the  busy  practitioner 
who  will  sometimes  consult  it  hastily.  The  book  has  evidently  been  'trained  down'  as 
much  as  possible  to  cecure  handiness  without  sacrificing  even  more  important  essentials.  We 
should  be  glad  to  be  able  to  think  and  speak  as  highly  of  every  medical  book  presented  for 
review  as  we  can  of  this.  In  truth,  had  our  enemy  written  it,  we  should  be  unable  to  find 
much  consolation  in  his  commitment."—  Boston  Medical  and  Surgical  Journal. 


New  York  :    D.  APPLETON  &  CO.,  1,  3,  &  5  Bond  Street. 


April,  1893. 

MEDICAL 

AND 

HYGIENIC    WORKS 


PUBLISHED   BY 


D.  APPLETON  &  CO.,  1,  3,  &  5  Bond  Street,  New  York, 


AULDE  (JOHN).  The  Pocket  Pharmacy,  with  Therapeutic  Index.  A  resume 
of  the  Clinical  Applications  of  Remedies  adapted  to  the  Pocket-case,  for 
the  Treatment  of  Emergencies  and  Acute  Diseases.     12mo.     Cloth,  $2.00. 

BARKER  (FORDYCE).  On  Sea-Sickness.  A  Popular  Treatise  for  Travelers 
and  the  General  Reader.     Small  12mo.     Cloth,  75  cents. 

BARKER  (FORDYCE).  On  Puerperal  Disease.  Clinical  Lectures  delivered  at 
Bellevue  Hospital.  A  Course  of  Lectures  valuable  alike  to  the  Student  and 
the  Practitioner.     Third  edition.     8vo.     Cloth,  $5.00;  sheep,  $6.00. 

BARTIIOLOW  (ROBERTS).  A  Treatise  on  Materia  Medica  and  Therapeutics. 
Seventh  edition.  Revised,  enlarged,  and  adapted  to  "  The  New  Pharmacopoeia." 
8vo.     Cloth,  $5.00 ;  sheep,  $6.00. 

BARTHOLOW  (ROBERTS).  A  Treatise  on  the  Practice  of  Medicine,  for  the 
Use  of  Students  and  Practitioners.  Sixth  edition,  revised  and  enlarged.  8vo. 
Cloth,  $5.00;  sheep,  $6.00. 

BARTHOLOW  (ROBERTS).  On  the  Antagonism  between  Medicines  and  be- 
tween Remedies  and  Diseases.  Being  the  Cartwright  Lectures  for  the  Year 
1880.     8vo.     Cloth,  $1.25. 

BASTIAN  (H.  CHARLTON).  Paralyses :  Cerebral,  Bulbar,  aud  Spinal.  A 
Manual  of  Diagnosis  for  Students  and  Practitioners.  With  136  Illustra- 
tions.    Small  8vo,  671  pages.     Cloth,  $4.50. 

BASTIAN  (H.  CHARLTON).  Paralysis  from  Brain  Disease  in  its  Common 
Forms.     With  Illustrations.     12mo,  340  pages.     Cloth,  $1.75. 

BILLINGS  (F.  S.).  The  Relation  of  Animal  Diseases  to  the  Public  Health,  and 
their  Prevention.     8vo.     Cloth,  $4.00. 

BILLROTH  (THEODOR).  General  Surgical  Pathology  and  Therapeutics.  A 
Text-Book  for  Students  and  Physicians.  Translated  from  the  tenth  German 
edition,  by  special  permission  of  the  author,  by  Charles  E.  Hackley,  M.  D. 
Fifth  American  edition,  revised  and  enlarged.     8vo.     Cloth,  $5.00;  sheep,  $6.00. 

BOYCE  (RUBERT).  A  Text-Book  of  Morbid  Histologr.  For  Students  and 
Practitioners.     With  130  Colored  Illustrations.     Cloth,  $7.50. 

BRAMWELL  (BYROM).  Diseases  of  the  Heart  and  Thoracic  Aorta.  Illus- 
trated with  226  Wood-Engravings  and  68  Lithograph  Plates — showing  91 
Figures — in  all  317  Illustrations.     8vo.     Cloth,  $8.00;  sheep,  $9.00. 

BRYANT  (JOSEPH  D.).  A  Manual  of  Operative  Surgery.  Sew  edition,  revised 
and  enlarged.     793  Illustrations.     8vo.     Cloth,  $5.00  ;  sheep,  $6.00. 


BÜKT  (STEPHEN  S.).  Exploration  of  the  Chest  in  Health  and  Disease.  8vo. 
210  pages.     With  Illustrations.     Cloth,  $1.50. 

CAMPBELL  (F.  P.).  The  Language  of  Medicine.  A  Manual  giving  the  Origin, 
Etymology,  Pronunciation,  and  Meaning  of  the  Technical  Terms  found  in 
Medical  Literature.     8vo.     Cloth,  $3.00. 

CARMICHAEL  .(JAMES).  Disease  in  Children.  A  Manual  for  Students  and 
Practitioners.  Illustrated  with  Thirty-one  Charts.  12mo,  591  pages. 
(Students'  Seeies.)     Cloth,  $3.00. 

CASTRO  (D'OLIVEIRA).  Elements  of  Therapeutics  and  Practice  according 
to  the  Dosimetric  System.     8vo.     Cloth,  $4.00. 

CHAUVEAU  (A.).  The  Comparative  Anatomy  of  the  Domesticated  Animals. 
Revised  and  enlarged,  with  the  co-operation  of  S.  Arloing,  Director  of  the 
Lyons  Veterinary  School.  Second  English  edition.  Translated  and  edited 
hy  George  Fleming,  C.  B.,  LL.  D.,  F.  R.  C.  V.  S.,  late  Principal  Veterinary 
Surgeon  of  the  British  Army ;  Foreign  Corresponding  Member  of  the 
Societe  Royale  de  Medecine,  and  of  the  Societ6  Royale  de  Medecine  Pub- 
lique, of  Belgium,  etc.  8vo,  1084  pages,  with  585  Illustrations.  Cloth, 
$7.00. 

CORNING-  (J.  L.).  Brain  Exhaustion,  with  some  Preliminary  Considerations 
on  Cerebral  Dynamics.     Crown  8vo.     Cloth,  $2.00. 

CORNING  (J.  L.).  Local  Anaesthesia  in  General  Medicine  and  Surgery.  Being 
the  Practical  Application  of  the  Author's  Recent  Discoveries.  With  Illus- 
trations.    Small  8vu.     Cloth,  $1.25. 

DAVIDSON  (ANDREW).  Geographical  Pathology:  An  Inquiry  into  the 
Geographical  Distribution  of  Infective  and  Climatic  Diseases.  2  vols. 
8vo.     Cloth,  $7.00. 

DEXTER  (FRANKLIN).  The  Anatomy  of  the  Peritonaeum.  12mo.  With 
39  colored  Illustrations.     Cloth,  $1.50. 

DOTY  (ALVAH  H.).  A  Manual  of  Instruction  in  the  Principles  of  Prompt 
Aid  to  the  Injured.  Designed  for  Military  and  Civil  Use.  96  Illustrations. 
12mo.    Cloth,  $1.25. 

ELLIOT  (GEORGE  T.).  Obstetric  Clinic :  A  Practical  Contribution  to  the  Study 
of  Obstetrics  aud  the  Diseases  of  Women  and  Children.    8vo.    Cloth,  $4.50. 

EVANS  (GEORGE  A.).  Hand-Book  of  Historical  and  Geographical  Phthisi- 
ology.  With  Special  Reference  to  the  Distribution  of  Consumption  in  the 
Lnited  States.     8vo.     Cloth,  $2.00. 

EWALD  (C.  A.).  Lectures  on  the  Diseases  of  the  Stomach.  By  Dr.  C.  A. 
Ewald,  Professor  of  Pathology  and  Therapeutics  in  the  University  of  Berlin, 
etc.  Translated  from  the  German  by  special  permission  of  the  author,  by 
Morris  Manges,  A.  M.,  M.  D.     Cloth,  $5.00  ;  sheep,  $0.00. 

FLINT  (AUSTIN).  Medical  Ethics  and  Etiquette.  Commentaries  on  the 
National  Code  of  Ethics.     12mo.     Cloth,  60  cents. 

FLINT  (AUSTIN).  Medicine  of  the  Future.  An  Address  prepared  for  the 
Annual  Meeting  of  the  British  Medical  Association  in  1886.  With  Portrait 
of  Dr.  Flint.     12mo.     Cloth,  $1.00. 

FLINT  (AUSTIN,  Jr.).  Text-Book  of  Human  Physiology;  designed  for  the 
Use  of  Practitioners  and  Students  of  Medicine.  Illustrated  with  three 
hundred  and  sixteen  Woodcuts  and  Two  Plates.  Fourth  edition,  revised. 
Imperial  8vo.     Cloth,  $6.00;  sheep,  $7.00. 

FLINT  (AUSTIN,  Jr.).  The  Physiological  Effects  of  Severe  and  Protracted 
Muscular  Exercise ;  with  Special  Reference  to  it?  Influence  upon  the  Excre- 
tion of  Nitrogen.     12mo.     Cloth,  $1.00. 


FLINT  (AUSTIN,  Jr.).  The  Source  of  Muscular  Power.  Arguments  and  Con- 
elusions  drawn  from  Observation  upon  the  Human  Subject  under  Conditions 
of  Rest  and  of  Muscular  Exercise.     12mo.     Cloth,  $1.00. 

FLINT  (AUSTIN,  Jb.).     Physiology  of  Man.     Designed  to  represent  the  Exist- 
ing State  of  Physiological  Science  as  applied  to  the  Functions  of  the  Human 
Body.     Complete  in  5  vols.,  8vo.     Per  vol.,  cloth,  $4.50  ;  sheep,  $5.50. 
*%*  Vols.  I  and  II  can  be  had  in  cloth  and  sheep  binding;  Vol.  Ill  in  sheep 
only.     Vol.  IV  is  at  present  out  of  print. 

FLINT  (AUSTIN,  Jb.).  Manual  of  Chemical  Examinations  of  the  Urine  in 
Disease;  with  Brief  Directions  for  the  Examination  of  the  most  Common 
Varieties  of  Urinary  Calculi.     Revised  edition.     12mo.     Cloth,  $1.00. 

FOSTER  (FRANK  P.).  Illustrated  Encyclopaedic  Medical  Dictionary,  being 
a  Dictionary  of  the  Technical  Terms  used  by  Writers  on  Medicine  and  the 
Collateral  Sciences  in  the  Latin,  English,  French,  and  German  Languages. 
This  work  will  be  completed  in  four  volumes.  {Sold  only  by  subscription.) 
The  work  will  consist  of  Four  Volumes,  and  will  be  sold  in  Parts;  Three 
Parts  to  a  Volume.     Ten  Parts  are  now  ready  for  delivery. 

FOÜRNIER  (ALFRED).  Syphilis  and  Marriage.  Translated  by  P.  Albert 
Morrow,  M.  D.     8vo.     Cloth,  $2.00 ;  sheep,  $3.00. 

FREY  (HEINRICH).  The  Histology  and  Histochemistry  of  Man.  A  Treatise 
on  the  Elements  of  Composition  and  Structure  of  the  Human  Body.  Trans- 
lated from  the  fourth  German  edition  by  Arthur  E.  J.  Barker,  M.  D.,  and 
revised  by  the  author.  With  608  Engravings  on  Wood.  8vo.  Cloth,  $5.00; 
sheep,  $6.00. 

FRIEDLANDER  (CARL).  The  Use  of  the  Microscope  in  Clinical  and  Patho- 
logical Examinations.  Second  edition,  enlarged  and  improved,  with  a 
Chromolithograph  Plate.  Translated,  with  the  permission  of  the  author, 
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chanical. Profusely  illustrated.  Second  edition,  revised  and  enlarged.  8vo. 
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COLUMBIA   UNIVERSITY 

This  book  is  due  on  the  date  indicated  below,  or  at  the 
expiration  of  a  definite  period  after  the  date  of  borrowing, 
as  provided  by  the  rules  of  the  Library  or  by  special  ar- 
rangement with  the  Librarian  in  charge. 

DATE  BORROWED 

DATE  DUE 

DATE  BORROWED 

DATE  DUE 

C28<638)M50 

